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63 Cards in this Set
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ME42a ANZCA version [2004-Aug] Q148, [2005-Apr] Q66, [Apr07] |
ANSWER B
Perioperative Considerations for Anorexia Nervosa Cardiovascular -hypotension : resulting from dehydration -bradycardic : decreased basal metabolic rate -ECG : AV block, ST depression, T wave inversion and QT prolongation; >80% will have an ECG abnormality -QT prolongation maybe caused by hypocalcaemia, hypomagnaesemia, drugs or starvation -hypophosphataemia reduces arrythmia threshold -Other arrhythmias : sinus arrest, wandering atrial pacemakers, nodal escape beats, SVT or VT; Reported incidence of 16-62% under anaesthesia. -reduced myocardial contractility : due to malnutrition, also ipecac is directly cardiomytoxic, avoid fluid overload -mitral valve prolapse Respiratory -metabolic alkalosis from self induced vomiting and laxatives produces compensatory bradypnoea -pneumothorax -aspiration pneumonia -pneumomediastinum Renal -hyponatraemia, hypokalaemia, hypochloraemia, hypomagnesaemia, hypocalaemia metabolic alkolosis -renal calculi from chronic ingestion of magnesium hydroxide |
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ME42b ANZCA version [2005-Sep] Q124, [Mar06] Q55
Complications of severe anorexia nervosa (body weight < 40% ideal) include all of the following EXCEPT A. cardiomyopathy B. delayed gastric emptying C. hypokalaemia D. hypercalcaemia E. prolonged QT interval |
ANSWER D
Perioperative Considerations for Anorexia Nervosa Cardiovascular -hypotension : resulting from dehydration -bradycardic : decreased basal metabolic rate -ECG : AV block, ST depression, T wave inversion and QT prolongation; >80% will have an ECG abnormality -QT prolongation maybe caused by hypocalcaemia, hypomagnaesemia, drugs or starvation -hypophosphataemia reduces arrythmia threshold -Other arrhythmias : sinus arrest, wandering atrial pacemakers, nodal escape beats, SVT or VT; Reported incidence of 16-62% under anaesthesia. -reduced myocardial contractility : due to malnutrition, also ipecac is directly cardiomytoxic, avoid fluid overload -mitral valve prolapse Respiratory -metabolic alkalosis from self induced vomiting and laxatives produces compensatory bradypnoea -pneumothorax -aspiration pneumonia -pneumomediastinum Renal -hyponatraemia, hypokalaemia, hypochloraemia, hypomagnesaemia, hypocalaemia metabolic alkolosis -renal calculi from chronic ingestion of magnesium hydroxide |
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ANZCA April 2007 [25].
An INCORRECT statement regarding the management of hypocalcaemia is that A. correcting a respiratory or metabolic alkalosis increases the level of ionised calcium B. undiluted calcium should be administered via a central vein as it is irritant to peripheral veins C. acidosis will decrease calcium binding to albumin and therefore increase ionised calcium D. when calcium alone is not sufficient for control of hypocalcaemia, Vitamin D metabolites can be added E. calcium chloride has been shown to be superior to calcium gluconate |
ANSWER E
Serum ionised calcium < 0.50mmol/L is a medical emergency Management 1. Correct any coexisting respiratory or metabolic alkalosis 2. Avoidance of Calcium lowering drugs 3. Administration of calcium IV -bolus 100-200mg over 10minutes -maintenance of 1-2mg/kg/hr -Ca gluconate 10%, 10ml contains 9.3mg calcium -CaCl 10%, 10 contains 27.2mg calcium -Calcium is irritating to veins and should be diluted before administration and all solutions are best administered through a central vein. o Ionised Ca affected by pH o Acidosis ↓ Ca binding to albumin →↑ ionised Ca o Alkalosis ↑Ca binding (calcium shifts onto the albumin molecule), → ↓ionised calcium. Respiratory alkalosis may occur with acute hyperventilation, thus lowering ionised calcium. |
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Medical Management of Hypercalaemia
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Treatment is directed by severity of hypercalcaemia, it is medical emergency and treatment should be initiated before diagnosis.
Low : Ca>2..0 Mod : Ca>2.0 with mild symptoms High : Ca>3.0 with moderate symptoms Symptoms may include dehydration, polyuria, tachycardia, pyschosis, anorexia, weakness, lethargy and vomiting Principles 1. Rehydrate: infusion of normal saline (150ml/hr) is the basic treatment. 4-6 litres may be needed. 2. Bisphosphonates: Pamidronate 60mg in 500 ml saline over 4 hrs. This is the drug of choice for life threatening hypercalcaemia. They are potent inhibitors of osteoclastic bone reabsorption. 3. Calcitonin 3-4U/kg IV then 4U/kg SC bd. This rapidly decreases the skeletal release of calcium and phosphorous but its effects are only temporary 4. Life threatening levels of calcium >4.5 mmol/l can be rapidly lowered with phosphate (500ml of 0.1M neutral solution over 6-8 hrs). Again, this effect is transient. Other : 1. Forced saline diuresis: is a second line treatment once the dehydration is corrected. Loop diuretics such as frusemide are used (40mg IV every 4hrs.). Frusemide inhibits the proximal tubular reabsorption of calcium. Forced saline diuresis, however, presents a significant risk of fluid overload, electrolyte disturbances and LVF in the elderly, so CVP monitoring should be considered. 2. Consider hydrocortisone 200-400mg IV in malignancy induced hypercalcaemia although this is ineffective in primary hyperparathyroidism. 3. Haemodialysis in patients with coexisting renal failure |
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ME01
Which of the following are characteristic of hyperaldosteronism? A. Low NaCl in serum B. Low NaCl in urine C. High NaCl in serum D. High NaCl in urine |
ANSWER A and C
Primary hyperaldosteronism is one of the more common causes of secondary hypertension. The term Conn's syndrome is used for primary hyperaldosteronism secondary to an adrenal adenoma secreting aldosterone. The syndrome is due to: * bilateral idiopathic adrenal hyperplasia 70 % * unilateral idiopathic adrenal hyperplasia 20 % * aldosterone-secreting adrenal adenoma (benign tumor, < 5%) * rare forms, including disorders of the renin-angiotensin system Aldosterone acts in kidney to increase Na+ reabsorption and increase K+ secretion. Consequently serum K+ is low: hypokalaemia. The result is hypokalaemic metabolic alkalosis due to H+ ion loss Hypomagnesemia and hypoglycaemia may also be present |
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ME02 [Sep90] [Apr99]
