Health Science II SAQ PP
1314
5) Give a brief account on RAAS in regulation of blood pressure, salt and water balance
6) Gastrin and cholecystokinin share amino acid identity at their carboxyl terminal and thus they exhibit structural-activity relationship. Describe briefly the physiological functions of gastrin and cholecystokinin. 6.
6) Briefly describe the major factors that slow down gastric emptying.
Protein Regulator
CCK
GIP
Secretin
Initial Stimulus
Presence of fats and proteins in duodenum
Fatty acids and glucose in duodenum
Low pH (acidic chyme) entering duodenum
Release Site
Intestinal I-cells in duodenum
Intestinal K-cells in duodenum
Intestinal S-cells in duodenum
Physiological response
* Stimulate gallbladder contraction to enhance bile release
* Stimulate digestive enzyme secretion by pancreatic acinar cells
* Relax hepatopancreatic sphincter
* Inhibits gastric motility by reducing antral contractions
* Inhibit gastric emptying to allow adequate time for fat and protein digestion
* Stimulate insulin release
* Inhibit gastric acid secretion = indirectly slowing digestion
* Reduces gastric motility by relaxing stomach fundus
* Inhibit gastric emptying to regulate nutrient absorption and prevent glucose spike
* Stimulate bicarbonate secretion from pancreas to neutralise acid
* Reduces gastric acid secretion by inhibiting parietal cells
* Stimulate growth of exocrine pancreas, ie: trophic action
* decrease gastric motility = inhibit gastric emptying
1415_1012A
5) Describe the major forces that determine GFR, what is the normal value of GFR? [10]
6) What is pulmonary gaseous exchange? Describe the factors that may affect the efficiency of pulmonary gaseous exchange [10]
1516
4) Discuss the forces that affect the ultrafiltration along glomerular capillaries
1516_1010
1) Give a brief account of the factors that contribute to the development of a resting membrane potential. Explain the significance of setting up a RMP [10]
2)
4a) Consider 2 alveoli: “A” has a diameter that is half of “B”. Which of the 2 has a greater tendency to collapse during ventilation? Explain your reasoning [6]
4b) In reality, the collapse of alveoli of different sizes can be presented. Describe how. [4]
1617
6)
1617_1010
1a) Describe how the different regions of a neuron are specialised in performing the function of communication and acting as an integrator in neurotransmission [5]
2a) Fluid movement between plasma and interstitial fluid depends on balance between two types of pressures. Describe how fluid movement is achieved at the 2 ends of capillary tube due to the interplay between these 2 types of pressures [4]
2b) what is the net movement of fluid across the capillary wall in normal condition [1]
2c) Name two conditions that can cause edema. Provide the mechanism on how they would occur [5]
3a) Recall the normal physiological range of extracellular osmolarity with correct unit [1]
3b) What is the primary defence of body when plasma osmolarity exceed the normal physiological range by 5% [1]
3c) Write a flow diagram to summarise the homeostatic control of the primary defence in part B due to rise in plasma osmolarity [8]
5) What kind of acid and base disturbance exists in a patient with the following data
* pH 7.28 (normal 7.4)
* pCO2 = 35 mmHg (normal 40mm Hg)
* Plasma concentration of bicarbonate ion [HCO3-] = 16mM (normal 24 mM)
1617 1011
1718
3) Explain how tubuloglomerular feedback regulates glomerular filtration rate (GFR) [10]
4) Describe the endocrine and paracrine pathways in the regulation of gastrointestinal functions [10]
5) write a flow diagram to summarise the events in the process of inspiration. In your diagram, you also need to specify clearly the changes in term of intrapleural and transpulmonary pressure [10]
6a) Name the three chemical classes of hormones [1]
6b) Explain how their differences in chemical nature affect
i. Receptor location in target cells
ii. Routes of hormone administration
iii. Susceptibility to heat denaturation and enzymatic digestion
1718_1010
3) Describe how the nervous system and its associated sensors and effectors are structurally and functionally organized into various components of a homeostatic control system. Explain what structural/ functional features are build in palace to ensure that the flow of neuronal signal are unidirectional [10]
5) Explain how metabolic acidosis can be compensated by ventilation [10]
1718_1012A
5) Briefly describe the neurocrine, endocrine and paracrine pathways and give 1 example for each of them in regulating the GI function
1819
1a) Define acidosis [2]
1b) With the aid of Henderson-Hasselbalch equation, briefly describe the changes in pH, pCO2, HCO3- in a subject with metabolic acidosis. Explain if this condition could be corrected. If yes, briefly describe the compensatory response. Write your answer by summarising the sequence of events in a flow chart [8]
2) Briefly explain why afferent arteriole constriction would lead to a fall in glomerular filtration rate (GFR) [10]
