1/27/25
Alimentary canal begins in the mouth
Digestive process:
* Ingestion
* Physical digestion mastication (chewing)
* Chemical digestion: enzymes
* Propulsion: swallowing
Mouth:
* Teeth - used in mastication
* Tongue - synthesizes and secretes enzymes; will also position food into bolus
* Salivary glands - synthesizes and secretes saliva (ions, glycoproteins, enzymes, waste products, water, lysosomes) helps maintain pH of 7 in the mouth and helps lubricate the bolus
Enzymes produced in mouth:
1. Salivary amylase: breakdown of starch and glycogen
1. Synthesized and secreted by salivary glands
2. Active in mouth, pharynx, and esophagus
3. Inactive in the stomach
2. Lingual lipase: breakdown of lipids
1. Synthesized and secreted from tongue
2. Inactive in mouth, pharynx, and esophagus
3. Active in the stomach
What type of digestion occurs in the mouth?
* Chemical and mechanical!
* Chemical: salivary amylase
* Mechanical: mastication
Pharynx and esophagus
* Pharynx: area where both air and food travels
* Esophagus: moves only food
* Upper esophageal sphincter: smooth muscls that controls movement of bolus into esophagus
* Upper ⅔ of esophagus composed of smooth muscle (involuntary) and skeletal muscle (voluntary)
* Lower ⅓ of esophagus composed of only smooth muscle (involuntary)
* Lower esophageal sphincter: prevent stomach juices (highly acidic) from entering esophagus
After the esophagus, what is the next part of the alimentary canal?
Stomach!
Stomach:
Regions:
* Fundus: top part
* Body: middle part
* Pylorus: last part
Other structures:
* Rugae: folds that allows stomach to expand
* Pyloric sphincter: controls the movement of chyme into small intestine
* Surface mucus cells: cover stomach, synthesize and secrets alkaline mucus to protect surface of the stomach
* Gastric pits: connects stomach to gastric glands
Cells in the gastric pits:
* Parietal cells: s/s HCl - kills microorganisms; also s/s intrinsic factor (molecule needed for B12 absorption)
* Mucus neck cells: s/s mucus - function is unknown!
* Chief cells: s/s pepsinogen (inactive form of pepsin (protease - digest proteins))
* Enteroendocrine cells: s/s hormone (ex: G cells s/s gastrin (hunger…))
What digestive processes occur in the stomach?
Propulsion: peristalsis and gastric emptying
Mechanical digestion: gastric mixing
Chemical digestion: pepsin (proteins), lingual lipase (lipids), gastric lipase
NO absorption happens in the stomach!
Match cell with what it produces:
Surface mucus cells: Alkaline mucus
Parietal cells: Hydrochloric acid (HCl)
Chief cells: Pepsinogen
Enteroendocrine cells: Gastrin
Small intestine:
What digestive processes occur in the small intestine?
* Propulsion: peristalsis
* Chemical digestion: enzymes
* Mechanical digestion: segmentation
* Absoption of nutrients!!
Duodenum
Jejunum
Ileum
Structures and cells:
1. Circular folds: increase surface area for absorption
2. Villi: increase SA for absorption
3. Microvilli: increase SA for absorption; also contain brush border enzymes (chemical d)
4. Goblet cells: s/s mucus (provides protection and lubrication)
5. Crypts of Lieberkuhn: s/s intestinal juices (lubricate SI and buffers HCl from stomach)
The molecules used in the small intestine to digest lipids are:
a. Bile
b. Pancreatic lipase
e. Co-lipase
Large Intestine:
Ileocecal sphincter: separates SI from LI
Internal anal sphincter: smooth muscle (involuntary)
External anal sphincter: skeletal muscle (voluntary)
What is the main function of the large intestines?
* Finish absorption
* Absorb H2O - form and defecate feces
Digestive processes within the large intestines?
* Some absorption
* Propulsion: mass movement; peristalsis
* Mechanical digestion: haustral contractions; mass movement
* Defecation
* NO chemical digestion in LI
ACCESSORY ORGANS
Liver/gallbladder:
1. Synthesizes bile
2. Removes old RBCs
3. Processes nutrients after a meal
4. Processes nutrients between meals
5. S/s hormones
6. S/s plasma proteins
7. Help eliminate wastes
8. Store essential vitamins (vitamin A)
Bile salts:
* Synthesized in liver from cholesterol
* Sectredted in bile to duodenum
* Amphipathic molecule (polar and nonpolar)
* Emulsify fat
* Turns big fat glob into lots of smaller fat droplets that are surrounded by water
* Increases SA of the fat (helps with digestion)
* Nonpolar parts face lipids; polar parts face water
* DO NOT digest fats; only emulsify
What part of the bile molecule should face water?