In hyperaldosteronism, the following may be seen: A. Malignant hypertension B. Severe muscle weakness C. Hyperkalaemia D. Skin pigmentation E. Cardiac arrhythmias F. Prolonged response to nondepolarizers |
# A - false - Hypertension is usually mild (Ref: Oxford handbook)
# B - true - Hypokalaemia can be marked and cause muscle weakness # C - false - Hypokalaemia occurs due to increased urinary secretion (in exchange for the increased Na+ reabsorption) # D - false - This distractor refers to Addison's Disease # E - true - Arrhythmias due to hypokalaemia # F - true - due to hypokalaemia |
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ME03 [Mar92]
Addison's Disease: A. Hyperkalaemia B. Water and sodium depleted C. Hyperpigmentation is usually present D. Metabolic acidosis |
ALL CORRECT
Addisons Disease : Primary adrenocortical insufficiency. -insidious, progressive hypofunctioning of the adrenal cortex The adrenal cortex produces a number of hormones * Mineralocorticoids e.g. aldosterone * Glucocorticoids e.g. Cortisol * Sex hormones/Androgens Failure of the adrenal cortex leads to a decrease in these hormones. Destruction of 90% of the cortex is required before insufficiency occurs. Causes -Destruction by antibodies (autoimmune disorder) is the cause in 70-80% of cases -Other causes of Addisons: * TB (previously a common cause but no longer so in Western countries) (eg For anaesthetic-related case report see [1] * Metastases * Bilateral adrenalectomy * Haemorrhage e.g. following meningococcal sepsis Effects of Addisons Disease Skin * Pigmentation due to increased ACTH by anterior pituitary gland. The ACTH cross stimulates Melanocyte Stimulating Hormone (MSH) causing pigmentation Fluid Balance * Hypovolaemia with postural hypotension is typical Acid Base * Metabolic acidosis (low HCO3) Electrolytes * Loss of aldosterone results in loss of Na+ reabsorption by the kidney * Hence urinary Na+ is high * Hyponatraemia * Hyperkalaemia * Haemoconcentration is often present * Hypoglycaemia * high urea Hormonal * Elevated ACTH (>50pg/mL) * Low cortisol (<5ug/dL) Anaesthesia * Volume is a key issue. These patients need intravascular reexpansion * Minimise neuromuscular blockade as hyperkalaemia can cause skeletal muscle weakness |
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ME04
In primary adrenal insufficiency: A. Hypokalaemia is present B. ACTH level is normal C. Hypernatraemia is common D. Pigmentation is usually present |
ALL WRONG
Addisons Disease : Primary adrenocortical insufficiency. The adrenal cortex produces a number of hormones * Mineralocorticoids e.g. aldosterone * Glucocorticoids e.g. Cortisol * Sex hormones/Androgens Failure of the adrenal cortex leads to a decrease in these hormones. Destruction of 90% of the cortex is required before insufficiency occurs. Causes Destruction by antibodies (autoimmune disorder) is the cause in 70-80% of cases Other causes of Addisons: * TB (previously a common cause but no longer so in Western countries) (eg For anaesthetic-related case report see [1] * Metastases * Bilateral adrenalectomy * Haemorrhage e.g. following meningococcal sepsis Effects of Addisons Disease Skin * Pigmentation due to increased ACTH by anterior pituitary gland. The ACTH cross stimulates Melanocyte Stimulating Hormone (MSH) causing pigmentation Fluid Balance * Hypovolaemia with postural hypotension is typical Acid Base * Metabolic acidosis Electrolytes * Loss of aldosterone results in loss of Na+ reabsorption by the kidney * Hence urinary Na+ is high * Serum Na+ is low * Serum K+ is usually high * Haemoconcentration is often present "Hyponatraemia, hyperkalaemia, hypoglycaemia and haemoconcentration are often present." "...Hyponatraemia, Hypovolaemia, Hypotension, Hyperkalaemia and metabolic acidosis..." Anaesthesia * Volume is a key issue. These patients need intravascular reexpansion * Minimise neuromuscular blockade as hyperkalaemia can cause skeletal muscle weakness |
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ME05
Which of the following electrolyte patterns may be found in Addison's Disease: A. High Na+ and Cl- B. Low Na+ and Cl- C. High Na+ and K+ D. Low Na+ and high Cl- E. Low K+ and high Cl- |
ANSWER B
Addisons Disease : Primary adrenocortical insufficiency. The adrenal cortex produces a number of hormones * Mineralocorticoids e.g. aldosterone * Glucocorticoids e.g. Cortisol * Sex hormones/Androgens Failure of the adrenal cortex leads to a decrease in these hormones. Destruction of 90% of the cortex is required before insufficiency occurs. Causes Destruction by antibodies (autoimmune disorder) is the cause in 70-80% of cases Other causes of Addisons: * TB (previously a common cause but no longer so in Western countries) (eg For anaesthetic-related case report see [1] * Metastases * Bilateral adrenalectomy * Haemorrhage e.g. following meningococcal sepsis Effects of Addisons Disease Skin * Pigmentation due to increased ACTH by anterior pituitary gland. The ACTH cross stimulates Melanocyte Stimulating Hormone (MSH) causing pigmentation Fluid Balance * Hypovolaemia with postural hypotension is typical Acid Base * Metabolic acidosis Electrolytes * Loss of aldosterone results in loss of Na+ reabsorption by the kidney * Hence urinary Na+ is high * Serum Na+ is low * Serum K+ is usually high * Haemoconcentration is often present "Hyponatraemia, hyperkalaemia, hypoglycaemia and haemoconcentration are often present." "...Hyponatraemia, Hypovolaemia, Hypotension, Hyperkalaemia and metabolic acidosis..." Anaesthesia * Volume is a key issue. These patients need intravascular reexpansion * Minimise neuromuscular blockade as hyperkalaemia can cause skeletal muscle weakness |
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ME06 [Mar92] [Aug94] [Aug95] [Aug99] [Mar00] (type K)
Total body depletion of sodium occurs in: A. Addison's Disease B. Nephrotic syndrome C. CCF D. Cushing's syndrome E. Diabetic ketoacidosis F. Chronic diuretic use/ frusemide |
ANSWER A, E and F
Although CCF and nephrotic syndrome are causes of hyponatraemia -they cause hyponatraemia due to water excess with smaller sodium excess, ie total body sodium is not depleted. |
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ME08 [1989]
Typical features of hyperparathyroidism include all of the following EXCEPT: A. Raised serum calcium B. Ectopic muscular calcification C. Raised urinary phosphate D. Staghorn calculi E. Lowered urinary calcium |
ANSWER E
