welcome to the med surge review where I help you prepare for your medsurge vinyl the study guide you can find it on my website blossomwithjesica.com so let's talk about the nervous system and when we're assessing the nervous system we have various types of neuro assessments so the first type of assessment is called the Glasgow Coma Scale and this scale is going to look at things such as eye-opening responses you're going to be scoring the patient based on how their eyes open so are they spontaneous are they only opening when you are talking to them do they only open to pain like if you do a sternum rub or do they not open it all and then they'll get a point for whichever one that they fit the next criteria is the verbal response so we're looking at are they oriented to what we're saying or are they confused are do they have inappropriate words are they incoherent or do they have none and again they're getting points for whichever one of those they hit for then we're looking at motor response so we're looking at do they obey commands do they only have a motor response to localized pain do they only withdraw from Pain do they have flexion to pain or do they have extension to pain or do they have none and again they're getting the points related to which one they score for so the total for the Glasgow Coma Scale is anywhere from 3 to 15 a score of one in each category indicates no performance of the skill so the lowest is three so just remember that it doesn't go to zero it goes to three the next type of assessment is called Perla and this is pupils equal round reactive to light and accommodating we want to remember that the normal pupil size is three to five millimeters and the way we're checking this is we're shining a light into the pupil and we're looking to see if um they are round if both sides are equal if they are when we say accommodating do they change size when you shine light and does both sides do it that is what we're looking for with that then we're looking at color sensory motor and temperature we're also looking at Vital Signs and we want to remember that the level of Consciousness is the best indicator of mental status also within the nervous system we can have elevated intracranial pressure and what we're going to look for with this is something called Cushing's Triad so you can see that right here now the three signs of Cushing's Triad is going to be hypertension bradycardia and a wide pulse pressure if patients have all three of these signs this is called the Cushing's Triad and this is a sign of elevated intracranial pressure we also want to look for signs like changes in the level of Consciousness headache increased blood pressure with widening pulse pressure that is a wide pulse pressure is the difference between the diastolic and systolic blood pressure being really far apart and widening so whatever your top number is you have 180 up top which would be very high right hypertension but on the bottom say you have something much lower like typically when we see 180 we'll also see a high number at the bottom but it will start the systolic will start to go up in the diastolic will start to go down and it will become wide we're also going to look at our nursing intervention so our priority most important so if you get a question about intracranial pressure is to elevate the head of the bed to 30 degrees to promote drainage from the brain you also want to keep the body straight flexion decreases drainage you want to maintain proper fluid volumes set up a quiet environment with minimal sensory stimulation stool softeners to prevent straining and avoid valsalva maneuver and limit suctioning performed the next type of assessment within the nervous system we can do is the cerebral spinal fluid assessment we're looking at things like the color of the spinal fluid we want normal is to be clear and colorless and we can look for something called Halo sign this is blood y fluid surrounded by a yellow stain when placed on a white backdrop so you can see this if you would drop a drop of these cerebral spinal fluid onto a white backdrop you'll see a bloody fluid surrounded by a yellow stain called the Halo sign also Labs so normally cerebral spinal fluid has little protein and glucose with no red white blood cells and no red blood cells and no microorganisms so we want to make sure that it doesn't have those types of things or else it's abnormal pressure so the normal pressure is 60 to 150 and the normal volume is 125 to 150 milliliters So within the nervous system Let's do an anatomy and physiology review so anatomy of the brain in the brain we first have the frontal lobe and this controls our emotions judgment controls motor aspects of speech primary motor cortex for voluntary muscular activation and Broca's area for speech we then have something called the Pareto lobe and this receives fibers with sensory information about touch temperature and pain from the other side of the body it is our spatial perception we then have the temporal lobe this is where the auditory information comes in and language comprehension this is where we have a wernick's area we then have the occipital lobe and this is the center for visual information we have our cerebellum this is our coordination of muscular function we also have our brain stem in here we have the midbrain the pons and the medulla this is where our respiratory and cardiac centers are our nerve Pathways to the brain then we have diencephalon this is our Thalamus subthalamus and hypothalamus so our Thalamus integrates and relays sensory information from the face retina Coachella and taste receptors it interprets sensation of touch pain and temperature then we have our hypothalamus which is going to control our autonomic nervous system and neuroendocrine system it maintains body homeostasis helps regulate body temperature regulates our appetite our thirst Center our sleeping cycle and controls hormone secretion so let's talk about the autonomic nervous system so when we talk about autonomic nervous system there's really two systems within the autonomic nervous system so we have our sympathetic which is our fight or flight and we have our parasympathetic which is also known as our rest and Digest so when we have our sympathetic nervous system is stimulated and we're in that fight or flight we're going to have dilated pupils increased heart rate and respiratory rate sweating epinephrine and norepinephrine is secreted increased blood pressure constriction of blood and abdominal arterioles so what we can think of is what would happen in our body when we were out in the jungle and we see a lion coming towards us think about the way your body would feel that your heart rate would increase your breathing would increase all of that is our synthetic nervous system when it comes to the parasympathetic nervous system you're going to have the opposite which makes it easier to remember so we're going to instead have constricted pupils a lower heart rate and respiratory rate increased peristalsis so this is our digestion the food moving our through our digestive tract acetylcholine will be secreted will have decreased blood pressure and relaxation of the skin and abdominal arterioles okay so let's talk about the cranial nerve assessment and tests so cranial nerve number one is our olfactory this is our smell and in order to test this we'll use something called a smell test two is our optic nerve this is our visual acuity to test this we will look at the pupils we'll use a Snellen chart to test visual Acuity this is the chart that when you stand away from the wall and you try to read a line of letters and also check visual fields ocular motor is eye movement you can remember this with the motor oculars eyes motor is movement so we're looking at eye function we're going to look at pupil constriction and extraocular movements extraocular movements these are our Cardinal fields and this is really if you just hold a pen in front of the patient and move it side to side up and down getting these kind of going diagonal across and making sure that their eyes can move in all of those directions we then have trochlear so this is our eye function again we're looking at those extraocular movements and the inferior abduction trigeminal so this is sensory of the face and chewing we can have them clench their teeth or light touch abductens this is the eye function a lot of these are eye function and again doing those extraocular movements then we look at seven is the facial so this is our facial expression we'll look at facial movement eye movement smile wrinkling forehead eight is acoustic so we're looking at auditory balance and posture hearing and romberg's test so romberg's test this is when you have a patient holds their arms out in front of them with their eyes closed and what you're looking for is to see if one side drifts and if it does drift they would fail that test then we have glossiofaryngeal so this is the Taste we'll look for the gag reflex we have the vagus nerve which is our cardiac and respiratory reflex we can have them say ah spinal accessories so strength of the trapezius and Sterno clendo mastoid muscles so turning their head or lifting their shoulders and hypoglossia this is a motor function of the tongue we can have them stick out their tongue so one thing to know with this is we can see that two three four all have to do with eye movement so you can remember those so if you get a question about which cranial nerve is related to motor functions of the tongue you already know that it's not two three four and six because those all have to do with eyes let's talk about CVA and stroke so our risk factors include diabetes arthrosclerosis hypertension cardiac disease and transient ischemic attacks there are different types of Strokes so the first one we have is the anterior cerebral stroke so this is the lower extremity is more involved than the upper extremities and contralateral hemiparesis and sensory deficits then we have a posterior cerebral stroke so contralateral sensory loss transient contralateral hemiparesis and then we have a middle cerebral artery stroke upper extremity is more involved than the lower extremity and contralateral sensory loss you probably will not have to remember all three of these and how they present however two things that you should remember are the two types of stroke when it comes to hemorrhagic stroke versus ischemic stroke so an ischemic stroke is due to the blockage of blood flow which causes an issue with brain tissue perfusion hypertension is common in order to maintain brain Fusion distal to the area of the blockage and we want to avoid sectioning for greater than 10 seconds to avoid increased intracranial pressure our nursing intervention and priority is going to be TPA to be given three to four hours from the onset of signs and symptoms and it's contr indicated in thrombocytopenia uncontrolled hypertension head trauma within the past three months and major surgery in the past 14 days so the big thing again ischemic stroke is that blockage so there's some type of clot something that is blocking the blood flow from reaching the blur the brain now a hemorrhagic stroke is going to be due to a bleed so you're bleeding in the brilliant brain due to blood vessel ruptures seizures can occur due to high intracranial pressure and dysphagia and so our nursing interventions are going to be NPO neuro assessment prevent activities that increase intracranial pressure or blood pressure so stool softeners bed rest with body midline and anticoagulants are contraindicated because they're bleeding we don't want to increase that bleeding all right let's talk about different types of seizures so the first type of seizure we're going to talk about is epilepsy so this is a recurrent seizures due to excessive insulin discharge of cerebral cortico neurons we then have tonic clonic Grand mild seizures so this the patient is confused and drowsy about the seizure it's usually two to five minutes in length then patients can have a absence seizure or petite mild seizure these are brief no convulsive contractions and it may be up to a hundred times a day they can also have something called a simple seizure which is no loss of consciousness or they can have a complex seizure so a brief loss of consciousness with psychomotor changes now this will not be on NCLEX but just so you guys know there is a type of seizure that does not show up on an EG so if a patient is having a seizure but it doesn't show on their EEG but it truly looks like they're having a seizure they can have psychological seizures essentially some people call them fake seizures but they're not fake they're real to the patient they just aren't having electrical activity in the brain and this can actually come from a trauma it can be a trauma response just so you can take that into your practice with you that you know it's real for the patient when they're experiencing it but that's not on here you don't need to know that for NCLEX that's my spiel okay so nursing intervention so our priority assists the patient to lie down position them on their side maintain a patent Airway because remember our ABCs Airway breathing circulation allow for drainage of secretions and prevent the tongue from occluding the airway we want a loosen restrictive clothes give the oxygen as needed record the time and duration of the seizure never abruptly stop anti-seizure meds we want to do good Oral Care to prevent gingival hyperplasia from phenytoin and use suction after the seizure and when a patient has a seizure during most interventions do not use a tongue blade and allow free movement in a safe environment so we went over this in the safe environment section we know our interventions include putting pads on the bed maybe you're putting down an incontinence pad in case you know they do urinate on themselves if they're on the floor and having a seizure you're putting their head in your lap or in your hands so they're not smashing it off the floor we always want to think about those types of things let's talk about Warner coughs encephalopathy so this is due to low thiamine intake B1 or from severe alcoholism and this is usually where we see it in practice because severe alcoholism can cause low absorption of B1 so signs and symptoms that we're looking for are in Altered mental status ocular motor dysfunction this is eye movement and Ataxia so let's talk about multiple sclerosis so multiple sclerosis is the progressive demyelinating disease of the central nervous system and it's autoimmune so you have a neuron and on your neurons there's this thing called the myelin sheath it goes around the neuron like that so what happens is the immune system comes in and for whatever reason decides that it wants to fight off this myelin sheet and when it does that it interrupts the connections between the neurons so that's what it means when it's demyelating because it is breaking down that myelin sheath so the signs and symptoms for multiple sclerosis are that they're going to have fluctuating exacerbations this is with most autoimmune disease there's usually things like flare-ups it's always not a constant presentation there could be changes in fluctuations it's confirmed with a lumbar puncture and they're looking for elevated gamma globulin they also might do a CT MRI myelogram or EEG these patients can have confusion because the central nervous system can connect to the brain and can have sensory deficits decrease perception to pain touch and temperature they may have bowel and bladder deficits they can have spasticity atoxic gait weakness Tremor spasm paresthesia vision changes dysplasia hyper reflex labia and a positive babinsky because we just have to remember all of these are connected through these neurons anything that is connected to our central nervous system and our neurons is going going to be affected it just depends what pathway is being attacked at that time so our nursing interventions our priority is to protect the patient from injury assist with frequent bladder and bowel elimination regular exercise and rest PT and speech language may need to be involved in fluid intake in a low fat high fiber diet and again these will be individualized depending on how our patient presents with all of these different symptoms that they could have let's talk about autonomic dysreflexia or hyperreflexia so this is caused by sympathetic nervous system stimulation after an either an injury at the T6 or higher or a lesion in the high thoracic or cervical cord or a blockage of the urinary catheter so signs and symptoms we're going to look for are severe hypertension sweating above the level of injury or flushing headaches bradycardia pylor erection nausea nursing interventions include our priority it's important is to monitor blood pressure and provide anti-hypertensive meds if needed we want to monitor bladder distension assess for bowel impactation remove restrictive clothes and keep the head of the bed at 45 degrees this is a neurological emergency as it can lead to a hypertensive stroke all right now let's talk about meningitis so this is an inflammation of the meninges of the spinal cord and brain caused by bacteria so signs and symptoms we're looking for verdinski's sign which is involuntary flexion of the hip and knee when the knee is flexed there's also kernig sine which the patient is unable to straighten the leg when it is flexed at the knee and hip they will have a stiff tight neck fever confusion they are cerebral spinal fluid will be cloudy with high protein high white blood cells and low glucose our nursing interventions include the priority is droplet and contact precautions if bacterial or menjucococcal meningitis we're going to assess for signs of intracranial pressure we're going to keep the head of the bed at 30 degrees and avoid flexion of the body and we're going to put them on seizure precautions and we're going to prepare for a lumbar puncture because we want to look at that cerebral spinal fluid let's talk about myasthenia gravis so this is a neurological disease characterized by muscular weakness this is because Communications between nerve cells and muscles are impaired due to defective nerve impulses so our signs and symptoms are that it is a progressive disease decreased muscle membrane acetylcholine receptors they have severe weakness proximal more than distal to muscles their facial ocular and bulbular weakness dysphagia vision changes difficulty breathing possibly life-threatening as respiratory muscle weakness can happen and they probable use of anticholinesterase drugs for treatment so our nursing interventions include our priority is going to be deep breathing and coughing we also may need to suction and have Emergency Equipment at the bedside again because of that respiratory muscle weakness we can we want to prevent aspiration so keeping them in a high Fowlers especially when they're eating we want to time exercise activities for when the patient has maximal muscle strength so muscles are stronger in the morning and then they get weaker at night so we want to do most of their kind of exercise and activities in the morning we'll administer anticholinistrate drugs and we want to avoid stress so we're also are going to compare a Myasthenia crisis versus a cholinergic crisis so let's look at the difference so with a Myasthenia crisis it is an acute exacerbation of myasthenia gravis so what we just talked about so this is an acute exacerbation whereas a cholinergic crisis is because there's too much acetylcholine due to an over medication with an anticholinesterase drug so we can really see a cholinergic crisis in any patient on an anticholinesterase drug myasthenia's gravis we're only seeing in those with myasthenia gravis disease for a Myasthenia crisis all right so let's look at the signs and symptoms so for Myasthenia crisis or signs and symptoms are tachycardia increased respiratory rate hypertension shortness of breath cyanosis bowel and bladder incontinence decreased urine output and no cough or swallow reflex again because all those muscles are getting weak our signs and symptoms for a cholinergic crisis are cramps nausea vomiting vision changes pale muscle twitching and hypotension so as we can see there's actually these are opposite right because one is having hypertension the other has hypo things that are similar as maybe the cyanosis Impaler those are similar so just some things to keep in mind but let's look at our nursing interventions so for Myasthenia crisis we our priority is to increase anti-cholinesterase meds so we want to increase those so our nursing priority for a cholinergic crisis is we want to hold the anticholinesterase meds so again they're the opposite and if there is an overdose for cholinergic crisis the antidote is atropine sulfate all right then we have something called an androphium test this is used to diagnose myasthena gravis and differentiate between Myasthenia crisis and cholinergic crisis so to diagnose myasthenia gravis they'll do the test and it will cause the muscle strength to improve so when they do this test and dronium they're looking to see if muscle strength will improve for people who have myasthenia gravis there's going to be no improvement so it's going to be negative in muscle strength or deterioration in muscle strength so if we're going to differentiate between Myasthenia graphis and cholinergic crisis if after the andropium muscle weakness improves then its myasthenios gravis Myasthenia crisis patient will need to will need more medication again because if we our priority is to increase those meds if after an Administration weakness worsens then it is a cholinergic crisis the patient is over medicated with the anticholinergic meds and needs atropine sulfate so that's how we can differentiate patient is at risk for v-fib and cardiac arrest during this test so keep that in mind as all right let's talk about Parkinson's disease so Parkinson's disease is a degenerative disease primarily involved in the basal ganglia signs and symptoms we're looking for include bradycardia resting Tremor monotone speech impaired postural reflexes rigidity loss of inhibitory dopamine a mask like affect drooling and difficulty swallowing and a shuffled gait the ones I underlined are really the ones that when you see a picture of someone with Parkinson's that's what you're going to really see nursing interventions include a soft diet high in calories proteins and fiber you want to increase fluid intake safety measures are they a fall risk Implement those safety measures they might need PT they might need rehab we want to avoid foods high in B6 because these can block the effects of some of the medications that we use for Parkinson's Disease and we want to avoid maois because again this can have some impairment it can cause that hypertensive crisis Bell's Palsy which is recognized as facial paralysis this is due to lower motor neuron lesion on the C7 that results in paralysis of one side of the face with the Hallmark sign recovery is usually in a couple weeks it does not affect Vision balance or extremity motor function so again and this is this can also be a sign of a stroke right so that's why we have to do those neuro tests as well so signs and symptoms flaccid facial mush nursing interventions include facial muscle exercises protect the eyes from becoming dry so we might have to have some artificial tears or wear a patch provide Oral Care and have patients chew on the unaffected side we're going to talk about Gillian Beret syndrome so this is a polynuropathy with Progressive muscular weakness it is an autoimmune disease it may be triggered by an infection causing neuritis of the cranial and peripheral nerves you'll also see this is a side effect of some vaccines it's rare but it can happen so signs and symptoms demyelation of peripheral and cranial nerves which is similar to Ms Ms attacks the Mylon sheets on the central nervous system Gillian Beret is the peripheral nervous system so motor paralysis in ascending pattern it has a three percent mortality because of respiratory failure autonomic dysfunction arrhythmias blood pressure changes tachycardia potential respiratory failure pain and hypersensitivity and when they do a cerebral spinal fluid test they'll see high protein next thing we're going to talk about is amiotropic lateral sclerosis this is also known as ALS and this is a degeneration of motor system with no changes in sensory autonomic or mental status there is no cure signs and symptoms include respiratory difficulty at the end of the disease because the respiratory muscles are affected leading to death muscle weakness and dysphagia let's now talk about Lou Garrett's disease so this is a degenerative disease affecting the upper and lower neurons signs and symptoms usually have they have death within two to five years you'll see spasticity hyperreflexia dysarthria dysphagia this is difficulty swallowing you'll see some autonomic dysfunction in about a third of the patients but their cognition will remain normal so different symptoms that we could see for this include Horner's syndrome so this is the result of another medical condition such as a stroke tumor or spinal cord injury symptoms include a smaller pupil drooping eyelid and little or no sweating on the effective side we can also have interior cord syndrome so this is damage is mainly in the anterior cord resulting in the loss of motor function and pain and temperature with preservation of a light touch preoccipation and position sense then we have brown sequired syndrome so this is a hemisection of the SC resulting in an ipsilateral weakness and loss of position and vibrational sense below the level of the lesion so this is the spinal cord I was like what does that stand for it's spinal cord okay vascular skull injury so signs and symptoms one main thing that we are looking for is called the battle signs and this is a bruising behind the ear another sign is periorbital hematoma so raccoon eyes like two black eyes and cerebral spinal fluid leaking from the nose or ear our nursing interventions are a priority is to support Airway breathing circulation we know that's always our priority we can do c-spine immobilization that's when you hold the neck still don't move the patient make it so they don't move their neck in neuromonitoring all right so some more on head injuries we also have concussions so a concussion happens when there's a jarring of the brain with no loss of consciousness they might have retrograde amnesia where they can't really remember what happened before or regarding the event and what we want to do our intervention is rest in a light diets are encouraged then we have a contusion this is bruising to the brain can occur with a subdural or extrateral blood collecting we have a skull fracture an example is linear depressed compound or community we have epidural hematoma this is the most serious hematoma a hematoma forms quickly so this is the blood is forming inside of the skull so due to an arterial bleed it could be the middle ingenial artery it could it forms between the skull and the dura mater there is a loss of consciousness in the patient may then feel better quickly where they have a lucid interval followed by a quick decline in mental function we can also have a subdural hematoma this is a slow bleed from a venous injury we can have an intracerebral Hemorrhage which is a blood vessel in the brain ruptures causing blood to leak inside of the brain and then we have spinal cord injuries so this can be a total transaction of the chord would be total loss of sensation movement and reflex below the level of the injury so this is a like a complete break if the injury is between C1 and C8 we can have a quadriplegic if it's C2 and C3 the injury is usually fatal and any injury between T1 and L4 can be paraplegia any injury C4 or above can lead to respiratory difficulties so our nursing priorities are going to be first priority is always assume the spinal cord injury with trauma until it's rolled out we also want to immobilize the patient on a backboard body should be midline with head in neutral position maintaining a patient patent Airway we want to log roll the patient if needed to