B-renal failure. C-SIADH (syndrome of inappropriate secretion of ADH). Remember: hyponatremia with NORMAL ECF volume: A-nephrotic syndrome B-hypothyroidism. C-diuretics. D-NSAIDS. Answer: 3 Remember: alcohol makes you urinate MORE and smoking makes you urinate LESS. Q11: Answer: c Such a urinary osmolality may indicate compulsive water drinking causing water intoxication and dilute urine, or diabetes insipidus (urinary osmolaity in SIADH is usually around 460 mmol / Kg .i.e. inappropriately high). Q12: Answer: d It is beta blockers, other causes: spironolactone, amiloride and triamterene. Remember: hypokalemia potentiates digoxin toxicity, but in digoxin toxicity hyperkalemia may occur. Q13: Answer: a Bicarbonate infusion reduces serum potassium by 0.2-0.4 meq / L, so it is a weak agent; anyhow, it is used in severe acidosis (but watch for circulatory overload). Calcium resonium is used in the chronic setting. Calcium gluconate infusion is just a cardio protective agent; it does lower the serum potassium. Q14: Answer: d a- True, due to muscle fiber necrosis, and even rhabdomyolysis. b- True, usually seen as a difficult weaning from a ventilator in the ICU setting. c- True, due to impaired red cell membrane ATPase. d- False, HYPERcalciuria and HYPERmagnisuria. e- True, usually resistant to anti-arrhythmics. Q15: Answer: e Volume expansion may be a cause of hypophosphatemia. You should know the causes of hypophophatemia, they are commonly seen in MRCP examination. Other causes: nutritional recovery syndrome, parenteral nutrition, insulin infusion, glucose infusion, alkalosis (respiratory and metabolic), oral phosphate binders, and in the way of treatment of diabetic ketoacidosis. Remember: Hypophophatemia is USUALLY multi factorial and commonly co-exist with other electrolyte imbalance. Q16: Answer: e Remember: drug induced hypomagnesaemia: cisplatin, gentamycin, and loop diuretics. Remember; magnesium is very poorly absorbed orally, hence oral preparations are of no use in deficiency states. Other causes: chronic diarrhea, excessive lactation, hyperparathyroidism, primary and secondary aldosteronism, upper GIT fistula and protein energy malnutrition. Q17: Answer: e a- True, Diamox (carbonic anhydrase inhibitor). b- True, by creating uretrosigmoidostomy (a form of ureteric diversion used in the past). c- True, due to HCL content. d- True, and type I and II. e- False, DKA in the way of recover and early (not late) uraemia , may cause normal anion gap metabolic acidosis. Normal anion gap metabolic acidosis is one of the favorite subjects in the MRCP (both part I and II). Q18: Answer: d In ethylene glycol poisoning there is accumulation of oxalic acid and glycolic acid. Q19: Answer: c Type B is caused by metformin (also sorbitol, isoniazide, and salisylates). *Type A (also seen in any severe shock, carbon monoxide poisoning) in general is caused by profound hypotension and or severe anemia. *Type B (also seen in hepatic failure, severe infections, ethanol, and methanol poisoning) in general is caused by impaired mitochondrial respiration and increased lactate production. Q20: Answer: e a- True, if excessive. b- True, due to direct stimulation of the respiratory center + metabolic acidosis. c- True, the clue is tetany + normal or increased PaO2 + high PH + very low PaCO2). d- True, and pulmonary embolism. e- False, METABOLIC alkalosis due to loss of HCL in vomitus. Chapter VII / Endocrinology Answers Q1: Answer: e a- True, and hence a sequential or a dynamic testing should be used. b- True, and hence, a biochemical diagnosis should be done before imaging. c- True, like adrenal adenomas versus carcinomas. d- True, and if you suspect a hormonal deficiency then choose a stimulation test. e- False, the usually story. Q2: Answer: e As the name implies, it is an apoplexy, so the presentation is a catastrophic one. Lateral extension may involve the 3 rd , 4 th and 6 th cranial nerves. Remember: a TSHoma is responsible for 1 % of all functioning pituitary tumors. Q3: Answer: d a-True, and radiotherapy is a second line treatment. b-True, and radiotherapy is a second line treatment. c- True, notice that radiotherapy is more effective in children, and also used to irradiate the pituitary to prevent Nelson's syndrome. d- False, dopamine agonists are the first line agents even in macroadenomas unless it is cystic and or large. e- True, unfortunately octreotide does not cause tumor shrinkage. Q4: Answer: e Pergolide is a dopamine agonist used in the treatment of hyperprolactinemia. Causes of hyperprolactinemia are many, and it is one the favorite topics in the MRCP examination. Other causes are: pregnancy and lactation, medications (oral contraceptive pills, metoclopromide, reserpine, methyldopa, antipsychotics, antidepressants, opiates and antiandrogens). However, the commonest causes are: 1- Disconnection hyperprolactinemia, as in non-functioning pituitary macroadenomas. 