"bones, groans, stones and moans" - most are diagnosed on random U+E's so asypmtomatic is 'typical' A: true B:? very unlikely to be 'typical' C: true D: true E: false - even though PTH decreases Ca excretion, urinary excretion actually high due to high plasma conc. |
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ME09 [1987] [1988] [Mar91]
Primary hyperparathyroidism: A. Hypercalcaemia B. Hypophosphataemia C. Hypochloraemic acidosis D. Increased alkaline phosphatase E. Raised urinary calcium |
ANSWER A B D E
Hyperparathyoidism a. hight PTH b. high Ca c. low phosphate -85% primary hyperparathyroidism from ademoma of single parathyroid gland -15% from hypertrophy of all parathyroid glands -parathyroid malignancy is rare -Associated with MEN1 and MEN2 Presentation -50% asymptomatic -discovered incidently from hypercalaemia -may present with anorexia, dyspepsia, nausea/vomiting, constipation -hypertension, shorten QT, polyuria, polydipsia, renal calculi -depression, poor memory, drowsiness Diagnosis -elevated parathyroid hormone in the setting of hypercalaemia -other causes of hypercalaemia will suppress parathryoid hormone Action -PTH is released from the parathyroid glands. It acts principally to increase the plasma calcium level, principally by three mechanisms: 1. Increased osteolysis. Increased osteoclastic activity causes calcium to be released from the bones into plasma. More than 99% of body Ca is stored in bones. This release can occur within minutes. 2. Renal conservation of calcium. The kidneys reabsorb filtered calcium in the ascending loop, distal tubule and collecting tubules. Renal conservation occurs via two mechanisms: * Increased reabsorption of filtered calcium * Increased secretion of PO4. This causes decreased plasma PO4, hence increasing the unbound plasma calcium level. 3. PTH increases synthesis of 1,25 dihydrocholecalciferol. This in turn increases calcium absorption from the GI tract. |
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ME10
In hyperparathyroidism one finds: A. High serum calcium and low urine calcium B. High serum calcium and high urine calcium C. Serum calcium lowered by corticosteroids D. Serum calcium raised by corticosteroids |
ANSWER B
A False B True. Even though there is increased renal tubular calcium reabsorption, the very high amount of calcium filtered still results in an overall high urinary calcium concentration. C FALSE - "plasma calcium in hyperparathyroidism is resistant to suppression by steroids; this also occurs with some malignancies. Hypercalcaemia due to sarcoidosis, vitamin D-mediated hypercalcaemia and some malignancies, suppression to normal or near normal levels is seen" AKA "the hydrocortisone suppression test" Ref Kumar & Clarke "Clinical Medicine" D False |
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ME11
In hyperparathyroidism, the following findings are present: A. Increased serum and urinary calcium B. Urinary phosphate excretion is usually normal C. Serum phosphate is usually low or normal D. Increased serum but decreased urinary calcium E. None of the above |
ANSWER A
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Treatment of hypercalaemic crisis
When would you proceed with the operation? |
Serum Calcium > 4.5 mmol/L
Occurs most commonly in elderly with undiagnosed hyperparathyroidism -dehydration Treatment First line Treatment 1. Transiently treat with phosphate : 500ml of 0.1M PO4 over 8 hours 2. Aggressive rehydration : 6-8L of fluid 3. Pamidronate (60mh in 500ml NaCl over 4 hours, rapid and long lasting treatment 4. Calcitonon (3-4U/kg IV then 4U/kg SC BD), rapid decrease in skeletal release of Ca and PO4, temporary measure Second Line Treatment -once volume repletion is complete 1. Forced diuresis with frusemide, consider CVP monitoring 2. Hydrocortisone (200-400mg IV daily) in patients with malignancy 3. Dialyisis Periopertive plan 1. Proceed if a. serum Ca <3.0 b. normal ECG c. stable CVS and renal 2. Careful use of NMB with monitoring |
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How would you adjust Ca concentration for albumin?
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Add 0.1 mmol/L to Ca for each 6g/L of albumin
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ME16 ANZCA version [Jul00] [2002-Aug] Q144
Drugs used in the management of a post-operative thyrotoxic crisis include 1. diazepam 2. propranolol 3. dexamethasone 4. potassium perchlorate How would you treat a thyroid storm |
ANSWER 1, 2, 3
Thyroid Crisis -known as thyroid storm -rare complication of hyperthyroidism -life-threatening exacerbation of hyperthyroid state with multiorgan involvement -rapid elevation of thyroid hormone T3/T4 -mortality 20-30% Symptoms Metabolic-temp > 40deg CVS-tachycardia/arrhythmia/hyerptension GIT-vomiting/diarrhoea -dehydration -coma Presents 6-24hours post surgery Treatment 1. Rehydrate with Iv saline and glucose 2. Cutaneous cooling 3. Paracetamol (NO NSAIDS as this will displace TH from serum binding sites and increase free T3/T4) 4. Propranolol (1mg increments up to 10mg) until HR<90 OR Esomolol (loading 250-500ug/kg followed by 50-100ug/kg/min) 5. Hydrocortisone 6. Propylthiouracil (loading 1g, followed by 200-300mg TDS) : inhibits TH release and decreases conversion of T4 to T3. 7. After PTU give a. Sodium Iodide (500mg TDS IV) or b. Potassium Iodide (5 drops QID) c. Lugol's iodine (5-10 drops QID) |
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ME13 [1985] [Sep90] [Apr98]
Hyperparathyroidism due to chronic renal failure is contributed to by all of the following EXCEPT: A. Hypocalcaemia B. Decreased renal calcium absorption due to acidosis C. increased renal calcium absorption due to increased 1,25 D3 D. Increased serum phosphate E. Decreased levels of 1,25 dihydroxycholecalciferol |
ANSWER C
1-25 Dihydroxycholecalciferol acts on the GI tract to cause increased gastric absorption of Calcium. The kidney is involved as part of the formation of 1-25 dihydroxycholecalciferol, but it does not in turn act on the kidney. Secondary Hyperparathyroidism -excessive secretion of PTH in response to hypocalcaemia -associated with hypertrophy of PT glands -especially seen in CRF Presents -excessive bone resorption (seen earliest in the radial aspect of the middle phalanx of the second digit) -soft tissue calcification kidneys, heart, lung and skin Treatment (medical) -dietary phosphate restriction -Ca -Vit D -if this failes them long-term dialysis |
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ME15
Causes of goiter include: A. Decreased iodine intake B. Thioureas C. Hashimoto's disease D. Hypopituitarism |
