Endo-II Past Papers

Thyroid
 True about thyroid hormone synthesis? Multiple proteases digest thyroglobulin n releases T3 T4 in free
form. These then Diffuse thru base of thyroid cell into capillaries, I2 is recovered from mono,
diiodotyrosine in TGB by cleavage inside the thyrocyte.
 Hormone of hypo and hyperthyroidism?
 Male: Female ratio in thyroid dysgenesis? 2:1
 When should u perform thyroid scan in a newborn infant? 5-8 days after birth, after 6 hours of life, at first
day of life
 Most common cause of hypothyroidism in developed countries? Hashimotos
 Which doesn’t occur in hypothyroidism? Diarrhea
 60yr, male, at high mountain region, constipated, H/R is 60, thick skin, tongue edges scalloped, teeth
indentation, what is probable diagnosis? Iodine deficiency
 In cretinism? Impaired skeletal & CNS development (BASIS), Impaired physical and mental
development, it is GULL disease
 A patient with short stature, mental retardation, protruding tongue, umbilical hernia, diagnosis? Cretinism
 40-year-old patient had hypothyroidism, most common cause? Iodine deficiency, Autoimmune thyroiditis
 Not found in hyperthyroidism? Cold intolerance
 Patient taking amiodarone, atenolol and aspirin, (showing hypothyroid symptoms)? Drug induced
hypothyroidism
 Not an indication for thyroid replacement therapy? To lose weight
 Radio iodine (131) is suitable for treatment in? >45yrs old, young patients, Pregnancy, Drug side effects
 All the following are used for the treatment for hyperthyroidism but which one of these complicates the
process? Propylthiouracil, Triiodothyronine, Surgical removal
 A woman presented with tachycardia, sweating, diarrhea, neck swelling and eye changes. Diagnosis?
Graves disease
 35 yr. old Black women. Recognized a 2x1 cm mass 2 days ago on the lower right thyroid lobe. No
palpitation tachycardia diaphoresis. No pain dysphagia or voice hoarseness. Mass is nontender. She has a
medicinal history of Hypertension. For which she uses atenolol. Physical exam remarkable. Blood urea
creatinine calcium phosphate normal. What do u do now? thyroid function test, history of neck and head
irradiation, family history for thyroid cancer, parathyroid function test., FNAC
 A person with probable hyperthyroidism, your first investigation? T3, T4, TSH
 All the following are used for the treatment for hyperthyroidism but which one of these complicates the
process? Propylthiouracil, Triiodothyronine, Surgical removal
 Patient With palpitations, anxiety and exophthalmos, Diagnosis? Graves disease (BASIS)
 Graves disease most discrete feature? Exophthalmos (BASIS)
 False about hyperthyroidism? Hashimoto can cause hyper
 Levels of hormones in Graves?
 How does exophthalmos occur in grave’s disease?
 Thyroid storm patients, die of? Cardiac arrhythmia
 Patient undergoes thyroidectomy develop swelling in the neck. And become dyspnea next management
is? Explore in the ward, send to OT, Intubation, tracheostomy
 Which of the following is not a feature of goiter? Euthyroid, Cabbage
 Which of following is not a feature of solitary thyroid nodule? Multiple nodules, endemic, associated with
cabbage &cauliflower
 Characteristic of diffuse goitre? Endemic when more than 10% of population is involved, Multinodular
 Which of the following is not a feature of simple colloid goiter? Euthyroid, Cabbage and cauliflower
increases it, Multiple nodules may be seen
 The treatment for a 72-year-old with multinodular goitre? Radioiodine
 All follow the RAI treatment in thyroid condition except? thyroid lymphoma, papillary carcinoma,
follicular carcinoma, MNG, Grave disease
 An asymmetric painless swelling in the neck with palpitation? Multinodular goitre
 Solitary nodules? More neoplastic if it is in young

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 Multinodular goiter? By recurrent episode of hyperplasia n involution
 A person had slightly elevated thyroid levels following a viral infection which became normal after 6
weeks without any treatment? Subacute thyroiditis
 Mutation seen in pendred syndrome? SLC26A4 (BASIS)
 Hallmark in medullary Carcinoma of thyroid? Amyloid deposits (BASIS)
 False about anaplastic Carcinoma? Amyloid deposits, Spindle cells and giant cells, Has worse prognosis
Parathyroid
 Which is not true about the parathyroid glands? Oxyphil cells secrete PTH, parathyroid from the 3rd and
4th branchial cleft
 Mechanism of release of PTH is such that calcium? binds to a protein receptor and activates intracellular
enzyme formation.