put them onto a stretcher and again monitor abgs to assess respiratory status and spinal cord immobilization you'll often hear this called c-spine you can use this if needed again this is to keep the neck from moving you're just holding the neck the you're holding the head keeping the neck we can do a neuro exam if we're concerned there's significant trauma we want to look at level of Consciousness are they intoxicated do they have another injury and we can do a spinal exam as well so let's talk about the respiratory system so first let's talk about assessments so there are different breath sounds that you could potentially hear so the first is called a friction rub this is caused by rubbing of the pleural surfaces against one another usually as there is results of an inflammatory process this is going to sound almost like a kind of rubbing squeaky noise okay then we have rails also known as crackles this is an adventitious breath sound associated with pathology meaning there's some type of infection pneumonia something like that something that is making the lungs crackle these rails or crackles could be the result of air bubbles or secretions or movement of fibrotic tissue during breathing so again this is going to sound like a crackle it almost sometimes people say that it sounds like when you rub your hair together that's the noise you'll hear then we have bacillary rails these are often accompanied by left ventricular congestive heart failure so electasis fibrosis and pulmonary edema and it's related to the opening of previously closed small Airways in abioli then we have ronkai this is a continuous that's the key word continuous low pitch sonorous breathing sound that are more prominent during expiration that's another key thing prominent during expiration and could the be the result of air passing through the Airways narrowed by inflammation a bronchiospasm or secretions and again heard during expiration that is a key then we have the Strider so again this is a continuous adventitious sound of inspiration this key inspiration associated with an upper Airway obstruction so again you're only hearing the sound when they breathe in so wheezes this is a continuous breath sound that are high pitched and musical so if you ever see something asking about a musical sound that's going to be wheezes and they're often associated with asthma COPD and foreign body aspiration and we should always remember that our with our nursing interventions patients with any type of respiratory disorder should have the head of the bed elevated all right so let's talk about risk factors for respiratory disorders so we have allergies and crowded living conditions chest injury exposure to chemicals and environments pollutions family history of infectious disease frequent respiratory illnesses geographical residents and travel to foreign countries smoking or chewing tobacco and viral illnesses so the first chest injury we're going to talk about is called flail chest so the signs and symptoms are a paradoxical respiration so this means an inward movement of a segment of the thorax during inspiration with outward movement during expiration so the way you can think about this is the chest is moving the opposite way you would expect so typically when people breathe in their chest expands when they breathe out it it relaxes it decreases in size but this is having the opposite so you're getting that inward movement that you would usually get when you exhale during an inhale and then the opposite when you exhale you're getting the outward movement that's a paradoxical respirations and that's a sign of flail chest a severe pain in the chest dysmia cyanosis tachycardia tachypnea hypotension shallow respirations and diminished breath sounds and again we want to remember that when we're looking through all of these different diagnoses we want to pick out what are like the key big differences so for flailed chest you're going to see those paradoxical respirations that most likely will be in the question if they're asking about this so our nursing interventions these are going to include maintaining the client in Fowler's position that is usually the answer for anything respiratory related we want them in Fowlers because when you sit them up to high Fowlers you're actually passing the diaphragm a little bit so they can't get as deep of breath so really the best position to get them in is a Fowler's position we're going to limit activity administer oxygen and pain meds monitor for increased respiratory distress and encourage coughing and deep breathing all right so let's talk about a pneumothorax so signs and symptoms include absent breath sounds on the affected side so that is the key for a pneumothorax something really important to remember the things we want to pick out so when you're listening to breath sounds if you're not hearing sounds on one side it's because they could have a pneumothorax you also see the cyanosis decreased chest expansion unilaterally so because they have a pneumothorax their chest isn't fully expanding on that side so you'll also see this is another key Point dispia hypotension sharp chest pain subcutaneous emphysema is evidenced by crepesa creptus on palpation so if you feel their chest and you're feeling what sounds like cracking it's air Under the Skin and that is another key thing of a pneumothorax if they have a sucking sound with an open chest wound that's another that right there is pretty obvious right if there's that there's a hole in their chest tachycardia tachypnea the other really important thing is tracheal deviation to the unaffected side with a tension pneumothorax so part of your head to toe assessment you're looking at the trachea you're making sure the trachea is a midline if it's not midline it's pushed over to a side it could be that they have attention pneumothorax and it's going to be on the opposite side of the way the trachea is deviated so again the deviation is towards the unaffected side so our nursing interventions are going to include applying a non-porous dressing open over the open chest wound we're going to administer oxygen as prescribed place them in Fowler's position prepare for chest tube placement which will remain in place until the lung has expanded fully monitor the chest tube drainage system and monitor for subcutaneous emphysema the next thing we're going to talk about is a pulmonary embolism what you're going to see with these patients this is a blood clot to the lung this is a clot in the lung so you're going to see apprehension and restlessness they're going to start to have blood tinge sputum chest pain cough crackles and wheezing on oscillation cyanosis distended neck veins dyspnea accompanied by angina and pleuritic pain exacerbated by Inspirations when they breathe in it starts to hurt more feelings of impeding Doom this is a big one that you will see on questions if they talk about that patients are feeling there's an impeding Doom sometimes that can indicate a pulmonary emboli hypotension fatiguei over the chest and axilla so that's another kind of specific thing to a pulmonary embolism shallow respirations tachypnea tachycardia so our nursing interventions are going to include notifying the rapid response team and healthcare provider reassess the client and Elevate the head of the bed prepare to administer oxygen obtain vitals check lung sounds prepared to obtain an arterial blood gas prepare for the administration of Heparin therapy or other therapies and document the event in interventions taken right the next diagnoses we're going to talk about is tuberculosis so this is an infectious respiratory process caused by tuberculosis bacilli so the diagnostic tests that we are going to use include APD which is a purified protein derivative so this is given as a subcutaneous injection typically in the forearm so what we need to remember is that a negative test will be between 0 and 4 millimeters after 48 hours with a redness but without induration induration is a bump a positive induration is going to be anything greater than 15 millimeters in a healthy individual or 10 millimeters after 48 hours in immunocompromised individuals or five millimeters in high risk individuals such as those with HIV a positive test with no symptoms the patient gets a chest x-ray and a positive test with symptoms the patient gets a speedo culture the next type of test is a sputum Plus for myobacion tuberculosis so again this is the speedo culture so this will happen within two to three weeks of onset of symptoms and it will be negative if the disease is in the latent phase so our treatment is going to be the drug of choice in most cases is going to be isonazid or Rifampin and they typically do these together so treatment will depend on which type the disease is in so if it's in the latent phase and it's asymptomatic and there'll be no tuberculosis transmission normal chest x-ray no speedometer needed to be collected that's fine patient's fine however if they're in the active phase with cough fever chills weight loss anorexia fatigue TB can be transmitted have abnormal X-rays and a positive sputum culture so symptoms we're going to see fatigue lethargy anorexia weight loss chills fever chest pain in our nursing interventions are going to be airborne precautions for TB always because it spreads through the air so we need the filter on an n95 mask the room should have six air exchanges per hour and patient is to wear a mask if leaving the room all right so asthma this is Airway inflammation that can be caused by hyper-responsiveness to allergens exercise or irritants signs and symptoms are wheezing shortness of breath coughing or chest tightness our nursing interventions our priority is always keep the airway patent right because our ABC is our way breathing circulation and then to administer systemic steroids so what does this mean this means if you get a question about somebody having an asthma attack while systemic steroids although they work they work long term this is a long-term treatment so what that means is if they're having an asthma attack they need a short term they need a quick treatment so this is when you would use something like Albuterol okay so let's talk about COPD COPD is an airflow limitation resulting from a small airway disease or parenchymal destruction so there are two types you have chronic bronchitis and you have emphysema so we can remember this as chronic bronchitis these patients tend to look more like blue where emphysema they tend to be called red puffers because they're just kind of more red and they have what's called a barrel chest so they're more round in their shoulder area but all right let's go through it so chronic bronchitis these people that have a smoking history or core pulmonary they have decreased expiratory flow rates crackles wheezes and hypoxemia for our emphysema patients these are going to have those Barrel chests so that's like a big one that indicates emphysema again the dyspina the cyanosis they're going to have some clubbing and accessory muscles of ventilation so are nursing interventions include a normal oxygen is going to spo2 is going to be 88 to 92 which would be low for a normal person but that's typically where people with COPD lives so that's okay as long as they're not showing symptoms we don't want to raise the oxygen level higher than 88 to 92 because a lower spo2 is what stimulates COPD patients to breathe so if we turn up the oxygen their body is not going to make them breathe so we want to keep them between this 88 and 92. pneumonia so pneumonia is an acute inflammation of the lungs due to bacteria viral fungal infection leading to stiffening of the lungs diagnoses we would do a sputum culture and sensitivity with confirmation of the organism and this is how we can figure out which antibiotic to give because we're checking the sensitivity and aspiration pneumonia results from the inhalation of foreign matter signs and symptoms are fever pleuretic pain so pain that is sharp and increases during inspiration tachypnea wheezing accessory muscle use with breathing we can see a changing level of Consciousness and sputum production our nursing interventions our priority is going to be droplet precautions so we always want to remember with pneumonia we're using droplet precautions we want to supplement with oxygen monitor their level of Consciousness we can have them do some deep breathing and coughing semi-fowlers to assist with breathing chest physiotherapy to mobilize secretions fluid intake to thin secretions and antibiotics then we're going to talk about a pleural effusion so this is a collection of fluid in the plural space preventing lungs from fully expanding these patients are going to have polaric pain shortness of breath dry cough tachycardia fever and decreased breath sounds over the area our nursing interventions include the priority is to prep the patient for a thorough synthesis we're going to keep the patient in Fowlers and we're going to monitor for breath sounds the next diagnosis we're going to talk about is empyema so this is a collection of pus within the pleural cavity our interventions are going to be to treat the infection so we want to figure out what it is and we want to give some antibiotics that will treat that type of infection we want to use high Fowlers coughing and deep breathing and a thorocentesis or chest tube for drainage let's talk about some respiratory interventions so first we have supplemental oxygen delivery devices so we want to remember these different face masks and cannulas that we can use to deliver oxygen so the first one is a nasal cannula this is going to deliver at one to six liters per minute with a fio2 of 24 to 44 and this is for patients on long-term oxygen use or with airflow limitations then we have a face mask this is going to be delivered at five to eight liters per minute with an fio2 of 40 to 60 percent and we want to monitor for risk of aspiration for short-term oxygen therapy or for emergencies is when we would use a face mask then we have a Venturi mask so this is four to ten liters per minute with an fio2 of 24 to 55 percent and this is for patients in acute respiratory failure the tree then we have a partial rebreather mask this is going to be delivered at 6 to 15 liters per minute with an fio2 of 70 to 90 percent we will adjust the flow rate to keep the Reserve bag two-thirds full during inspiration and then we have a non-rebreather where the rate of flow needs to keep the bag full the fio2 is 60 to 100 percent and this is for patients with deteriorating respiratory status so then we also want to talk about ventilator alarms so things to remember with this is a high pressure alarm can be caused by increased secretions tube Kinks patient biting on the tube or coughing whereas a low pressure alarm can be caused by tube disconnection or the patient stops breathing chest tubes and with the chest tube there are two different suction types so we have a wet section and a dry section a wet section is regulated by the height of water so we can remember wet water in the suction controlled chamber the suction control chamber is filled with water and the amount of suction depends on the height of the water we want to see bubbling bubbling is good a dry section the suction monitor Bellow controls the amount of suction and the amount of suction is controlled by moving the dial on the suction control area now within the suction machine we have different areas so we have we have a drainage chamber so this is going to monit monitors drainage color and amount the normal is less than 100 cc's an hour and it's located right below the tube that comes from the patient then we have a water seal chamber so this again is going to be on our wet section water fluctuates with inspiration and expiration so we want to see it moving up and down as they breathe if there's no fluctuation and that means that the lung has re-expanded or there is a kink then we have the air leak monitor so this if this has excessive bubbling it indicates an air leak and if patient has a pneumothorax air in the pleural cavity intermittent bubbling is okay so what are our nursing interventions it's going to depend what happens so if we have dislodgement we want to cover the area with a sterile dressing tape three sides so that air can escape but not enter if there's a tubing issue we want to make sure that the tubing is below the patient's chest keeping it free from clots Kinks and stagnant fluid and during removal we want to position the patient in semifowlers perform of el Salvo maneuver and have them hold their breath so some medications to remember related to the respiratory system include atropine so used for severe asthma to help with spasms and involuntary muscles and inhibit secretions bronchodilators like epinephrine alleyupent then a twin provental relaxed smooth muscles and open the airway and corticosteroids like prednisone and cortisol are used to decrease edema and inflammation in COPD so let's talk about the cardiovascular system so the first thing we're going to talk about is cardiac marker labs and the first one we're talking about is ckmd or creatinine kinase myocardial muscle so what this is looking at is if the value is elevated that means that there has been cardiac damage following an acute ischemic attack this is usually around 18 hours after an acute ischemic attack and the normal value is going to be two to six in males and two to five in females the next one we're going to talk about is troponin so troponin C cardiac troponin one and cardiac troponin T so troponin one is specifically has a high affinity for myocardial tissue so that's troponin one it rises within three hours and persists up to seven to ten days after myocardial injury normal values are typically low with troponin one being less than 0.3 in troponin t being less than 0.2 next one we're going to talk about is myoglobulin so this is an oxygen binding protein found in cardiac and muscle cells the level rises within two hours after cellular death with a rapid decline in the level after seven hours however it is not cardiac specific now let's talk about B type naturetic peptide or BNP this is released in response to atrial and ventricular stretch it serves as a marker for heart failure the levels should be less than a hundred and the higher the level the more severe the heart failure let's talk about cardiac diagnostic procedures so the first one is an electrocardiogram so this is going to record electrical activity of the heart it detects this rhythmias myocardial infarctions and cardiac hypertrophy then we have something called a halter monitor so this is a monitor that the client will wear throughout the day over 24 hours or more and it records the electrocardiogram tracing throughout the entire day but the patient must avoid hot tubs baths and showers because again it is electrical then we have an echocardiography this is like an ultrasound it evaluates the structural and functional changes in the heart there's something called an exercise electrocardiography test or a stress test this is done while the patient is on a treadmill if the patient cannot tolerate the treadmill testing the patient may be given with an IV medication called type so they'll give this IV the patient doesn't have to get on the treadmill and it's important to note that the patient should be NPO for three to six hours before the procedure in our nursing interventions include instructing a client to avoid smoking alcohol and caffeine before the procedure as these can interfere with the then we have a myocardial nuclear perfusion imagery or an mnpi this is the use of radionucleotide techniques in scanning for cardiovascular assessment and then we have a magnetic Renaissance Imaging or an MRI and this is going to use radio waves magnetic fields and atomic nuclei it provides information on chamber size valve and ventricular function and blood flow and our nursing interventions include making sure all metal is removed and to assess for claustrophobia and because this is using magnetic fields it can actually pull the metal out of a patient so we just need to make sure that they don't have metal in their body all right so the next one we're going to talk about is a cardiac catheterization and this is an invasive procedure which inserts a catheter into the heart and surrounding vessels our nursing interventions include assessing for allergies to Seafood this is a big one iodine or radiopalak dyes this is because when they're doing this they inject a medication that is similar to seafood and iodine has the same kind of allergic reaction if you're allergic to Seafood you'll have allergic reaction to it so we need to know that doesn't necessarily mean that they won't get this procedure but they might need to be pre-medicated or something like that we have to withhold solid foods for six to eight hours if the patient is taking metformin it must be withheld for 24 hours because of the risk for lactic acidosis usually held for 48 after the procedure post procedure monitor peripheral pulses color warmth and sensation distal to the insertion site every 30 minutes for the first two hours apply a compressed device or sandbag to the insertion site and monitor for bleeding keep the extremity extended for four to six hours maintain bed rest for 6 to 12 hours and do not Elevate the head of the bed more than 15 degrees so let's talk about cardiovascular disease process so some keywords to know are atherosclerosis so this is the development of a fatty area throughout the arteries of the heart then we have angina pectoris so this is a term used to describe chest pain in which the pain is not localized but may include the left arm area as well as the sensation of an inability to breathe and demise the rhombus this is a term used to describe a blood clot then we have a myocardial infarction it is used to describe a complete arterial narrowing that does not allow for blood flow to take place it's also described as a heart attack then we have thrombosis this is the development of a thrombus or clot inside a vessel and ischema which is a decreased supply of blood and oxygen to an area of tissue so when we talk about angina and again this is a term used to describe chest pain in which the pain is not localized so we can have stable which is chest pain with exertion or activity relieved with rust or Nitro we can have unstable which is chest pain that is unpredictable may or may not be relieved with Nitro and variant or prismols is chest pain due to a coronary artery spasm and it may occur at rest so let's talk about a myocardial infarction signs and symptoms patients are going to have chest pain and pressure diaphoresis dyspnea anxiety females can present stating that they feel like they have indigestion shoulder pain or jaw pain and one important thing we want to look for is EKG changes and acute MI you're going to see an st elevation in localized leads so there's St elevation that is a big sign that it is a myocardial infarction so we're nursing interventions we always want to remember our ABCs so breathing circulation we're doing Vital Signs they might need we want to look at an EKG but also those cardiac markers that we talked about because that's going to tell us if there has been tissue death specifically cardiac tissue death depending on which marker we're looking at and they may need nitroglycerin or morphine those are the treatments for heart attack let's talk about aortic aneurysm so an aortic aneurysm is an abnormal dilation of the arterial wall so there's like a bulging of the arterial wall caused by localized weakness and stretching in the medial layer of the wall of the aorta we want to assess for the main kind of big problem with an aortic aneurysm is that it could burst and that's any aneurysm right we're nervous and it's going to burst and then they're going to have bleeding signs and symptoms we're looking for are pain syncope or cyanosis dyspnea and increased pulse they might have hoarseness difficulty swallowing because of the pressure from the aneurysm all right so let's talk peripheral artery disease versus coronary artery disease so peripheral artery disease is a decreased blood flow to the lower extremities due to atherosclerosis our signs and symptoms are intermittent claudication so they're going to present with muscle pain in their extremities they could have hair loss so typically we see this on the legs you're looking from the knees down they'll typically have some muscle pain especially when they're moving hair loss on their legs decreased peripheral pulses cool and dry skin gangrene thick nails and ulcers when we talk about coronary artery disease this is going to be an obstruction or narrowing of a coronary artery due to atherosclerosis so one is an obstruction of the coronary artery and the thing that is nice is this is called coronary artery disease you know it's the coronary arteries due to atherosclerosis where the other one is called Peripheral arterial disease so you know that it's not the coronary arteries so with coronary artery disease these patients are going to have chest pain palpitations shortness of breath syncope fatigue and a cough now let's talk about heart failure congestive heart failure so there's two types we're going to have left-sided heart failure and right-sided heart failure and these are going to look different so our left-sided heart failure if we think about the way that the blood pumps through the heart right it comes in to our heart on the left side it goes our left atrium so it goes our atrium Right comes in on the right side and it goes into our right atrium down to our right ventricle then it goes over through the lungs where it gets oxygenated and then it comes back into our left atrium down into our left ventricle where it is then shot up and pumped through the entire body so if we have left-sided heart failure that means that this side of the heart is not pumping adequately it's failing so what's going to happen the blood is going to back up and it's going to back up into the lungs so our signs and symptoms for left-sided heart failure are going to be pulmonary congestion shortness of breath tachypnea crackles cough and hypertension because it's being backed up into the lungs our nursing so for right-sided heart failure it is similar where we have it our right side of our heart is failing so it's not pumping adequately so the blood is coming in from the body like comes in from the body and now it's backing up it's not pumping adequately out so where is it backing up to it's backing up into the body so we're going to see signs and symptoms of Edema jugular vein distension because if you think about it this is the vein that is going into that right atrium we're going to see abdominal distension weight gain and hypertension so our nursing interventions for both types of heart failure are going to be high Fowlers supplemental oxygen monitoring the output fluid and sodium restriction monitoring daily weights monitor the number of pillows used to facilitate breathing while sleeping all right let's talk about valvular heart disease so the first one is mitral stenosis so this is a valvular tissue thickens and narrows the valve opening it prevents blood from flowing from the left atrium to the left ventricle then we have mitral insufficiency so this is a regurgitation the valve is incompetent preventing complete valve closure during systole and then we have mitral valve prolapse which the valve leaflets protrude into the left atrium during systole so let's also talk about aortic's genosis versus aortic insufficiency so with aortic stenosis the valvular tissue thickens and narrows the valve opening preventing blood flow from the left ventricle to the aorta so this is the aorta this is when it gets pumped into the body it goes the left ventricle into the aorta so signs and symptoms we're going to have dyspena angina syncopeon exertion fatigue orthopnea paradoxical nocturnal dyspnea and harsh systolic murmur with aortic insufficiency the valve is incompetent preventing complete valve closure during diastol our symptoms are dyspena angina tachypnea fatigue orthopnea paroxysmal nocturnal dyspnea a blowing decrescendo diastolic murmur