Polar
Pancreas - s/s pancreatic juice (Exocrine factor)
* Contains zymogens: Inactive proteases (activated in the small intestine
* Bicarbonate buffer juice: base that neutralizes HCl from the stomach w/ small intestine
* Co-lipase: molecule that helps load lipase onto lipids
* Enzymes: pancreatic lipase; pancreatic amylase (starch/glycogen)
Zymogens: inactive storage form of proteases produced via exocrine acinar cells of the pancreas
* Trypsinogen
* Chymotrypsinogen
* Procarboxypeptidase
Pathway:
1. Acinar cells
2. Pancreatic duct
3. Ampulla of vader (pancreatic duct joins w hepatic/cystic duct)
4. Sphincter of oddi (controls how much juice gets into small intestine)
5. Duodenum
Pancreatic Acinar cells: s/s zymogens
-hydrophilic
-exocytosed
-can’t pass through membrane
-proteins are hydrophilic
Make zymogens via protein synthesis
* Dna transcripted into mRNA → translated by ribosomes on the rough endoplasmic reticulum → peptides will undergo modification within rough ER → travel to golgi apparatus→ packaged into zymogen granules (secretory vesicles) → exocytosed into pancreatic duct (out of acinar cells) → ampulla of vader → through open sphincter of Oddi → duodenum of SI → in SI - zymogens are actived by brush border enzymes (BBE)
Which of the following is NOT matched correctly with the corresponding term?
Parietal cells: Pepsinogen
Crypt of Lieberkuhn: Intestinal juice
Lactose: Disaccharide
Microvilli: Brush border enzymes
Carbohydrate digestion and absorption
Generic term for the enzymes that breakdown polysaccharides: amylase
Where are these enzymes synthesized and secreted? Salivary glands and pancreas
Starch/glycogen → maltose + limit (alpha) dextrins
Maltose (bbe) → 2 glucose
Dextrinase (bbe) → glucose
Sodium/ potassium pump role in absorption:
3 Na out → ICF [low Na]
Establish a Na gradient in epithelial cells to allow cotransport of nutrients against gradient into cells
Absorption of Carbs: (only absorb monosaccharides)
Glucose apical: cotransport with Na (form of active transport)
Basolateral: facilitated diffusion (glucose from lumen of GI tract into blood) (passive but needs TM bc its hydrophilic)
Galactose Apical: same as glucose
Basolateral: same as glucose
Fructose apical: facilitated diffusion
Basolateral: facilitated diffusion
Proteins:
* Typical diet: 125 g/day (only require 40-50g)
* Proteins to be absorbed / digested
* Consumed
* Secreted into lumen of intestinal tract (enzymes)
* Sloughed off with cells lining intestinal tract (enterocytes)
* Generic term for enzymes that break down proteins = proteases
* Proteins:
* Amino acids (AA)
* Dipeptides (AA-AA)
* Tripeptides (AA-AA-AA)
What types of enzymes digest proteins?
Proteases
Types of proteases:
* Endopeptidases
* Split polypeptides at interior peptide bonds
* Cleave inside bonds
* Product = small peptide fragments (di/tripeptides)
* Exopeptidases
* Cleave off amino acis from one end of polypeptide
* Product = amino acids
* Cleave outside bonds (individual)
Protein digestion in the stomach (start):
Chief cells - s/s pepsinogen
Parietal cells - HCl & intrinsic factors
Ingested protein → pepsin→ dipeptides and tripeptides (ENDOpeptidase)
Protein digestion in the small intestine:
Water released from pancreas (zymogens (inactive)) → activated by enzymes → Trysinogen activated by BBE enterochymase → trypsin (activated) → digest proteins into di/tri peptides → trypsin also converts chymotrysiogen into chymotrypsin → di/tri peptides → trypsin converts PCX into carboxipeptidase → digest proteins into amino acids
Trypsin = endopeptidase
Chymotrypsin = endopeptidase
Pepsin = endopeptidase
Carboxypeptidase (ONLY) = exopeptidase
Absorption of Amino Acids:
Need Na/K pump (establish sodium gradient) (pump out K, pump in Na)
* We want low Na
* Allow amino acids to go against gradient (co-transport)
Apical: co-transport w/ Na (high to low)
Basolateral: facilitated diffusion
Convert di/tri peptides into amino acids with brush border enzymes (aminopeptidase/ dipeptidase)
Carrier protein
Absorption of di/tri peptides:
Apical - co transport w Hydrogen ions within epithelial cells of GI
Di/tri peptides → individual AA (cross basolateral membrane via facilitated diffusion)
What happens to di/tri peptides in the small intestines?