3) List 3 major functions of vasoactive intestinal polypeptide (VIP) and briefly describe VIPomas [10]
4) In what ways a neuron is specialised in unidirectional propagation of signals and acting as an integrator in the neuronal circuit. How the specialised role of different parts of a neuron is reflected in the charges in ion channel expression on its cell surface [10]
5) Give an account of the proposed mechanism that explains the onset and breaking of fever. Propose how certain drugs may reduce the development of fever [10]
6a) Summarise 4 factors that causes transient changes in venous return [8]
6b) Under steady state conditions, venous return must equal cardiac output? Describe briefly why thai is necessary [2]
1819_1011
2) Thermoregulation represents an example of homeostatic control of body function. Describe how on a cold and windy day, a subject can detect the perturbation to his/her body temperature and make the appropriate responses to minimise the drop in body temperature [10]
3a) List the major components of the intrinsic conduction system of the heart in correct sequence of the electrical conduction [3]
3b) Reproduce the action potential generated by the natural pacemaker of the human heart with clear labels on both the x axis and y axis. Identify each of the different phases and state clearly the direction of ion movement and the type of ion channel in each phase [6]
3c) Based on the action potential in (b), which phase will undergo major change if heart rate is to be modified by ANS [1]
4a) Define Poiseuille’s law [3]
4b) Which of the physiological variables indicated in the POiseuille’s law contributes majorly to the minute to minute control of arteriolar resistance in a healthy person. WHy? [6]
4c) Name 1 medical condition that can cause an increase in vascular resistance [1]
5a) Fluid movement between the plasma and interstitial fluid depends on the balance of 2 opposing pressures. Name the 2 pressures? [2]
5b) describe how the movement of fluid differs at the 2 ends of the blood capillary due to the pressure in (a) [6]
5c) If the capillary wall starts to leak out plasma protein to tissue fluid, what medical condition will most likely occur? Describe briefly [2]
6a) A 25 year old male student has been vomiting for 2 days due to consumption of contaminated seafood. What type of acid base disturbance will most likely occur, explain [2]
6b) Describe its compensatory mechanism [8]
1920
1. A 25-year-old woman was running for her first marathon in a hot summer. To avoid dehydration,
She drank a large quantity of water before the race began. In the middle of the race, she started
to feel a headache and nausea. Later on, it was learnt that the woman was suffering from
hyponatremia. Hyponatremia is defined as a plasma Na level below 135 mmol/L and the plasma Na
level of this person is 125 mmol/L. Hyponatremia induced by ingestion of large quantities of water
is also called dilutional hyponatremia
a) What is the estimated plasma osmolarity of this person? Please show your calculation. (1 mark)
Plasma NaCl level of this person = 125 mmol/L
125* dissociation constant (2) = 250 mosm/L
b) Which body fluid compartment(s) is/are diluted in this type of hyponatremia? (3 marks)
Plasma is part of ECF, therefore ECF is diluted in this type of hyponatremia
Hyponatremia refers to plasma Na+ lower than normal
Since large ingestion of water, water content in blood increases, and with constant amounts of Na+ in blood, sodium ion concentration is decreased and diluted.
Hence, water will move out of plasma into interstitial fluid and even ICF as both ISF and ICF have higher effective osmolarity, creating a suction force
This leads to expansion of both ECF and ICF volume, hence reducing fluid osmolarity as a whole.
c) What effect the dilutional hyponatremia has on the tissue cells of this person especially on her
brain? (3 marks)
Due to reduced effective osmolarity in plasma, water will move into tissue cells, causing swelling of cells as ICF volume expands. For instance, the woman felt headache and nausea as the swollen cell may compress on cranial nerve/ rise of intracranial pressure
If situation worsens → cerebral edema → death
d) What would happen to vasopressin secretion in response to the status of this person? (1 mark)
Less vasopressin secretion so more water can be removed via urination to excrete water
e) Summaries the primary physiological function of vasopressin. (2 marks)
Regulate osmolarity of body fluid → Increase permeability of DCT and collecting duct of nephron to facilitate increase water reabsorption → adjust volume and concentration of urine
Vasopressin increase permeability of collecting duct and DCT to increase water reabsorption. Vasopressin bind to GPCR on basolateral membrane, activate adenylyl cyclase to convert ATP → cAMP, increase protein kinase A increase protein phosphorylation, causing vesicles with aquaporin to fuse with apical membrane.
Change in water content = long term regulation of blood pressure. Larger volume will increase blood pressure
2)
a) Define alkalosis (2 marks).