so again these are key differences right we always want to remember the key differences and valvular heart disease is prepared by a balloon valvuloplasty so again looking at these there's a lot of similarities in how they present right but we want to look at the key differences so to me it's that murmur so definitely memorize which type of murmur goes with which type of valvular heart disease all valvular diseases are repaired by a balloon valvoloplasty a mitro annuloplasty a chemistry autonomy or a valtonymy and valve replacement means that the patient has to be on anticoagulants for the rest of their life again this is this is a key Point important to know all right let's talk about cardiac tapinod so this is a fluid accumulation in the pericardium signs and symptoms are a pulseless paradoxis a high CVP jugular vein distension with clear lungs muffled heart sounds low cardiac output and a narrow pulse pressure remember we talked about how to find the pulse pressure you take the systolic blood pressure and you minus the diastolic blood pressure our nursing interventions are going to be IV fluids and a pericardiocentesis where they suck the fluid let's discuss cardiac inflammation so there's some different types so we have pericarditis myocarditis and endocarditis so pericarditis is an acute inflammation of the pericardium signs and symptoms are a sharp pluric chest pain that's worse during inspiration again this is a key point you may see this in a question and you should be able to identify that is a symptom of pericarditis coughing relieved when leaning forward a pericardial friction rub fever fatigue and acute pericarditis you'll see an st elevation in all leaves our nursing interventions include High Fowlers this is our priority pain meds NSAIDs antibiotics and monitor for tapinod so a pulseless paradox jvd narrowed pulse pressure tachycardia and muffled heart sounds then we have myocarditis this is an acute or chronic inflammation of the myocardium so the thing that's nice it kind of tells you where this is the pericardium is for pericarditis myocardium inflammation is myocarditis so our signs and symptoms include fever a pericardial friction rub murmur so again there's a key signs and symptoms of chronic heart failure so or congestive heart failure so fatigue tachycardia and chest pain and our nursing interventions are assist to a seated position oxygen if needed periods of rest avoid overexertion pain meds antidis rhythmics and antibiotics then we have endocarditis so this is an inflammation of the inner lining of the heart or the endocardium kind of tells you in the name what area it is so our signs and symptoms include fever weight loss fatigue murmur congestive heart failure petechiai and splintering hemorrhages in the nail beds so again there's a key and clubbing of the fingers signs and symptoms rest Ted stockings monitor for signs and symptoms of an emboli or thrombus and antibiotics let's talk about cardiogenic shock so this is the inability for the heart to pump blood adequately signs and symptoms include hypotension tachycardia or a weak thready pulse urine output is lower than 30 milliliters per hour this is always a sign that something is wrong that's never good cold clammy skin and disoriented then let's talk about deep vein thrombo phlebitis so our signs and symptoms include the patient presents as warm skin on the calf or groin pain with or without swelling if a patient is saying that one calf is sore so specifically one I mean it could be both but typically it's one and it's warm when you touch it and they're complaining of pain that is a sign of a DVT so risk factors include verchoff's Triad so decreased flow stasis endothelial damage and hypercoagulability State our nursing interventions include elevating the extremity above the level of the heart avoid a pillow under the knees do not massage the area because you can dislodge it we want to apply anti-embolism stockings measure the circumference of the thigh or calf apply a warm moist compress as needed they're going to have to have antith thrombolytics we want to avoid prolonged sitting because the stasis of the blood is what can make it coagulate now let's talk about atrial fibrillation so this increases the risk of a stroke due to increased risk of blood clots because the heart is during atrial fibrillation it's almost like spluttering it's not like fully beating so the blood is just pulling there and staying it's not being pumped and the stasis of blood is what can make blood clots so our nursing intervention is the patient needs to be on anticoagulants we monitor INR if on Warfarin monitor a change in heart rate and monitor circulation and just to clarify this is the atrial part of the heart so remember we have our Atrium up top and then our ventricle below it's kind of like our right atrium right ventricle and then we have our left atrium and left ventricle in the heart and then the blood gets pumped it comes from the body into the right atrium into the right ventricle and it gets pumped into the lungs where it then goes into the left atrium down to the left ventricle and then out into the body all right so let's talk about percutaneous coronary interventions so this is when a catheter is inserted into the femoral or radial vein and advanced into the pulmonary artery to obtain information about the structure and performance of the chambers Valves and coronary circulation the procedure will improve coronary artery patency and increase cardiac perfusion however there are some complications we need to look for so thrombosis ostent occlusion a hematoma and limb ischema then lastly mechanical valves so when a patient is has a mechanical valve they'll need to be on anticoagulants for the rest of their life to avoid a thromboembolism let's talk about cardiac electrical activity different places in the heart that conduct electrical activity so the first one is the SA node this is the main pacemaker it initiates every heartbeat generates impulses 60 to 100 beats per minute that is the normal this is known as the pacemaker of them when this isn't working properly patients typically need a pacemaker then we have the AV node this is a place that receives impulses from the SA node if the SA node does not work then the AV node will take over and sustain a heart rate of 40 to 60 beats per minute and then we have the bundle of hiss this separates into the left and right bundle branches it's located in the ventricles and it can act as the pacemaker of the heart if the SA node and AV node fail and the heart rate will be between 20 to 40 beats per minute so when we talk about a pacemaker this is a device that provides an electrical stimulation to maintain a heart rate when the patient's SA node fails to provide a rhythm you'll see a ventricular Spike on an EKG that indicates a pacing stimulus so it will look like you'll have your your EKG strip and then you'll just see like a line and then you'll see like the next heart rate and then a line and that is the pacemaker you'll see the spike before the P wave for atrial pacing and a spike before the QRS complex for ventricular pacing so this one would be atrial and if you were going to see a ventricular it would be over here right before the QRS so our nursing interventions are going to be vital signs are monitored and cardiac monitoring is done continuously we monitor for dizziness and weakness or fatigue report swelling redness or drainage teach patient how to monitor their pulse and signs of a low battery we want to inform them of no cell phone use over the site over where the pacemaker is they don't want to put their cell phone on top of it we want to teach we want to teach them not to go for an MRI because we know the metal right can get pulled out during an MRI because it uses magnets waves are safe it's just a rumor that you can't use microwaves with a pacemaker so microwaves are fine and we want to teach them to avoid heavy lifting after surgery so let's talk about the vagal maneuver so in order to have a patient do the vagal maneuver you'll have them bear down this is when you're like holding your breath but then also trying to Exhale if you're ever on a plane and somebody says try to pop your ears it's that kind of maneuver and this can be used to terminate a super ventricular tachy dysrhythmia tea so a patient is in SVT the first thing you can do is have them bear down and sometimes that will pop them out of it cardioversion is a synchronized and it has to be synchronized to the r wave if delivered on a T wave it can lead to a lethal arrhythmia so it has to be synchronized on the r wave it is a counter shock to convert an undesired Rhythm to a stable rhythm and then we have defibrillation this is an asynchronous counter shock so this one does not have to be synchronized that terminates pulseless ventricular tachycardia or ventricular fibulation so let's talk about cardiac rhythms so first thing is determining the heart rate using a six second strip so this method can be used to determine the heart rate for regular and irregular rhythms when we are determining the atrial rate we're counting the number of p waves in a six second strip and then we're multiplying it by 10 because we know there's 60 seconds in a minute if we want to find the ventricular rate we count the number of R waves or QRS complexes in that six second strip we multiply that by 10. it's also important to know that there are 30 boxes in a six second strip and timing should begin on the P wave or QRS and end exactly after 30 blocks which is a six second strip let's talk about cardiac rhythms so the first Rhythm we're going to talk about is sinus bradycardia and we can see that this is a six second um cardiac strip when we have a six second cardiac strip we can take the amount of beets in that strip and multiply it by 10 and we'll get the beats per minute so in this one we find our QRS and we have one two three so 3 times 10 equals 30. so this is showing 30 beats per minute which would be sinus bradycardia anything less than 60 is a sinus bradycardia we can also see that because we have a normal we have a normal Rhythm so we have our P our q r s and then our T wave so that is all normal so it's sinus bradycardia so again our Rhythm our P wave and QRS is regular a heart rate p waves and QRS complex both less than 60 beats per minute we said we had 30. our P wave is consistent and one before each QRS that's true right PR interval is 0.12 to 20 seconds and consistent and our QRS is less than 0.12 seconds inconsistent so true so the pathophysiology we have a slow heart rate less than 60 beats per minute this can arise from a normal pacemaker in the heart it can be the site the SA node it can just be slow resting heart rate sometimes in athletes our P wave is normal and followed by a normal QRS and a T wave so our assessment we want to look at subjective and objective information so objective we're looking at is there any syncope or subjective we're looking at any syncope dizziness lightheadedness chest pain shortness of breath exercise intolerance these are things that the patient says they feel objective is what we can see so decreased level of Consciousness cyanosis peripheral edema pulmonary vascular congestion dyspnea poor perfusion and syncope our nursing diagnoses are going to include decreased cardiac output risk for injury risk for fluid volume overload and our interventions they may need atropine if symptomatic to raise up their heart rate it would be given by an IV at 0.5 milligrams at three to five minutes apart for a total of three milligrams treatment is directed at the cause which could include discontinuing meds preventing vagal stimulation and our treatment goals is for the client to remain syncope free to show a normal sinus rhythm and have them remain free of injury so now let's talk about sinus tachycardia so same thing we just talked about we're looking at a six second strip we can see all of the different waves so we can see our P our q r s and our T so that is normal but when we look at our six second strip we see one two three four five six seven eight nine ten eleven twelve thirteen if we take 13 times 10 because we want to figure out how many beats per minute we know it's a six second strip and 6 times 10 is 60 seconds which is one minute so we take our 13 times 10 equals 130 beats per minute so we can see our P wave QRS is regular our heart rate is above 100 beats per minute our P wave is consistent one before each QRS our PR interval is normal our QRS is normal so the pathophysiology so we see the elevated heart rate of 100 beats per minute or more causes could include shock fever stress exercise which would be normal anxiety pain or stimulants so again the subjective is what the patient says they feel so I feel a racing heart anxiety chest pain objective is weight so decrease blood pressure or an increased heart rate our nursing diagnoses could include anxiety risk for injury knowledge deficit and our interventions are going to be things like a calcium channel blocker carzepam digoxin or beta blockers to help slow down that heart rate our treatment goals is for the client to have less anxiety have a decrease their absent chest pain to them demonstrate understanding of how to decrease their heart rate so this has to match up with whatever our diagnoses was all right so now let's talk about atrial fibrillation so if we look at this heart rate we can see that first of all our our QRS and our QRS is our ventricle that kind of shows us our ventricle so our QRS is not regular right the distance from here to here is different from here to here so that's the first thing then if we look for our P wave and our T wave it's not here right we just this like fibrillation we can call it so this is atrial fibrillation so again our ventricle Rhythm our QRS is irregular our heart rate the atrial has multiple rapid impulses from many areas of the Atria resulting in the characteristics of a fibratory line so that's talking about this ventricular usually responds at a heart rate of 120 to 200 beats per minute so we can see The ventricle is beating so P wave no clear P wave no clear PR interval so our pathophysiology the Atria of the heart so the top of the heart we have our right atrium our right ventricle our left atrium our left ventricle so this top part our atrium is quivering and the blood is not being pumped out of the Atria so we know that when blood is stagnant in the heart like that there is an increased risk of blood clots because the blood is pooling the causes are usually hypertension valvila or ischemic and other types of structural diseases so again subjective the patient may say they feel they're heart racing you're going to see decreased blood pressure increase pulse rate we have some nursing diagnoses there but our interventions are going to be Coumadin if the client has been in a rhythm greater than 48 hours if it's unstable they may need a cardioversion it depends on the cause or durations clients can convert to a normal Rhythm spontaneously within 24 hours so we want to check if they're symptomatic if not there may not be much we can do so we may have to do those cardioversions and the medications things like that all right let's talk about atrial flutter so again we're seeing something similar where we have our QRS here so we're seeing those beats however when we look at our p and RT it's definitely irregular right you can't see those waves and the main thing that you'll see in questions is they call this a Sawtooth pattern if you see that that's atrial flutter so our rhythm is irregular again the distance between here and here is different than the distance from here to here heart rate greater than 100 beats per minute no P wave no PR interval and a narrow QRS you can see this is narrow so pathophysiology tachyarthemia is most often contained within the right atrium it's defined on an EKG by a Sawtooth pattern of flutter waves has negative polarity and leads to three and the f the assessment so again patient may say they feel chest pain or racing heart rate you may see blood pressure decrease loss of consciousness mental status change a regular fast heart rate are interventions for this are cardioversion and treatment goals big things are restoring sinus rhythm preventing thromboembolytic complications minimizing adverse effects of the therapy all right so let's talk about pre-ventricular contractions so when we talk about this is also called a PVC and you can see them here and here so the rhythm is irregular because we can see it kind of changes right heart rate varies you'll see a P wave there will be a wide PR interval so again it's gonna be here okay in here and our QRS is going to be narrow but very big so just this is our PR okay pathophysiology so extra abnormal heartbeats that begin in one of the ventricles these extra beats disrupt your regular heart rhythm causing the patient to feel a flip-flop or skipped beat in chest it can be caused by hypoxia low potassium caffeine and stress patients will say they feel their hearts skipping a beat anxiety stressed some people may say oh I drank caffeine you'll see decreased oxygen you might see their potassium low you might see a low blood pressure heart rate less than 60 beats or decreased level of Consciousness and that the intervention is again a cardioversion all right so ventricular tachycardia so you can see there's no QRS here right it's just this tachycardic Rhythm that is irregular we don't have a P wave we have a wide qrs's like these are all really wide and we can't identify a PR interval so pathophysiology so it's a type of regular and fast heart rate that arises from improper electrical activity in the ventricles of the heart ventricular tachycardia may turn into v-fib and cardiac arrest if it's sustained the heart rate can be greater than 120 beats per minute and it can last greater than 30 non-sustained a heart rate is greater than 120 beats per minute but lasts less than 30 seconds assessment subject you might say I feel almost dead the client might not be able to talk they might have shortness of breath chest pain dizziness lightheadedness you're going to see palpitations Cardiac Arrest heart rate of greater than 100 beats per minute and our intervention is we can have them try to do a vasovagal maneuver but if they have a pulse and amarodion if they have no pulse then they need immediate defibrillation so let's talk about ventricular fibrillation so again we talked about we have the atrium at the top The ventricle at the bottom so this is when now that ventricle is just fibrillating it's not pumping right we if we look at this rhythm we really can't determine anything there's no regularity there's no heart rate there's no P wave there's no PR interval we can't determine the QRS so the pathophysiology is coordinated contractions of the ventricular myocardium is replaced by a high frequency disorganized excitation resulting in the failure of the heart to pump the blood patients may say they feel short of breath chest pain dizziness lightheadedness nausea you might see low blood pressure fainting cardiac arrest and a heart rate of less than or greater than 100 beats per minute and palpitations or interventions include defibrillation and CPR so asystole we have nothing so pathophysiology there's no electrical activity on the EKG monitor clients probably unconscious you're not going to see a pulse so our interventions this is our high quality CPR they might need epinephrine the recommended dose is one milligram IV push every three to five minutes vasopressin 40 units IV is acceptable in place of first or second dose of epinephrine and defibrillation will not work for asystole that is important to know then we have proximal superventricular tachycardia so if we look at this we have an irregular Rhythm our heart rate is greater than 100 beats per minute there's no T wave no PR interval and a wide QRS pathophysiology is the rapid heartbeat that develops when normal electrical impulses of the heart are disrupted and this can convert to ventricle tachycardia we're going to patient may say they feel like they're going to faint dizzy or chest pain we're going to see a rapid pulse and diaphoresis our interventions are adenosine rapid push six milligrams followed by 20 milliliters of normal saline and the heart rate will stop so first degree heart block we can remember this if R is far from p so we have our P wave here q r s t so we're looking at this distance so rhythm is regular heart rate is less than 60. normal P wave PR interval greater than 0.2 and a wide QRS so pathophysiology the wiring of the heart is slowing to send electrical activities but all of the signals are able to pass successfully there's no electrical block but rather a slowing or delay of the signal and this usually does not cause a problem causes include enhanced vagal tone acute myocardial infarction myocarditis electrical disturbances subjective the patient may rarely show symptoms they may have you may see a slow pulse interventions there's usually no medical intervention required when we talk about second-degree heart block this is also called morbid's type 1 wenkebec we can remember this as further further drop so if we look at our p in our R distance we can see that it gets bigger and bigger and bigger it will drop so Rhythm increasingly prolonged heart rate's normal P wave normal PR increases with each beat until the QRS drops so we can see we're missing our QRS here so the QRS drops every third or fourth block pathophysiology so a progressive prolongation of the PR interval until eventually an atrial impulse is completely blocked and when the atrial impulse is completely blocked there will be a P wave without a QR complex patient will say rarely do they show symptoms they might be dizzy you'll see a slow pulse and interventions are atropine followed by a pacemaker when we talk about second-degree heart block or morbids type 2 we can remember this if some peas don't get through you'll have a morbids type 2. so we're going to see a QRS dropped in an unpredictable pattern so we can see a QRS here dropped our PR is constant same duration P wave is normal heart rate's less than 60 beats per minute our Rhythm for our Atrium is regular but our ventricular is irregular because again that's the QRS pathophysiology usually the disease of distal conduction system there is an intermittent non-conductive P wave without Progressive prolongation of the PR interval and can progress to complete heart block patient might complain of fainting dizziness lightheadedness chest pain shortness of breath you might see a slow pulse and our interventions will be a pacemaker so third degree heart block complete heart block so for this our QRS will be present but not equal to the amount of p waves and we can remember this as p and Q don't agree so we can see our P wave here and they're all kind of different distances we'll see our PR interval is delayed our P wave is inconsistent sometimes more than the QRS so again we can actually see two heat rhythm is regular and our heart rate is less than 60 beats per minute so pathophysiology there's no communication between the atrial and the ventricles and there's diminished cardiac output patient may say they feel like they're going to faint dizzy lightheaded chest pain shortness of breath you're going to see a low pulse and our interventions include IV titrated dopamine drip followed by a paste maker and now a paste Rhythm so our regularity is irregular heart rate varies P wave is inconsistent more than QRS PR releases delayed QRS is present but not equal to the amount of p waves so this is why we place a pacemaker so the pathophysiology we're going to see ventricle spikes on short duration usually every two milliseconds so you can see these right here so those are our pacemaker in the EKG and our interventions include clinical monitoring telling them not to do an MRI because of the magnet and there are certain ways we can turn it on and off so first let's talk about sinus tachycardia so the rhythm is regular the rate is going to be greater than 100 beats per minute our p waves our sinus they're normal PR our interval is 0.12 to 0.20 and QRS is around 10 seconds for sinus tachycardia you have a regular rhythm right it has that same kind of regular rhythm but there's just a lot of them because it's beating fast when it comes to sinus bradycardia it is a slow Rhythm so we're looking at beats of 40 to 60 beats per minute and there's no treatment unless symptomatic so if they have low blood pressure and loss of consciousness when we talk about superventricular tachycardia we're seeing again a very fast heart rate the rhythm is normal it's just beating really fast but the p and T waves have now formed into one wave the pr complex interval is not measurable and the QRS is around 10 seconds so this is an unstable Rhythm you'll see they may need a cardioversion they may have a low blood pressure loss of consciousness or chest pain and that's if they're unstable so there's two types unstable and then stable you could see sedation you can have them try that vagal maneuver we talked about earlier where they bear down and they may need a bolus of adenosine then we have atrial flutter so again the rate is 250 to 400 beats per minute the ventricular is beating normal but the but it's less than the atrial and again that atrial is in a flutter it's just fluttering for the P wave you're going to see a Sawtooth pattern this is a key if you see in a question it's saying you see a patient's Rhythm that's in a Sawtooth pattern that is going to be atrial flutter and it's important to know that to control the ventricular rate they'll use dilazzavin a flutter less than 48 hours long they'll need a cardioversion and if it's greater than 48 hours long they will anticoagulate before attempting the cardioversion then we have atrial fibrillation so a key for this is the P wave is fibrillatory and we're seeing a heart rhythm of 350 to 600 beats per minute in the atrial and ventricular is going to be less than that but again that atrial is just fibrillating so we want to control the rate first so again we're using that dilazepam afib less then 48 hours long the cardioversion or anticoagulation in afib greater than 48 hours long again anticoagulate before attempting cardioversion and unstable afib we will cardiovert Ace that all right so first degree heart block so this is a regular Rhythm it's just going to depend on the underlying Rhythm how fast it's beating if there are no symptoms it requires no treatment then we have second degree heart block type 1 and the atrial is beating regularly but the ventricle is not the atrial is going to beat at a rate that matches whatever the underlying rhythm is but the ventricular will be less than that you're going to see the pr lengthening progressively until QRS drops and this is also called wankerback and then second degree type two block this is again atrials beating at the underlying Rhythm ventricle less than atrial rate our sinus will be two to three p waves before each QRS once again these are the key things to know usually ventricular rate is slow you can we can see Strokes atom syncope caused by suddenly slowing of the heartbeat and treatment is usually a pacemaker all right so third degree heart block again atrial regular ventricular regular atrial is the same as the underlying Rhythm ventricular is going to be 40 to 60 beats per minute sinus P wave has no relationship with the QRS p waves may be hidden atrial and ventricular beat independently of each other symptoms include hypotension dyspnea heart failure chest pain Strokes atom syncope and treatment again as a pacemaker then we have ventricular tachycardia so this is we're going to see 140 to 250 beats per minute we're going to have we're going to have an absent P wave and the QRS is going to be wide so if it's stable we're going to do amiodarone bolus over 10 minutes once Rhythm converts an amiodarone infusion if this is unsuccessful they'll need a cardioversion if it's unstable we'll sedate the patient cardiovert and maintain an infusion of amiodarone then we have premature ventricular type contractions these patients are going to be tachycardic they are maybe no P wave before