Absorbed across the apical membrane with co-transport with hydrogen ions
Broken down by brush border enzymes into individual amino acids
Absorbed across the basolateral membrane with co-transport with hydrogen ions
A and B are correct
B and C are correct
2/3/25
Lipids - 25-160g lipids
* 90% triglycerides
* Not water soluble
* Do not mix
* Enzymes of digestion = lipases
* Secreted from
* Lipases can only act on molecules near edge of fat droplet
* Bile salts increase SA of droplets by breaking large droplet into several small droplets = emulsification
* Co-lipase is needed to help load lipase onto lipid
Lingual lipase - s/s from tongue, activated in the stomach
Gastric lipase - s/s from stomach
Pancreatic lipase & colipase - s/s from pancreas
Bile - made in liver; stored/concentrated in gallbladder
Lipoprotein lipase (blood) - s/s from liver
Action of bile salts and colipase
Bile salts - emulsify lipids → increases SA of lipids to allow water soluble lipase efficient digestion
Co-lipase - move bile salts out of the way to load lipase onto the lipid
Absorption of Lipids:
1. Micelles release lipophilic molecules
2. Lipophilic molecules cross apical membrane via simple diffusion
3. Smooth ER - reassemble molecules into a triglyceride
4. Triglycerides travel to golgi apparatus
5. In GA, add proteins and other lipids to triglycerides → molecule is now hydrophilic
6. Transformed into chylomicron (hydrophilic!)
1. Crosses basolateral membrane via exocytosis
2. Too large to be absorbed via capillaries
3. Bypass capillaries
7. Enter lymphatic system via lacteals
1. To blood (lipoprotein lipase (blood)
2. Digests chylomicrons into glycerols and fatty acids
3. Fatty acids and glycerols enter cells via simple diffusion
Important to not have globs of fat in bloodstream! → fat embolisms
Chylomicrons = way for fat/lipids to be absorbed in bloodstream
What happens to bile salts?
Enterohepatic circulation
* Absorb the bile in ileum → recycled by liver
How do fat soluble vitamins (lipophilic) get absorbed across the apical membrane of epithelial cells of the GI tract?
Simple diffusion
LIPOPHILIC = simple diffusion
Fat soluble vitamins - A, D, E, and K
* Absorbed w lipids
* Dissolve with micelles, simple diffusion
Water soluble vitamins - B and C
* Carrier proteins
B12 - intrinsic factor (parietal cells)
Calcium: absorbed in duodenum/jejunum
* Binds to BBE = calcium binding protein
* Into epithelial cell
Water: water in GI tract
* 7 liters from GI secretions
* 2 liters
* Passive
* Follows absorption of solutes by osmosis
* Where does most water absorption occur in GI tract? Large intestine
Sue has a genetic mutation that decreases the amount of enterokinase proteins on the brush border of her small intestines. What will be the result of her disorder?
Less carbohydrate digestion
Less lipid digestion
Less protein digestion
More carbohydrate digestion
READING 3
Presence of oxygen
AKA: aerobic respiration/complete oxidation
1. Glycolysis
2. Pyruvate oxidation (linking step; transition stage)
3. Krebs cycle (TCA; citric acid cycle)
4. Oxidative phosphorylation
1. Electron transport chain
2. Chemiosmotic coupling
Absence of oxygen
AKA: anaerobic respiration/ incomplete oxidation
1. Glycolysis
2. Fermentation
Carbohydrate Metabolism
NEED to know
* What goes into each pathway
* What comes out
* Location
First Pathway: Glycolysis:
Location: Occurs within cytoplasm
In: 1 glucose, 2 ATP, 2 NAD+, 4 ADP
Out: 2 ADP, 2 NADH, 4 ATP, 2 pyruvates
Costs 2 ATP
Make 4 ATP
NET: 2 ATP
ONLY PATHWAY THAT REQUIRES ATP
2/5/25
Second pathway: linking step (Pyruvate Oxidation)
Location: mitochondrial matrix
In:
2 pyruvates
2 NAD+
2 CoA
Out:
2 CO2
2 NADH
2 Acetyl CoA
What are the products of the linking step per glucose molecule?