Alkalosis is when blood pH is larger/ equal to 7.45. They can be further classified to respiratory alkalosis (increase CO2 in blood) / metabolic alkalosis (decrease HCO3- concentration in blood)
b) With the aid of the Henderson-Hasselbalch equation, briefly describe the changes in pH, pCO2
and HCO3- in a subject with metabolic alkalosis. Explain if this condition could be corrected. If yes,
briefly describe the compensatory response. Write your answer by summarizing the sequence of
events in a flow chart (8 marks).
Henderson-Hasselbalch equation —- pH = 6.1 + log(HCO3-)/(0.03xpCO2)
Metabolic alkalosis = increase in plasma pH in the body. Caused by insufficient production of acids/ overproduction of HCO3-. Refer to equation, increase in pH suggest increase in HCO3-/ decrease in pCO2, however since this is metabolic, pCO2 not contributing factor, so it is increased [HCO3-] in blood/ decreased [H+] in blood.
Respiratory compensatory response. Refer to equation, increase pCO2 could reduce pH → bring back to normal range (7.35-7.45).
Cause of alkalosis: Alkaline load to body → buffer by H2CO3 ⇌ H+ + HCO3- → ECF [H2CO3-] decrease → ECF pH increase → depress respiration → pCO2 increase → further minimize change in pH.
After alkaline load to body, buffer by H2CO3, causing a decrease in ECF pH as H+ used, increase in plasma pH sensed by peripheral chemoreceptors → decrease firing of medullary inspiratory neuron → decreased firing of diaphragm and external intercostal muscle neuron = decrease contraction = decrease ventilation = hyperventilation rate so more CO2 preserved = increase pCO2.
3)
a) Briefly explain the three physiological processes of the nephron involved in urine production. (3
marks)
Filtration - Blood pressure forces water and solutes from glomerular capillaries into Bowman’s capsule across basement membrane
Reabsorption - removal of water and solutes from tubular fluid and their movement across tubular epithelium into peritubular fluid back to circulation
Secretion - The transport of solutes from peritubular fluid (blood) across tubular epithelium into tubular fluid
b) How do these processes affect the amount of solutes being excreted in urine? Illustrate your
answer with an example solute. (7 marks)
Excretion = Filtration - reabsorption + secretion
Filtration: As solutes squeezed through the size and charge selective filtration membrane (includes pores of endothelial cells, glomerular basement membrane, filtration slits between podocytes), the filterability of different solutes varies, thus affecting composition of urine. Smaller and cationic molecules are more likely to be filtered, ie: Na+ with 23Da has full permeability. However, large molecules like protein cannot pass through the basement membrane and hence stay behind in glomerulus, therefore not in urine.
Forces that favour filtration: hydrostatic pressure in glomerular capillary
Forces that drive absorption: oncotic pressure in glomerular capillary, hydrostatic pressure in bowman’s space
Net glomerular filtration pressure = PGC - PBS - πGC
GFR = Kf [(Pgc - Pbs) - (πgc - πbs)]
Filtration fraction = GFR/RPF → normally, only 15-20% of plasma that enters glomerulus is actually filtered.
Reabsorption: Given that the filtered load is enormous, certain solutes are reabsorbed/regulated, whilst others are not. Reabsorption of useful palsa compounds is relatively complete (water, glucose) whilst reabsorption of waste is relatively incomplete (urea). As mentioned, the reabsorption of glucose is relatively complete. Therefore, it does not normally appear in urine. However, the reabsorption of glucose is carried out by a limited transport mechanism at PT. At normal plasma [glucose], all filtered glucose is reabsorbed. When the plasma [glucose] exceeded 400 mg/min, glucose would appear in urine because the rate of reabsorption reaches the tubular transport maximum (Tm), where glucose transporters are saturated.
Secretion: Certain substances are actively secreted for physiological regulation, for example, hydrogen ion and potassium ions are actively secreted into the tubular fluid to regulate pH or plasma potassium level. The more a substance is secreted, the higher its concentration in urine.