ANSWER A, B, C
A: true B: true - Thioureas have goitrogenic effect, so B is true (See thioureas (http://en.wikipedia.org/wiki/Thioureas)) C: true D: false |
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ME17b ANZCA version [2003-Apr] Q145
The first drug to be used in the management of an intra-operative thyrotoxic crisis is A. esmolol B. hydrocortisone C. magnesium D. potassium iodide E. propyl thiouracil |
ANSWER A
Thyroid storm Thyroid storm is defined as fulminant thyrotoxicosis, occuring perioperatively. -TH secreted from thyroid gland -TSH secreted from anterior pituitary gland -TRH from hypothalamus Immediate management issues are: * Airway * Breathing * Circulation Issues of note 1. Tachycardia & arrhythmias e.g. AF as a result of acidosis, electrolyte imbalance. Rate related ischaemia can be an issue also. Hence early use of beta blockers is recommended (Allman et al, 2005, p256). Note that this has two effects * Beta blocker related heart rate changes * Beta blocker treatment of hypertension 2. Hypertension complications * Short term -> APO * Long term -> End organ damage 3. Hyperpyrexia * Prolonged hyperpyrexia can lead to seizures. * Associated with muscle damage, myoglobin release and myoglobinuria. Associated ARF. 4. Muscle function * Manifest in several ways * Loss of breathing hence requires ventilation * - Loss of muscle tone - often requires airway support i.e. ETT Timing of drugs * Minutes - beta blockers. Esmolol is drug of choice due to most rapid action * Hours - Antithyroid drugs. PTU prevents peripheral conversion. * Hours - Steroids * Days - Lugols iodine takes several days to work. |
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ME18
Which of the following is NOT a feature of primary myxoedema? A. Bradycardia B. Pretibial myxoedema C. Macrocytic anaemia D. Flattened ECG complexes |
ANSWER B
Myxoedema = Severe Hypothyroidism -rare form of decompensated hypothroidism -hypothyroidism in 2% women and 0.2% men -myxedema in 0.1% of all cases of hypothyroidism -mortality 15-20% -typically seen in elderly women -precipitated by infection, medication, environmental exposure or metabolic-related stresses ECG changes -bradycardia -prolonged QT -low P, T, QRS amplitude -complete heart block -BBB Treatment ABC approach 1. rehydrate with IV glocose and saline 2. inotropes and vasopressors if required 3. warming 4. IV liothronine 5. Hydrocortosone (100mg TDS) 6. ICU |
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ME19 [Mar90]
The signs of primary myxoedema except: A. Bradycardia B. Macrocytic anaemia C. Pretibial oedema D. Flattening of T wave E. Loss of hair |
ANSWER C
Myxoedema = Severe Hypothyroidism -rare form of decompensated hypothroidism -hypothyroidism in 2% women and 0.2% men -myxedema in 0.1% of all cases of hypothyroidism -mortality 15-20% -typically seen in elderly women -precipitated by infection, medication, environmental exposure or metabolic-related stresses ECG changes -bradycardia -prolonged QT -low P, T, QRS amplitude -complete heart block -BBB Treatment ABC approach 1. rehydrate with IV glocose and saline 2. inotropes and vasopressors if required 3. warming 4. IV liothronine 5. Hydrocortosone (100mg TDS) 6. ICU |
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ME20 [1986]
To make the diagnosis of diabetes mellitus: A. Need 2 fasting BSLs > 6.0 mmol/l B. Need 2 fasting BSLs > 8 mmol/l with symptoms C. Patient must fast for 4 hours before a glucose tolerance test D. Patient must have at least 150g/day of carbohydrate for 3 days prior to a glucose tolerance test |
ANSWER D
* A: FALSE No. WHO: random BSL > 11.1 mmol/L (200 mg/dL) ONCE with symptoms or MORE THAN ONCE without symptoms. * B: FALSE No. WHO: random BSL > 11.1 mmol/L (200 mg/dL) ONCE with symptoms or MORE THAN ONCE without symptoms. * C: FALSE No. GTT involves overnight fast. (>8hours) Harrison's Ch. 334 * D: TRUE Diagostic Criteria - WHO DIABETES * Must confirm the diagnosis on second test if patient is asymptomatic * Random plasma glucose': >11.1 mmol/L * Fasting plasma glucose: >7 mmol/L Oral glucose tolerance test (OGTT) * 2 hours post 75g load plasma glucose > 11.1 mmol/L * Note: 3 days of > 150g/day carbohydrate. Fast 8 – 16hrs then give 75g glucose. This is because marked carbohydrate depletion can impair glucose tolerance. (Red book RCPA) HbA1c * >7% DM is likely (sensitivity 99%, specificity 99.6%) IMPAIRED GLUCOSE TOLERANCE Impaired Fasting Glucose * plasma glucose 6.1 -7.0 mmol/L Impaired Oral glucose tolerance test (OGTT) * 2 hours post 75g load plasma glucose 7.8 - 11.1 mmol/L |
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ME21
Insulin resistance is due to: A. Acidosis B. Infection C. Dehydration D. Vomiting E. Circulating antibodies |
NONE
Insulin resistance Insulin resistance is a state in which a given concentration of insulin produces a less-than-expected biological effect. Insulin resistance has also been arbitrarily defined as the requirement of 200 or more units of insulin per day to attain glycemic control and to prevent ketosis. The syndromes of insulin resistance actually comprise a broad clinical spectrum, which includes obesity, glucose intolerance, diabetes, and syndrome X, as well as an extreme insulin-resistant state. Many of these disorders are associated with various endocrine, metabolic, and genetic conditions. These syndromes may also be associated with immunological diseases and may exhibit distinct phenotypic characteristics. Syndrome X, the insulin-resistance state also known as metabolic or dysmetabolic syndrome, has drawn the greatest attention because of the public health importance |
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ME23 ANZCA version [2003-Aug] Q19, [2004-Apr] Q64 [Aug10] (Similar Q in [Mar90] [Mar91] [Aug91] [Mar92] [Aug92])
Plasma glucose concentration is approximately A. 32% lower than blood glucose concentration B. 14% lower than blood glucose concentration C. the same as blood glucose concentration D. 14% higher than blood glucose concentration E. 32% higher than blood glucose concentration |
ANSWER D
a BSL of 5.6-6.1 = pl glucose 6.1-7 |
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ME24 [1985]
The depth of unconsciousness in a patient with diabetic ketoacidosis correlates best with the degree of: A. Hyperglycaemia B. pH alteration C. Hyponatraemia D. Hyperosmolarity E. Hypokalaemia |
ANSWER D
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ME25 [1989] [Mar92]