2 Acetyl CoA, 2 NADH, 2 CO2
Third Pathway: Krebs Cycle, TCA cycle/citric acid cycle
Location: in mitochondria matrix
In:
2 Acetyl coA
6 NAD+
2 FAD
2 ADP
H2O
Out:
6 NADH
2 FADH2
2 ATP
CoA
CO2
Fourth Pathway: Oxidative Phosphorylation:
1. Electron Transport Chain (ETC)
2. Chemiosmotic coupling
Goal of ETC: create a proton/hydrogen gradient between the intermembrane space (IMS) and the mitochondrial matrix
Mechanism: takes NADH and FADH2 (made in glycolysis, pyruvate oxidation, krebs cycle) → are oxidized (lose electrons) (donated to ETC)
As electrons are removed → THIS RELEASES ENERGY
Pump H+ ions from mitochondrial matric into intermembrane space
Where do the electrons go?
Puts all donated electrons onto Oxygen
Oxygen serves as final electron acceptor
Goal of chemiosmotic coupling: to create ATP
Mechanism: H/protons move down gradient through ATP synthase →
energy released from Hydrogen going through ATP synthase allows Pi + APD → ATP
In:
10 NADH
2 FADH2
O2
34 ADP
Out:
10 NAD+
2 FAD
H2O
34 ATP
Calculate the total number of ATP produced via the complete oxidation of one glucose molecule
Glycolysis:
2 ATP
2 NADH
0 FADH2
Pyruvate Oxifation:
0 ATP
2 NADH
2 FADH2
Krebs:
2 ATP
6 NADH
2 FADH2
Every 1 glucose produces 36 ATP
What happens to the NADHs and FADH2 that were created during glycolysis, linking step, and Krebs Cycle?
They become reduced in the electron transport chain within the intermembrane space.
They become oxidized in the electron transport chain within the mitochondrial matrix.
They become oxidized in the chemiosmotic coupling within the intermembrane space.
They become reduced in the chemiosmotic coupling within the mitochondrial matrix.
They become oxidized in the electron transport chain within the intermembrane space
What region does the electron transport chain actively pump hydrogen ions into?
Nucleus
Mitochondrial matrix
Cytoplasm
Intermembrane space
(from mitochondrial matrix INTO intermembrane space)
Excess of glucose → covert glucose into glycogen via glycogenesis (liver or skeletal mm)
OR convert into triglycerides via lipogenesis (adipose tissue (fat))
No glucose
LIVER → glycogenolysis (glycogen into glucose)
→ OR glyconeogenesis (convert non-carbs into glucose)
1. Pyruvate
2. Glycerol
3. Lactate
4. Amino acids
READING 4
Lipid Metabolism
Lipogenesis: building lipids
Glycerol + 3 Fatty Acids = triglycerides
Occurs in adipose tissue and liver
Excess glucose → glycolysis → pyruvate oxifation → excess acetyl CoA
→ fatty acids → triglycerides → adipose tissue OR live
→ cholesterol → steroid hormones → dependent on location
→ bile → liver (stored and concentrated in gallbladder)
Lipolysis: break down triglycerides
adipose tissue or liver
Lipolysis and beta oxidation are rich sources of ATP. If your dietary intake included one fatty acid chain of 14 carbons, your body would produce approximately 114 ATP while the carbohydrate metabolism of a single glucose gives rise to approximately 36 ATP. Which type of metabolism produces more ATP?
LIPID metabolism
Ketogenesis → releases a lot of CO2
CO2 + ketones are acidic → blood concentration becomes acidic
Metabolic acidosis (ketoacidosis)
If lipid metabolism produces more ATP than carbohydrate metabolism, then why is glucose our primary energy currency? In other words, why is it utilized before fat metabolism?
* Lipid metabolism produces ketones which can cause ketoacidosis (acidic blood) which would prevent proteins in the blood from functioning normally.
2/7/25
Protein Metabolism:
What are the individual monomers of protein digestion and how do they cross the apical membrane of the epithelial cells of the small intestine?
Glucose : Facilitated diffusion
Amino acid : Co-transport with hydrogen ions
Amino acid : Anti-transport with sodium ions
Amino acid : Co-transport with sodium ions
Proteogenesis: building of proteins from amino acids
Lipogenesis: building of fats
Gluconeogenesis: glucose →
Some amino acids can be turned into pyruvate → pyruvate oxidation (skips glycolysis)
Excess amino acids → transporters → amino acids (deaminate (remove NH2)) → urea → kidneys → excrete urea in urine
(excess amino acids are released via urine)
PUTTING IT ALL TOGETHER:
Insulin is considered an anabolic, while glucagon is considered a catabolic hormone.