4)
a) List two peptide hormones of the gastrointestinal (GI) system (2 marks)
CCK (cholecystokinin) - secretion by intestinal I cells
Gastrin - secreted by antral G cells in stomach
GIP - secreted by intestinal K cells
Secretin secreted by intestinal S cells
Somatostatin - secreted by gastric D cells
b) Describe the characteristics of gut endocrine cells that produce these GI hormones. (8 marks)
Enteroendocrine cells are specialised epithelial cells that secrete peptide hormones in response to luminal stimuli
Location in GI tract
Scattered within mucosal epithelium, predominantly in
* stomach
* Antral G cells → gastrin
* Antral D cells → somatostatin
* small intestine
* K cells → GIP
* S cells → secretin
* I cells → CCK
Morphology
1. Open type cells (most common) - have microvilli extending to lumen to sense nutrients (ie: glucose, amino acids, fats), mechanical stimuli
2. Closed type cell: do not directly contact lumen, respond to paracrine/ neuronal signal
Hormone secretion mechanism
Stimuli: food component/ pH change → trigger hormone release into bloodstream (endocrine)/ locally (paracrine)
* ie: Gastrin secreted from antral G cells when peptides and amino acid in stomach
* ie: CCK secreted from intestinal I cells in response to fats, hence stimulate enzyme secretion from pancreatic acinar cells, promote gallbladder contraction, relax hematopoietic sphincter
Polarized secretion
Gut endocrine cells are polarized (have 2 distinct sides)
1. Apical side (face gut lumen) have microlli to detect nutrients
2. Basolateral side (face blood) hormones are secreted basolateral into capillaries not into gut lumen (unlike digestive enzymes)
Neural and paracrine regulation
Receive signals from enteric nervous system and neighbouring cells to release GI hormones,
* ie: somatostatin from gastric D cells inhibit gastric release by binding to SSTR2 receptors on parietal cells to inhibit acid release + bind to antral G cells to inhibit gastrin release
* ie: histamine opposite effect of somatostatin, released by gastric enterochromaffin like cells to stimulate acid secretion through paracrine control
Acting as receptors to detect luminal changes of stimuli
5)
a) Give an account of the factors that determine the setting up of a resting membrane potential in
excitable cells. (7 marks)
* Vm (resting membrane potential = -70mV)
Setting up Vm
* Basal state: K+, Pr= higher conc inside cell, Na+, Cl- higher concentration outside side
* Membranes are inherently more permeable to K+ because more K+ leak channels, therefore K+ flow out much faster than Na+ flow in. K+ diffuse out, down concentration gradient Pr- stay behind because too large, creates charge separation. Inside of cell becomes more negative
* K+ attracted to negative inner surface of membrane because of Pr- and move back in (electrical force for K+ oppose chemical force)
* K+ outflow slow down, Na+ inflow speed up → membrane potential stabilise
* To prevent Na+, K+ conc gradient dissipation, Na+/K+ ATPase pumps move 3Na+ out 2K+ in
1. Intracellular and extracellular [Na+] and [K+] concentration in determining equilibrium potential
2. Differences in membrane permeabilities
3. Presence of impermeable intracellular Pr-
4. Activity of Na+&.K+ ATPase pump
b) Briefly explain the significance of establishing such a potential difference across the cell
membrane. (3 marks)
* Vm forms basis of cells to become excitable through AP generation
* Operate voltage gated ion channels for release of signaling molecules
* Generate intracellular messengers/ producing change in cellular activity ie: contraction
Describe how the nervous system and its associated sensors and effectors are structurally and
functionally organized into forming different components of a homeostatic control system. Explain
what structural and functional features are built in place to ensure that the flow of neuronal signals
is unidirectional.
ive components of homeostatic control system: sensor/sensory receptor(PNS) 🡪 afferent (sensory pathway – sensory neuron (+interneuron))(PNS) 🡪 control center (CNS) 🡪 efferent pathway(autonomic/somatic motor neuron)(PNS) 🡪 effector(organs/tissue)
The sensors will detect the change in body conditions, such as temperature, pH, pressure, osmolarity and so on, the sensors will then send nerve impulses via the sensory neuron to the regulatory centers in the brain, which will then send out signals via autonomic nervous system or motor neurons to minimise the change and to provide a more stable internal environment for the body to conduct various reactions or functions.
Structural feature that ensures the unidirectional flow of neuronal signals: Membrane differentiation of presynaptic and postsynaptic cleft at a chemical synapse – on the presynaptic side, synaptic vesicles are clustered in the cytoplasm adjacent to the region of membrane specialization named active zone. On the postsynaptic side, neurotransmitter receptors are concentrated in the postsynaptic density. Therefore, release of neurotransmitters from the presynaptic cell to bind receptors on the postsynaptic cell only, but not vice versa, allowing a unidirectional flow of information.
Functional feature that ensures the unidirectional flow of neuronal signals: The presence of refractory period and after-hyperpolarization, at which both activation and inactivation gates of voltage-gated Na+ channel are closed and the channel cannot open again until the membrane potential repolarized to more negative value that it cannot be activated shortly, preventing the AP from propagating in the reverse direction, thus only the more distal and nascent region will depolarize to reach the threshold.