a premature QRS it will be wide for client experiencing PVCs we want to notify the health care provider if they complain of chest pain or if they the PVCs increase in frequency are multifocal occur on a T wave or occur in runs of ventricular tachycardia ventricular fibulation I have no no rhythm no rate absent this so if it's a witness you know them going down we defibrillate if it's unwitnessed we do CPR for two minutes before initiating shock and BLS and then asystole again no rate no rhythm P wave is absent not measurable QRS we have an absent QRS so if we witness again defibrillate unwitness CPR for two minutes before initiating shock and BLS let's review the renal system so the first thing we're going to cover is just a small review of anatomy and physiology so the role of the kidneys so the kidney regulates water and ionic compounds of the body excretes waste excretes foreign chemicals produces glucose during prolonged fasting and secretes hormones the three basic renal processes of glue meal frustration tubular reabsorption and tubular secretion in addition the kidneys synthesize and catabolize certain substances the excretion of a substance is equal to the amount filtered plus the amount excreted minus the amount reabsorbed so let's talk about normal renal function values so the first one we have is blood urea nitrogen or bun and this is anywhere from 10 to 20. the bun level indicates the extent of renal clearance of urea nitrogenous waste products an elevation does not always mean the renal disease is present then we have serum creatinine level in a male this is going to be from 0.6 to 1.2 and in a female it's 0.5 to 1.1 creatinine levels reflect the glomial filtration rate and increases only when 50 percent of renal function is lost then we have a bun creatinine ratio and this is going to be anywhere between 6 and 25 and then we have creatinine clearance test the normal is 125 milliliters per minute the creatinine clearance test provides the best estimate of glomial filtration rate it evaluates how well the kidneys remove creatinine from the blood and is an estimate of the glomial filtration rate the glomial filtration rate decreases with age about 10 percent per decade and by age 65 it is 65 milliliters per minute it's the average all right so let's talk about acute kidney injury so this happens quickly and is reversible so let's look at the different phases in laboratory findings so first we're looking at the onset it begins with a precipitating event that's because it's acute and anything acute it's not chronic it's not long-term it's not untreatable so acute is something happens that causes a problem that is reversible and fixable and if it's not reversible or flexible then it turns into a chronic problem so it begins with some precipitating event and it has some phases so the first phase is called the oliguric phase and during this phase we're going to see an elevated bun in serum creatinine levels we're going to see decreased urine specific gravity if it's caused by a pre-renal cause or the urine specific gravity will be normal if it's an intra-renal cause then we'll see a decreased glomial filtration rate and creatinine clearance we'll see hypergalemia normal or reduced sodium hypervolemia hypocalcemia hyperphosphatemia then we move on to the diuretic phase so this is we're going to start to see a gradual decline in the bun and serum carotene and clearance will still be elevated these so both of these will still be elevated but it's going to start to go down then we're going to see a continued low creatinine clearance with improved glomal filtration rate we'll see hypokalemia and hyponatremia and we'll see hypovolemia then we have the recovery phase so now we're going to start to see an increase in the glomial filtration rate so it's going up again we'll start to see a stabilization or continued decline in the bun in creatinine levels toward normal and we'll start to have a complete recovery but it could take as long as one to two years so what are our nursing interventions as we can see so to be honest you probably do not need to remember all of the hypocalcemia hyperphosphatemia in the algeric phase and then in the diuretic phase hypokalemia hyponatremia like that's a lot to remember but an important thing because that would be a very specific question to get on NCLEX if you're getting a question like that you're probably doing really well because that's a very difficult question to memorize all that material but you'll probably get a question related to electrolytes in nursing intervention so we should know that with acute kidney injury you're having electrolyte imbalances so that's a big thing so monitoring electrolyte levels is important and specifically we remember that potassium is the most risky when that one is out of balance so if it's asking you like what is your priority electrolyte to monitor with an acute kidney injury or something like that and potassium is one of the answers go with that because that's where you're going to have the cardiac abnormalities and things like that but monitoring electrolytes important with kidney injuries monitor blood pressure and Vital Signs and monitor intake and output with daily weights all of these are really important the interventions are really what you should memorize want to remember renal disease so that's a low protein high carb diet they may need dialysis and we may need to monitor for acidosis the treatment for acidosis is sodium bicarbonate chronic kidney disease so this now is a slow Progressive and irreversible loss of kidney function so a normal glomerular filtration rate is going to be 90. mild chronic kidney disease will be anywhere between 60 and 89 normal mild okay and then moderate chronic kidney disease glomial filtration rate is 30 to 59 severe is going to be 15 to 29 an end stage is a glomial filtration rate less than 15. this is going to require dialysis which is the process of filtering the patient's blood and removing wastes patients are at risk for fluid overload and hyperkalemia so these are things we should be monitoring for so now when we talk about our nursing interventions during dialysis we're monitoring for hypovolemia and shock or monitoring for bleeding we're going to hold anti-attensive and meds that could be removed during dialysis such as water soluble vitamins antibiotics or digoxin we're going to monitor for arterial steel syndrome in patients with internal AV fistulas which is too much blood is sent to the vein that the arterial perfusion to the hand is compromised and we'll palpate for a thrill or also take a brewery to ensure the fistula is pending this is when you use your stethoscope and you put it on the fistula whether it's wherever it is on the arm Etc and you're listening for a whooshing sound and that's showing that the blood is passing through there and it's working properly let's talk about an air embolism in a client with dialysis so how do we treat this we stop the hemodialysis we turn the client on the left side with the head down which is Trendelenburg position notify the health care provider in rapid response team administer oxygen assess Vital Signs and pulse and document the event actions taken in clients response so you may get a question on NCLEX like the way NCLEX will ask questions like what do you do first what is the priority it is never contact the health care provider there's always something that you should do first and we're thinking patient safety so if they're like there's an air embolism what do you do so first stop the hemodialysis turn the patient on the left side with the head down and Trendelenburg position then you notify the health care provider okay now let's talk about kidney transplant so a transplant can come from a living or deceased donor they must have the same blood type and antibodies the patient will be on an immunosuppressive medication for life so our nursing interventions are going to be to monitor urine output which starts immediately after the transplant daily weights and semi-fowlers position we want to remember to instruct the client following a kidney transplant to avoid prolonged periods of sitting monitor intake and output of a urine recognize the signs and symptoms of infection and rejection use medication as prescribed and maintain immunosuppressive therapy for life avoid contact Sports and avoid exposure to people who have infections so what are the signs of rejection so a temperature higher than 100 degrees pain or tenderness over the grafted kidney a two to three pound weight gain in 24 hours edema hypertension malice elevated blood urine nitrogen and serum creatinine levels decreased creatinine clearance and elevated white blood cell count all right let's talk about a UTI so UTIs may experience cloudy malodirous or bloody urine there are two types of UTIs so we have a lower UTI this is in the urethras cystitis due to ascending pathogens such as E coli signs and symptoms are frequency urgency and burning then we have an upper UTI these are things like polynephritis due to urine reflux from the bladder into the ureters OR obstruction causing inflammation these signs and symptoms are calculi structure and an enlarged prostate nursing interventions you want to give them antibiotics and monitor for confusion in the elderly the this is a big thing when elderly people get UTIs they can really be Delirious in things and then continuous bladder irrigation removes clotted blood from the bladder post-turp which is a three-way catheter that is used nursing interventions report pain and spasms which indicate obstruction report if output is less than the input which indicates a clot or Kink and titrate irrigation rate so that urine is light pink let's review the reproductive system so first let's talk about irregularities associated with the Menses so we have amenorrhea which is characterized by a lack of or uncharacteristic Paws of menses then we have dysmenorrhea this is painful Menses hypomenorrhea which is a limited period or period of short duration hypermenorrhea this is extensive menses algiomenorrhea this is irregular menses polymenorrhea this is abnormally frequent menses and ano-ovulation cycle is characterized by a menstrual cycle in which a woman does not ovulate okay now let's talk about endometriosis so endometriosis is the occurrence of endometrial tissue in an area other than the uterine cavity the signs and symptoms are painful intercourse dysmenorrhea which is painful menses dyschesia difficulty product producing stool pelvic pain pre-menstrual spotting and spontaneous abortion then we have pelvic inflammatory disease this is an acute or chronic inflammation of the endometrium uterine tubes and pelvic peritoneum chronic or acute inflammation caused by either gonorrhea chlamydia and is usually the end product of an untreated STD so signs and symptoms pain and vaginal bleeding nausea vomiting purulent drainage fever and elevated white blood count okay let's talk about sexually transmitted diseases so first we have chlamydia this is a sexually transmitted bacterial infection in males we're going to see things like urethritis epidymitis proctitis and reader syndrome in females we're going to see cervictitis and urethritis inflammation or infected barthonian glands and pelvic inflammatory disease then we have gonorrhea this is a contagious inflammation of the genital mucosa and may affect the genital tract both upper and lower the urethra endoservix peritoneum the heart and any joints in the body and any other area via the bloodstream we're going to see polyuria painful urination in discharge then we have syphilis this can invade any system within the body and cause damage to Bone tissues and nerve we'll see fever eruptions of mucosal patches on the skin lymphedectomopathy a painless canker papule that manifests 0.3 up to two centimeters non-tender ulcer that has a form border with a yellowish base flu-like symptoms and a rash then we have human papillomerular virus or HPV things we'll see include venereal warts so characterized by a growth of warts on the anal or genital area may appear as a single or in clusters and are fleshy skin colored and may be soft to touch signs and symptoms are soft Cecil having a broad base of attachment tumors may be smooth or roughed Paratus itching and bleeding at the site in our nursing interventions or we should educate that females should have a pap smear at 21 years old and then we have pubic lice and our interventions for this are lice shampoo remove knits with a fine tip comb wash belongings separately from others and sexual partners need to be treated as well so let's talk about the endocrine system so a quick Anatomy overview is we have endocrine glands throughout our body which are our adrenals hypothalamus ovaries pancreas parathyroid pituitary testes and thyroid then we have something called metabolic syndrome so this is three or more of the following factors are present and it increases a patient's risk for stroke diabetes and cardiovascular disease so abdomen obesity High triglyceride levels low HDL and a fasting blood sugar greater than 110. so let's talk about endocrine disorders so we have our hypo and hyper so when we talk about hypo pituitary growth hormone and gonadinoid hormone we're talking about hypo pituitarianism and then when we talk about an increase of the growth hormone it's hyper pituitarism so let's compare the two so hypo is a hyposecretion or one of more of the pituitary hormones caused by tumors trauma Encephalitis autoimmunity or stroke so we're talking about pituitary hormones right because we have all these different endocrine glands with hyperpituitarism we have a hypersecretion of the growth hormones are signs and symptoms for hypopituitarism so when it's low is mild to moderate obesity reduced cardiac output infertility sexual dysfunction fatigue low blood pressure tumors of the pituitary that may cause headaches or visual deficits and our nursing interventions are we may need hormone replacement and we need to educate them on signs of hyper pituitaryism because if they have too much medication it can cause that so we talk about hyper pituitarism are signs and symptoms include large hands and feet thickening and protrusion of the jaw arthritic changes of the joints visual disturbances diaphoresis oily rough skin organometally hypertension arthrosclerosis dysphagia deepening of the voice thickening of the tongue narrowing of the airway hyperglycemia colon polyps and colon cancer risk so I think Tony Robbins has this I don't know if you guys know who Tony Robbins is but if you look him up I think he has this and you can see he's a very large man large hands and feet he's got very big kind of jawline and he has some really good talks so nursing interventions we're going to provide pharmacological interventions to suppress or block the action of the gonotropic hormones we're going to prepare the client for pituitary gland radiation stereothetic radiosurgery or hypophysectomy if planned we're going to get off into pain relief and emotional support all right so now when we talk about the hormone ADH posterior pituitary is the endocrine gland involved what we're going to see is diabetes insipidus if it's low so again this is let's just add hypo and height hyper so we can see it all right so if it's low we have diabetes insipidus this is caused by stroke trauma and surgery this is when the kidneys fail to reabsorb water signs and symptoms include a large amount of dilate urine polydispia dehydration low urine specific gravity fatigue headache tachycardia postural hypertension in our nursing intervention so we're going to monitor Vital Signs monitor electrolytes maintain fluid intake may need an IV monitor intake and output in weight now when we talk about syndrome of inappropriate antidiuretic hormone secretion again this is the hyper ADH causes or trauma stroke malignancies medication and stress signs and symptoms are that it leads to a water intoxication and hyponatremia nursing interventions monitor for fluid overload change in level of conscious weight gain hypertension tachycardia we want to monitor their neuro status so looking for signs of that increased intracranial pressure monitor intake and output monitor weight serum osmolarity urine specific gravity we want to restrict fluids administer diuretics and have them on seizure precautions these patients will need lifelong glucocorticoid replacement all right then we have Addison's disease and Cushing's disease so this has to do with cortisol and this is from the adrenal gland so we have Cushings it's going to be hyper and Addison's is going to be hypo so for Addison's signs and symptoms are lethargy fatigue muscle weakness gastrointestinal disturbances weight loss menstrual changes in females impotents in males hypoglycemia hyponatremia hyperkalemia hypercalcemia hypotension hyperpigmentation of the skin then we have something called addisonian crisis a different color go and this is an acute adrenal insufficiency caused by stress infection trauma surgery or withdrawal from corticosteroids signs and symptoms are severe headache weakness hyponatremia hyperkalemia hypoglycemia get severe abdominal leg and lower back pain irritability and confusion severe hypotension or shock and our nursing interventions are to administer fluids and glucose IV post-crisis we're giving po glucocorticoid monitor Vital Signs neurostatus intake and output maintain bed rest in a quiet environment patients with Addison will need lifelong glucocorticoids during times of stress glucocorticoids will need to be increased just an important fact and let's talk about Cushing syndrome so again this is when we have a high level of cortisol so this is a metabolic disorder resulting from chronic and excessive production of cortisol from the adrenal cortex or from the administration of glucocorticoids in a large dose for several weeks or longer or from ACTH secreting hormones so Cushing's disease this is a metabolic disorder with increased secretions of cortisol caused by increased amounts of ACTH secreted by the pituitary gland signs and symptoms for both include muscle weakness and wasting you'll see the moon face and buffalo hump truncial obesity here sutium which is masculine features in a female they might get hair on their face hyperglycemia hypernatremia hypertension fragile skin bruises easily and Street day on the abdomen which is stretch marks nursing interventions we're going to monitor Vital Signs and monitor intake and output all right so then let's talk about the thyroid so again we have so for hypothyroidism our T4 is low and TSH is elevated we have decreases in the body's metabolism signs and symptoms are going to be lethargy fatigue weakness muscle aches cold intolerance weight gain dry skin and hair constipation edema around the eyes and face bradycardia and cardiac enlargement and sometimes a goiter a lot of times you can think that this is like everything is slowing down so our nursing interventions are going to include monitoring Vital Signs and heart rhythm administer thyroid replacement usually levothioxine monitor for overdose on thyroid men so we're looking for signs of hyperthyroidism instruct the client on a low calorie low saturated fat diet to go along with hypothyroidism we all have something we also have something called myxedema coma so we can see up here that one of these signs and symptoms was edema around the eyes and face which is my extema a myxedema coma is due to persistently low thyroid production we're going to see hypotension bradycardia hypothermia hypoontremia hypoglycemia generalized edema respiratory failure and then coma this is not good we don't want this to happen so our nursing interventions if this happens is to maintain a patent Airway because our Airway breathing circulation aspiration precautions IV fluid we're going to give them that labo dioxin intravenously along with glucose we're going to assess clients for temperature hourly keep client warm monitor for changes in mental status and monitor for electrolytes and glucose levels now when we talk about hyperthyroid two hyperthyroid so for hyperthyroid our T3 and T4 are high but our TSH is low it increases the body's metabolism and this can be caused by Graves disease so signs and symptoms are irritability nervousness and fine Tremors heat intolerance weight loss smooth skin palpitations and cardiac dysrhythmias diarrhea EXO fly Thalamus this is bulging eyes hypertension and goiter the way we can think about this is everything is speeding up our nursing interventions are going to include providing rest administering sedatives providing a cool quiet environment provide a high calorie diet avoid stimulants administer anti-thyroid medication or iodine preparations administer Propranolol for tachycardia if the patient has exothermals so the bulging of the eyes we're going to elevate the head of the bed give them a low salt diet artificial tears use dark glasses or tape eyes closed at night because sometimes they're popping so much the eyelids won't close then we have something with along with hyperthyroid called thyroid storm and this is uncontrollable hyperthyroidism we're seeing things like fever tachycardia systolic hypertension agitation Tremors confusions delirium seizures and coma and our nursing interventions include maintaining a patent Airway administer anti-thyroid medications Propranolol and glucocorticoids monitor Vital Signs and cardiac dyspritmias now we're going to look at the parathyroid so we have hypoparathyroid and hyperparathyroid so for hypoparathyroid we're seeing hypocalcemia and hyperphosphatemia tingling of the and muscle cramps a positive torsos introvertex sign we're going to see tetany hypotension anxiety irritability and depression so we can see for a lot of these there's some overlap with all the electrolytes and things like that but a positive trusos in chubasak sign with hypoparathyroid that's important to know because it's very specific so nursing interventions we're going to monitor Vital Signs tetany and hypocalcemia initiate seizure precautions place a trait kit O2 in section at the bedside they may need calcium gluconate IV they may need Vitamin D for enhanced absorption of calcium and instruct the client on a high calcium low phosphorus diet we talk about hyper parathyroid we're going to see hypercalcemia and hypophosphatemia fatigue muscle weakness bone deformity skeletal pain anorexia nausea vomiting weight loss constipation hypertension cardiac dysrhythmias and renal stones and our nursing interventions are monitoring Vital Signs specifically blood pressure monitor for dysrhythmias inos and renal Stones administer furosemide to lower the calcium levels administer calcitonin and phosphates and biophosphates okay so let's talk about insulin and pancreatic disorders so we have two types we have type 1 diabetes and type 2 diabetes let's talk about insulin and pancreatic disorders so the first is going to be type 1 diabetes so this is an absolute insulin deficiency they do not have any if insulin is not given that's a metabolized for energy which leads to Ketone production which leads to acidosis so signs and symptoms are polyuria polydipsia polyphasia and weight loss these are key to remember because this is what differentiates from type 2 because you're also going to have all of the same signs and symptoms that are in type 2. in addition to polyuria polydipsia polyphagian weight loss nursing interventions are to instruct the client to monitor their blood glucose levels before during and after exercise and to provide insulin then we might see something called diabetic ketoacidosis this is a life-threatening complication of type 1 diabetes it is a sudden onset due to inadequate insulin doses infections or other stressors in ketosis there is who's Maul's breath or kuzma's respirations which is a fruity breath this is a key sign so just remember that that goes along with dka we'll also see that polyuria polydipsia polyphrasia dry skin sunken eyes and coma diagnostically what we're looking for is going to be urine ketones that are positive our serum pH is going to be less than 7.35 and serum glucose is going to be greater than 300 which is also a key right we're looking at those blood sugar levels so our nursing interventions are to give IV normal saline first so if you get a question remember priority is IV normal saline first we're going to do cardiac monitoring we're going to monitor and correct electrolyte imbalances short duration insulin through an IV monitor Vital Signs and takes an output and monitor the client for signs of increased intracranial pressure then we're going to talk about type 2 diabetes so this is a lack or resistance to insulin they're is enough insulin to metabolize fats and protein but not carbs we're going to see hyperglycemia blurred vision weakness slow wound healing and inadequate circulation to the feet are nursing interventions are to instruct the client with diabetes to monitor their blood glucose before during and after exercise and provide insulin or oral medications then we're going to see something called hyperglycemia hyperosmolar non-chaotic syndrome or hns this is Extreme hyperglycemia that occurs without Ketone or acidosis which is the major difference in dka it's usually seen in patients with type 2 diabetes that's because we know that they have enough insulin to metabolize fat so you're not going to see those ketones signs and symptoms gradual onset due to infections stressors or poor fluid intake neurological symptoms such as lethargy coma might see dehydration with increased thirst electrolyte loss and also the same symptoms as dka so we want to remember these are the differences right we always want to remember the differences you don't want to have to memorize a bunch of information twice so nursing interventions are similar to DK interventions correct the IV normal saline first correct electrolyte imbalances insulin replacement plays a less critical role than in dka and rehydration alone may fix this all right so let's discuss blood sugars so we have hypoglycemia which is a low blood sugar and hyperglycemia which is a high blood sugar so for hypoglycemia we're going to see things like cold clammy pale irritable weak diaphoretic for a moderate hypoglycemia we may see mental status changes confusion irritability headaches slurred speech and for severe hypoglycemia they'll be disoriented or loss of conscious and also seizures are nursing interventions include checking their blood sugar if it's less than 70 we're going to administer 15 grams of simple carbs or half a cup of juice then we recheck the blood sugar in 15 minutes if it's still less than 70 we want to give another 15 grams of simple carbs or half a cup of juice then we will recheck again in 15 minutes if it's still less than 70 we want to administer 25 to 50 mL of 50 dextrose IV or we can treat with one milligram of glucagon Sub-Q or intramuscularly after the blood glucose has recovered we can have the patient eat complex carbs in a protein snack and if the patient has an altered mental status we're going to start with the injectable glucagon then for hyperglycemia we're going to see things like the patient's going to be hot and dry have polyphagia polyuria polydipsia blurred vision and that fruity breath and again that diabetic ketoacidosis and hyperglycemic hyperosmolar non-chaotic syndrome and we can see details of that in our previous section we went over now we're going to talk about types of insulin so first we have rapid acting insulin so this is our lispro as part and glue Ellison these have an onset of less than 15 minutes they Peak at one to two hours and they have a duration of three to six hours then we have our short acting this is just our regular insulin it's onset is 30 to 60 minutes with a peak in two to four hours and a duration of six to ten hours then we have our intermediate acting this is our NPH this has an onset of two to four hours Peaks four to eight hours and a duration of 10 to 18 hours and then we have a long acting which is our glargon or dedimir and this onset is one to two hours it has no peak and the duration is up to 24 hours and you do want to remember your insulins you will