* Anabolic: building blocks
* Catabolic: breaks down stored molecules
Absorptive state = fed state = when body is absorbing nutrients
If actively absorbing nutrients, blood glucose levels increases and plasma amino acids levels increases this causes:
The release of insulin from the beta cells of the pancreas
How would these fx affect plasma con of glucose, fa, and aa → decrease because we are removing from blood into cells
Post absorptive state = fasted state = no food intake
* Not actively absorbing nutrients → glucose levels falls then release glucagon → from alpha cells of pancreas
* Important to avoid hypoglycemia (low blood glucose)
* Actions of glucagon
* Alpha cells in pancreas: glucagon secretion
* Liver: glycogenolysis, gluconeogenesis, ketone synthesis, protein breakdown
* Adipose tissue: lipolysis, triglyceride synthesis
1. What causes glucagon secretion? Low blood glucose
2. What will happen to level of glucose in the blood? increase
3. What will happen to the level of fatty acids in the blood? Increase
4. Amino acids → increase
5. Were any fuel storages increased? No
Intercellular Communication:
How cells are able to communicate with each other
How can you classify chemical messengers?
Chemical only
Structural only
Functional only
Chemical and functional
Which of the following best characterizes hormones?
Hormones are released by a neuron into the interstitial fluid and then targets a certain organ.
Hormones are released by an endocrine gland and travel via a gap junction to an adjacent cell.
Hormones are released by an endocrine gland via the axon terminal and travel through the synaptic cleft to reach their target cell.
Hormones are released by an endocrine gland into the IF and then into the blood and then targets a certain organ
CHEMICAL CLASSIFICATION:
Amino Acid - neurotransmitter
Amines - paracrines, neurotransmitter,
Peptides/Proteins
Steroids
Which chemical classes are lipophilic? Steroids
* Fat loving, can pass through cell membranes via simple diffusion
* Not stored!
* Release rate depends on how synthesis
Which chemical classes are lipophobic? Amino acids, amines, peptide/proteins
* Cannot use simple diffusion
* Stored in secretory vesicles
* Leave cell determine by exocytosis
Amines (except thyroid hormone), peptide/proteins, amino acids are polar, while steroid hormones are non-polar.
Amine synthesis: derived from amino acids
Tryptophan → amine
Through enzyme catalyzed reactions
NEED TO KNOW
Serotonin derived from tryptophan
Melatonin derived from tryptophan
Histamine derived from histidine
Thyroid hormone derived from tyrosine
Catecholamines derived from tyrosine
Catecholamines: group of amines
* Derived from tyrosine
* Through ECR→ turn tyrosine into any catecholamine
Peptide and protein synthesis: formed by cleaving larger proteins
* Cleaves off aa
Steroids:
Start w cholesterol turn into steroid hormone
NEED TO KNOW
Start with cholesterol and use enzyme catalyzed reactions!
2/10/25
From secretory cell to target cell
Transport
→ diffusion only through IF (AKA IF only) - nearby cells
→ diffusion through the IF first then blood borne transport (AKA IF and blood) - to far away cells
* Bound to carrier protein
* Dissolved in plasma
Messenger Transport:
* Diffusion through IF only
* Secretory cell and target are nearby
* Ligand is quickly degraded
* Hydrophilic
* Functional class: Paracrines, NTs,
* Blood borne transport
* Secretory cell and target are far away
* Lipophobic (hydrophilic): dissolved in plasma
* Chemical classes: peptide/proteins, amines
* Lipophilic (hydrophobic): bound to a carrier protein
* Chemical classes: steroids (& thyroid hormone)
* Functional: hormones, neurohormones
* 99% bound to a carrier protein
* 1% dissolved in plasma
* Simple diffusion
Messenger half life
How long it takes for 50% of messenger to be degraded
Do messengers dissolved in plasma have a long or short half-life compared to messengers bound to carriers?
Short half life
What organ degrades these messengers and which organ excretes their breakdown products?
Liver degrades
Kidney breaksdown
I'm a ligand that is transported through the interstitial fluid then blood. I am never bound to a carrier protein so I must be.....
Lipophobic
READING 2 - Intercellular Communication
* Altering number receptors
If we change # of receptors, we will change response
If we change # of ligands, we will change response level
What happened to the number of receptors? Based on what happened to the number of receptors would this cell have an increase in sensitivity or decrease in sensitivity to the ligand?
Decrease, decreased
(harder for ligand to find the receptor - sensitivity of target cell is correlation to # of receptors)
Based on your response to the previous question, would this target cell have an increased response or decreased response to the ligand?