2- Prolactinomas, usually microprolactinomas. 3- Primary hypothyroidism. 4- Polycystic ovarian syndrome. Q5: Answer: e External irradiation is used for some macroadenomas to prevent re-growth if dopamine agonists are stopped. All other options are true. Q6: Answer: e External irradiation although causes shrinkage of the tumor, yet the growth hormone level takes long to return to normal and there is a high risk of panhypoituitarism. Q7: Answer: a Sampling should be done post exercise, not pre exercise. Other tricks are true. Q8: Answer: b The 250 microgram tetracosactrin injection can be given at ANY time during the day. Because it relies on ACTH dependent adrenal atrophy in secondary adrenal failure so it may not diagnose acute adrenal failure secondary to acute ACTH deficiency. Q10: Answer: e Unlike primary hypothyroidism, measuring TSH is not helpful because the pituitary may secrete glycoproteins which are usually detected by TSH assay but they are NOT BIOACTIVE. So the aim is to KEEP the T4 in the upper part of reference range during replacement therapy with T4. Q11: Answer: e a- True, and in the assessment of GH deficiency. b- True, and in SEVERE hypopituitarism c- True, with signs of neuroglycopenia. d- True, at time 0, 30, 45, 60, 90, 120 minutes post administration. e- False, it is given as soluble insulin 0.15 u / kg intravenously. Remember: at the end of the test, the serum GH should be > 20 mu / L, and serum cortisol >550 nmol/ L. Q12: Answer: d DDAVP should not be given if you suspect a severe compulsive water drinking as this will prevent water excretion and risks severe water intoxication if the patient continues to drink water. Q13: Answer: e pruritis (with increased sweating), palmar erythema, and spider nevi, skin pigmentation (but vitilligo is much more common), and clubbing, all are seen in thyrotoxicosis per se . Q14: Answer: c a- True, and slightly raised serum bilirubin. b- True, very mildly. c- False, up to 5 % only, and almost always mild. d- True, due to associated diabetes mellitus and lag storage. e- True, a well documented feature. Q15: Answer: d a- True, 0.2% will develop severe reversible agranulocytosis during carbimazole therapy. b- True, and in those dependent on voice e.g. singers. c- True, and planned pregnancy with in 6 months. d- False, 10% will develop TRANSIENT hypocalcaemia following surgery, and 1% only will develop long term permanent hypocalcaemia. e- True, thus regular follow ups are important. Remember: clinical improvement in a patient on carbimazole is seen after 2 weeks but the biochemical abnormalities will normalize after 4 weeks. Q16: Answer: c a- True, ike coxsackie, mumps, and adeno viruses. b- True, and by swallowing, and movement of the neck. The pain may radiate to the jaw and ears. c- False, the ESR is usually raised and a low titer of thyroid antibodies non- specifically detected transiently. d- True, but steroids are occasionally used for severe cases. e- True, apart from oral propranolol in certain cases and no need for anti-thyroid drugs. Q17: Answer: d The combination of: Suppressed TSH, negligible radio-iodine uptake, low serum thryroglubulin, and greatly raised T4:T3 ratio (usually around 70:1) are diagnostic. Q18: Answer: d There is NO association between post partum depression and post partum thyoriditis. It is supposed to be an autoimmune in origin. Q19: Answer: d a- True, also precipitated by surgery and radio-iodine treatment in a previously inappropriately treated patient. b- True, but should always be kept in mind and the patient should be rendered euthyroid before the operation. c- True, anti-thyroid measures are: oral or IV propranolol, oral sodium iopodate (a radio-contrast medium will restore serum thyroid hormone levels to normal with in 2- 3 days), oral potassium iodate or Lugol's solution, oral or per rectal carbimazole. d- False, there is NO parenteral preparation for carbimazole , if can not be given orally , then give it rectally or by an NG tube. e- True, and the patient should continue on carbimazole. Q20: Answer: e Post ablative and primary atrophic hypothyroidism are both not goitrous. Q21: Answer: e Iron deficiency anemia is a common finding in premenopausal females due to heavy menses. There 8 RARE but well recognized features, although SEEN in many textbooks and QUESTIONS and BOFs, yet in clinical practice if you are in an endocrinology clinic you will see that they are rare: 1-Myotonia. 