Hypercalcaemia associated with malignancy: A. Commonest cause: tumour in bone B. Corrected by fluid loading/diuresis C. No response to calcitonin D. Results from increased PTH E. QT interval normal |
ANSWER A, B, D
A: true B: true C: false : calcitonin (3-4U/kg IV followed by 4U/kg SC BD) rapid decrease in skeletal release of Ca and PO4 D: true 40% ectopic PTH production E: false - short QT |
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E26 [1989] [Mar91] [Aug94] [Mar95] [Jul98]
Which drug is NOT used in the preoperative management of phaeochromocytoma? A. Phenoxybenzamine B. Aprotinon C. Atenolol D. Alpha-methyl tyrosine E. Prazosin |
ANSWER B
Drugs used in phaeochromocytoma * α blockade (first) o Phentolamine o Phenoxybenzamine o Prazosin o Doxazocin (doesn't need subsequent β blockade because it doesn't block α2 receptors) * β blockade (only after α blockade established) o Atenolol o Labetolol * α-Methyl-p-Tyrosine - blocks tyrosine hydroxylase * Calcium channel antagonists |
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ME28b ANZCA version [2001-Apr] Q118
The syndrome of inappropriate ADH secretion may be seen in 1. carcinoma of the lung 2. pulmonary tuberculosis 3. septicaemia 4. sarcoidosis |
ALL TRUE
SIADH -characterised by excessive release of ADH from posterior pituitary or another source Presentation -fluid overload (signs of failure and hypertension) -hyponatraemia (symptoms of cerebral edema become prominent (irritability, confusion, seizures, and coma). Diagnosis -Hyponatraemia Na<135 -Urine hyponatramia >20 Causes * Meningitis * Head injury o Subarachnoid hemorrhage * Cancers o Lung cancer (especially small-cell lung cancer, as well as other small-cell malignancies of other organs) * Infections o Brain abscess o Pneumonia o Lung abscess * Guillain Barre syndrome * Drugs o Chlorpropamide o Clofibrate o Phenothiazine o Cyclophosphamide o Carbamazepine o Selective serotonin reuptake inhibitors (SSRIs, a class of antidepressants) o Methylenedioxymethamphetamine (MDMA, commonly called Ecstasy. SIADH due to taking ecstasy was cited as a factor in the death of Leah Betts) o Oxytocin o Vincristine morphine,amitriptaline * Hypothyroidism * sarcoidosis Management of SIADH includes: * Treating underlying causes when possible. * Fluid restriction of 1,200–1,800 mL/day to increase serum sodium. * Hypertonic saline * Drugs o Demeclocycline most potent inhibitor of Vasopressin (ADH/AVP) action. side effect profile, including but not limited to new onset Nephrogenic Diabetes Insipidus (70%), skin photosensitivity, and nephrotoxicity. o Urea: oral daily ingestion has shown favorable long-term results with protective effects in myelinosis and brain damage. o Conivaptan - an antagonist of both V1A and V2 vasopressin receptors. o Tolvaptan - an antagonist of the V2 vasopressin receptor. |
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Hormones of the anterior and posterior pituitary.
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Anterior
Somatoropins -Growth Hormone Thyrotropins -Thyroid stimulating hormone Corticotropins -Adrenacorticotropic hormone -Beta endorpine Lactotropins -Prolactin Gonadotropins -Luteinizing hormone -Follicle stimulating hormone Melanotropins -melanocyte stimulating hormone Posterior Pituitary -Oxytocin -Antidiuretic hormone |
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ME27 [1989]
SIADH: A. Water overload B. ECG changes C. Hyponatraemia D. Urine osmolality > plasma osmolality |
ANSWER A, C, D
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ME29 [1989] [Sep90] [Mar91] [Mar94] [Aug94]
Panhypopituitarism: A. Is most commonly due to post-partum necrosis B. Causes increased body hair C. Multiple endocrine deficiencies the most important being hypothyroidism D. Resembles Anorexia nervosa E. Changes in ovarian function are early F. Tumour is commonest cause in adults G. Severe weight loss H. Higher insulin requirements I. Diabetes insipidus is most common abnormality |
A: False
* Most common vascular cause (Sheehan's syndrome) * Most common cause in general is tumour growth B: False * Decreased (Described as 'alabaster skin' - combination of pallor and hairlessness) C: False * Multiple endocrine abnormalities are present, but most important is ACTH D: True * Get anorexia, amenorrhoea, lethargy and malaise in both * Severe weight loss known as 'pituitary cahexia' (can have inc. weight with hypothyroidism) E: True * LH / FSH lost first (Kumar and Clarke), or second (OHCM) - but definitely early F: True G: True * 'Pituitary cahexia' H: False * Opposite of acromegaly (GH excess) I: False * Panhypopituitarism refers to anterior hormone deficiencies * Post pituitary function (eg. DI) only affected if there is major suprasellar extension |
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Hypopituitarism
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Hormones
Six anterior pituitary hormones * ACTH * GH * FSH * LH * TSH * PRL Causes of hypopituitarism * Hypophysectomy * Pituitary irradiation * Pituitary adenoma * Craniopharyngioma * Sphenoid meningioma * Sheehans syndrome = pituitary necrosis following post partum haemorrhage * Tuberculosis Symptoms * Insidous onset * Loss of libido * Impotence * Amenorrhea * Headache * Depression * Hypothyroidism Signs * Breast or testicular atrophy * Hair loss * Thin flaky wrinkled skin (monkey face) * Hypotension * Visual field defect |
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ME30b ANZCA version [2001-Aug] Q30, [2003-Aug] Q63
The hyperglycaemic hyperosmolar non-ketotic syndrome A. may be associated with a high serum sodium B. only occurs in elderly patients C. is commonly complicated by thromboembolism D. is characterized by only a moderate degree of hyperglycaemia E. is NOT characterized by dehydration |
ANSWER A
A. TRUE : -mild cases : less dehydration, dilutional hyponatraemia -as dehydration worsens hypernatraemia compounds the hyperosmolality B .FALSE : middle aged to elderly C. FALSE : potential complication but not common D. FALSE E. FALSE Complications: * Ischemia or infarction to any organ, including heart and brain * Thromboembolism * ARDS/DIC or multiorgan dysfunction syndrome * Cerebral edema (rare) Prognosis: * The overall mortality rate is between 10-20% and is dependent on coexisting conditions and complications." |
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ME30c ANZCA version [2002-Mar] Q69
Hyperosmolar non-ketotic coma A. is relatively common in young diabetics B. occurs in patients who have a history of diabetes in the majority cases C. is more acute in presentation than diabetic ketoacidosis D. is NOT associated with intracellular and intravascular dehydration E. is associated with a decrease in serum sodium concentration |