Decreased
Down Regulation and Up regulation
Normal # of ligands = x level of response
Double # of ligands = larger response
We want normal response! (homeostasis obvi)
Down regulation: when the body decreases # of receptors in response to having more ligands than normal
Ex: drug tolerance
Up regulation: when cells increase number of receptors in response to having to few ligands
Signal Transduction Pathway:
Signal molecule - chemical messenger - binds to
Receptor protein - activates
Intracellular signal molecules - alters
Target proteins - create
Response
Intracellular mediated response - within cell
* In cytoplasm or nucleus
* Lipophilic (simple diffusion)
* Chemical classes: steroids (& thyroid hormone)
* Gene activation
Membrane bound receptor mediated response - within the membrane
* Lipophobic (doesnt have to get in cell)
* Chemical classes: Amino acids, peptides/proteins, amines
* Enzyme activation
* Changes membrane permeability
* Permeability of target to ions may be altered
* Types:
* Ligand linked: channel linked or g protein linked
* Enzyme linked
Types of channels
Leak - always open
Gated - open/close in response to stimuli
* Voltage gated: change in response to a change in membrane potential
* Chemically (ligand) gated: when ligands bind to them
* - Mechanically gated: physically open/close by force
* Thermally gated: changes in temperature
Ligand gated channels: ligand must bind
→ Fast channels: when receptor and channel are same protein (ionotropic)
→ Slow channels: when receptor and channel are separate proteins (metabotropic)
2/12/25
I am a ligand that is made through a series of enzyme catalyzed reactions that starts with an amino acid so I must be a(n)......
Amine
Peptide/protein (through protein synthesis)
Steroid (ECR starting with cholesterol)
Channel-linked receptors: fast ligated (can only open channels)
Slow: channel and receptor are different proteins (need some type of protein) (g proteins link receptor and channel/enzyme)
Structure of a g-protein: 3 subparts
* At rest all 3 subunits are together & GDP attached to alpha subunit
* To activate a g-protein:
* Ligand has to bind to the receptor
* GDP to fall off the alpha subunit
* GTP attaches to alpha subunit
* Causes alpha subunit with GTP to slide over (activate ion channel (open or close))
* To inactivate a g-protein:
* Ligand has to fall off receptor
* Hydrolyze alpha GTP → GDP
* Alpha subunit with GDP returns back to beta and gamma units
Slow g protein:
1. Direct coupling
1. Ligand binds to receptor
2. Activates g-protein - GDP falls off, GTP attaches, alpha unit with GTP slides over
3. Open or close a channel (allows ions to move in or stop ions from moving)
2. 2nd messengers
1. Triggered by first messenger (ligand) activating the g protein which actives an amplifier enzyme which activates 2nd messenger production which activates or inhibits cellular pathways
2. Two types:
1. Gi- inhibitory amplifier enzyme (decreases cell response)
2. Gs - stiulatory amplifier enzyme (increases cell response)
cAMP:
The cAMP second messenger system is used to reabsorb water from the kidneys back to the plasma. If water is not reabsorbed it is excreted in the urine. You are nurse at Normal Regional Hospital. A patient has arrived in the ER and is immediately diagnosed with hypothermia. What effect will this have on the this patient’s cAMP messenger system?
Protein kinase A will not function properly and therefore PKA cannot activate cAMP and the patient will urinate profusely.
The likelihood of vasopressin binding to the receptor is decreased causing increased activation of the G-protein.
Adenylate cyclase will slow the conversion of ATP to cAMP resulting in a large volume of urine produced by the patient’s kidneys.
The alpha-subunit will be slow to activate phosphatase.
IP3/DAG/Ca:
Cytokines are proteins that act as signaling messengers for your immune response. They are released from secretory cells to only act on nearby cells. Choose the CORRECT statement.
Since cytokines are chemical messengers, they are functionally classified as hormones. (far away cells)
Cytokines leave the secretory cell via simple diffusion. (exocytosis)
Cytokines are derived from cholesterol. (protein synthesis)
Cytokines will bind to receptors on the membranes of the nearby cells to initiate a signal transduction pathway to start a cell response.
2/14/25
How are the IP3/DAG systems turned off?
1. Ligand falls off receptor
2. Hydrolyze GTP → GDP
3. Dephosphorylate the protein
4. Degrade 2nd messenger (IP3, DAG)
5. Reuptake Ca
Enzyme Linked Receptors:
1. Binds to receptor
2. Enzyme undergoes a conformational change (active)
3. Phosphorylate a protein
4. Protein casus cell response
Ex: insulin receptor = tyrosine kinase
Long distance communication:
* Endocrine system
* What chemical messenger: Hormones
* Through what avenue must this messenger travel to reach target cell?