2- Cereberallar ataxia. 3- Frank psychosis. 4- Pleural and pericardial effusions and heart failure. 5- Ileus. 6- Impotence (while in thyrotoxicosis it is common!!). 7- Galactorrhea. 8- Ascites. Q22: Answer: d READ the question well "Biochemical findings that are useful in the assessment of hypothyroidism". T3 is not a reliable test to differentiate between a euthyroid and hypothyroid patient. Also, we may see: normochromic anemia, low voltage ECG, bradycardia and non specific ST-T changes indicate PROLOBGED SEVERE hypothyroidism. Q23: Answer: d Remember: Subjective improvement is seen after 2-3 weeks, and the reduction in body weight and periorbital puffiness occurs relatively rapidly, BUT restoration of skin and hair texture and resolution of any effusion may take 3-6 MONTHS. Q24: Answer: e a- True, a rare presentation rather than to be a complication of an already diagnosed patient. b- True, as well as raised CSF protein, so you it may be missed as a PRIMARY CNS DISEASE. c- True, it is not a "cold case". d- True, and start treatment with intravenous hydrocortisone before the biochemical diagnosis. e- There is NO parenteral preparation of T4, BUT there is a parenteral form of T3 and so T3 can be given intravenously. Q25: Answer: c Option "c" is the classical finding in those who are non-compliant and take large doses before the follow up visit to fool the doctor! Q26: Answer: e Phneytoin is an enzyme inducer, so the dose of thyroxin may need to be increased in hypothyroidism and concomitant use of phenytoin. Q27: Answer: e Obesity is rarely due to a single gene mutation. Endocrine diseases associated with obesity are: Cushing' syndrome, hypothyroidism, and polycystic ovarian syndrome. Q28: Answer: d Follicular carcinoma and adenoma are very similar on FNA cytology, but thyroid biopsy is needed to demonstrate vascular invasion in cases of carcinomas. Q29: Answer: e Secondary tumors are rarely seen. Q30: Answer: b a- True, it is an aggressive one. b- False, it is part of MEN type II. c- True, as there is no curative treatment. d- This, clinically speaking it is only a tumor MARKER! e- True, because the para-follicular cells don’t trap iodine and hence it has no role in the treatment. Q31: Answer: e Even when caused by an adenoma, the tumor is rarely felt in the neck (usually located at surgical exploration).Other options are true. Q32: Answer: e Secondary bone malignancy is a cause of hypercalcemia with undetectable parathyroid hormone level (also seen in vitamin D intoxication, milk alkai syndrome, sarcoidosis , Addison's disease…cet. ). The 1 st 4 options are the cause of hypercalcemia with normal or high serum parathryoid hormone level. Q33: Answer: d The hypercalcemia of primary hyperparathyroidism does not respond to steroids. High dose glucocorticoids are very effective in the treatment of malignancy- associated hypercalcemia patients. Q34: Answer: a It may caused by hypoparathyroidism and pseudohypoparathyroidism. Also may cause seizures, and Parkinsonian like picture. Pseudopseudohypoparathyroidism resembles pseudohypoparathryoidism pheonotypically, but it has a normal biochemical profile. Q35: Answer: e Pseudopseudohypoparathyroidism resembles pseudohypoparathyroidism phenotypically, but it has a normal biochemical profile. Q36: Answer: d pseudohypoparathyroidism is treated by vitamine D metabolites like alpha calcidol tablets and follow up the patient with serum PTH and serum calcium. Q37: Answer: e 1- True, and weight gain is the commonest symptom. 2- True, so it is seen in 75% of cases. 3- True, as well as prominent hypokalemic alkalosis. 4- True, frank psychosis is uncommon. 