probably get a question about insulin there was something called Don phenomenon so this is reduced tissue sensitivity to insulin causing pre-breakfast hyperglycemia our nursing intervention is to increase the client's insulin dose or change in scheduling the insulin time then we have samojis phenomenon this is normal or elevated blood glucose levels at night then we see hypoglycemia at two to three a.m causing an increase in counter-regulatory hormone and by 7 am due to this hormone the glucose levels rebound and are increased signs and symptoms are early morning headache night sweats or nightmares or nursing intervention is to decrease the client's insulin dose and increase a bedtime snack or both let's talk about the integumentary system so the first thing we're going to talk about is wounds and when it comes to wounds we have a couple of different kinds of exudates so things that it can leak like fluid costs like things like that so when we talk about exudate we can have Cirrus exudate this is a clear or straw colored it is normal and part of the healing process we have serosanguinous exudate which is pink due to a small amount of blood mixed with serous drainage this is also normal part of the healing process we can have sanguinous this is red because it's due to blood vessel trauma it's uncommon in wounds we can have a hemorrhage which is Frank blood leaking from a blood vessel this is also uncommon and may require emergency treatment and purulent this is a yellow gray or green and it's due to an infection so that's important to know they may ask you if you see purulent drainage what do you have to worry about all right so let's talk about pressure ulcers so this is an impairment of Skin Integrity that can occur anywhere in the body it's due to the skin being compressed on a bony prominence restricting blood flow and it has difficult time healing because of that so the risk factors are skin pressure skin shearing and friction immobility so our patients that might be bed bound or maybe they are in a chair most of the day if they're not moving around this is why we always want to try to reposition our patients so that we can reduce the risk of injuries if they are immobile malnutrition incontinence decrease sensory perception so if they can't feel that there's pain there then they might not know to readjust and things like that when it comes to pressure ulcer staging there are different stages so a stage one is when the skin is intact non-blanchable with local redness that means when you push on it that it doesn't blanch so it doesn't turn white and then turn red again so it just stays red then we have stage two this is going to be open shallow red pink in color no sloth intact or an open blister so just think like the top layer is just sheared away stage three is a full thickness skin loss possibly visible fat but no bone or muscles showing stage four is full thickness skin loss with bone tendon or muscle showing and then unstageable is a full thickness with Sloth so it looks like scabbing or s-car which is black necrotic tissue that would be unstageable because we can't see how deep it goes so first we have shingles this is also known as herpes zoster it's due to a reactivation of varicella zoster in a patient with a history of chickenpox shingles is contagious to people who have never had chickenpox and to those who haven't been vaccinated against the disease signs and symptoms are an eruption occurs in a unilateral segmental Distribution on the skin along the infected nerve so it'll be unilateral so it'll be on one side of the body and it will be distributed along the nerve pathway we'll see fever burning pain puritis or nursing interventions patients should be on contact precautions patients should avoid scratching the area and we can assess the seventh nerve because Bell's Palsy is a complication MRSA signs and symptoms that can appear as a folliculitis or for uncles culture and sensitivity to confirm MRSA or nursing interventions include contact precautions it can spread by direct contact with infected skin we're monitoring first signs and symptoms of infection and we're administering antibiotics then we have cellulitis this is an infection of the dermis and Hyper they're going to have pain tenderness edema fever arrhythmia and warmth our nursing interventions are rest the affected area apply warm compresses to promote circulation and administer antibiotics then we have psoriasis this is an autoimmune disease causing a rapid turnover of cells there is no cure we see shedding a silvery plaque on renin's skin they might have apparatus so itching a yellow discoloration or thickening of the nails if they're infected and they can have joint inflammation with psoriatic arthritis or nursing interventions are to avoid triggers stress trauma infection they'll use topical corticosteroids sometimes phototherapy we want to advise them not to scratch stress makes it worse medications are Methotrexate sometimes we'll use that and to avoid alcohol then we have Steven Johnson syndrome so this is a medication induced skin reaction which occurs through an immunological response example NSAIDs antibiotics and anti-seizure medications can cause this it can be systemic involvement like the eyes respiratory system and it can result in blindness so signs and symptoms initially they'll have flu-like symptoms and erythema on the skin and mucous membranes then they'll start to have vesicle erosions and crust on the skin and then they'll have severe systemic symptoms can cause ulcerations on the larynx bronchii and esophagus our nursing interventions are to discontinue the meds administer antibiotics corticosteroids and supportive Therapies now let's talk about Burns so when it comes to burn depth we have superficial thickness Burns this is damage to the epidermis they're pink red with no blisters and it heals in three to six days we all know these types of burns get them on our hand no blisters it's just red it burns a little bit then we have superficial partial thickness burn so this is damage into the dermis it'll be pink and red with a blister and edema and it will heal in 10 to 21 days you can then have deep partial thickness Burns this goes deeper into the dermis red skin with white dry areas and no blisters due to dead tissue that heals in three to six weeks so an important thing to note is if it says a patient with blisters we know that superficial partial thickness Burns again we want to find the differences right so full thickness burn this is destruction of the epidermis and dermis it'll be waxy white deep red brown or black dry and hard skin healing takes weeks to months and it can involve skin grafting and then we have deep full thickness burn so the injury extends to the muscle bone or tendons skin is black and hard healing take months and it involves skin grafting as well so our priority nursing actions are to assess Airway for patency because always Airway breathing circulation first administer oxygen if needed obtain Vital Signs initiate an IV line and begin a fluid replacement so again this is our Airway this is our breathing this is our circulation because we want to prevent hypovolemia shock and preserve organ function Elevate extremities if there's no fractures keep the client warm and place on NPO assess for signs and symptoms of infection urinary output is the most sensitive non-invasive way to monitor cardiac output and tissue perfusion avoid IM or Sub-Q medications because absorption through the soft tissue is not reliable and proper nutrition is essential to promote wound healing the basal metabolic rate is 40 to 100 times higher than normal with burn injuries so they need an increase in calories and it's a big increase 40 to 100 times so let's talk about the rule of nines to estimate burn percentages so the head is nine percent the arm is nine percent legs are 18 each torsos 36 in perineum is one and we want to remember that we have a front and a back so the head is nine but it's 4.5 for the French 4.5 for the back the arm is nine percent each so each arm is nine percent and 4.5 for the front 4.5 for the back legs are double the arms because they're pretty much twice as big nine percent for the front nine percent of the back of the Torso is the largest area so it's 36 percent we have 18 for the front 18 for the back and then one percent for the perineum then we have something called the Parkland formula so this determines the amount of resuscitation that's needed in 24 hours after a burn so this is going to be four milliliters times the percent of the body burned so again we find that percentage using rule of nines and we give half of that milliliter amount in the four in the first eight hours and then we give the remaining half over the next 16 hours let's talk about hematological and oncology so first we have cancer this is a malignant neoplastic disorder that can spread throughout the body it can be solid tumors or hematological cancers of the blood cells forming tissue metastases is when cancer moves from its original location to other locations and it can do this in various ways so first it can do this by local seeding which is distribution of shedding cancer cells and occurs in the local area the primary tumor it can use bloodborne metastases so the tumor cells enter the blood this is the most common cause of cancer spread or lymphatic spread so the primary sites rich in lymphatics are more susceptible to early metastic spread now let's talk about grading and staging of cancer so first to grade zero this is carcinoma in situ then we have stage one this is going to be our grade is cells differ slightly from normal cells and are well differentiated and the stage is that tumor is limited to tissues of origin localized growth so this it has not metastasized it's only in the tissue of origin with localized growth when we move on to two these cells are abnormal and moderately differentiated and there's just a limited local spread three cells are very abnormal and poorly differentiated and this has extensive local and Regional spread and stage four cells are immature undifferentiated in cells of origin are difficult to determine and these have distant metastases so warning signs of cancer we can remember the acronym caution so changes in bowel and bladder habits any sore that does not heal unusual bleeding or discharge thickening or lump in the breast or elsewhere indigestion obvious changes in warts or a mole and nagging cough or hoarseness to diagnose a biopsy is the definitive means of diagnosing cancer the tissue is then examined under a microscope let's talk about different types of treatment so first we have chemotherapy this is going to kill or inhibit the reproduction of neoplastic cells and also kill normal cells in skin hair and GI lining then we have radiation this destroys cancer cells with minimal exposure to normal cells it's effective only for tissue in the direct pathway of the radiation beam side effects are local site changes so they might have reddening of the skin they might have pain in that area where they got the radiation this is really just they focus it on an area where they can shoot the beam in at it where chemotherapy is going through your entire body and it's attacking normal cells nursing interventions we want to wash aerated area with water and soap daily do not remove the markings for the radiation beam so they'll actually Mark where they're shooting the radiation do not use powder lotions creams on skin at radiation site avoid any clothing or binding that will rub the skin too much at the radiation site and we want to avoid exposure to the Sun and infection is a major cause of death for immunocompromised patients so those on chemotherapy we want to make sure they know to take Prosper precautions to not catch infections and also the signs and symptoms of infections all right so nursing interventions for patients with a sealed radiation implant so this is they actually implant something with radiation in the body so we want to place the client in a private room with a private bath place a radiation precaution sign on their door organize our nursing task to minimize exposure to the radiation Source because when we go in there we'll be exposed nursing assignments to a client with a radiation implant should be rotated limit time to 30 minutes per care provider per shift that's why we are doing all of our tasks as much as we can at once wear a Dawson or film badge to measure radiation exposure lead shielding may be used to reduce exposure to radiation the nurse should never care for more than one client with a radiation implant at one time the nurse should never care oh do not allow a pregnant nurse to care for the client do not allow children younger than 16 years old or pregnant women to visit the client limit visitors to 30 minutes a day visitors she should be at least six feet away from the patient save bed linens until the source is removed and disposed of the Linens in the usual manner other equipment can be removed from the broom at any time if the radiation implant dislodges we want to encourage the client to lie still using we're going to use long-handled forceps to retrieve the radioactive Source we're going to deposit that Source into a lead container contact the radiation oncologist and document the occurrence in the actions taken all right so let's talk about patient education for those with Cancers so first breast cancer so this is an invasive and metastasis by the lymph nodes it increased the risk in females over 50 or those who have the broccoli or brocca II Gene we can teach our patients to do a breast exam they can do this in the shower when the skin is slippery we want to tell them to use the opposite hand to assess the breast so our right hand to the left breast so the right hand to the left breast we want to use small circular motions in a spiral pattern to examine the entire breast check for lumps hard knots thickening up the tissue we can have them teach them to look in the mirror with the hands at the side raise their arms up over their head assess for any changes in shape or dimpling we want to place him tell them to place their hands on the hips and press firmly to tighten the pectoral muscles and absorb for any changes in Symmetry and when lying down they can also do this where they feel their breast with the opposite hand in a spiral motion so post mastectomy so when if they remove the breasts we're going to teach the patient to avoid overusing the effective arm during the first few months keep an affected arm elevated to avoid lymphedema avoid strong sunlight on the effect of arm do not let the effective arm hang dependently want to avoid constricting clothing have them avoid blood work and blood pressure on that affected arm education for testicular cancer so this most often occurs between 15 to 40 years old obviously in men it can metastasize to the lungs liver bone adrenal glands and lymph nodes when teaching patients of a testicular self-exam it's best to have them assess right after the shower gently lifting feeling around it should feel like an egg with no lumps you can roll them around to feel for lumps and swelling and mass and notify your doctor if there's any changes from one month to the next let's talk about the gastrointestinal system so things that we're going to monitor for within the gastrointestinal system so the first one is a retroperitoneal Hemorrhage so signs and symptoms we're going to see hypotension back pain something called Turner's sign so this is a gray blue discoloration of the flank seen in acute hemorrhagic pancreatitis we could see a hematoma and we'll see decreased distal pulses we also want to monitor for a bowel perforation so signs and symptoms abdominal guarding pain distension fever they'll be pale tachycardia tachypenia dysphagia this is a patient is at an increased risk of aspiration pneumonia because they have difficulty swallowing nursing interventions have evaluated by speech therapy they may need to thickened liquids soft meals put the head of the bed in high Fowlers 30 minutes post meal and have them swallow twice before taking another bite as far as what we can see with stool and bowel movement so we can have constipation this will be small dry hard stool we can have biliary obstruction so the stool will be light gray or clay color for ulcerative colitis they'll have mucus in the stool pancreatitis it will be a greasy fatty foamy stool if they have an upper GI bleed we'll see black tarry stool a lower GI bleed will be bright red and hemorrhoids will be lead on the surface of the stool when we talk about constipation our nursing interventions are going to be to ambulate the patient because this will increase peristalsis put them on a high fiber diet make sure they're drinking two to three liters of water a day and have them on a bowel regimen let's talk about some different medical diagnoses you'll see within the gastrointestinal system so the first one is GERD this is better known as heartburn love heartburn epigastric pain dyspepsia nausea and vomiting pain swallowing our nursing interventions can include having them avoid irritants like coffee chocolate fried foods carbonated drinks and alcohol and they can also be medicated with things like antacids H2 receptor antagonists or ppis inflammatory bowel disease so this is not to be confused so this is not irritable bowel syndrome IBS so this is not that okay these are two different things IBS is like a food intolerance more that situation inflammatory bowel disease is an autoimmune condition so the body is fighting the intestinal tract we have two types ulcerative colitis and we have Crohn's so ulcerative colitis is the chronic inflammation leading to poor absorption of nutrients it begins in the rectum and spreads upward the colon becomes a dimitius and has these bleeding lesions form on the mucous membranes so Scar Tissue causes diminished absorption of nutrients there'll be periods of exacerbations and remissions like any real autoimmune disease so symptoms anorexia malice frequent bloody diarrhea and mucus abdominal pain fever fatigue weight loss the thing to know for ulcerative colitis is this is only affecting the very first lining of the mucous membrane of the intestine so it's only affecting that outside lining and they get ulcers on this lining and that's what's creating the blood and the mucus so our nursing interventions in an acute phase they may be NPO need an IV or parental nutrition we restrict their activity to reduce intestinal activity we monitor stool color consistency and for any signs of blood monitor for hemorrhaging perforation or peritonitis they may be on a low fiber diet during an exacerbation they want to avoid alcohol caffeine raw fruits raw vegetables whole wheat and milk these patients may need surgery to create a stoma the stoma should be pink if it's purple or black in color this indicates compromised circulation when it comes to Crohn's this inflammation can occur anywhere in the GI tract for Crohn's how we talked about with ulcerative colitis is just the outside lining Crohn's can go all the way through these ulcerations it can create fistulas because it can be the entire membrane of the intestines we can see leads to thickening and scarring a narrow Lumen fistulous ulcerations and abscess again remissions and exacerbations we can see things like fever cramping after meals weight loss dehydration abdominal distension anorexia and nausea vomiting weight loss anemia in our nursing interventions are during a cute episode it's the same as ulcerative colitis and again surgery may be necessary but is avoided as long as possible because recurrence of the disease in the same region is likely to occur let's talk about diverticulitis so this is an out pouching or herniation of the intestinal mucosa it usually is discovered during a colonoscopy usually these people are asymptomatic and no treatment is needed diverticulitis which is an inflammation of the diverticula which can form an abscess signs and symptoms are left lower quadrant pain that increases with coughing lifting or straining they may have an elevated temperature nausea or vomiting they may have abdominal distension they may have a palpable tender rectal mass and there may be blood in stool our nursing interventions are to provide bed rest during an acute phase mpo status or clear liquids monitor for perforation or Hemorrhage increase fluids to 2500 to 3000 milliliters a day treat with antibiotics in a clear liquid diet and introduce a fiber-containing diet gradually when the inflammation results so then let's talk about peptic ulcer disease so this is ulcerations in the mucusal wall this is ulcerations in the mucosal wall of the stomach pylorus duodendum or esophagus due to gastric secretions patients will complain of a gnawing sharp pain in the left lower mid epigastric region that occurs 30 to 60 minutes after a meal food indigestion accumulates and causes the pain hematemesis is a common than Millennia so coughing up blood is more common than passing blood or dark colored blood in the stool our nursing interventions are to monitor for signs of bleeding if they're bleeding we want to get Vital Signs check for signs of dehydration shock sepsis and respiratory insufficiency we want to maintain NPO and administer IV fluids monitor H administer blood transfusion and medication as prescribed if needed that would be they're bleeding a lot administer small Bland feedings during the active phase administer antacids anticholinergics mucosal barrier protectants and prostaglandins as prescribed and educate the client on avoiding caffeine chocolate alcohol and sets and aspirin so those are interventions if it's in the gastric area now if it's in the duodenal area we're going to see things like burning pain that occurs in the mid epigastric area one and a half to three hours after a meal that often awaits the client at night they may have dark colored stool for from blood passing in the stool more so than coughing up blood and pain is often relieved by the ingestion of food nursing interventions monitor Vital Signs teach them to eat small meals frequently with a bland diet encourage smoking cessation and administer H2 receptor antagonists or PPI now let's talk about gastritis so there's two types of gastritis we have acute gastritis and chronic gastritis so acute gastritis is a stomach inflammation due to contaminated food this is going to have abdominal discomfort anorexia nausea and vomiting a headache hiccuping and reflux or nursing interventions are food and fluid that are withheld till symptoms subside we can give them ice chips clear fluids and then solid food when it's chronic gastritis this is caused by ulcers H pylori autoimmune diet medications alcohol smoking or acid reflux symptoms include anorexia nausea vomiting or belching heartburn after eating a sour taste in their mouth they may have a B12 deficiency in our nursing interventions are going to be NPO monitor signs for hemorrhatic gastritis so that would be hemateemesis tachycardia hypotension and avoid irritating foods and fluids then we have something called dumping syndrome so this is a rapid emptying of gastric contents into these small intestines after gastric gastric resection so this is after a gastric bypass signs and symptoms so it occurs 30 minutes after eating we'll see nausea vomiting diarrhea abdominal fullness and cramps tachycardia weakness dizziness and gory gig sounds which are loud gurgling abdominals so our nursing interventions we want to teach patients that have had a gastric bypass to use small meals and avoid fluids while eating we can teach them to lie down after meals avoid sugar salt and milk and eat high protein high fat and low carb meals now let's talk about cholecystitis so this is an inflammation of the gallbladder that may be acute or chronic if it is acute It's associated with gallstones and if it's chronic it's due to the inefficient bile emptying and inflammation of the gallbladder signs and symptoms will see are nausea vomiting flatulence epigastric pain radiating to the right shoulder or scapula a two to four which occurs two to four hours after fatty foods or a large meal we can feel a mass in the upper right quadrant they'll have a right right upper quadrant pain guarding and rebound tenderness we can look for something called Murphy's Sign this is where they feel like they can't take a breath because of the pain when fingers are pressed on the hepatic margin we can see tachycardia elevated temperature and dehydration now let's talk about obstruction in the gallbladder so signs and symptoms are jaundice dark orange and foamy urine stratea and Clay colored stool and Paratus our nursing interventions are NPO NG decompression for patients with chronic colitis and struck them to eat small low-fat meals so now let's talk about cirrhosis so this is destruction of hepatocytes which leads to scar tissue formation this is in the liver chronic causes are hepatitis C alcoholism non-fatty liver disease and non-alcoholic stetho hepatitis complications are portal hypertension due to flow obstruction ascites due to congestive hepatic capillaries that lead to plasma leakage coagulation deficits coagulation defects bleeding esophageal varices jaundice the liver cannot metabolize bilirubin portal systemic encephalopathy and hepato renal syndrome so signs and symptoms we can see a change in the level of Consciousness due to failure of the liver to get rid of ammonia in the system you can see ecchymosis batikiai and Palmar erythema leukopenia dysrhythmias fatigue anema ascites abdominal pain dyspena and many others because most systems of the body are affected and our nursing interventions are going to include elevating the head of the bed if they're having shortness of breath provide vitamin supplements restrict sodium and fluid intake enteral and paraentrial feeds diuretic meditation medications for ascites whey patients daily monitor the level of Consciousness monitor for asterisks this is a coarse tremor characterized by non-rhythmic extensions inflections in the wrists and fingers we want to administer lactulose this is a medication which facilitates the excretion of ammonia administer antibiotics this inhibits the synthesis in bacteria and decreases ammonia production avoid opioids and sedatives teach the importance of alcohol abstinence monitor ammonium levels and to help with piratus cut nail short calamine lotion cool wet cloths avoid hot showers and cholester thymine another diagnoses we may see is esophageal varices so these are dilated veins in the subucosa of the esophagus it's caused by portal hypertension associated with liver cirrhosis and if they start bleeding this is a medical emergency signs and symptoms are Hemi to emesis so coughing up blood dark blood in the stool Melania ascites jaundice heptamagdolly and splenomegdally dilated abdominal veins and signs of shock we're going to monitor for signs of rupture because this is life-threatening monitor Vital Signs watch for orthostatic hypertension monitor lung sounds and note any presence of respiratory distress Elevate the head of the bed administer O2 to prevent hypoxia monitor level of Consciousness they'll be on NPO status receiving fluids with IVs monitor h h administer clotting factor and blood transfusion as prescribed insert an NG tube or balloon tapenade as prescribed and instruct the client to avoid activities that will promote vasovagal response so things like bearing down or straining during a bowel movement we want to instruct them not to do that then we have appendicitis so this is an inflammation of the appendix and rupture can occur quickly which leads to peritonitis and sepsis so our signs and symptoms so pain in the perical area radiating to the right lower quadrant pain near the belly button that radiates to the right lower quadrant this is key if you see that on an exam that's a appendicitis abdominal pain at mcburney's point so this is another key thing to know abdominal rigidity fever nausea vomiting anorexia abdominal guarding our interventions are going to be NPO IV fluids to prevent dehydration do not palpate or apply heat to the abdomen and this increases the risk of rupture and peritonitis apply