ANSWER B
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ME30d ANZCA version [2003-Apr] Q87, [2005-Apr] Q54
Hyperosmolar non-ketotic coma is associated with A. a normal coagulation profile B. a normal serum sodium concentration C. a normal urinary potassium concentration D. intracellular dehydration E. known diabetic patients |
ANSWER D and E
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ME31 [1989] [Mar93] [Apr99]
Conn's syndrome (primary aldosteronism) is characterised by: 1. Hypertension 2. Oedema 3. Hypokalaemia 4. Oliguria |
ANSWER 1, 2, 3
Primary hyperaldosteronism is one of the more common causes of secondary hypertension. The term Conn's syndrome is used for primary hyperaldosteronism secondary to an adrenal adenoma secreting aldosterone. The syndrome is due to: * bilateral idiopathic adrenal hyperplasia 70 % * unilateral idiopathic adrenal hyperplasia 20 % * aldosterone-secreting adrenal adenoma (benign tumor, < 5%) * rare forms, including disorders of the renin-angiotensin system Aldosterone acts in kidney to increase Na+ reabsorption and increase K+ secretion. -Water follows Na, therefore increase in extracellular fluid volume -hypokalaemia -metabolic alkalosis -Hypomagnesemia -hypoglycaemia Clinical Features -refractory hypertension, hypervolaemia, metabolic alkolosis -hypokaelaemia -muscle weakness or paralysis -nephrogenic diabetes insipidus -impaired glucose tolerance Treatment is adrenalectomy 1. Medical optimisation a. spironoloctone (400mg/day, compeditively inhibits aldosterone) b. correct K+, HCO3 c. Treat hypertension d. exclude LVH, treat as for CCF if present |
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ME31b ANZCA version [2005-Apr] Q117
Features of Conn's syndrome (primary hyperaldosteronism) include each of the following EXCEPT A. acidosis B. high urinary potassium C. hypertension D. hypokalaemia E. low plasma renin |
ANSWER A
Primary hyperaldosteronism is one of the more common causes of secondary hypertension. The term Conn's syndrome is used for primary hyperaldosteronism secondary to an adrenal adenoma secreting aldosterone. The syndrome is due to: * bilateral idiopathic adrenal hyperplasia 70 % * unilateral idiopathic adrenal hyperplasia 20 % * aldosterone-secreting adrenal adenoma (benign tumor, < 5%) * rare forms, including disorders of the renin-angiotensin system Aldosterone acts in kidney to increase Na+ reabsorption and increase K+ secretion. -Water follows Na, therefore increase in extracellular fluid volume -hypokalaemia -metabolic alkalosis -Hypomagnesemia -hypoglycaemia Clinical Features -refractory hypertension, hypervolaemia, metabolic alkolosis -hypokaelaemia -muscle weakness or paralysis -nephrogenic diabetes insipidus -impaired glucose tolerance Treatment is adrenalectomy 1. Medical optimisation a. spironoloctone (400mg/day, compeditively inhibits aldosterone) b. correct K+, HCO3 c. Treat hypertension d. exclude LVH, treat as for CCF if present |
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ME32 [Mar90] [Aug92] [Mar93]
In hypercalcaemia associated with malignancy: A. Bone metastasis is an essential feature B. The ECG characteristically shows a shortened Q-T interval C. Emergency treatment includes fluid restriction to control the associated polyuria D. Calcitonin has no place in management |
ANSWER B
* A: false - not essential - 40% ectopic PTH producing tumours * B: true * C: false * D: false |
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ME33 [Sep90]
Acromegaly: A. Recurrent laryngeal nerve palsy B. Glossoptosis C. Fixed vocal cords D. Prognathism |
ANSWER A and D
A True B False * Glossoptosis = abnormal downward or back placement of the tongue * Acromegaly → macroglossia C False * Abnormal cord movement, not fixed * Deepening of voice D True Acromegaly -rare clinical syndrome caused by excessive Growth Hormone Production (Anterior Pituitary) CVS : hypertension 30%, IHD, cardiomyopathy, heart failure, valvular disease Airway : large jaw, head, tongie, lips, hypertrophy of larynx and trachea, OSA, enlarged thyroid Drugs : -somatostatin causing nausea and vomiting -bromocriptine : postural hypotension Neurological -raised ICP -nerve entrapment Endocrine -25% diabetic |
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ME35 [Mar93] [Jul06] Q82, [Apr07]
A patient has a history of polyuria and has an elevated serum calcium, normal parathyroid hormone level and an elevated angiotensin converting enzyme level. The most likely diagnosis is: A. milk-alkali syndrome B. primary hyperparathyroidism C. malignancy D. sarcoidosis E. multiple myeloma |
ANSWER D
There are three diseases which elevate SACE 1. sarcoidosis, 2. Gaucher disease, 3. leprosy Physiological ACE overproduction in 1. childhood growth, 2. hyperthyroidism, 3. diabetes mellitus with retinopathy, 4. hepatitis and liver cirrhosis undergoing active liver regeneration, and, 5. possibly HIV disease. |
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ME34 [Mar92] [Aug94] [Mar95] [Aug95]
Acromegaly is associated with ONE of the following: A. Aortic incompetence B. Postop respiratory obstruction C. Aspiration D. ?Aortic incompetence E. ? (Type A) |
ANSWER B
Acromegaly -rare clinical syndrome caused by excessive Growth Hormone Production (Anterior Pituitary) CVS : hypertension 30%, IHD, cardiomyopathy, heart failure, valvular disease Airway : large jaw, head, tongie, lips, hypertrophy of larynx and trachea, OSA, enlarged thyroid Drugs : -somatostatin causing nausea and vomiting -bromocriptine : postural hypotension Neurological -raised ICP -nerve entrapment Endocrine -25% diabetic |
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ME36 [Aug93] [Mar94] [Aug94] [Mar95] [Aug95] [Jul97]
Hypokalaemia is seen in: (type K) A. Conn's syndrome B. Bartter's syndrome C. Cushing's syndrome D. Addison's disease |
ANSWER A, B, C
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ME38 ANZCA version [2003-Aug] Q32, [2004-Apr] Q53, [2005-Sep] Q57 [2006-Apr] Q57 (Similar question reported in [Apr97] [Jul97] [Apr98] [Apr99] [Aug99])
In patients with phaeochromocytoma A. paroxysmal hypertension is the most common presentation B. initial treatment should be with beta blockade if tachycardia is present C. excesses of adrenaline and noradrenaline occur with equal frequency D. urinary Vanillyl Mandelic Acid (VMA) studies may be normal E. extra-adrenal tumours occur in 2% of patients |