2021
1a) Write an aid of a buffer curve, briefly describe how to choose a good buffer [6]
* Buffer: mixture of weak acid/base + conjugate acid/base
* pH of buffer adjusted to pKa of weak acid/ pKb of weak base because at such pH, the concentration of acid and conjugate base are equal to maximise ability to neutralize exogenous acid/base added to solution
* Concentration of buffer should be high to increase buffering capacity
1b) Briefly describe ONE example of body buffers [4]
3a) List 3 major functions of vasoactive polypeptides (VIP) [3]
* Vasodilation and increase blood flow
* Stimulate intestinal and electrolyte secretion
* Relax GI sphincter and circular smooth muscle
3b) Briefly describe the underlying mechanisms of VIPomas-induced diarrhea [7]
* Rare endocrine tumour overproduce VIP in pancreas
* VIP stimulate GPCR, activates adenylyl cyclase ATP → cAMP → increase PKA → increase protein phosphorylation
* Increase CFTR Cl- channels at apical membrane for Cl- secretion
* Active NaCl secretion >>>> rate of NaCl absorption
* Water follows Na+
* Water diarrhea
4) Give a brief account of the structural and functional organization of a typical neuron into 4 parts. Explain how the specialised role of these different parts of a neuron is related to the specific ion channel expression on the cell surface [10]
Dendrites
Cell Body (Soma)
Axon Hillock
Axon
Structure
Highly branched, tree like extensions to receive signals from other neurons
Contains nucleus, rER, nissl bodies for protein synthesis
Junction between soma and axon, high density of voltage gated channels
Long, myelinated schwann cells (PNS)/ oligodendrocyte (CNS) with periodic nodes of ranvier
Function
Detect and integrate synaptic input
Synaptic potential (graded potential → spatial/ temporal summation) - excitatory/ inhibitory postsynaptic potential
Integrate incoming signals from dendrites, metabolic center
AP initiation zone (threshold decision point)
Rapid, long distance AP propagation
If have myelin sheath = saltatory conduction
Ion channels
Ligand gated channels respond to neurotransmitters
Passive leak K+ channels - maintain Vm (=70mV)
Ligand gated receptors - modulate excitability
Passive leak K+ channels - maintain Vm (=70mV)
High density voltage gated Na+ channel - rapid depolarization when threshold (-55mV) is reached → generate all/none AP
Voltage gated Na+ and K+ channels (depolarization & repolarization) concentrated at nodes of ranvier for saltatory conduction
Myelin sheath - prevent ion leakage, speed up conduction
5) Use a named example to describe the organization of neuroendocrine control and to explain its significance [10] - neuroendocrine control of anterior and posterior pituitary hormones
ADH under neuroendocrine control - vital in maintaining ECF osmolarity and long term BP management
Specific stimuli + receptor + afferent neuronal control
1. Increase in plasma osmolarity sensed by hypothalamic osmoreceptors
→ interneurons to hypothalamus
2. Decrease atrial stretch due to low blood volume detected by atrial stretch receptor (volume receptor)
→ sensory neurons to hypothalamus
3. Decrease blood pressure detected by carotid and aortic baroreceptor
→ sensory neurons to hypothalamus
Hypothalamus + posterior pituitary: Such neural inputs are converged on the hypothalamus, where hypothalamic neuroendocrine cells produce ADH and release it via hypothalamic neurons – paraventricular and supraoptic nuclei. ADH transport via hypothalamic hypophyseal tract to the posterior pituitary’s axon terminal for storage. Once hypothalamic neurons fire, ADH is released into the blood and travels to target organs like the kidneys collecting duct.
At collecting duct: ADH binds to ADH receptors on basolateral membrane, causing increase in adenylyl cyclase activity to ATP → cAMP, increase PKA increase protein phosphorylation, cause vesicles with aquaporin 2 to move to apical membrane and exocytosis AQP2 to apical membrane. This increased collecting duct permeability allows more water to be passed from tubular lumen through Aquaporin2 and Aquaporin 3,4 back to blood for reabsorption. This reduces water excretion, producing small volume of concentrated urine, which allows for plasma osmolarity to be reduced, with increased blood volume, ECF BP will also increase → negative feedback homeostatic control.