ice packs and let's talk about hepatitis so our goal is to increase blood supply rest the inflamed liver and reduce demands so there's a few different stages in hepatitis so we have the pre-ictic stage this is the first stage of hepatitis we'll see fever malice fatigue anorexia pain headache and muscle aches then we have the ictric stage and this is the second stage of hepatitis we'll see signs and symptoms of jaundice paritis elevated bilirubin dark urine clay colored stool and the post-ictric stage they're starting to get better so jaundice will decrease urine and stool color return to normal energy increases pain subsides and minimal GI symptoms so now let's talk about types of hepatitis so the first one is Hepatitis A this is spread through a fecal oral root and it's a person-to-person contact with contaminated food or water or poorly washed utensils our incubation period is two to six weeks infection is another two to three weeks before and then one week after jaundice and hepatitis A viral antibodies are found in the blood at an increased level will indicate infection so our complications are femalant hepatitis this is a severe acute and often fatal hepatitis nursing interventions we want good hand washing when handling stool we just being careful always using the precautions treating Municipal Water Supplies hepatitis A vaccine there is an immunoglobulin for travel or exposure then we have Hepatitis B this is spread through blood or bodily fluids increased risk for IV drug users health care workers those who work in prisons common in all age groups incubation period of 6 to 24 weeks a hepatitis B surface antigen will disappear in six weeks if not then the patient is a carrier and again those complications are the fomalent hepatitis chronic liver disease cirrhosis primary hepatocellular carcinoma or nursing interventions include hand hygiene screening blood donors testing pregnant women using our needle precautions avoid sexual contact with hepatitis B positive individuals hepatitis B vaccine and a HEPA immunoglobulin for those who are exposed then we have Hepatitis C this is also spread through blood or bodily fluids increased risk for IV drug users health care workers those in prisons our incubation period is five to ten weeks hepatitis C viral antibody will be found in the blood and our complications are chronic liver disease cirrhosis and primary hepatocellular carcinoma and again nursing intervention strict hand hygiene needle precautions screening blood so no hepatitis D is interesting because it only occurs with the presence of hepatitis B it's common in Mediterranean Middle Eastern areas has an intubation period of seven to eight weeks and we'll see a hepatitis D antigen found in the blood our complications again are that fomalent hepatitis and chronic liver disease and nursing interventions are prevention which includes hepatitis B vaccine since hepatitis D also needs to coexist with hepatitis B and then Hepatitis E is a fecal and water-borne virus intubation period is nine weeks we'll see IGM and IGG antibodies to the Hepatitis E viral found in the blood complications there's a high mortality rate in pregnant women and Fetal demise and nursing interventions are strict hand hygiene and treating Water Supplies let's talk about home care instructions for those with hepatitis so we want to teach patients good hand washing don't share bathrooms unless the client strictly adheres to personal hygiene and this again is for hepatitis this would be hepatitis A and Hepatitis E so the ones that are spread through fecal World washcloths towels drinking and eating utensils toothbrushes and razors must only be used by the patient the patient may not prepare food for other family members they should for all types of hepatitis patients should avoid alcohol and over-the-counter medications particularly Tylenol and sedatives because they're hepatotoxic the patient should increase activity gradually to prevent fatigue if the patient should consume small frequent meals consisting of high carbs low-fat foods the patient cannot donate blood close personal contacts such as kissing and sexual activity should be discouraged with hepatitis B until surface antigen tests are negative and the client should carry a medical alert card noting the date of the hepatitis onset all right let's talk about pancreatitis so this is when pancreatic enzymes Escape into surrounding tissue there are two types acute which occur suddenly as one attack or recurrent with resolutions signs and symptoms include abdominal pain mid-gastric or upper left quadrant radiating to the back so that's important to know the locations of the pain can really tell us what it is so it's important to remember the locations of pain with certain diagnoses pain aggravated by fatty meal alcohol or lying in a recumbent position this is also important the fatty meal piece you may be asked about that abdominal tenderness weight loss absent bowel sounds this is also important to know something called Cullen sign which is discoloration of the abdominal and periumble area and Turner sign which is blue discoloration of the flanks are nursing interventions include withholding food or fluid during an acute period and maintain IV fluids administer parental nutrition for severe nutritional depletion in an NG tube may be inserted if they are vomiting have a paralytic ileus or a biliary obstruction then we have chronic this is a continual inflammation and destruction of the pancreas with scar tissue signs and symptoms are abdominal pain and tenderness left upper quadrant Mass they may have stratoria and foul smelling stools that may increase in volume we may see weight loss muscle wasting and jaundice and we may see signs and symptoms of diabetes so our nursing interventions we want to limit fat and protein intake avoid heavy metals and avoid alcohol administer pancreatic enzymes we also want to look at this is the lab alt and AST these enzymes release when hepatic cells are injured so two other diagnoses we may see related to the gastrointestinal system are a small bowel obstruction or a large bowel obstruction so for a small bowel obstruction we're seeing signs and symptoms of Rapid onset nausea and vomiting intermittent abdominal pain and abdominal distension for a large bowel obstruction this is going to have a gradual onset cramping and abdominal pain abdominal distension and complete constipation and no passing of gas nursing interventions for both of these are NPO NG tube insertion IV fluids and managing pain in the last diagnosis we're going to discuss is a paralytic ileus this is a temporary halting of peristalsis for 24 to 48 hours after a bowel procedure and no bowel sounds will be also tated all right so let's talk about different bowel procedures so first we have gastric surgery and our nursing interventions for this include following the gastric surgery do not irrigate or remove the NG tube unless specifically prescribed because of the risk for distribution of gastric sutures monitor closely to ensure proper function of an NG tube to prevent strain on the anatomical site and contact the healthcare provider if the tube is not functioning properly we want to monitor respiratory complications that could be caused by pain at the insertion site we want to encourage coughing and deep breathing encourage ambulation instruct the client about splinting the abdomen to prevent discomfort during coughing administer antiemetics administer analgesics maintain NPO status and the NG tube section as prescribed an advanced diet from clear liquids to solids when prescribed and as tolerated by the client when it comes to bariatric surgery we want to teach the client to avoid alcohol high protein foods high in sugar and fat we want to teach them to eat slowly and chew food progress food types and amounts as prescribed take nutritional supplements as prescribed which may include calcium iron multivitamin and b12 and monitor in reports signs and symptoms of complications such as dehydration and gastric pain then we have a colonoscopy so this is the lining of the large intestine is examined and biopsies can be performed nursing intervention is clear liquid diet day before with a colon cleanse given there'll be NPO at midnight and the patient is in a left side lying position with knees to chest oil it's being performed then we have a colostomy this nursing interventions are to keep liquid stool from leaking out this causes skin irritation due to digestive enzymes we want to change the bag so this is a bag that's attached on the front of the patient where stool comes out of they're creating a hole in the stomach into the intestines want to change the bag every four to seven days increase fluid intake to prevent dehydration and empty the bag when it's a third full and then colostomy care so we want to empty contents of the bag before removing it push skin away from the bag wash the stoma using soap and water but do not scrub inspect for redness irritation bleeding and blisters and pat dry measure the stoma using a measuring guide with scissors we cut along the measurement with 1 8 bigger than the stoma apply a barrier ring and apply a Skin Barrier and attach the stoma all right so let's talk about a paracentesis and thoracentesis so these are the removal of fluid from the peritoneal cavity for a paracentesis or the pleural space for a thoracentesis it's performed at the bedside our nursing interventions are the patient is in an upright position at the edge of the bed with arms on the table for thoracentesis Vital Signs and weights pre-procedure have the patient void if they're getting a paracentesis and a dry sterile dressing at the puncture site and measure fluid removal we have total parental nutrition for our nursing interventions this is avoid stopping it abruptly as it can lead to hypoglycemia we want to monitor signs and symptoms of hypoglycemia such as polyphagia polydipsia and polyuria though we have something called an ercp this is an examination of the apatobiliary system with an endoscope down the esophagus nursing interventions are NPO before the procedure and post-procedure monitor for return of a gag reflex and for signs of perforation and then we have entero feeding so this we're looking for abdominal cramping can occur if the feed is too fast or too cold interventions are head of bed 30 to 45 degrees pre and post feed tube flushes pre and post feed because we don't want it to clot and assess bowel function okay let's review the musculoskeletal system so first we're going to talk about injuries so risk factors include autoimmune disorders Calcium deficiency Falls hypoglycemia infection medications metabolic disorders needle plastic disorders obesity and postmenopausal states so we can have either a strain or a sprain so the difference is that a strain is an excessive stretching of the muscle or tendon whereas a sprain is a stretching of a ligament usually caused by a twisting motion signs and symptoms include pain and swelling for a sprain our nursing interventions for a strain are going to be cold and heat application exercise anti-inflammatory and muscle relaxant medications whereas for a sprain we're going to use something called rice so rest ice compression or cast and elevation so if you get a question asking about heat remember that heat is only on a strain so now let's talk about types of fractures so we have a closed or simple fracture this is skin over the fracture area May remain intact commuted fracture the bone is splinted or crushed with numerous fragments complete is bone is completely separated by a break into two parts then we have compression this is fractured bone is compressed by two other bones we have depressed where the bone fragments are pushed inward there's green stick one side of the bone is broken and the other side is bent most common in children impacted so part of the bone is driven into another bone then we have incomplete so the fracture line does not extend the entire width of the bone we have oblique which the fracture line runs on an angle we have an open or compound this is the bone is exposed to air through a break in the skin for this it's important we want to watch for infection cover the wound with a simple sterile dressing then we can have pathological which the fracture is due to weakness of the bone structure and then we can have transverse where the bone fracture is straight across so signs and symptoms of a fracture include the five P's of a fracture so pain paler pulselessness paresthesia and polar which is cold they're going to have decreased muscle strength and obvious deformity crepitus so if you feel it you can feel it like creaking and edema and muscle spasms so then complications of a fracture so things we want to look for make sure a complication is a fat emboli a pulmonary emboli compartment syndrome infection and a vascular necrosis are interventions include immobilizing the fracture they may need an open or closed reduction internal or external fixation and traction or Cap all right so let's talk about a fractured hip so risk for hemorrhage nursing interventions are monitored for signs of delirium maintain leg and hip proper alignment and prevent rotation Elevate the head of the bed 30 to 40 degrees for meals only avoid weight-bearing on affected leg keep post-op leg extended supported and elevated when standing up and monitor neurovascular status of the extremity and avoid crossing the legs in any activity that requires bending these are important complications of fractures complications of fractures so we discussed earlier a fat embolize so this can occur after a fracture so a long bone fracture is the greatest risk our sine are signs and symptoms include restlessness hypoxemia changes in level of Consciousness tachycardia hypotension and shortness of breath our nursing interventions or give them oxygen if needed IV fluids monitor respiratory status Vital Signs and bed rest then we have compartment syndrome so this is a pressure increases in a muscle group usually after a cast has been placed which decreased blood flow leads to tissue ischemia and neurovascular impairment and after four to six hours of this syndrome neurovascular damage is irreversible so this is very important that we monitor for this signs and symptoms paresthesia limb pain pressure Aller pulselessness distal to the area and paralysis or nursing interventions we want to notify the doctor they're probably going to have to do a fasciotomy to relieve pressure buildup or loosen the restrictive cast and then avascular necrosis so when a fracture interrupts blood supply to the Bone which can result in bone death okay so let's talk about some nursing interventions related to the muscular skeletal system so first we have bucks traction this alleviates muscle spasms and immobilizes the limb our nursing interventions include ensuring proper body alignment weights hang freely and don't touch the floor do not remove weights without a doctor's order ensure that pulleys are not obstructed and Elevate foot of bed and check ropes for fraying then we have cast care so teaching is going to be to keep the cast elevated allow to to allow 24 to 72 hours for a cast to dry handle a wet cast with palms of hands turn the extremity every one to two hours to allow circulation use a hair dryer on a cool setting to help with the drying process do not insert any object into the cast to relieve itching this is very important monitor for signs of infection and keep the cast clean and dry our nursing interventions are to monitor the casted extremity for circulation impairment so we're looking for pain discoloration numbness swelling coolness tingling and diminished pulse then when it comes to crutches so we want to make sure the crutches are measured properly they should be two to three finger widths between the axilla space and the arm piece elbows should be flexed 20 to 30 should stand on the patient's affected side when ambulating do not rest axilla on the auxiliary bars and stop ambulation if number numbness or tingling occurs in hands or arms when assisting the client with crutches to sit to stand we place the unaffected leg against the front of chair we move the crutches to the affected side grasp the arm of the chair with the hand on the unaffected side when lowering self into the chair Flex the knees of the unaffected leg while placing the affected leg straight out in front reverse the steps to remove from sitting to stand alright so let's talk about going down going up and down the stairs the client moves the unaffected leg first the client moves the effective leg and the crutches up going down the stairs the client moves the crutches and the effective leg down and then the client moves the unaffected leg down so let's talk about some medical diagnoses related to the musculoskeletal system so first we have rheumatoid arthritis this is an autoimmune disease that leads to Chronic systemic inflammation destruction of connective tissue and synovial membranes in the joints and ultimately leads to dislocation and permanent deformity of the joints signs and symptoms include inflammation of the joints pain and stiffness in the morning greater than 30 minutes muscle atrophy spongy joints and weight loss our nursing interventions include rheumatoid Factor blood tests to confirm diagnoses range of motion exercises using hot and cold rest and activity balance prevent flexion of contractures avoid weight-bearing on inflamed joints use chair with a high back and a small pillow when laying down then we have osteoarthritis this is a progressive deterioration of articular cartilage in the peripheral and axillo Joints mostly on weight-bearing joints hips knees hands the causes unknown though it could be trauma aging obesity genetics and smoking signs and symptoms are pain that increases with activity so these are like the key things so rheumatoid arthritis pain and stiffness in the morning for greater than 30 minutes key point for osteoarthritis pain that increases with activity and decreases with rest and increases with temperature change you'll also see heparins or Bouchard's nodes so here is another key point and you'll also see crepitus our nursing interventions for osteoarthritis are pain and corticosteroid meds avoid flexions of knees and hips avoid large pillows when laying apply cold packs when joint is inflamed and balance activity and rest and limit activity when in pain then we have osteoporosis so this is bone demineralization leading to fragile bones and risk for fractures risk factors include smoking early menopause alcohol use family history being a female increased age low calcium intake sedentary lifestyle thin and small frame European or Asian race signs and symptoms are possibly asymmatic they might have back pain with palpitations after lifting bending or stooping pelvic or hip pain balance problem a decline in height or typhosis and there is a risk for pathological fractures our nursing interventions are to move them gently assist with ambulation if unsteady gentle range of motion exercises and a firm mattress now let's talk about amputation of a lower extremity post-op so this is going to be surgical removal of the limb and nursing interventions are monitored for bleeding and drainage exp explain Phantom limb syndrome or Phantom limb pain do not Elevate residual limb on pillow in the first 24 hours Elevate the foot of bed to reduce edema after keep the bed flat to prevent flexion contractures and after 24 to 48 hours put the patient in a prone position to stretch the muscles then we have gout this is a buildup of the urate crystals in the joints due to high uric acid in the body we're going to have Painful joints something called tofi which are hard nodules paritis renal stones and inflammation of the small joints specifically the big toe someone is reporting inflammation of their big toe gout is something we should be looking at nursing intervention so a low purine diet so we're avoiding organ Meats wines aged cheese and alcohol high fluid intake of 2 000 milliliters a day monitor joint range of motion bed rest during painful attacks and heat and cold applications for pain okay let's review the immune system the first thing we're going to talk about is HIV our nursing interventions for this are standard precautions HIV is only spread when non-intact skin is in contact with patients blood breast milk semen or vaginal secretions we want to protect these patients from infection and always using aseptic technique for all procedures HIV testing so we're looking at CD4 and T cell count which is normally between 500 and 1600 in HIV it will drop below 500 and in some cases lower than 200. we may do a viral culture of the patient's blood looking at viral load testing p24 antigen assay we have in oral testing for HIV where a device is placed against the gums and a home test then we have Aid so this is a viral disease due to HIV high risk for infection and malignancy and incubation period of up to 10 years signs and symptoms include low white blood cells platelets CD4 along with high cd8 IGG and IGA we can see weakness fever weight loss which is called a wasting syndrome leukopenia night sweats infections neoplasms such as carposi sarconoma occur in immunocompromised individuals it's a slow growing tumor they can also have the presence of fungal viral and bacterial infections our high risk such as IV drug users patients receiving blood products health care workers and babies born to infected moms our nursing interventions their oxygen as needed maintain fluid and electrolyte imbalance monitor for infections using standard precaution and meticulous skin care talk about anaphylaxis so this is an immediate hypersensitivity reaction with release of histamine we'll see angioedema dizziness paresthesia paritis eudocaria narrowing of the airway wheezing Strider shortness of breath respiratory arrest hypotension tachycardia Cardiac Arrest abdominal pain nausea and vomiting nursing interventions always are ABCs so first is making sure there's a patent Airway they can have that angioedema which can close up the airway we may need to give them supplemental oxygen they may need IV normal saline infusion and we want to be giving them the antidotes whether it's Benadryl or epinephrine and disease so this is an infection due to Varela bugadoffery from a tick bite so there are three stages the first stage we're going to see symptoms that occur several days to months following a bite of ring-shaped rash may occur anywhere on the body this is key they give you something that's talking about a ring shape rash you want to be thinking lime to these they have flu-like symptoms such as headache stiff neck muscle ache and fatigue the second stage occurs several weeks following the bite there'll be joint pain neurological complications and cardiac complications can occur and the third stage large joints become involved in arthritis progresses our nursing interventions are to remove the tick complete a blood test for diagnoses four to six weeks after the bite for reliability administer antibiotics teach patients to avoid Woody areas teach them to wear long sleeve tops and pants when outside and use tick repellent so then we have different types of immunoglobulins so we have immunoglobulin a this is gives us viral protection we have immunoglobulin D which has an unknown function immunoglobulin e is our allergy and parasitic infestation protection IGG is our secondary antibody protection and IGM is our primary antibody protection so now let's talk about a couple autoimmune diseases we've talked about some other ones in their specific systems that they're related to but we're going to talk about systemic lupus this is a chronic progressive systemic inflammation which causes the organs to fail the cause is unknown but it's thought to be genetic symptoms are a mylar rash on the face this is also called a butterfly rash this is a key point if you see this in a question the answer is most likely going to be lupus dry rash on the upper body fever weakness weight loss photosensitivity joint pain red Palms anemia they'll have a positive Ana blood test and an elevated ESR and C-reactive protein so our nursing interventions is we want to monitor for skin integrity mild soap on the skin frequent oil Oral Care high vitamin and iron diet can serve energy and avoid direct sunlight topical corticosteroids and monitor BUN and creatinine levels to watch for renal impairment because they do have that organ failure sclerodema so this is similar to lupus it causes inflammation fibrosis and sclerosis of connective tissue there is no cure patients will have pain stiff muscles pitting edema tight shiny thick and hard skin dysphagia and contractures for nursing interventions we want to encourage activity is tolerated maintain constant room temperature provides small meals eliminates spicy foods caffeine alcohol and we want to remember that renal crisis is a life-threatening complication and causes hypertension due to narrowing up the blood vessels going to the kidney assessments so regular kind of Vital Signs lab values so the first is our adult Vital Signs heart rate normally 80 to 100 respiratory 12 to 20 blood pressure 110 to 120 over 60 and temperature 98.6 or 37 degrees Celsius then when we talk about serum electrolytes so how I remember these is first we have potassium and when I think of potassium I think of bananas and when I go to the store and I buy a bunch of banana bananas there is between 3.5 and 5 bananas in a bunch and we want to make sure that we definitely remember potassium because when patients are outside of the normal range we can see cardiac irregularities it's really pretty much the most important electrolyte to be monitoring it's always our priority so it's really important we remember that so then when we talk about sodium so when I think of sodium I think of like fast food burger places like things that have a lot of sodium on French fries like salt I'm thinking salt like salty food so when you go to a place that has salty food you're going to spend around 13.50 to 14.50 so I remember it is 135 to 145 so that's just how I remember it but that's me you might find a different way then calcium so when I see calcium C-A-L I think call 9-1-1 it must just be the psych nurse in me um but when we call 9-1-1 that's very close to 8.5 to 10.5 so that's how I remember that then we have chloride so when I think of chloride I think of chlorine and I think of a pool and I personally only like to swim in a pool when it's really hot so like 95 to 105 degrees that's when I'll go swimming so that's how I remember that one then we have magnesium and I just remember that's 1.5 to 2.5 again you're probably not going to get a question about magnesium if you're going to get a question about electrolytes it's going to be sodium or potassium and then phosphorus is 2.5 to 4.5 now when we talk about blood values red blood cells 4.5 to 5 white blood cells 5 to 10 anything higher than this can indicate an infection neutrophils 60 to 70 lymphocytes 20 to 25 monocytes I'm not going to read through all of these but these are the labs you should know the big ones I would say you're not going to get asked on NCLEX about neutrophils and lymphocytes and monocytes you might get asked about red blood cells hemoglobin or hematocrit and white blood cells related to infection all right so then we have cardiac markers and the things that are important to know about this is troponin is very important you probably won't get asked about these other ones but you might get asked about troponin in relation to an MI okay and then acid-base balance so when we're figuring out acid base balance and we'll go over this a little bit later these are our normal values anything outside of this can indicate a problem and we'll go over how to do that in a little bit but a normal pH is 3.5 7.35 to 7.45 normal CO2 is 35 to 45 normal hco3 is 24 to 26 pao2 is 80 to 100 and sao2 is greater than 95 those are our normal values when it comes to chemistry values again these are our normal values for chemistry things that would make sure you definitely know for NCLEX is the glucose value so 70 to 110 is the normal probably aren't going to get asked anything on