 MOA of PTH? Increase resorption of both Ca n po4
 Most common cause of Hypocalcemia? Dec. vitD, hypoparathyroidism, hypoalbuminemia
 Not present in Hypocalcemia? Carpopedal spasm, Stridor, Polyurea (DAVID), Convulsions
 Most common cause of hypercalcemia? primary hyperparathyroidism
 A person has hypercalcemia with normal PTH of 52 (range 15-55). What is your conclusion about his
condition? the problem is not within the parathyroid, I marked that the person has abnormally high
sensitivity to PTH such that normal levels of PTH have caused calcium levels to rise.
 A case of hypercalcemia was given with its sign and symptoms mentioned. Levels of urea and creatinine
were given in mmol/L (the irritating part). What is the most probable cause of hypercalcemia? Chronic
renal failure, primary hyperparathyroidism, Increased Vitamin D
 Lab findings in hyperparathyroidism? High calcium, low PO4, high PTH
 Most common cause of primary hyperparathyroidism? Single adenoma, Multiple adenoma, Carcinoma
 Most common cause of hyperparathyroidism? Adenoma, Carcinoma, Hyperplasia
 Increased parathyroid hormone, increased calcium cardiac findings? aortic and mitral calcification
(BASIS), aortic calcification, mitral calcification
 Suture for PTH adenoma? Ant triangle, post triangle, 2 cm above the sternal notch
 Patient after thyroidectomy complain of tingling sensation investigation? PTH level
Adrenals
 Not true about adrenal?
 Adrenal medulla is derived from? Ectoderm, endoderm, mesoderm, neural crest cells
 Not a function of glucocorticoids? Increased skin protein synthesis, Hyperglycemia, Leukotriene synthesis
 True about steroid hormones? Derived from cholesterol
 Zona glomerulosa causes the release of? Aldosterone
 Cortisol does not cause? Hypoglycemia
 Serum and urinary cortisol high, ACTH low, further investigations? CT adrenals, MRI abdomen
 A patient having cushingoid symptoms, high dose dexamethasone suppression test does not suppress
cortisol levels? Ectopic ACTH secretion (DAVID)
 Patients With smoking history and increased episode of hemoptysis, have Cushing syndrome? Small cell
carcinoma
 A 34-year-old female presents with an increased free urinary cortisol level. High dose dexamethasone test
decreases the cortisol level more than 50%. What is the probable diagnosis? Pituitary tumor
 A patient has Cushingoid face, raised cortisol and ACTH, your next investigation? MRI head, 48 hours
high dose dexamethasone suppression test
 A patient has slightly elevated Cortisol levels, undergoes dexamethasone overnight test, cortisol levels
become normal, he has? Pseudo Cushing
 Free cortisol urine is high. Serum cortisol urine is high. Serum ACTH is high. MRI brain shows no lesion.
What do u do next? dexamethasone suppression test, CT brain, CT chest and X-ray chest, CT abdomen
 A couple had 7 children out of which two were obese. Couple were black haired, and they had a son who
was 13 yrs. old with weight ____, and BMI was 52. He was red haired and was diagnosed at time of birth
having adrenal problem so has been treated for cortisol. What should be given? Leptin
 Which of the following statement is wrong about Cushing’s? aldosterone causes Cushing syndrome

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 Untrue about Addison’s Disease? Clinical pigmentation does not occur, Mucosal pigmentation occurs
 Hyperaldosteronism is Cushing’s syndrome
 Not true about Addison’s disease? Mucosal pigmentation not present clinically
 Following has no value in adrenal insufficiency? Single cortisol level, Urinary renin activity
 Patient With increased aldosterone and decreased renin? Adrenal cortex adenoma
Pancreas
 Which of the following is not function of insulin? Lipoid degradation, Lipid synthesis, protein
breakdown
 Glucagon acts by? promoting glycogenolysis and gluconeogenesis
 Insulin release stimulated by?
