gastroenterology past year papers

PAST YEARS COMPILATION PAPERS (2006 & 2007) QUESTIONS AND - Sympathetic cause vasoconstriction in the renal.
ANSWERS. - Renal blood flow decrease
- Renin is secreted by the juxtaglomerular cell
CREDIT TO: RCSIanS’08 - aldosterone secretion is increase that cause high Na+
reabsorption into the blood.
Summer 2006 - This will result in increase K+ secretion into the tubular
system and being excreted by the urine.
Q1. Following severe vomiting, a patient has developed hypokalaemia (low - Thus, K+ in the blood low  hypokalemia.
plasma
[K+]) and metabolic alkalosis. The patient is showing signs of hypovolaemia - Intrarenal volume receptor:
(low blood volume). Explain how (a) vomiting itself, (b) hypovolaemia and - In hypovolemia, this receptor will control the renin secretion.
(c) metabolic alkalosis may contribute to the patient’s hypokalaemia. - Increase in renin secretion cause increase in aldosterone level.
- Aldosterone cause increase in reabsorption of Na+
a) Vomiting may contribute to the patient’s hypokalemia by 2 ways, direct - Reabsorption of Na+ into the blood is exchange with the
and indirect. secretion of K+ into the tubular system. Thus, K+ loss through
Direct via mouth: the urine.
- Severe vomiting cause loss of GIT content especially gastric
juice. c) Metabolic alkalosis may contribute to the patient’s hypokalaemia:
- Gastric juice contain high K+, NaCl and H+ - metabolic alkalosis stimulate the Na+/K+ pump at the distal
- This will cause decrease in plasma [K+] tubule and collecting duct.
- Thus, increase in reabsorption of Na+ into the blood cause
Indirect via kidney: exchange mechanism of K+ into the tubular filtrate and excreted
- When plasma [K+] decrease due to loss of GIT fluid, this will cause into the collecting duct as one of the urine compounds. 
disturbance of salt/water balance result in decrease ECF and BV hypokalemia.
- Also disturb the acid/base balance. This will cause metabolic alkalosis.
- metabolic alkalosis stimulate activity of Na+/K+ pump thus cause K+ Q2. A young man, who sustained a complete spinal cord transection in the
being secreted into the filtrate. thoracic region a few years ago, has no voluntary control over the
- increase [K+] loss in the urine micturition reflex i.e. he has developed an “automatic” bladder. Describe
- Plasma [K+] decrease.  hypokalemia how the reflex occurs in this patient.
- micturation reflex in normal person consist of 2 steps: - filling of
b) Hypovolaemia may contribute to the patient’s hypokalemia: the bladder and storage – reflex emptying of bladder via internal
- Low blood volume may cause stimulation atrial volume receptor and external sphincter.
and intrarenal receptor. - In person developed an automatic bladder,
- Atrial volume receptor: - The filling of the bladder occur normally and cause stretch of
- Stimulate production of ADH in the hypothalamus and increase detrusor wall
reabsorption of water into the blood. - This activate the stretch receptor on the wall  increase in PNS
-This cause low in ECF and plasma osmolarity. sensory afferent
-This cause disturbance of salt/water balance. Thus, Na+ is - Afferent connects to s2 – s4 with PNS motor efferent to bladder.
also reabsorbed. - This cause increase in PNS motor efferent activity  detrusor
-When Na+ is reabsorbed into the blood, K+ is secreted into muscle contraction.
the tubule as they used exchanger Na+/K+ pump. - Bladder pressure increase and cause opening of internal
- Low K+ in blood  hypokalemia sphincter.
- Stimulate renal medulla to modulate sympathetic renal nerve - Thus, urine is propelled involuntarily.
activity.

,Q3. Following prolonged diarrhoea, a patient’s laboratory report showed Q5. An elderly man is diagnosed with mild congestive heart failure. The
the following: symptoms include breathlessness on walking and swollen ankles. The
Blood pH = 7.32 (reference = 7.4) patient is prescribed a thiazide diuretic drug, Chlorothiazide. Outline
Plasma [HCO3] = 15 mmol/l (reference = 24 mmol/l) (a) the mechanism of action of this drug and
Plasma PaCO2 = 30 mmHg (reference = 40 mmHg) (b) the possible adverse effects.
Answer the following questions, giving reasons for your answers:
congestive heart failure: is a condition of HF that is marked by inability of the
a) What acid-base disturbance is present? heart to maintain adequate blood circulation in the peripheral tissues and the
- Metabolic acidosis lungs and can be caused by many reasons primary: left ventrical impairment.
Secondary:from hypertension, valve failure, congestion, arteriosclerosis, etc.
b) Has compensation occurred? If so, describe the mechanism. Using chlorothiazide, a diuretic, can decrease the symptoms and complication sof
- Respiratory compensation occurs. this HF i.e. oedema adn dyspnoea by enhancing Na+ excretion in urine in d
- Mechanism: kidneyreducing vascular volume and preload (hence systolic n diastolic BP)
- Decrease blood pH will cause increase the activity of chemoreceptor. and decreasing overall distribution of ECF.
- This will increase the rate of breathing and thus decrease paCO2 in the blood. Mechanism of action: Act mainly in distal tube to ↓ the reabsorption of Na+ by
- Consequently, the pH is raised since the ratio increase. binding to the Cl- site of the Na+/Cl- cotransporter on the luminal membrane and
inhibiting its action
c) Why does diarrhoea cause the acid-base disturbance you have • Results in ↑ concentration of Na+ & Cl- in tubular fluid
identified? Adverse Effects: serious unwanted effects relatively rare
- Diarrhoea causes loss of GIT fluid. a) Potassium depletion: frequent problem
- GIT fluid contains pancreatic, colonic and intestinal fluids which are high in b) Hyperuricemia: gouty attacks
HCO3 c) Volume depletion: can cause dizziness
- This will cause high loss of HCO3. d) Hypercalcemia: thiazides inhibit secretion of Ca++, can lead to ↑ Ca++ in blood
- Since the ratio decrease, the pH also decrease (metabolic acidosis) e) Hyperglycemia
f) Hypersensitivity: bone marrow suppression, dermatitis, are rare