ANSWER D
* A False - 85% have sustained hypertension. Whilst I don't know where 85% comes from there is discrepency with serum peaks of NA and Adr with BP due to receptor sensitivity and vascular reactivity (CEACCP) o 50 % have paroxysmal hypertension, 30 % have sustained hypertension, 20 % have none (Stoelting 5th ed.) - True * B False - α blockers first then β blockers o A distractor, as in text from Stoelting...if tachycardia (>120) after α blockade, then non-specific β blockers added * C False - Some Ad > Norad, Some Norad > Ad * D True - not the most sensitive and specific test o VMA's are oldest and least expensive test but non-specific o The glucagon stimulation test is the most specific test * E False - 6% in other sites in sympathetic system o 20 % extra-adrenal (Stoelting 5th ed.) |
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ME40 ANZCA version [2001-Apr] Q147, [2001-Aug] Q128 (Type K MCQ)
Disorders associated with systolic hypertension include 1. Cushing’s syndrome 2. primary aldosteronism 3. congenital adrenal hyperplasia 4. hyperparathyroidism |
ANSWER 1, 2, 3
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ME41 ANZCA version [2001-Apr] Q81
The most correct statement concerning thyroid diseases is that A. thyrotoxicosis has the same incidence in men and women B. thrombocytopaenia is associated with thyrotoxicosis C. the half life of T 4 (thyroxine) is 2 days D. beta-blockers are contraindicated in acute thyrotoxicosis E. carbimazole acts within 2-3 days to reduce T4 synthesis |
ANSWER B
A. FALSE : Men: Female is 9:1 B. TRUE C. FALSE : T3 half life is 7 days D. FALSE: esmolol is the first drug used for symptom control E. FALSE : improvement in 1-2 days Carbimazole • Onset of action: Antithyroid: Oral: 12-18 hours • Duration: 36-72 hours • Distribution: Concentrated in thyroid gland; crosses placenta; enters breast milk (1:1) • Protein binding, plasma: None • Metabolism: Hepatic • Bioavailability: 80% to 95% • Half-life elimination: 4-13 hours • Excretion: Urine (80%) |
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ME42b ANZCA version [2005-Sep] Q124, [Mar06] Q55
Complications of severe anorexia nervosa (body weight < 40% ideal) include all of the following EXCEPT A. cardiomyopathy B. delayed gastric emptying C. hypokalaemia D. hypercalcaemia E. prolonged QT interval |
ANSWER D
Complications CVS -sinus Brady -peripheral cyanosis -arrythmias ECG - av block, long QT, ST depression, T inversion -contractility only mildly impaired (but ipecac induced cardiomyopathy common) -MV proplapse Resp -Vomiting - aspiration, pneumothorax, pneumomediastinum hypovent due to alkalosis Renal -decreaesed GFR -proteinuria -calculi -hypo - K, Na, Cl, Ca GI -dental caries -parotitis -oesophageal injury -delayed gastric emptying Haem, Endo and skin -anaemia -leucopaenia -thrombocytopaenia -panhypopituitarism -high cortisol and GH -poor thermoregulation -osteoporosis -dry, cracked skin -perioral dermatitis |
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ME43 [Apr07] [Jul07]
Addison's disease lab features: Which is NOT correct A. Ca 2.50 mmol/L B. BSL 12.0 mmol/L C. Na 128 mmol/L D. K 6.1 mmol/L E. Urea 15mmol/L |
ANSWER B
Addisons Disease : Primary adrenocortical insufficiency. -insidious, progressive hypofunctioning of the adrenal cortex The adrenal cortex produces a number of hormones * Mineralocorticoids e.g. aldosterone * Glucocorticoids e.g. Cortisol * Sex hormones/Androgens Failure of the adrenal cortex leads to a decrease in these hormones. Destruction of 90% of the cortex is required before insufficiency occurs. Causes -Destruction by antibodies (autoimmune disorder) is the cause in 70-80% of cases -Other causes of Addisons: * TB (previously a common cause but no longer so in Western countries) (eg For anaesthetic-related case report see [1] * Metastases * Bilateral adrenalectomy * Haemorrhage e.g. following meningococcal sepsis Effects of Addisons Disease Skin * Pigmentation due to increased ACTH by anterior pituitary gland. The ACTH cross stimulates Melanocyte Stimulating Hormone (MSH) causing pigmentation Fluid Balance * Hypovolaemia with postural hypotension is typical Acid Base * Metabolic acidosis (low HCO3) Electrolytes * Loss of aldosterone results in loss of Na+ reabsorption by the kidney * Hence urinary Na+ is high * Hyponatraemia * Hyperkalaemia * Haemoconcentration is often present * Hypoglycaemia * high urea Hormonal * Elevated ACTH (>50pg/mL) * Low cortisol (<5ug/dL) Anaesthesia * Volume is a key issue. These patients need intravascular reexpansion * Minimise neuromuscular blockade as hyperkalaemia can cause skeletal muscle weakness |
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ME44 [Apr07]
A 70kg male who has been taking prenisolone 10mg per day orally for over 12 months, undergoes an uncomplicated laparotomy and bowel resection. The best management of his steroid therapy perioperatively, until oral intake resumes, is to administer A. Hydrocortisone 100mg iv for approximately 24 hours B. Hydrocortisone 200mg per day for approx 72 hours C. Hydrocortisone 400mg per day for 72 hrs D. No steroids E. 20mg nasogastric prednisolone daily |
ANSWER A
Recognised guidelines (for someone on 10mg or more in last 3 months) would be to give normal oral dose, 25mg hydrocortisone at induction and 25mg 6 hrly for 2-3 days (major surgery) or 1-2 days (moderate surgery). |
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ME46 Mar2011
Acromegaly due to excess of growth hormone. Why hard to do direct laryngoscopy? A. Distorted facial anatomy B. Macroglossia C. Glottic stenosis D. Prognathe mandible E. Arthritis of the neck |
ANSWER B
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SG56 ANZCA version [2005-Sep] Q106, [April 06] Q81
During surgery there is increased secretion of each of the following hormones EXCEPT A. aldosterone B. glucagon C. growth hormone D. thyroid stimulating hormone E. vasopressin |
ANSWER D
INCREASED -GH -ACTH -B endorphins -Prolactin -ADH -Catecholamines -Cortisol -Aldosterone -Glucogon -Renin SAME -TSH -LH -FSH DECREASED -insulin -testerone -estrogen -T3 |
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Burnett's Syndrome
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Milk Alkalii Syndrome
-hypercalaemia caused by repeated ingestion of Calcium eg milk, calcium carbonate, sodium bicarbonate (antacids) Results in metastatic calcification and renal failure -hypoparathyroidism -diabetes insipidus |