 Not true about exocrine pancreas? Somatostatin cause glycogen degradation
 Excretion of insulin occurs by? Liver and kidney
 cause release of insulin? Ca
 Not classic definition of diabetes? Random Glucose is greater than 300mg/dl*, with classic signs and
symptoms glucose is 20mg/dl, Fasting glucose greater than 126 mg/dl
 A person had hyperlipidemia with LDL 166 mg/dl. No history of cigarette smoking, hypertension or any
family history. What do ATP III guidelines suggest for controlling his LDL levels? ATP III suggests
taking medication to keep his LDL levels below 160 mg/dl, ATP III suggests taking medication to keep
his LDL levels below 130 mg/dl, ATP III suggests taking medication to keep his LDL levels below 100
mg/dl
 ATP guidelines for Hyperlipidemia?? LDL should be maintained at 100mg/dl, LDL should be
maintained at 130mg/dl, LDL should be maintained at 160mg/dl
 Regarding diabetes? FBG>126 on more than one occasion (BASIS)
 Most common cause of type1 diabetes? Autoimmune
 Type of Diabetes in < 20 years patient? Diabetes mellitus type 1
 Type 1 DM? ketonuria
 Type 2 Diabetes? Due to multifactorial causes
 Metabolic syndrome linked to? Diabetes
 Which of these is wrong about Type 2 Diabetes? There is insulin deficiency, there is resistance to the
action of insulin, it is a result of multifactorial causes
 Not true about DM 2? No relation with sedentary lifestyle and obesity
 Type 2 diabetes histologically have? Amyloid deposition (BASIS)
 Complications of DM except? MI, neuropathy, ischemic limbs, diarrhea, preeclampsia
 DM not characterized by? Single disease entity, Group of metabolic syndromes
 An old man was suffering from diabetes, hypertension, high cholesterol. Two of his anti-diabetic drugs
were mentioned. One metformin second doesn’t remember. He had chest pain and was brought to the
CCU department. Primary angioplasty was performed. What drug regimen should the patient be kept on
for his glycemic control? Same dosage of the two anti-diabetic drugs, sliding scale adjustment of
insulin, biphasic insulin regimen, monophasic insulin regimen
 Insulin therapy after angioplasty?
 DKA initial treatment? IV fluids
 Diabetic coma treatment? Crystalline insulin
 Diabetic nephropathy and retinopathy are? Microangiopathy
 Whipple’s triad?
 Treatment for diabetic ketoacidosis? Crystalline insulin, Anti diabetic drugs, Lente insulin, Glargine
 Insulin given in acute emergency? Rapid acting insulin (KATZUNG), Lente insulin, Long acting insulin
 Severe Diabetic ketoacidosis is when? pH<7.15, glucose 400 mg/dl, HCO3 16 mg/dl
 Diabetic ketoacidosis is severe if? HCO-3 < 10
 An overweight person with type 2 diabetes is taking gliclazide(sulfonylurea) but he has poor glycemic
control. All his lab reports were given with an HbA1c of 9%. What drug will you prescribe to improve his
glycemic control? Metformin, Thiazolidinediones, Glimepiride
 In which of the following cases insulin increased? Insulinoma

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 Pituitary
 Other than their specialized functions, which of these do not have endocrine secretions? Spleen, Heart,
Kidney, liver
 About Pituitary? shrinks during pregnancy, has two lobes, lies at the base of the skull, is controlled by the
hypothalamus, controls other major endocrine organs
 Not true about pituitary gland? Anterior is called neurohypophysis, Corticotrophin cells are basophils
 Untrue about endocrine is? Somatostatin promote breakdown of glycogen
 Which hormone is not released by anterior pituitary? ACTH, TSH, prolactin, GH, ADH
 Not a function of pituitary gland? Diabetic control
 Peptide hormones are derived from? Tyrosine, cysteine
 somatotroph? GH
 GH increase by? Decrease Glucose
 not true about pituitary? Hormones travel through lymphatics from hypothalamus to post pituitary
 Somatostatin affects? Pulsatile release of GH
 Regarding GH?