Q4. A 32-year old woman presents with mild to moderate hypertension.
Briefly describe the ways in which aldosterone may be involved in the
aetiology (cause) of hypertension. Q6. In panhypopituitarism, the levels of human growth hormone (HGH) are
low. Describe the factors which normally control human growth hormone
Hypertension= increase in BP over a period of time. Mild to moderate (HGH) secretion and explain why the levels of HGH are low in
hypertension usually related to secondary causes of hypertension e.g. kidney panhypopituitarism.
disease.
Aldosterone: is a hormone produced in zona glomerulosa of adrenal cortex. It’s  HGH: Most abundant hormone produced by anterior pituitary
main function is enhancing the reabsorption of Na+ from DCT of kidney by
causing translation/ synthesis of Na+ pump and Na+/K+ pump on apical and  Even in adults in whom growth has ceased
basolateral membrane respectively.
High amount of aldosterone e.g. due to aldosterone secreting tumours of adrenal  GH secretion typically declines after middle age
cortex (Conn’s syndrome) will cause high level of Na+ reabsorption and hence
high water retention and hence cause blood and ECF volume expansion. High Normal control of HGH
blood volume will cause high bloop pressurehypertension. High ECF volume,  Complex
exceeding its critical threshold will cause oedema
 Two hypothalamic hypophysiotropic hormones

,  GHRH  FSH & LH – collectively gonadotropins

 Stimulates secretion & synthesis of GH  Prolactin (PRL)

 GHIH
Q7. Ann is a 26 year old woman who has had insulin-dependent diabetes
 Inhibits GH release in response to GHRH & e.g. low mellitus for the past six years. Diabetic retinopathy has now been
blood glucose diagnosed.
a) Describe the symptoms and consequences of diabetic retinopathy
 Negative feedback loop involving IGF-1 o One of the major causes of blindness
o Symptoms: Blurred vision & blood spots visible (Due to haemorrhage and
 High blood levels IGF-1 lead to decreased GH secretion Microaneurysms)
Proliferative Diabetic Retinopathy
 Suppressing somatotrophs • Local ischaemia/hypoxia triggers theactivation of a transcription factor,hypoxia-
inducible factor (HIF)
 Stimulating release of GHIH from hypothalamus • HIF promotes the expression of genes that stimulate the formation of new blood
vessels
 GH also feedbacks to inhibit GHRH secretion • One of these factors is VEGF (vascular endothelial growth factor)
• This process of neovascularisation combined with other factors may
Panhypopituitarism: result in debilitating loss of vision in diabetics
 Decrease in secretion in all anterior pituitary hormones
b) List the other microvascular complications associated with insulin-
 Causes dependent diabetes mellitus
o Diabetic neuropathy (Autonomic & Peripheral Neuropathy)
 Congenital o Diabetic nephropathy (May lead to chronic renal failure)

 Pituitary tumour that destroys the gland Q8. Explain briefly why a patient with adrenal 21-hydroxylase deficiency
presents with a raised level of ACTH. Describe the symptoms which may
 Infarction of portal vessels during pregnancy occur in this condition.

Anterior pituitary hormones includes:  ACTH (Adrenocorticotropic Hormone) is produced by Anterior Pituitary Gland
 The Anterior Pituitary synthesizes its hormones to stimulate production of Cortisol and Aldosterone (Only at high
concentration of ACTH) by Adrenal cortex
 Growth hormone (GH, Somatotropin)..so…??  Adrenal 21-Hydroxylase is one of the enzymes that essential for production
of Cortisol from Cholesterol
 Adrenocorticotropin hormone (ACTH, Adrenocorticotropin)  Cortisol will then give negative feedback inhibition to the production of ACTH
 But in the case of 21-Hydroxylase deficiency, less or no Cortisol being
 Thyroid-stimulating hormone (TSH, thyrotropin) produced
 So, there will be no negative feedback to inhibit production of ACTH.
 Follicle-stimulating hormone (FSH) Concentration of ACTH will rise
 Since Cholesterol cannot be converted to Cortisol or Aldosterone, more
 Leutinizing hormone (LH, ICSH) cholesterols are available for production of estrogen & testosterone
 Symptoms :