6) Briefly explain the role of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) in the regulation of Na+ balance [10]
ANP & BNP are cardiac hormones released in response to increased blood volume and pressure. They promote natriuresis (Na+ excretion) and diuresis (water loss) to restore fluid-electrolyte balance when ECF volume is expanded. Oppose the effects of aldosterone and ADH to ensure homeostasis
Released by:
* Cardiac atria → ANP (response to atrial stretch)
* Cardiac ventricles → BNP (response to pressure overload)
Target Organs
* Kidney
* Increase GFR with little change in RMF → more Na+ filtered
* Inhibit Na+ reabsorption in DCT & CT
* Suppress renin secretion → reduce angiotensin II and aldosterone (reduce Na+ retention)
* Blood vessels
* Dilate afferent arteriole and constrict efferent arteriole → increase GFR
* Adrenal glands: inhibits aldosterone release
* Hypothalamus: suppress ADH → reduce water reabsorption
Net effect on Na+ Balance
* Increase Na+ excretion to reduce plasma Na+; increase water excretion to lower blood volume and pressure; counteracts RAAS by preventing excessive Na+ retention
2122
1a) Define “buffer” [2]
Solution that resists pH change when small amounts of weak acid/ base is added
1b) Briefly describe 2 examples of body buffers [8]
2) Describe the mechanisms that lead to autoregulation of glomerular filtration rate and renal blood flow [10]
GFR is maintained by keeping Pgc constant, involves differential alteration of afferent arterioles
1. Myogenic reflex (rapid response)
↓BP → ↓blood flow → ↓glomerular filtration pressure → ↓stretch → dilation of afferent arterioles → ↑volume → ↑glomerular filtration pressure
2. Tubuloglomerular feedback
↑GFR → ↑NaCl concentration in tubule fluid in loop of Henle → sensed by macula densa cells in juxtaglomerular apparatus of distal convoluted tubule → sends signal to afferent arteriole → increase resistance of afferent arteriole via constriction → ↓GFR
* Autoregulation absent when arterial pressure <90 mmHg
* Autoregulation not perfect, RMB and GFR do change slightly as arterial BP varies
* Can be influenced by hormones (RAAS, ADH, ANP) and sympathetic activation
3a) What is the first-pass effect? [2]
First-pass effect refers to the loss of drugs as they pass through the organs of elimination, e.g. stomach, intestines and livers, for the first time during drug absorption, reducing the bioavailability of drugs.
3b) Describe the characteristics of gut endocrine cells that produce these GI hormones [8] 翻炒
Enteroendocrine cells are specialised epithelial cells that secrete peptide hormones in response to luminal stimuli
Location in GI tract
Scattered within mucosal epithelium, predominantly in
* stomach
* Antral G cells → gastrin
* Antral D cells → somatostatin
* small intestine
* K cells → GIP
* S cells → secretin
* I cells → CCK
Morphology
3. Open type cells (most common) - have microvilli extending to lumen to sense nutrients (ie: glucose, amino acids, fats), mechanical stimuli
4. Closed type cell: do not directly contact lumen, respond to paracrine/ neuronal signal
Hormone secretion mechanism
Stimuli: food component/ pH change → trigger hormone release into bloodstream (endocrine)/ locally (paracrine)
* ie: Gastrin secreted from antral G cells when peptides and amino acid in stomach
* ie: CCK secreted from intestinal I cells in response to fats, hence stimulate enzyme secretion from pancreatic acinar cells, promote gallbladder contraction, relax hematopoietic sphincter
Polarized secretion
Gut endocrine cells are polarized (have 2 distinct sides)
3. Apical side (face gut lumen) have microlli to detect nutrients
4. Basolateral side (face blood) hormones are secreted from basolateral into capillaries not into gut lumen (unlike digestive enzymes)
Neural and paracrine regulation
Receive signals from enteric nervous system and neighbouring cells to release GI hormones,
* ie: somatostatin from gastric D cells inhibit gastric release by binding to SSTR2 receptors on parietal cells to inhibit acid release + bind to antral G cells to inhibit gastrin release
* ie: histamine opposite effect of somatostatin, released by gastric enterochromaffin like cells to stimulate acid secretion through paracrine control
Acting as receptors to detect luminal changes of stimuli
4) Explain which 2 factors are most important in determining velocity of action potential propagation along the length of an axon [10]
* Myelination
* In non-myelinated nerves, only continuous conduction is possible as high conductance along unmyelinated nerves cause rapid decrement of AP down length of axon. Continuous conduction involves generation of short local currents for the AP to spread slowly along the axon.
* In myelinated axon, AP is induced to only generate at nodes of ranvier and propagate rapidly by jumping from node to node → saltatory conduction. The depolarizing current doesn't leak through the internodal region due to high resistance of myelin sheath and low density of Na+ and K+ channels. Nodes of ranvier are exposed to ECF and have highest concentration of voltage gated Na+ and K+ channels and Na+/K+ATPase
* Diameter of axon
5) Describe the structural and functional relationship between pituitary gland and hypothalamus, and how they relate to the organization of neuroendocrine control [10]
Neuroendocrine control refers to the integration of sensory afferents by the neural system, and production of efferent responses via endocrine system for a more long term effect on the body.