 Mutation of a gene involved in the development of diencephalon can affect secretion of which hormone?
ACTH, Oxytocin
 Somatotrophs consists how much of anterior pituitary? 30-40% or 50%
 Acromegaly symptoms, not responding to OGTT. Investigation? MRI head
 A pt. with signs n symptoms of acromegaly with no lesion on MRI. It was asked which test will confirm
diagnosis? OGTT, IGF
 A pt. has visual disturbances, lesion on MRI. Which of these is the investigation of choice to establish the
diagnosis? OGTT, IGF
 Patient having pituitary adenoma with increased GH secretion, investigation of choice? IGF, OGTT
 Acromegaly confirmatory test? OGTT
 A 40-year-old male presents with visual field problems. On examination he has prognathism and prominent
periorbital ridges. There a pituitary lesion on MRI. What’s the best therapy? Surgery, GH receptor blocker)
 Best treatment for acromegaly? Surgery (DAVID), octreotide
 36yr, Male, head ache, visual disturbance treatment is, MRI shows pituitary tumor, glucose tolerance
positive, not suitable for surgery. What to give? Pegvisomant, Octreotide, Transsphenoidal surgery
 A person has visual disturbance, lesion on MRI, high levels of prolactin in blood. What is the most
probable diagnosis? Prolactinoma
 Which of these do not match with a GH/somatotropin secreting pituitary tumor? Old person with
gigantism, acromegaly when epiphyses closed, Increased secretion of growth hormone
 Lesion on optic chiasma? Bitemporal Hemianopsia
 Pituitary tumor presents as? Visual defect
 Not feature of hyperpituitarism? Hypoglycemia
 Which of the following is not a characteristic of Sheehan’s syndrome? It is defined as Ante-partum
hemorrhage
 Regarding treatment of hypopituitarism? it is mostly incurable, surgical and medical treatment,
medication for life time
 Empty Sella syndrome? Lack of pituitary in Sella but usually hormones are normal
 Most common cause of hypopituitarism? Pituitary macroadenoma
 Child with short stature and pituitary tumor? Craniopharyngioma
 Kallmann Syndrome? Hypogonadotropic hypogonadism
 Achondroplasia, how to confirm? Short limbs, Upper segment scan, lower segment scan
 Patient with renal stones, head mass, hyperglycemia? MEN I
 How to diagnose hypopituitarism? MRI, TRH insulin GnRH response, baseline level of hormone
Pharma
 A 32-year-old female presents with hyperprolactinemia having pituitary lesion on MRI. What’s 1st line Tx?
Dopamine agonist
 Following is the somatostatin analogue? Octreotide (LIPPIN)

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 Vasopressin effects potentiated by?
 Patient with tumor producing Vasoactive intestinal polypeptide, treatment? Octreotide (DAVID)
 GH decrease by? Octreotide
 Decrease ADH by? phenytoin
 Bromocriptine is not indicated in? dwarfism.
 Patient with GH adenoma with failed surgery? Next treatment is octreotide
 Octreotide given in? calci
 Levothyroxine dose in neonates? 10-15 ug/kg/day
 Recommended dose of levothyroxine in children? 4 ug/kg/day
 Best treatment for myxedema coma? IV Triiodothyronine 300-400ug, Levothyroxine, Keep patient
warm, IV fluids & electrolytes
 Drug decreasing protein binding of thyroxine? Aspirin
 Hypothyroidism patient with ischemic heart disease. Which of these drugs will be used for the initiation
therapy? Optimization of thyroxine, Beta blockers
 Hypothyroidism patient with ischemic heart disease. treatment? Beta blockers
 Adverse effects of PTU and methimazole? Agranulocytosis
 Mechanism of action of Propylthiouracil? Inhibits iodination and coupling
 levothyroxine is indicated for treatment in the following cases except? simple treatment of obesity
 Most dangerous complication of methimazole?