the rest of these but you may so they're good to know but I would definitely know the glucose anticoagulation therapy these I would know you may get a question about Heparin or Warfarin or something like that so PT normal is 20 to 36 seconds on heparin we want it to be 1.5 to 2 times the normal our PT 9 to 11 seconds and an INR of 0.9 to 1.8 but two to three if on warfarin and then our therapeutic drug levels things to know for NCLEX definitely the digoxin definitely the lithium levels I would say that's probably the need to know but you have the rest of these here to look at as well then also Vancomycin I would note that one adventitious lung sound so the different types of lung sounds you might hear when doing an assessment the first one is going to be crackles so these are fine short interrupted cracking sounds alveolar rails are high pitched sound can be stimulated by Rolling a lock of hair near your ear so if you take your hair and kind of crinkle it near your ear that's the sound that crackles will be it's best heard on inspiration but can be heard on both inspiration and expiration and can be cleared by a cough the sound comes from Air passing through fluid or mucus then we have gurgles or ronkai this is a continuous low pitched coarse gurgling harsh loud sound with a moaning or snoring quality the best heard on expiration and this is air passing through a narrow air passage as a result of secretion swelling or tumor then you might hear a wheeze so this is a continuous high-pitched squeaking musical sound that's the key if in the question they're asking you about a musical sound it's most likely going to be a wheeze heard on expiration not altered by coughing and this is air passing through a constricted bronchus as a result of secretion swelling or tumor then we have a plural friction rub this is a superficial grating or creaking sound heard during inspiration expiration this is comes from rubbing together of inflamed pleural surfaces then we have Strider this is a harsh high pitched that's the key word here breathing due to obstruction in the upper Airway and again that's from an obstruction in the upper Airway all right so let's talk about conversions these you definitely need to know you may get questions about this on NCLEX related to medication dose thing fluid balances if someone is on a fluid restriction how many cups of something can you give or weights or all of those things so important to know is that one one teaspoon is five ml one tablespoon is three teaspoons this is important to know you may get a medication question related to that also other ones that are important that one ounce is 30 ml that is important that one cup is eight ounces one kilogram is 2.2 pounds I'd probably say you should know that one gram is a thousand milligrams and those are probably the real important ones maybe that one pound is 16 ounces you might get something on that and one milligram is a thousand micrograms or 0.001 grams so make sure you know these because you may get questions related to medication dosing all right so medication calculations so the first one is going to be the amount to administer so we want to take the dose and put it over what we have and that's going to give us the amount to administer when so in order to do that we're going to plug in so XML so the amount to administer equals the unit dose over the unit concentration equals milligrams over milligrams then we can look at flow rate calculations so to do this we're putting the rate equals the amount of milliliters over per hour and our drip rate equals the ordered volume times the drip rate over time in minutes and then we have infusion time so infusion time is the total volume to be infused over milliliters per hour being infused and those are medication calculations and I can make another video on medication calculations if you guys want to go more in depth with this but again this is just a review so these are your medication calculation equations all right and that so we just went over in depth fluid and electrolytes this is a review that comes in the packet that was a free study guide that you can also get so you guys can put them together whatever you feel like is going to help you to add on to what we just talked about we have different types of fluids so the first type is called intravascular so this is a fluid inside a blood vessel and we have intracellular fluid inside a cell mostly bodily fluids are inside a cell and we have extracellular so this is fluid outside the cell which includes interstitial fluid between cells blood bone connective tissue and water then we have different types of solutions so we have an isotonic solution these are things like 0.9 normal saline D5W and lactated ringers they have no osmotic Force cells don't swell or Shrink then we have a hypotonic solution this is I like to think of it as lower than our isotonics of 0.45 normal saline or 0.33 normal saline and these have a lower concentration of salt which causes water to enter the cell we have to watch for edema with these then we have hypertonic so I like to think of these as higher than our isotonics so this is three percent normal saline 5 normal saline d10w D5W with one half normal saline D5 lactated ringers and D5 normal saline these are more concentrated Solutions so they have more solute than water and water is removed from the cell so the cells shrink then we have colloid so this is dextrin or albumin these are plasma expanders fluid moves from interstitial to intravascular compartment and this is given in severe hypovolemia patients with severe nausea and vomiting are at risk for electrolyte imbalances we want to keep that in mind now that we're talking about electrolyte imbalances so for electrolytes so let's talk potassium imbalance and we can remember the normal range of potassium as potassium is found in bananas so when you buy a bunch of bananas at the store you have between three and a half to five bananas per bundle so when we talk about hypo that means low so that's going to be anything less than 3.5 and when we talk hyper that's high so that's anything greater than five and those are our parameters so what are some things that we are going to see for hypokalemia cardiovascularly we're seeing a thready weak irregular pulse now if we look over to hyperkalemia we're actually seeing the same thing so that really isn't something that we should memorize because it's not going to be something that differentiates between the two now if you look also cardiovascularly again we're seeing a decrease of blood pressure for hyperkalemia and we're seeing orthostatic hypotension for hypokalemia pretty similar now when we talk about respiratory with hypokalemia we're seeing shallow ineffective respirations due to skeletal muscle weakness when we look at hyper we're seeing profound weakness of skeletal muscles leading to respiratory failure again these are pretty similar so let's keep moving on so neuromuscularly with hypokalemia we're seeing anxiety lethargy confusion and coma skeletal muscle weakness leg cramps loss of tactile discrimination paresthesis and deep tendon hypoflexia with hyperkalemia we're seeing muscle twitches cramps paresthesia and late we're seeing profound weakness ascending flaccid paralysis in arms and legs become affected when potassium levels become lethal okay so again we're seeing those paresthesias we're seeing loss of the tactile discrimination we're seeing muscle weaknesses and we're seeing deep tendon hypoflexia and flaccid paralysis of arms and legs so those are all pretty similar the one thing that really sticks out to me is muscle twitches and cramps for early signs of hyperkalemia so I would definitely memorize that that something different and because it's so specific the Deep tendon hypoflexia although that is similar to the muscle weakness and flaccid paralysis and things like that because it's so specific I would also memorize this for the hypokalemia so let's keep moving on so gastrointestinally for hypokalemia we're going to see decreased motility hypoactive bowel sounds nausea vomiting constipation abdominal distension and paralytic Ileus now if we look over gastrointestinally for hyperkalemia we're seeing increased motility hyperactive bowel sounds and diarrhea okay so here we go here is big difference number one okay so we want to memorize those gastrointestinal signs for hypo versus Hyper now the thing that makes this nice is that with Hyper everything is increasing we're having increased motility hyperactive bowel sounds and diarrhea things are moving with hypokalemia things are slowing down we have the hypoactive the nausea the paralytic ileus so things are really slowing down on the side and they're speeding up over here okay so when we talk about EKG changes there are some important things to remember here as well so we can see for hypokalemia we have shallow flat inverted T waves this is important because it's the opposite of the tall peaked T waves we're going to see in hyperkalemia so again the thing that is nice is hyper is going up hyper hypo is going down so this is easy to remember now we are also going to have a prominent u-wave in hypokalemia so just remember that one as well and you can remember that in hyperkalemia we're going to see those flat p waves a widened QRS and a prolonged PR interval so you want to definitely remember those EKG changes so let's talk about risk factors so anything that is hypokalemia is a potassium loss so remember we're low our K is low so this could be from an inadequate intake maybe they're fasting or NPO it could be potassium moving into the cell from hyper insulinism or alkalosis it could be a dilution of serum potassium maybe from IV therapy with potassium deficient Solutions or water intoxication when we're talking about hyperkalemia medications like ACE inhibitors NSAIDs potassium sparing diuretics can all increase our potassium excessive potassium intake can also increase it kidney disease or dialysis with decreased potassium excretion Addison's disease tissue damage acidosis hypergurcemia and hyper catabolism so another thing that really sticks out to me is hyperkalemia you're going to have acidosis and hypokalemia you're going to have alkalosis so that might be something important to remember those opposites now see if you're looking at this whole list and you're trying to memorize each side it's going to be really hard it's a lot of information so what we want to do is pick out the key differences and it may also be good to memorize that um hyperinsulinism is for hypokalemia or hyperuricemia and Hyper catabolism is for hyper kalemia all right so our nursing interventions we're talking about hypokalemia we're going to do oral potassium supplements liquid potassium chloride potassium retaining diuretics any of these whatever the doctor orders potassium is never administered by IV push IM or subcutaneous Roots IV potassium is always diluted and administered by an infusion device so make sure you know that if there's ever an answer that's asking you to give potassium IV push that is wrong hyperkalemia things we're going to do for our nursing interventions is Monitor EKG restrict potassium diet avoid salt substitutes discontinue IV or po potassium prepare potassium secreting diuretics prepare client for dialysis is going to bother me diuretics okay prepare client for dialysis prepare IV calcium gluconate and IV sodium bicarb and then just to remember foods with potassium because this might be something they ask you on NCLEX your patient is hyperkalemia which food would you not give them so foods with potassium avocado banana carrots fish oranges potatoes pork beef spinach and tomatoes and also just remember that potassium and sodium are the opposite and when we talk about sodium you will see that more the signs and symptoms are reversed okay now let's talk about a sodium imbalance so we're going to talk about hyponatremia which is a low sodium less than a hundred and thirty five and hypernatremia which is greater than 145. so when we have hyponatremia we're going to see low specific gravity and when we have hypernatremia we're going to see high specific gravity so let's look at the different signs and symptoms based on different systems within the body so in the cardiovascular system we'll talk about hyponatremia first so if someone is normovolemic meaning they have a normal amount of blood volume they'll have a rapid pulse with a normal blood pressure if they're hypovolemic meaning that they have a low blood volume there'll be a thready weak pulse hypotension flat neck veins and if they're hypervolemic you'll see a rapid bounding pulse with normal or elevated blood pressure they're going to have shallow and ineffective breathing but this will be a late sign you'll see skeletal muscle weakness and decreased deep tendon reflexes central nervous system you'll have headaches confusion seizure coma and personality changes gastrointestinal increased motility increased bowel sounds nausea abdominal cramps and diarrhea renal will be increased renal output and integumentary will be dry mucous membranes so again when we are looking at the signs and symptoms between hyponatremia and hypernatremia what we want to do is pick out the differences and that's what we want to memorize because if we get a question on it they're going to be asking about something that's different so if we look over at hypernatremia we can see heart rate and blood pressure will be dependent on vascular volume so not much to differentiate there respiratory we'll see pulmonary edema if hypervolemic so that is something different granted it's only if they're hypervolemic but again pulmonary edema neuromuscular will see muscle twitches irregular muscle contractions and then late signs will be muscle weakness and decreased deep tendon reflexes so we want to remember that if it's an early sign we're going to see those muscle twitches and muscle contractions those are things we're not going to see in hyponatremia central nervous system we're seeing altered cerebral function normal bulimia or hypovolemia you might have agitation confusion and seizures hypervolemia lethargy stupor coma so again all of those are very similar to hyponatremia so there's really no kind of differences to memorize we can remember that with hyponatremia we have shallow and ineffective breathing as a late sign that's important during testimony we'll have in extreme thirst so that is different so we want to remember that and then if we come over to hyponatremia we can see increased motility bowel sounds nausea abdominal cramps and diarrhea so again this is different so those GI symptoms are are very different so knowing those again here's a big one to know the difference so renal if it's hypernatremia we're having decreased output but if it's hyponatremia we're having increased output so that might be something you're asked about and integumentary dry and flush skin dry sticky mouth and mucous membranes and edema so the dryness is the same for both but the difference is you might see edema so memorize that so let's talk about risk factors so with hyponatremia your risk factors include increased sodium excretion this could be from diaphoresis like a high fever diuretics like Loops or thiazides diarrhea vomiting drains and G-tube suction and decreased excretion of aldosterone you can have s-i-a-d-h adrenal insufficiency inadequate sodium intake from fasting or NPO kidney disease or heart failure when it comes to risk factors of hypernatremia could be increased sodium intake oral sodium intake IV fluids with sodium hypertonic IV Solutions or loss of fluids through fever diarrhea diabetes insipidus excessive sweating and infection so important things to know is for diabetes insipidus you're going to see the hypernatremia and for s-i-a-d-h you'll see the hyponatremia as well as adrenal insufficiency and kidney disease and also knowing increased sodium intake is going to give you hypernatremia which would make sense because it's too high and increase sodium excretion is going to give you hyponatremia because it's too low so what are our nursing interventions for hyponatremia we're going to administer IV sodium chloride we'll give diuretics if it's due to hypervolemia because remember there's too much fluid in the vascular system it's diluting the blood essentially and making you hyponatremix so that's why if we give diuretics we can get rid of some of that fluid and come back to a normal amount of sodium daily weight safety orthostatic hypotensions because they're at risk for fall Airway protection and po of lethargic limbic water intake if hypervolemic and teach about foods that contain salt for hypernatremia if due to fluid loss we'll administer IV because if you're losing fluid that means that there's an increased amount of sodium in your blood because there's less fluid if due to an adequate renal excretion give diuretics that increase sodium loss and restrict sodium and fluid intake per order foods with sodium are bacon butter canned food cheese milk condiment salt and bread and potassium and sodium are opposite so usually when our potassium is high our sodium is going to be low and vice versa all right so let's talk about calcium imbalances so we have hypocalcemia Which is less than nine in hypercalcemia which is greater than 11. and the way I remember these numbers is when I think calcium I think call and call 911 so that's how I remember that but so signs and symptoms so again we're looking for differences so for hypocalcemia we're seeing a decreased heart rate decreased blood pressure and decreased peripheral pulses so this right here decreased heart rate that is a key point because if we come over to hypercalcemia we can see that there's an increased heart rate at first and then it does turn into bradycardia when we look at oh calcimia we're seeing decreased peripheral pulses but when we look at hypercalcemia we're seeing bounding now let's talk about neuromuscular so for hypocalcemia we're seeing irritable skeletal muscles twitching cramps tetany and seizures so this is a big thing because if we look over at hypercalcemia we're seeing profound muscle weakness decrease deep tendon reflexes so again they're the opposite hypocalcemia we're gonna have Painful muscle spasms in calves or feet during periods in activity paresthesia followed by numbness may affect the lips nose ears and limbs increase deep tendon reflexes anxiety irritability so these neuromuscular signs are really important to note because they're different when it comes to gastrointestinal same thing very important to know because they're the opposite with hypocalcemia we're seeing increased motility bowel sounds abdominal cramps diarrhea with hypercalcemia we're seeing decreased motility in bowel sounds this is important and the big thing to know is that there's something called trussos and chovistuk sign for hypocalcemia because everything is going up increase deep tendon reflexes increase motility increase bowel sounds Twitches cramps tetanis seizures all of that increase of those symptoms is going to give you something called a positive truso sign which is a carpal spasm induced by inflating a blood pressure cuff above the systolic pressure for a few minutes so you put a cuff on the patient's arm you pump it up and they're going to have a carpal spasm of their like a positive stuck sign is contraction of the facial muscle in response to a light tap over the facial nerve in front of the ear so that is important to know EKG changes we're going to see so for hypocalcemia we can see prolonged St interval and prolonged QT interval for hypercalcemia we see a shortened ST segment and a widen T wave risk factors for hypocalcemia include inhibition of calcium absorption in the GI tract increase calcium excretion through wound drain diarrhea steaturia kidney disease if they're in the diuretic phase and conditions that decrease the ionized fraction of calcium for hypercalcemia our risk factors include increased calcium absorption decreased calcium excretion kidney disease thiazide diuretics hyperparathyroidism and hyperthyroidism malignancy leading to Bone destruction from tumors and hemoconcentration our nursing interventions for hypocalcemia or to give calcium supplements either po or IV administer vitamin D and aluminum hydroxide initiate seizure precautions and consume foods high in calcium our nursing interventions for hypercalcemia or to DC the thiazide diuretics or ivpo calcium EKG is a neurostatus monitoring Loop Diuretics encourage fluids and restrict dietary calcium and a patient with a calcium imbalance is at risk for fractures so move the client carefully and assist with ambulation foods with calcium include cheese milk spinach yogurt tofu sardines and greens and calcium and phosphate are opposite so if calcium is high phosphate will be low okay so let's talk about magnesium and balance so we have hypomagnesemia Which is less than 1.3 and we have hyper magnesemia which is 10.5 or higher so again we're looking for differences so for hypomagnesemia we look at the cardiovascular so this is important because we have tachycardia and hypo and hypertension when we go over to hypermagnesemia we have bradycardia and hypotension so they're opposites so that's important to know now if we look at respiratory for hypomagnesemia we have shallow respirations and for hyper magnesemia we have respiratory insufficiency when the skeletal muscles of respirations are involved okay not many differences we go back to hypomagnesemia we're seeing neuromuscularly Twitches paresthesia's positive trusos and chovistox sign hyper reflex stevia tetany and seizures so these are all important because these are different than hyper magnesemia which is going to have diminished or absent deep tendon reflexes and skeletal muscle weakness in the central nervous system of hypomagnesemia we're seeing increased motility and hyperactive bowel sounds and abdominal cramps so this is the GI system so this is important to know because again it's something different important fact is calcium gluconate is the antidote for a magnesium overdose so when we look at EKG changes we can see tall T waves in depressed St segments for hypomagnesemia and for hypermagnesemia we can see shortened T waves and white shortened St segments in a widened T if you don't need to memorize the EKG changes most likely you won't be asked about that but you will be asked about signs and symptoms risk factors for hypomagnesemia is insufficient magnesium intake they could be malnourished have celiacs or Crohn's disease vomiting or diarrhea increased magnesium excretion through diuretics alcoholism hyperglycemia and Insulin Administration or sepsis for hypermagnesemia they can have increased magnesium intake from antacids or IV magnesium they can be in dka or have renal insufficiency so they have decreased excretion of magnesium our nursing interventions for hypomagnesemia is magnesium sulfate IV or po seizure precautions and increasing magnesium containing foods which are avocado leafy greens milk wheat peanut butter pork beef chicken potatoes and yogurt for hypermagnesemia we're going to give diuretics IV administration of calcium gluconate because we know that's the antidote or strict intake of magnesium-containing foods avoid laxatives or antacids that contain magnesium and hemodialysis and magnesium and calcium are the same so when we have a high calcium we also have a high magnesium all right let's talk about a phosphorus imbalance so we have hypophosphatemia Which is less than 2.5 and we have hyperphosphatemia which is greater than 4.5 again we're looking for differences so cardiovascularly hypophosphatemia will see decreased contractility and cardiac output with slowed peripheral pulses for hyperphosphatemia we'll see an increased heart rate early but then it will turn to bradycardia that can cause cardiac arrest and will have a bounding full peripheral pulse so that is a difference we can remember that with respiratory hypophosphatemia and hyperphosphatemia both have shallow respirations and ineffective respiration so not much different there when it comes neuromuscularly again we're not seeing huge differences Rhabdomyolysis in hypophosphatemia but they're both kind of showing absent or diminished deep tendon reflexes weakness so not much there to remember but we will see in hypophosphatemia those central nervous system changes like irritability confusion and seizures so that's important to know and then in hyperphosphatemia we'll see some gastrointestinal signs of decreased motility and hyperactive bowel sounds risk factors for hypophosphatemia or glucose Administration or insulin release respiratory alkidosis milk absorption syndrome diarrhea vomiting aldosterone ISM and diuretic therapy and risk factors for hyperphosphatemia or renal disease hypoparathyroid or hyper thyroidism excessive vitamin D intake muscle necrosis excessive phosphate intake and chemotherapy nursing interventions for hypophosphatemia are neurological assessments and phosphate supplements as prescribed and for hyperphosphatemia assessed for signs of hypocalcemia teach patients to avoid foods and medications with phosphorus administer phosphorus binding antacids and prepare patient for possible dialysis foods with phosphorus include fish pumpkin nuts pork beef chicken whole grains and dairy and calcium and phosphate are opposite so if we have high calcium we'll usually have a low phosphate we just went over in depth with the free electrolyte study guide but within this study guide you have a more briefer overview of the main points of electrolytes I'm not going to go through all this again I included the electrite but this is here in a less colorful form so you can review these and again making sure to know what foods these are in so let's talk about electrolyte relationships so sodium and potassium have an inverse relationship so a high sodium means that you're going to have a low potassium calcium and phosphorus have an inverse relationship so a high calcium is a low phosphorus and magnesium and phosphorus have an inverse relationship so low magnesium high phosphorus calcium and vitamin D are the same so a high calcium means a high vitamin D magnesium and calcium are the same so a low magnesium you're also going to see a low calcium and magnesium and potassium are the same so a low magnesium can also mean a low potassium and again here are just a review of those electrolytes okay let's talk about acid-base balance so we have two different manifestations so we have acidosis and alkalosis now within each manifestation it can be respiratory or metabolic it can be respiratory or metabolic so these are the signs and symptoms we're going to see so first let's talk about acidosis if it's a respiratory acidosis we're going to see drowsiness disoriented dizzy headache or coma and if it's a metabolic acidosis we're also going to see drowsiness confusion headache and coma if we come over to alkalosis for neurological lethargy lightheadedness confusion metabolic drowsiness dizziness not nausea confusion so all of these are very similar so you don't need to go through each one and remember respiratory I'm going to see this for acidosis metabolic I'm going to see this for acidosis because you're really seeing the same thing for almost all of these we want to look at the differences so one thing I see is metabolic alkalosis nervousness so that might be a key thing to remember I'm also seeing that for acidosis we may see a headache for both metabolic or respiratory so that might be something to just remember but now let's move down so cardiovascularly for respiratory acidosis we're seeing decreased blood pressure dysrhythmias warm flushed skin for acidosis metabolic we're seeing decreased blood pressure dysrhythmias warm flesh skin again same symptoms so okay we don't have to really remember the differences with those if we come over to alkalosis and we look at respiratory alkalosis we're seeing tachycardia dysrhythmias for metabolic alkalosis we're seeing tachycardia and dysrhythmias Okay so we can see with this one that how we can differentiate it is with acidosis we're seeing a decreased blood pressure and dysrhythmias so the main thing is the decreased blood