5- False, type II fiber atrophy. Remember: Striae are seen in 50% Proximal myopathy 50% Bruising 50% Obesity as a sign is seen in 97% of cases, so 3 % are not obese. Q38: Answer: c a- True, as the stress of hospitalization may interfere with many tests and some normal persons will even FAIL to suppress on overnight dexamehtason suppression test (i.e. behaves like Cushing's) because the hypothalamic- pituitary-adrenal axis will ESCAPE such suppression due to powerful endogenous stress mechanisms. b- True. c- False, it does not cross react and that's why it is used in the suppression test. d- True, hence called pseudo Cushing's. e- True, and very high levels indicate an ectopic source. Q39: Answer: e Without treatment, the 5 year survival rate is 50%. All other options are true. Q40: Answer e a- True, and liquorice abuse. b- True, and congenital adrenal hyperplasia due to 11 beta hydroxylase and 17 alpha hydroxylase deficiency. c- True, causing hypokalemia, hypertension and low aldosterone. d- True, and 11 beta HSD deficiency. e- False, Glucocorticoids suppressible hyperaldosterosnism and Conn's adenoma and idiopathic bilateral adrenal hyperplasia , all are the cause of PRIMARY aldosteronism. Q41: Answer: e Although there is an avid sodium retention, leg edema is uncommon and suggests secondary aldosteronism or a complicating heart failure. Serum potassium is normal in up to 70% of cases at the time of diagnosis because many patients are already treated by salt restriction making less sodium available to be exchanged for potassium at the distal tubule. Q42: Answer: c 1- True, like MEN type II, neurofibromatosis, and Von Hipple Lindau. 2- True, and predominantly elevated adrenalin indicates an adrenal tumor that is not large enough to outgrow its blood supply. 3- False, it commonly occurs in the absence of diabetes. 4- True, indicating a high level of dopamine. 5- True, in urinary bladder tumors. Remember: although pallor is commonly seen during the attack, occasionally FLUSHING is seen. Q43: Answer: e a- TB is the next, hence CXR should be done in all cases. b- True, and when presents with buccal hyperpigmentation, both are highly suggestive. c- True, Addison's disease per se causes fasting hypoglycemia. d-True. e- False, it is a rare disease with an incidence of 8 new case/ million of population. Male to female ratio is 1:2. Q44: Answer: d a- True, up to 90% of cases, and a late onset form with hirsutism is a recognized presentation. b- True, many enzymatic deficiencies are documented. c- True, and salt losing nephropathy and crises in neonates, usually in males. d- False, associated with hypertension due to increased 11 deoxycorticosterone, a powerful mineralocorticoid. e- True, and plastic surgery has a place for the ambiguous genitalia in females Q45: Answer 5 Other drugs: estrogens, and GnRH analogues given for prostatic carcinomas. Q46: Answer: e LH: FSH ratio more than 2.5:1.Also there is: hypertension, hyperglycemia, hyperlipidemia, hirsutism, oligomenorrhea or secondary amenorrhea, and infertility. Remember : PCOS is treated according to the PRERSENTING feature .eg She is complaining of infertility, so treat the infertility, or complaining of hirsutism so treat the hirsutism . DON’T TRY TO TREAT EVERYTHING! However, weight reduction in obese is important in the overall management. Q47: Answer: e In idiopathic hisutism, female family history is very important, especially seen in Asians or Mediterraneans. Q48: Answer: b a- True, and mutation in RET proto-oncogen on chromosome 10 in type II. b- False, hypercalcemia is the commonest presenting feature of type I, while in type IIa it is uncommon and in type IIb it is absent. c- True, hence family history is very important. d- True, unlike the sporadic ones (10% bilateral). e- True, also Cushing syndrome is uncommon in type I. Q49: Answer: e a- True, next is the cecum and appendix. b- True, due to obstruction of the mouth of the appendix. c- True, because they have a low malignant potential. d- True, Pulmonic stenosis, tricuspid regurgitation and right sided endocardial fibrosis. e- False, Cramping abdominal pain and diarrhea with flushing and wheeze are the commonest presenting features of carcinoid SYNROMS not tumors. Q50: Answer: d 1- True, and steatorrhea and achlorhydria. 2- True, and skin rash and diabetes. 3- True, or watery diarrhea and multiple severe peptic ulceration. 4- False, with HYPOKALEMIA, hence called pancreatic cholera. 5- True, due to hypoglycemia. [...]... Total fat should be 3 0-3 5% Saturated fat should be . B-renal failure. C-SIADH (syndrome of inappropriate secretion of ADH). Remember: hyponatremia with NORMAL ECF volume: A-nephrotic syndrome B-hypothyroidism. C-diuretics. D-NSAIDS. Answer:. commonest causes are: 1- Disconnection hyperprolactinemia, as in non-functioning pituitary macroadenomas. 2- Prolactinomas, usually microprolactinomas. 3- Primary hypothyroidism. 4- Polycystic ovarian. pathogenesis. Q4: Answer 5 1-MODY type I, a rare progressive early onset form 2-MODY type III. Progressive early onset 3-MODY type II , mild and relatively stable early onset type 4- very rare 5-it has