 Drug given in thyroid storm? Propranolol
 decrease the iodination? PTU, methimazole, iodide, RAI
 cretinism? Levothyroxine
 Metabolic interaction of theophylline with cimetidine?
 tetany treatment? IV Ca-gluconate infusion
 which is not treatment of hyperparathyroidism? Calcimimetics
 Which of the following used in DM acts by delaying digestion/absorption of food? alpha glucosidase
inhibitor
 Treatment plan for type 1 DM? SC/IV administration of Insulin.
 Advantage of Lispro over short acting insulin? Less chances of hypoglycaemia
 1st generation sulfonylureas include? Tolbutamide (LIPPIN)
 Which is not an anti-diabetic drug? Tolbutamide
 Sulfonylurea acts on? Potassium channels (LIPPIN)
 Mechanism of action of alpha-glucosidase inhibitor? Carbohydrate malabsorption
 drug that causes both synthesis n formation of insulin? Sulfonylurea
 MOA of sulfonylurea incorrect? Regeneration of beta cell
 Glucocorticoid inhibits? Phospholipase A2
 Desmopressin is not given in? Bronchoconstriction (LIPPIN and KAPLAN), Diabetes insipidus,
Colonic diverticula, Esophageal varices, Von Willebrand disease
 Which of these is a long acting corticosteroid? Betamethasone (LIPPIN)
 Treatment of choice for Cushing’s?
CM
 Best desk type in school? Minus type (LECTURE), Zero type, Plus type
 School services made for? School children
 Doctor should have what other than attitude? thinks of the best treatment for the patient, show respect
towards time and punctuality
 professional skill for verbal communication? For patient counseling
 Psychosocial model consists of? Ask the patient perception first
 Short stature, which centile? <3rd centile
 Short stature with short trunk occurs in? Mucopolysaccharidoses, Downs syndrome, Nona’s syndrome
 A short statured child having short limbs is suffering from? Achondroplasia (Lec outlines)
 Increase in the height of baby during first 12months is? 9-11 inches (25cm)

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 Short stature with obesity...which syndrome? (Downs syndrome) pseudohypoparathyroidism, Cushing syn
and Prader Willi syndrome
OSPE-1 (Fig.1)
 Diagnosis? papillary Carcinoma
 All of these is true except?
 Orphan Annie eye nuclei
 intranuclear inclusions
 it is the most common thyroid malignancy
 Hurthle cells
 The tumor spreads by? Lymphatic route
 Following causes the paraneoplastic syndrome?
Medullary Carcinoma of thyroid
 Most aggressive? Anaplastic Ca
(Fig.1)
OSPE-2 (Fig.2)
 Identification? Parathyroid adenoma
 Gene involved? Cyclin D1 (BASIS), RET
 Most common manifestation? Hypercalcemia, Hypocalcemia
 Osteolytic lesions on legs? Browns tumor

(Fig.2)
OSPE-3 (Fig.3)
 Name the structure marked A? Inferior parathyroid gland, Facial artery
 The structure marked B is a branch of? External carotid artery
 Name the structure labeled D? Recurrent laryngeal nerve
 The structure marked C is a branch of? Thyrocervical trunk, External carotid artery
 Inferior thyroid vein drains? Superior parathyroid, Inferior parathyroid, Both

OSPE ON SHORT STATURE.

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 Initial diagnosis by? US:LS ratio, wt., height
 Further question should b ask? Family hx, birth weight n height, developmental hx
 Investigation initially? GH level, bone age
 If chronological = bone age, then? Familial, normal, constitutional delay.
 What will you say to the parent about the progress of height? Height will b normal, height achieved but
delay
OSPE: SCHOOL Dr. Farzana as health officer.
 Responsibility? To do periodical medical examination, to do periodical vaccination
 Routine vaccination? Cholera, typhoid, hep, polio
 Function of public health service? Referral, to prevent disease?