* IF → blood → IF → receptor on target cell
* Slower systems have a longer effect
* Endocrine system is slower than nervous system
* Nervous System
* Two major cell types: neurons and glial cells
* Are neurons capable of communicating short or long distances? Short
* Uses chemical and electrical signals
* Chemical: axon terminal at synaptic cleft
* Electrical: axon
* Uses voltage gates and ligand gated channels
Nervous Communication:
Dendrites - receive info via ligand channels
Soma - “”
Axon hillock - start an action potential
Axon - propagate action potential
Axon terminal- release neurotransmitters
Axon hillock and axon have voltage gated channels
Would a steroid hormone or a peptide/protein hormone bind to a receptor on the surface of the target cell?
Steroid hormone - lipophilic - receptor will be in cell
Peptide/protein hormone - lipophobic - receptor on the surface
ENDOCRINE:
1. Hypothalamus will release a releasing hormone
2. RH travels to the anterior pituitary bind to excitatory receptor for RH = Erh
3. Anterior pituitary will synthesize and secrete stimulating hormones (SH)
4. SH travels through endocrine gland (binds to Esh
5. Causes endocrine gland to s/s fnal hormone
6. Hormone travels to target tissues/cells (bind Eh)
7. Cell response
* Neurosecretory cells in the hypothalamus will release releasing hormones (neurohormones)
* RH are release via exocytosis from axon terminals (lipophobic)
* Travel in blood to anterior pituitary
* RH will bind to excitatory receptors are on the endocrine receptor cells of anterior pituitary → s/s SH into the blood
* SH will travel to the endocrine gland
* Cause the cell response
IF: hypothalamus releases inhibiting hormones → IH bind inhibitory receptors on anterior pituitary → causes ant pit to stop releasing hormones
Feedback loops
Control of endocrine systems - VIA NEGATIVE FEEDBACK (back to normal)
Hypothalamus release tropic hormone 1 → bind to excitatory receptors (ant pit) → release tropic hormone 2 (SH) → travel to endocrine gland and bind to excitatory receptors → s/s final hormone → travel to target tissues and bind to Ehs → cell response
To stop: bind to Ihs on ant pit to stop making tropic hormone 2, so we dont make final hormone
EXAMPLE:
Cortisol → stress hormone
Stress → causes hypothalamus CRH secretion → ant pit (bind to excitatory receptors) → causes ant pit ACTH secretion (release via exocytosis (lipophobic)) travel in blood to → adrenal glands (binds to EATCH) → release of cortisol (final hormone) (release cortisol via simple diffusion (lipophilic)) → travel in blood to target tissues/cells → bind to excitatory receptors to cause cell response
* Too much of cell response – eventually stops due to inhibitory receptors (stop releasing ATCH)
2/17/25
Control of endocrine systems
Circadian rhythms controlled by time of day
-melatonin
When you stop releasing melatonin, you wake up
Adenoma- benign tumor that forms on glands in the body
Functioning: cause hypersecretion
Nonfunctioning: cause hyposecretion
If there was a non-functioning adenoma on the adrenal gland would cortisol by gland be hypo- or hypersecreted?
Hyposecretion and primary disorder (because it is on the gland)
If the adrenal gland atrophied, would cortisol be hypo- or hypersecreted?
Hyposecreted
Based on your response above, would the level of CRH be high or low? ACTH?
Up
If there was a functioning adenoma on the adrenal gland would cortisol be hypo- or hypersecreted?
Hypersecreted
Based on your response, would the levels of CRH be high or low? ACTH?
Up, down, primary endocrine disorder
READING 2
Oxytocin and ADH are synthesized in the posterior pituitary.
True
False
Posterior pituitary is not a true endocrine gland
Stored and released in posterior pituitary, hypothalamus makes them
GROWTH HORMONE - peptide
Hypothalamus releases gh (releasing hormone) travels to ant pit and binds to EGHRH which causes secretion of GH and binds to EGH on liver and causes secretion of IGF1 and bind to ET0F1 on target cells which causes cell response
Hypothalamus releases gh (inhibitory hormone) which binds to IGHTH on ant pit which inhibits secretion of GH →cells throughout body → binds to EGH on cells throughout the body which causes cell response
Where will the excitatory Growth Hormone Releasing Hormone receptors be located at?