Pituitary divided into anterior and posterior parts, as a downward extension of hypothalamus:
1. Anterior pituitary
* Under higher brain centre’s neural input (ie: stress, circadian rhythm, central glucopenia) , neural signals via neurotransmitters travels to hypothalamus, it triggers hypothalamus secrete hypothalamic releasing [GHRH, CRH, TRH, GnRH, VIP] / inhibiting hormones [dopamine, SRIF] into primary capillary plexus, into median eminence, via hypophyseal portal system into anterior pituitary. These hypothalamic releasing/ inhibiting hormones that induce the production of anterior pituitary hormones (FSH, LH, GH, ACTH, TSH, prolactin) and they are released from secondary capillary plexus into blood.
2. Posterior pituitary
* Under sensory input from various body parts converging to hypothalamus, ie: osmoreceptors, baroreceptors, suckling of breast). These specific stimuli trigger neural signals via neurotransmitters to the hypothalamus, where neuroendocrine cells produce ADH and oxytocin. They are released via hypothalamic neurons - paraventricular and supraoptic nuclei to posterior pituitary via hypothalamic hypophyseal tract. They are stored in axon terminals until hypothalamic neurons fire and cause ADH and oxytocin to be released into blood.
6a) A person is unable to produce sufficient respiratory surfactants due to unknown medical reasons. In order to inhale a normal tidal volume of 500ml at rest, will his/her intrapleural pressure have to be more/ less sub-atmospheric during inhalation, relative to a healthy person? [3]
* Normal Pip = -4mmHg
* Insufficient respiratory surfactant increase surface tension of alveoli → collapse during expiration, decreasing alveolar pressure
* Ptp determine degree of lung expansion = Palv-Pip
* In order to have same tidal volume, greater Ptp is required, therefore more negative Pip required
6b) What would happen to the transpulmonary pressure that occurs to the person in (a) [1]
Increase
6c) Describe how breathing deeply by a healthy person can affect the production of surfactants [2]
Deep breath stretch alveoli, stimulate secretion of surfactant by type II alveoli
6d) Describe how taking similar deep breaths by the same person in (b) can also transiently improve their venous return at the same time? [4]
Deep breathing facilitate respiratory pump mechanism
Inhale: diaphragm descend, pushing abdominal content and increase abdominal pressure
Pressure in thorax decrease
Creates pressure gradient between veins and lung → enhance venous return towards heart
2223
1 (a) Describe the events that occur at a chemical synapse between the axon terminal of a presynaptic
neuron and the cell body of a postsynaptic cell. (6 marks)
(b) Explain how the arrangement of a chemical synapse would determine a unidirectional flow of
information from the pre-synaptic cell to the post-synaptic cell. (4 marks)
As MED1 students, they were not particularly precise in what they put down in the answers.
• With the arrival of the action potential (and not simply as a “nerve impulse”) at the axonal terminal, it
triggers the opening of the voltage-gated calcium (Ca2+) channel (VGCC) rather than “calcium (Ca2+)
voltage-gated channel”.
• In the nerve terminal (unlike in heart muscle cells and smooth muscle cells), influx of extracellular Ca2+
does not result in Ca-induced Ca release from intracellular store.
• Ca2+ ions do not bind to receptors at the nerve terminal. In MED2, students will be introduced to Ca2+
binding to synaptobrevin acting as a Ca2+
sensor to trigger the exocytosis of synaptic vesicles.
• In a chemical synapse, the neurotransmitter triggers the generation of postsynaptic potential in the
postsynaptic cell. Though they are graded potential, it would be better to refer to these as postsynaptic
potentials as there are other examples of graded potential such as receptor potential produced by the
activation of sensory receptors in response to other forms of stimuli (e.g. mechanical, light, heat, etc.)
unrelated to action of neurotransmitters at a chemical synapse. When abbreviations are used, they should
be written in full form when first introduced – excitatory postsynaptic potential for EPSP and inhibitory
postsynaptic potential for IPSP.
• When describing the events that occur at a chemical synapse (chemical signal), there is no need to go into
describing the generation of action potential, and its unidirectional propagation (electrical signal) as the
other determinant in the unidirectional flow of information in the nervous system.
2a) The mean systemic arterial pressure is the arithmetic product of two factors. Name and define these
two factors. (1 mark)
(b) With an aid of a flow diagram, summarise how a baroreceptor reflex makes use of the two factors
mentioned in (a) to compensate for a fall in arterial pressure due to haemorrhage. (8 marks)
(c) In this type of homeostatic control mechanism, what kind of feedback system is activated? Define this kind of feedback system using the example summarised in (b). (1 mark)
Teacher feedback:
• Performance of this question was generally good.