pressure for acidosis both it could be either right this isn't differentiating between respiratory and metabolic but we're seeing decreased blood pressure when it comes to alkalosis the real difference that we're seeing is the tachycardia and we could see that for metabolic or respiratory so let's just remember that okay so let's move along so for respiratory acidosis we're seeing no GI symptoms for metabolic acidosis we're seeing nausea vomiting and diarrhea okay so that's important to know that those are some differences now when it comes to gastrointestinal for Respiratory alkalosis we're seeing nausea and epigastric pain when it comes to metabolic alkalosis we're seeing anorexia nausea and vomiting so just this is supposed to say vomiting vomiting okay there we go I will fix that in the study guide we can see that the difference a key thing is with respiratory alkalosis epigastric pain okay so let's remember that epigastric pain okay so now let's move along to respiratory acidosis so we're going to see neuromuscular we're going to see seizures that's important so remember that and then for metabolic acidosis we have no neuromuscular symptoms for Respiratory alkalosis we're seeing tetany numbness tingling of extremities hyper reflexia and seizures so we need to remember all of these right tetany numbness and tingling hyperreflexia so this one is a key for Respiratory alkalosis specifically right we don't see that for any of the other ones and again if we come over to alkalosis metabolic we again have those Tremors hypertonic muscles muscle cramps technique tingling seizures so these are the same so just noticing that alkalosis you're having a lot of those neuromuscular symptoms all right so moving along respiratory acidosis for Respiratory is going to be hypoventilation with hypoxia very important this is different than our metabolic acidosis which is going to have deep rapid respirations or kuzmals so these are different so remember those for alkalosis respiratory we're having hyperventilation again this is different so remember this one and for metabolic alkylosis we're seeing hypoventilation so you want to remember all the differences in respiratory for these you can see a significant difference for respiratory acidosis the causes are asthma electasis brain trauma central nervous system depression pulmonary edema COPD and hypoventilation for metabolic acidosis or causes or diabetes excessive ingestion of acetacilic acid high fat diet malnutrition and diarrhea for Respiratory alkalosis our causes our fever hypoxia hyperventilation pain and Hysteria and for metabolic alkalosis are causes our diuretics vomiting hyper aldostronianism ingestion of sodium bicarb and a massive transfusion of blood our nursing interventions for respiratory acidosis are monitor signs of respiratory distress administer oxygen place them in semi-fowlers turn cough deep breathe and hydrate to thin secretions for metabolic acidosis or nursing interventions include monitor for respiratory distress assess level of Consciousness monitor Ino monitor potassium and if diabetic ketoacidosis give insulin for Respiratory alkalosis our nursing interventions are to monitor for science respiratory depression emotional support assists with breathing techniques and monitor electrolytes in our nursing interventions for metabolic alkalosis our monitor signs of respiratory distress monitor abg's potassium and calcium IV medications and replace potassium all right now let's talk about interpreting arterial blood gas results so key points in acidosis the pH is decreased less than 7.35 in alkalosis the pH is elevated greater than 7.45 respiratory function indicator is the CO2 and a metabolic indicator is the hco3 okay so important to note that we know that a normal pH is 7.35 to 7.45 so if we go below that we're in acidosis and if we go above that we're in alkalosis okay so again here's our normal values over on the right side for all of these the thing that's nice is our pH is 7.35 to 7.45 and our CO2 is 35 to 45 so it's the same hco3 is 24 to 26 so you do have to remember that and our pao2 is 80 to 100 we know that and our sao2 is greater than 95. okay so let's talk about the steps to interpret arterial blood gases so step one we're going to look at the pH so this is Step One is it high or low and again we just talked about if it's low it's acidosis if it's high as alkalosis okay step two look at the CO2 is it high or low what is the relationship to pH so we can so opposite relationship one is high and the other is low means a respiratory imbalance a same relationship both high or both low go to step three so a way to remember this is something called Rome and this stands for Respiratory opposite metabolic equal okay so if it's opposite it's respiratory if it's the same we're going to go on to step three most likely metabolic but there is there is a thing that it is not always metabolic all right so we're going to look at the hco3 and what the relationship is to the pH so if it's the same both low or both high it's a metabolic imbalance all right so let's move on to step four so if the pH is normal but other things are not normal it could be due to something called compensation and that means that the body adjusts and compensates with other things to make the pH normal so partially compensated is if the pH is not normal we look at the system that is supposed to fix the problem so if the condition is a respiratory imbalance look at the state of hco3 to determine the state of compensation if the condition is a metabolic imbalance look at paco2 to determine the state of compensation what this means in a equation format is that a low PH plus a high CO2 respiratory acidosis because we have a low PH we know it's acidosis and we have a high CO2 so we know that it's respiratory a low PH plus a low hco3 is metabolic acidosis so again we are looking at because we know that if we follow Rome respiratory opposite so we can see low and high is opposite and then a low and low is equal so metabolic equals we have a metabolic acidosis if we have a high pH and a low CO2 we're opposite right low and high so we know it's respiratory alkalosis and a high pH plus a high h CO3 we know metabolic equal so we know metabolic is equal so it's metabolic alkalosis all right let's look at pharmacology so this is a pharmacology review this is a very kind of brief overview of different meds we learned in nursing school if you want a more in-depth overview something you can make flash cards with and really study these medications I recommend getting the pharmacology study guide that you can actually print out different flash cards and things like that but this is going to be an overview of you're getting ready to take your exam you don't want to study like a hundred note cards Etc or 50 pages of information so this is a six page pharmacology summary all right so first we have antacids so these decrease gastric acidity protect the stomach mucosa and decrease epigastric pain the mechanism of action is that it binds to excessive acids drugs include magnesium aluminum hydroxide or maglocks our side effects we're looking for are constipation due to the aluminum or diarrhea if it is a magnesium form nursing interventions of food avoid food that cause GI distress and don't overuse then we have anti-diarrheals so these decrease diarrhea mechanism of action is that it decreases motility causes more water to be absorbed by the large intestines drugs include lomatil and Imodium side effects include tachycardia respiratory depression urinary tension dry mouth respiratory depression nursing interventions include monitor fluids and electrolytes then we have antibiotics so these decrease or destroy microorganisms mechanism of action depends on the class of drugs so we have no glycosides these decreased protein synthesis things like Gentamicin we have cephalosporins which bind to the cell while causing death these are things like cefazolin we have fluoroxicinals which decrease DNA synthesis things like Cipro we have a macrolids which decrease protein synthesis things like cithromax we have penicillins which bind to the cell wall and cause death things like amoxicillin we have sulfonamides which decrease protein synthesis things like vibramycin and we have anti-infectives which decrease protein and DNA synthesis and these are things like Flagyl our side effects include hypersensitive reaction rash or anaphylaxis in our nursing interventions include culture insensitivity should be done before initiating antibiotic therapy and teach the patient to take entire prescription monitor for hepatotoxicity and nephrotoxicity all right now let's talk about anticoagulants so these interfere with normal coagulations leading to decrease in thrombus formation or extension mechanism of action depends on the type we're using again so we have thrombin Inhibitors which decrease conversion of prothrombin to thrombin and conversion of fibrin to fibrin fibrogen to fibrin thing these are things like heparin low molecular weight heparins block coagulation Factor XA these are things like fragment or Lovenox and we have clotting Factor Inhibitors these interfere with vitamin K synthesis these are things like Warfarin and we have platelet Inhibitors which decrease platelet aggregation and things are these are things like Plavix so our side effects include excessive bleeding bruising Molina which is dark stools that have blood in them epistaxis which is a bloody nose bleeding gums low hemoglobin thrombocytopenia our nursing interventions are to monitor PT PT INR and monitor for bleep all right then we have antiemetics these decrease nausea and vomiting and prevent and decrease motion sickness mechanism of action is a 5-ht3 antagonist which blocks serotonin at the receptor site in the vagal nerve Terminals and chemoreceptor Trigger zones in the central nervous system these are drugs like ondansetron or Zofran side effects include headache dizziness constipation diarrhea and our nursing intervention is to give 30 to 60 minutes before chemotherapy and to teach the patient to avoid alcohol then we have antifungals these decrease fungal growth it does this through the impairing the fungal plasma membrane drugs include mycilex and neostatin side effects we look for renal liver and autotoxicity it can be teratogenic nausea vomiting and diarrhea nursing interventions include teaching the patient to complete the entire regimen then we have analgesic or antipyuretics and NSAIDs the mechanism of action again depends on the drugs so we have analgesics they inhibit prostolic landins involved in pain and fever these are things like Tylenol then we have NSAIDS which inhibit prostaglandins involved in inflammation pain and fever these are things like ibuprofen or naproxen side effects we're looking for hepatic toxicity rash tinnitus and flu-like symptoms nursing interventions it's important to know that you do not exceed 4000 milligrams of Tylenol per day monitor for GI bleeding and avoid alcohol then we have anti-alzeimer's medications these decrease signs of dementia mechanism of action is increasing acetylcholine levels drugs include dinopazil and glantamine side effects are anorexia nausea vomiting headache dizziness insomnia in our nursing interventions are to teach the patient and family that this medication is not a cure and use caution and COPD patients then we have antidepressants so these are going to lift a depressed mood their mechanism of action depends on the type so we have tcas which decrease the reuptake of norepinephrine and serotonin in the presynaptic nerve terminals these are things like Elavil or Pamelor we have ssris which decrease reuptake of serotonin in the presynaptic nerve terminals these are things like Celexa Prozac Paxil and Zoloft we have maois which decrease the breakdown of norepinephrine dopamine and serotonin these are things like Nardo and we have atypicals which increase the effects of dopamine serotonin norepinephrine these are things like buprenorphine Remeron or Effexor if you guys want a more detailed overview of antidepressants I do have a whole discussion on that on the YouTube channel so side effects include anticholinergic effects sexual dysfunction dizziness headache weight gain increased appetite our nursing interventions are to assess for suicidal ideation high risk because medications give patients more energy to commit the ACT medications need to be used for two to six weeks to start to see the effects monitor for serotonin syndrome these are going to be things like the patient is really hot they have dilated pupils do not stop the medication abruptly and for tcaas do not give to a patient with narrow angle glaucoma and for maois avoid food with tyramine so this one is very important all right let's talk about anti-dis rhythmics so these decrease abnormal electrical conduction in the heart mechanism of action again depends on the drug so class 1 calcium ion antagonist the slow conduction used for ventricle dysrhythmias these are things like procambid or lidocaine we have class 2 beta adrenergic blockers which decrease cardiac excitability output and workload decreases heart rate and blood pressure things like metoprolol class three we have potassium channel blockers these slow the heart rate and conductions used for ventricular and superventricular dysrhythmias things like ambryodiorone in class 4 we have ccbs so decrease entry of so these are calcium channel blockers decrease entry of calcium into the myocardial cells decreases sa and AV node conduction and used for afib and SVT these are things like Verapamil and side effects include heart failure hypotension anticholinergic effects diarrhea and new dysrhythmias and our nursing interventions are to monitor heart rate before administering and do not give if heart rate is less than 60. this is very important you may get a question about that so now let's talk about antihistamines so these decrease the sign of an allergies they do this by blocking histamine and decreasing allergic reactions side effects include dry eyes and mouth constipation blurred vision and sedation are nursing interventions are that they're contraindicated in narrow angle glaucoma and we want to administer with food to decrease GI irritation gum or hard candy can help with a dry mouth then we have antihypertensives so these decrease blood pressure their mechanism of action depends on the type so we have ACE inhibitors these decrease the release of aldosterone which increases the excitation of sodium and H2O these are things like enelopril lisinopril or Ramipril so a lot of these end in Prill then we have calcium channel blockers which these cause relaxation dilation of vascular smooth muscle of coronary arteries these are things like amylodipine dilatism nifedipine a lot of these end in peens some of them don't though sleep out of this one angiotensin two receptor blockers these decrease vasoconstriction and decrease the release of aldosterone these are things like Avapro losartan Valsartan a lot of these end in sartin that's how you can remember these then we have beta blockers and we have selective which blocks stimulation of beta 1 myocardial receptors these are things like metroprolol a lot of beta blockers end in Lull we also have beta blockers non-selective which block stimulation of beta1 and beta2 so this is pulmonary receptors and myocardial and these are things like carvedol or label law side effects include dizziness weakness flushing and bradycardia nursing interventions is that abrupt withdrawal can lead to hypertension into rhythmias we don't want to abruptly stop them we want to assess for increased fluid volume monitor blood pressure and heart rate then we have anti-lipidemic these decrease LDL triglycerides and total cholesterol and they increase HDL which is the good cholesterol mechanism of action depends on the type so we have an HMG COA reductase inhibitor which inhibits this hmgcoa enzyme which is a catalyst in the synthesis of cholesterol these are things like atorvostatin Razo Statin and simvastatin and a lot of these again and in Statin then we have bile acid sequestrins so these bind to cholesterol inhibit absorption of cholesterol in the small intestines these are things like cholesteriamine and easy Tim eBay sorry I don't know how to say all of these side effects include nausea vomiting abdominal cramps diarrhea consterpation and nursing interventions are they need to avoid grapefruit juice with HMG coase reductase Inhibitors because it will increase toxicity all right now we have antineoplastics these destroy and decrease the growth of neoplastic cells mechanism of action depends on the type so we have alkaliding agents with decreased DNA synthesis and prevent replication things these are things like carboplatin or cisplatin we have antimetabolics which decrease DNA synthesis and Metabolism these are things like ferox uracil or methotrexate are side effects include renal GI and skin problems nephrotoxicity autotoxicity and alopecia our nursing interventions are to teach patients about alopecia as a side effect do period blood tests throughout to monitor their levels protect patients from infection and provide frequent meals these are immunosuppressives all right then we have anti-parkinson's drugs these balance dopamine and acetylcholate mechanism of action depends on the drug types we have a dopaminergic which increases dopamine these are things like amantidine bromocystopine and Carbidopa levodopa then we have anticholinergics which decrease excessive cholinergic activity these are things like Cogentin our side effects are hypotension increased heart rate fatigue nausea vomiting dry mouth constipation muscle twitching can be a sign of toxicity nursing interventions do not strap abruptly and it can cause a parkinsonian crisis if you stop them abruptly we have antipsychotics these decrease hallucinations psychotic symptoms and decreased agitated Behavior mechanism of action again depends on the type we have typical for positive symptoms like Haldol or pro-chlorpazine then we have atypicals which are for negative symptoms and positive symptoms these are things like clozarils like Praxis Seroquel and Risperdal side effects we're looking for extra pyramidal side effects so these are things like dystonias acostisias parkinsonian symptoms tardive dyskinesia sedation hypotension sexual dysfunction and anticholinergic effects are nursing interventions is that it can take two weeks to see results increase fluid and fiber to avoid constipation avoid caffeine monitor for those extra perimetal symptoms and give meds to help with those extrapyramidal symptoms we can give things like Cogentin then we have anti-sacredatory agents these decrease gastric acidity and improve pain mechanism of action depends on the type we have H2 antagonists which decrease histamine of the H2 receptor and the paretal cells and decrease gastric secretions these are things like Pepcid or Zantac we then have proton pump inhibitors which decrease the entry of hydrogen ions in the gastric Lumen these are things like Prilosec Prevacid and Protonix side effects or confusion dizziness drowsiness headache nephrotoxicity and our nursing interventions are to administer one to two hours before or after antacids they may increase anticoagulant effects of Warfarin and do not Crush proton pump and now we have anti-seizure medication so these decrease the severity frequency and occurrence of seizures mechanism of action depends on the type some of them will block sodium channels inhibiting Action potentials these are things like tegatrol or phenotoin then we have analog of Gaba but does not act on the Gaba channels mechanism of affection is unknown these are things like Gabapentin then we have another one that blocks sodium channels and high voltage dependent calcium channels like Lamictal or Topamax for Capra our mechanism is unknown but used for focal onset myoclonic and tonic colonic seizures phenobarbital enhances the inhibitory effect of gaba-mediated neurons and valproic acid block sodium channels Gaba Channel trans ammonase and T-Type calcium channels side effects we're looking for include dizziness drowsiness nausea vomiting headache hypertension respiratory depression things we want to look for that are important to know so phenotoin we want to look for Ataxia and gingival hyperplasia nursing interventions include dose graduate increased dose gradually provide Oral Care avoid Alcohol and Other CNS depressants and do not abruptly stop as it can lead to seizures the next one is anti-tubu tuber anti-tubercular so these are used in tuberculosis they decrease cough fever and night sweats mechanism of action is to decrease mycobacterial cell wall synthesis drugs are isonozide Rifampin ethambutyl side effects or peripheral neuropathy hepatotoxicity diarrhea and optic neuritis nursing interventions are to avoid aluminum containing antacids for one hour before or after medication dose and educate patients that Rifampin will produce orange colored urine this is important to remember all right then we have antivirals so these prevent or decrease the severity of a viral infection through decreasing viral DNA synthesis or entry of the virus into the host drugs are Tamiflu or acyclovir side effects anorexia nausea vomiting diarrhea headache vaginitis nursing interventions are culture and sensitivity needed before giving medications then we have analytic sedatives and hypnotics these decrease anxiety help with sleep and ease alcohol withdrawal our mechanism of action depends on the type so we have diazepines which increase the action of Gaba inhibitory neurotransmitter we have short acting like Xanax medium acting like Ativan and long-acting like Librium clonazepam or diazepam then we have non-barbituates which CNS depressant effect so these are things like Buspar Benadryl or Ambien side effects include decreased mental alertness hypotension dizziness headache Euphoria nursing intervention are benzodiazepines can create dependency and to avoid alcohol and caffeine then we have bronchodilators so these promote bronchial expansion allow for gas exchange and decreased shortness of breath mechanism of action depends on the type we have xanathines which relax bronchial smooth muscle and decrease spasms like Theophylline we have anticholinergic so to decrease the action of acetylcholine receptors and bronchial smooth muscles so like atrovent we have leukotirene or separate antagonists so these decrease edema bronchioconstriction and inflammation these are things like Singulair we have inhaled steroids which decrease local inflammation response and edema increase Airway diameter things like pulmicort or flow vent side effects include increased heart rate decreased blood pressure palpitations dizziness headache weakness dry mouth urinary retention nursing interventions use bronchodilators first then wait one to five minutes between inhalers rinse mouth after use and encourage fluid intake to avoid dry mouth so this is important inhalers and rinse the mouth okay now we have cardiac glycosides so these increase the force of contractions decrease heart rate and increase cardiac output mechanism of action inhibits sodium increases cardiac intracellular calcium increases myocardial contractility these are things like digoxin side effects are low heart rate drowsiness fatigue and weakness nursing interventions include give a loading dose first assess atypical pulse before giving medications heart rate must be greater than 60 so this you may be asked if you're giving a patient on digoxin about their heart rate has to be above 60. the therapeutic range is 0.5 to 2 and first signs of toxicity are usually GI related it's important too so then we have cardiac stimulants so these increase heart rate they stimulate Alpha and beta receptors to increase the heart rate and contractility these are drugs like atropine sulfate dobutamine norepinephrine or ephedrine or epinephrine side effects are dysrhythmias increased heart rate headache anticholinergic effects nursing intervention are continuous EKG when giving them IV then we have coronary vasodilators so these dilate arteries decrease preload and after load decrease myocardial oxygen consumption mechanism of action they block calcium channels and relax smooth muscles to treat angina and hypotension drugs are things like amlodipine Procardia nitroglycerin Verapamil side effects or orthostatic hypertension increased heart rate headache dizziness nausea vomiting flushing and our nursing interventions are to wear gloves when we put it on put oral Nitro under the patient's tongue and avoid sudden standing then we have diuretics this urine output decrease hypervolemia and decrease blood pressure decrease edema and decrease intracranial pressure mechanism of action depends on the type we have thiazide which decreases sodium and chloride reabsorption in the distal convoluted tubule and decrease chloride reabsorption in the loop of henle these are things like Hydrochlorothiazide or metrolozone then we have Loop Diuretics which decrease sodium and chloride reabsorption in the ascending Loop of henle and distal tubules these are things like Lasix or vumix we have potassium sparing these in the distal tubules decrease action of aldosterone sodium is excreted but it retains potassium these are things like ldactone so this is important to know what is a potassium sparing specifically and then what is not because you may get a question about that side effects are things like dehydration or the static hypotension decreased potassium except with potassium sparing fluid and electrolyte imbalance nursing interventions we want to monitor potassium levels given the morning due to patients urinating it could keep them up at night and change positions slowly then we have hypoglycemics so these mechanisms of action depends on the type so we have sulfon ureas which stimulate beta cells to release insulin these are things like amaril Glipizide Glyburide then we have bigger rides which increase sensitivity to insulin increases binding of insulin at the receptor these are things like metformin and then we have meglotides which increase the release of insulin in the pancreas and these are things like reproglenide side effects are hypoglycemia nursing interventions are contraindicated in type 1 diabetes and monitor for hypoglycemia then we have laxatives which relieve constipation mechanism of action depends on the type we have bulk forming which increases the bulk and stimulates peristalsis these are things like spillium we have stool softeners which water and fat enter the feces to soften and decrease drying of stool these are things like Colace we have stimulants which can irritate these are a rapid propulsion of continents so these are things like duralax or Senokot and then we have saline osmotic which draws water in and stimulates peristalsis these are things like milk of magnesia and sodium phosphate Fleet side effects are cramps fluid and electrolyte imbalances nursing interventions is is contraindicated if vomiting nausea or abdominal obstruction we want to give it bedtime encourage fluids and saline osmotic is the most rapid acting then we have opioids so these decrease transmission of the pain impulse mechanism of action is combined with opioid receptors in the CNS drugs are codeine fentanyl hydrocodone Hydromorphone methadone morphine oxycodone side effects is they decrease the respiratory rate they can cause sedation constipation nausea drowsiness nursing interventions are to monitor for respiratory depression and have naloxone available which is Narcan and it is the reversal agent and we have opioid antagonists so these reverse opioid induced respiratory and CNS depression mechanism of action is to deep place opioids at recept respiratory receptor site by a competitive antagonism drugs is naloxone or Narcan so that's what we were just talking about um side effects or nausea vomiting and v-fib nursing interventions are monitored for opioid withdrawal if given for patient with pain all of pain relief will be reserved reversed and patient will feel pain so just be prepared for that if you would like a copy of the study guide you can find it on my website blot them with jessica.com