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MZ62 ANZCA version [2001-Apr] Q72, [2001-Aug] Q37, [2002-Aug] Q48, [2003-Apr] Q59, [2004-Aug] Q77, [2005-Apr] Q33, [Apr07] [Jul07]
An INCORRECT statement regarding the management of hypocalcaemia is that A. Correcting a respiratory or metabolic alkalosis increases the level of ionised calcium B. Calcium should be administered via a central vein as it is irritant to peripheral veins C. Acidosis will decrease calcium binding to albumin and therefore increase ionised calcium D. When calcium alone is NOT sufficient for control of hypocalcaemia, Vitamin D metabolites can be added E. Calcium chloride has been shown to be superior to calcium gluconate |
ANSWER E
* A - True o Reducing alkalosis → ↑ H+ → displaces calcium from albumin → ↑ ionised calcium * B - False - although "should be" is true - if type A question then ?E the least correct? o Calcium causes tissue necrosis with extravasation so CVC or large vein preferable * C - True (see A) * D - calcitriol (also calcidiol and dihydrotachysterol) are Vit D metabolites. Calcitriol is the preferred because of its rapid onset (hours) * E - False - just more concentrated o CaCl2 + 5ml ampoule + 1mmol/ml o Ca Gluconate + 10ml ampoule + 0.22mmol/ml |
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MH09b ANZCA version [2002-Aug] Q41, [2005-Apr] Q83, [2005-Sep] Q85, [Jul07] (Similar question reported in [Mar91] [Mar94] [Aug94] [Aug95] [Apr98])
Anaemia in chronic renal failure is characteristically A. due to haemolysis in the renal vascular bed B. normochromic and microcytic C. due to defective haemoglobin synthesis D. responsive to iron and folate therapy E. associated with increased 2,3-DPG levels in blood cells |
ANSWER E
Anaemia in chronic renal failure is characteristically * A. due to haemolysis in the renal vascular bed * B. normochromic and microcytic - false: "The anemia is characteristically normocytic and normochromic" * C. due to defective haemoglobin synthesis * D. responsive to iron and folate therapy * E. associated with increased 2,3-DPG levels in blood cells - true: "The intracellular concentration of 2,3-bisphosphoglycerate is appropriately increased in response to anemia and hyperphosphatemia,9 with a moderate decrease in the affinity of hemoglobin for oxygen." (Williams Hematology) |
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AC93 ANZCA version [2001-Apr] Q8, [2002-Aug] Q10, [2003-Aug] Q55, [2004-Apr] Q60, [Apr07] Q55, [Jul07] (Similar question reported in [Apr99] [Jul00])
The most important factor in reducing peri-operative morbidity in diabetic patients undergoing peripheral vascular surgery is A. tight control of blood sugar level in the peri-operative period B. frequent blood sugar level estimations C. use of regional rather than general anaesthesia D. stabilisation of co-existing disease E. the use of an insulin infusion rather than a subcutaneous sliding scale regimen |
ANSWER D
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Black Bank April 2008
ME Hyperparathyroidism and increased Ca+ A. Long QT B. Polydipsia and polyuria C. Short PR D. Increased GFR E. |
ANSWER B
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Black Bank April 2008
MZ Hyponatraemia and hypovolaemia all except A. SIADH B. Pancreatitis C. Nephritis D. Renal tubular acidosis E. Addisons |
ANSWER A
CAUSES OF HYPONATRAEMIA Hypovolaemic -renal losses - diuretic, mineralocorticoid deficency, cerebral salt waste, renal tubular acidosis -GIT : vomiting dirrhoea -Skin : burns, sweat -Pancreatitis |
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AZ26. PAC seeing patient with thyroid disease. Most reassuring factor for normal thyroid function is:
A. Absence of 'hot' nodules on nuclear scan B.? C. Normal heart rate D. Normal temperature E. Absence of any antithyroid medications |
ANSWER C
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Black Bank April 2009
MM Features of eaton lambert include all EXCEPT... a) Associated with SCLC b) improvement with exercise c) defect in ACh release from motor end plate d) dry mouth e) Fatigue with exercise |
ANSWER E
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[TMP-132] [Aug09]
Laparoscopic cholecystectomy patient with hyperparathyroidism and ionised calcium of 2.0 mmol/l. The BEST initial treatment is: A. Calcitonin B. Magnesium C. Dialysis D. IV fluids E. Frusemide |
ANSWER D
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Black Bank April 2009
MM Carcinoid syndrome - finding on examining heart: A. Fine inspiratory crepitations B. Systolic murmur at apex C. Systolic murmur at left sternal edge D. Murmur at apex with opening snap E. Pericardial rub |
ANSWER C
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SZ14b ANZCA version [2004-Aug] Q130, [Jul07], [mar10]
Following a cadaveric renal transplant under general anaesthesia, your patient's plasma K+ increases to 6.0 mmol.l-1 in recovery after being 5.0 mmol.l-1 pre and intra-operatively. This patient requires A. an intravenous infusion of CaCl2 (10 mls over 20 minutes) B. arterial blood gases to ascertain the acid/base status C. potassium exchange resins rectally D. sodium bicarbonate infusion (50- 100 mEq over 5- 10 minutes) E. urgent haemodialysis |
ANSWER B
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TMP-Jul10-049
The EARLIEST sign of hypocalcaemia is: A. Tingling of face and hands B. Chvostek’s sign C. Carpopedal spasm D. ? E. ? |
ANSWER A
Hypocalaemia -Ca <2.1 mmol/L or ionized Ca <1.1 mmol/L Correction for albumin -50% is bound to albumin -CorrCa = Measured serum Ca + [(4.0 - measured serum albumin) * 0.8] Symptoms * Petechia which appear as on-off spots, then later become confluent, and appear as purpura * Oral, perioral and acral paresthesias, tingling or 'pins and needles' sensation in and around the mouth and lips, and in the extremities of the hands and feet. This is often the earliest symptom of hypocalcaemia. * Carpopedal and generalized tetany * Latent tetany o Trousseau sign of latent tetany (eliciting carpal spasm by inflating the blood pressure cuff and maintaining the cuff pressure above systolic) o Chvostek's sign (tapping of the inferior portion of the zygoma will produce facial spasms) * Tendon reflexes are hyperactive * Life threatening complications o Laryngospasm o Cardiac arrhythmias * ECG changes include: o Intermittent QT prolongation Treatment -Urgent -10ml 10% Ca gluconate over 3 minutes -Vit D 1-5g orally -Consider Ca infusion -Consider acidosis : to increase the freely ionized Ca concentration For every 0.1 increase in pH, ionized calcium decreases by about 0.05 mmol/L. |