• Cardiac output is the blood ejected by either the left or right ventricle per minute. It is ok to say per unit
time but it is not true to say it is the blood volume ejected by the left ventricle only. Some students did not
define both CO and TPR separately. Only half mark was given.
• It was acceptable to use the CO equation to define CO as SV multiplied by HR. Still, unit of CO should have
been indicated in the answer.
• TPR is the sum of total resistance in the systemic circuit or from aorta to ends of vena cava. Full score would
not be given if only total resistance of blood vessels is provided.
• Full marks would be given only if a complete flow diagram summarizing a baroreceptor reflex was shown.
You may refer to slide 18 of lecture 5 (Body circulation- the heart) for the answer to this question.
• A proper flow diagram should always include primary stimulus, receptors, integrator and the multiple
effector responses. In this question, if the original stimulus is a fall in MAP, the effector responses should
show how a rise in MAP can be achieved.
• Some students could not write a flow diagram properly and some flow diagrams were broken with long
sentences in between and thus no full marks could be given.
• Many students forgot to include the location of baroreceptors and name of the integrator in their answer.
• Most students could indicate negative feedback clearly in their answers but some students forgot to refer
to the change of MAP as the required example.
• Vasoconstriction of arteries or of blood vessels was not specific enough to raise TPR and thus some students
did not get full score as arterioles are major site of resistance and this needed to be stated clearly in the
answer.
3) Explain how the renin-angiotensin system affects renal vascular function and tubular sodium transport? (10
marks)
4) Most gastrointestinal (GI) hormones regulate certain aspects of the GI luminal environment in a feedback
mechanism and affect more than one effector. Using cholecystokinin (CCK) as an example, explain how the
changes in the luminal environment lead to various effector responses. (10 marks)
Teacher feedback:
Students performed satisfactorily on this question. Please take note of the following important concepts
together with the associated misconceptions encountered by students:
- The release of CCK from duodenal i cells is triggered
o by the presence of fatty acid and amino acid in the duodenum;
o BUT NOT by the acidic duodenal environment which only triggers the release of secretin
from duodenal s cells.
- CCK in circulation will then trigger the release of
o enzymatic secretion from the pancreatic acinar cells;
o BUT NOT the release of bicarbonate secretion from the pancreatic ductal cells.
5) Name the THREE major types of stimuli (or signals) that control hormone secretion. For each of these, describe using one NAMED example to illustrate how it is organized into controlling the hormone secretion and forms a component of the feedback control loop. (10 marks)
Teacher feedback:
This is a new question and some students were taken by surprise and wrote on something totally unrelated
(e.g. on endocrine, autocrine, paracrine control).
• When answering this question, some students use insulin as an example of a hormone responding to
humoral stimulus (i.e. blood glucose level). However, it is totally wrong to state that insulin is secreted by
the liver (instead of the pancreatic -cells).
• In addition, blood glucose level is directly sensed by the pancreatic -cells and not by the gastrointestinal
tract. Also, there are no glucose receptors to sense blood glucose levels.
• For hormone controlling the secretion of other hormones, only growth hormone and prolactin are
examples of anterior pituitary hormones that exert short-loop negative feedback on the secretion of their
respective hypothalamic hormones.
• In the control of antidiuretic hormone secretion, though it responds to changes in plasma osmolarity, ADH
secreting cells are not directly responding to humoral stimulus (e.g. plasma osmolarity). ADH secreting
neuroendocrine cells are responding to neural input originating from hypothalamic osmoreceptors(a type
of hypothalamic neurons), baroreceptors located in aortic arch/carotid sinus and volume receptors
located in right atrium/vena cava.
6) Describe the visual pathway from photoreceptor cells to the primary visual cortex. What is the possible visual
impairment in a patient with lesion in the right temporal lobe of the brain? (10 marks)
Teacher feedback:
Most students correctly answered the question. Some students just answer LGN in short form and it would
be better to give the answer in full name “Lateral geniculate nucleus”. Please note that this lesion affects both
eyes but few students say it just affect either left or right eye.
2324
1a) Define venous return
1b) Briefly explain 4 factors that facilitate venous return.
1c) Illustrate how increase in venous return facilitate increase in mean arterial pressure with flow diagram
4) Name the three chemical classes of hormones. Explain how their differences in chemical nature affect: (a) receptor localisation on cell membrane
HSII SAQ reference answers (from Anes 24).docx MEDF 1010 17-18
HS2 LQ Answers (13-19).docx