In the cytoplasm of the cells in the anterior pituitary
In the membrane of the cells in the anterior pituitary
In the cytoplasm of the cells in the liver
In the membrane of the cells in the liver
In 2003, FDA approved a use of recombinant human GH for treating children with non-GH deficient short stature (more than 2.25 standard deviations below the mean height for their age and sex). Average cost: $22,000 per year for hGH injections, this comes out to more than $33,000 per inch of height gained. Side effects: glucose intolerance and pancreatitis
Hyposecretion of GH causes Dwarfism. Which of the following may explain hyposecretion of GH?
Non-functioning pituitary adenoma
Upregulation of GHRH receptors on the anterior pituitary
Downregulation of GHRH receptors on the liver
Atrophy of the hypothalamus
THYROID HORMONE - amine
Hypothalamus releases → TRH → binds to ETRH on ant pit → secretion of TSH → binds to ETH on thyroid gland s/s
What type of receptors will thyroid hormone bind to? [Choose all that apply]
Inhibitory receptors on the hypothalamus
Excitatory receptors on the hypothalamus
Excitatory receptors on the anterior pituitary
Inhibitory receptors on the anterior pituitary
Excitatory receptors on the thyroid gland
Inhibitory receptors on the thyroid gland
(And ETH on target tissues)
Thyroid gland - releases 3 hormones: T3, T4, calcitonin
C cells secret calcitonin
Follicular cells secrete TH
Follicular cells produce/secrete thyroglobin (precursor to TH) and bring iodide to the colloid. (iodid is brought into the follicular cells via AT from the blood)
2/19/25
Hypothyroidism - not making enough TH
decrease BMR
decrease HR
Increase weight
Decrease heat (cannot tolerate cold)
Treatment: synthetic TH
If lack TH from birth, cretinism (short, dwarfism, mentally underdeveloped)
Hyperthyroidism - too much TH
Increase BMR
Increase HR
Decrease weight
Increase heat (cannot tolerate heat)
You have a patient with a secondary hypersecretion disorder of the anterior pituitary. Indicate the levels TSH, TH, and TRH and diagnose the patient.
TRH high ; TSH high ; TH high ; hypothyroidism
TRH low ; TSH high ; TH high ; hyperthyroidism
TRH high ; TSH high ; TH high ; hyperthyroidism
Hypothalamus → TRH
→ ant pit → TSH
→ Thyroid gland → TH
TRH low: Since TH (thyroid hormone) is high, it will exert negative feedback on the hypothalamus, suppressing TRH secretion.
TSH high: The anterior pituitary is overproducing TSH, which is the hallmark of secondary hypersecretion.
TH high: The thyroid gland responds to the high TSH levels by producing more thyroid hormone, leading to hyperthyroidism.
READING 3
Adrenal Hormones
What type of control regulates the synthesis/secretion of parathyroid hormone and calcitonin? (both Ca regulation (in the plasma))
Humoral control
Hormonal control
Neural control
Adrenal glands - sit on top of the kidneys
2 major layers - adrenal cortex (outer), adrenal medulla (inner)
Zona glomerulosa: secretes mineralcotricoids (adrenocorticoids)
Steroid = lipophilic
* Aldosterone
* Target: kidneys
* Fxn: reabsorption of Na and K excretion
Zona fasciulata : cortisol
Zona reticularis: sex hormones
How would the majority of aldosterone be transported in blood?
Bound to a carrier protein
Dissolved in plasma
Chemical class = steroid = lipophilic = bound to carrier protein
Control of aldosterone:
Steroid hormone controlled via humoral control
S/s of aldosterone - Increase Na in blood, decrease K in blood
Cortisol: Steroid - hypothalamic - CRH, ATCH = peptide
Adrenocorticotropic hormone will be converted to cortisol.
True
False
Causes release of cortisol (peptide via protein synthesis)
Cortisol - steroid from cholesterol
Thymus - involved in immune response
Secretes thymosin
* Regulate t cell function (type of WBC)
* Cortisol suppresses the thymus
Adrenal medulla
Secretory cells = chromafin cells = modified neurons
Secrete: 80% epi, 20% norepinephine, 1% dopamine (ALL amines, all catecholamines, LIPOPHOBIC)
Under neural control
Epi causes: gluconeogenesis, glycogenolosis, lipolysis, ketogenesis
INCREASE fuel substrates (adrenaline during fight/flight)
PINEAL GLAND:
Glandular tissue in brain
Secrete melatonin
* Amine - tryptophan
* Circadian rhythms (sleep schedule)
GONADS:
male- testes
* Testosterone: steroid
* androstenedione
Female - ovaries
Testosterone:
Hypothalamus secretes GnRH to ant pit