 Public health service is a branch of? Preventive medicine
 Further health checkup is required except? Student, teacher, school personnel
 Most common problem in school children? dental caries
 A class should contain? No more then 40 students
OSPE: CUSHING diagram
 Diagnosis? Cushing disease
 Which will not be finding? Thick skin
 Best investigation? 24 hr urine cortisol excretion
 Treatment? Cortisol
CASE-2
 Diagnosis? Adrenal insufficiency
 Most common cause? (Exogenous drug inappropriate withdrawal something like that)
CASE-3 A lady with low BP, pallor, atrophic breast
 Diagnosis? Sheehan syndrome, Pituitary apoplexy, Adrenal crisis
 Which hormone should be corrected first? Cortisol (DAVID)
 Why patient has pallor? FSH and LH deficiency (DAVID), Decreased TSH
 Which hormone won’t be affected? ADH, TSH, ACTH, GH
CASE-4 Glucose 400mg/d, pH 7.2, HCO3 12mg/dll………
 Diagnosis? Diabetic ketoacidosis, hyperosmolar coma
 What is the initial management? Fluids I/V
SBL: Cushing
 least likely? Increase k+
 least likely? Thick skin.
 diff b/w pituitary n Cushing syndrome? High dose dexamethasone
SBL: Hashimotos
 diagnosis? Hashimotos thyroiditis
 Histology? Hurthle cell + lymphocyte infiltrate
 Characteristic feature? Gradual thyroid failure
 Most common lymphoma? MALToma (diffuse B cell lymphoma)
 Most common Ca of thyroid is? Papillary
SBL: graves
 investigation? TSH/T4
 other investigation? Cortisol
 primary hypothyroidism investigation? TSH
 not a complication? Constipation
SBL: hypothyroidism case and also symptom of pericardial effusion
 investigation? TSH/T4
 cardiac sin is due to? Pericardial effusion
 most characteristic? Levothyroxine
 treatment? Levothyroxine
SBL; pain in whole body
 diagnosis? Primary hyperparathyroidism

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 function of PTH? Maintenance of extra cellular Ca.
 drug can be given
 treatment? Surgery
ENDOCRINOLOGY – II MODULE PAPER D22 (31st Oct 2019)
1. Appropriate regarding thyroid? Sometimes supplied by thyroid imma artery
2. Adverse effect of thyroxine? Increased BMR, angina, Exophthalmos, dyspnea
3. Potency of T4 to T3 is? 1:10
4. A pt. with hypothyroidism has raised JVP and other cardiac symptoms, dx? Pericardial effusion
5. 20-year-old nurse which with symptoms of hyperthyroidism and decreased uptake of iodine?
 Graves’ disease
 Toxic adenoma
 Toxic multinodular goiter
 Factitious thyroiditis
 Deque vain thyroiditis
6. Sensitive test for primary hypothyroidism? TSH, free T4, total T3, thyroglobulin, thyroid antibodies
7. Hurtle cell variant seen in? Follicular carcinoma
8. Female patient with thyroid nodule. FNAC is performed showing follicular pathology? What to do next?
 Repeat FNAC
 Lobectomy
 Excisional biopsy
 Incisional biopsy
 Turcot biopsy
9. Female patient with thyroid nodule. What to do next? FNAC
10. Most common thyroid carcinoma? Papillary cell carcinoma
11. A 45 years old female presented with nodule, most common thyroid carcinoma in this age group?
Papillary carcinoma
12. Thyroid carcinoma associated with increased calcitonin levels? Medullary cell carcinoma
13. Kid with protruding tongue, mental retardation, umbilical hernia and coarse facial features caused by
deficiency of which hormone? Thyroxine
14. Kid with protruding tongue, mental retardation, umbilical hernia and coarse facial features caused by
caused by which condition? Cretinism
15. Pregnant woman which reduced T4 and T3 and increased TSH. Her child showed symptoms of
hypothyroidism basically and like what is this condition called
 Cretinism
 Thyroid dysplasia
 Thyroid dyshormogenesis
16. Which does not cause diabetes mellites?
 Cushing’s syndrome
 Acromegaly
 Hyperthyroidism
 Hypothyroidism
 Glucagonoma
17. A patient with subtotal thyroidectomy, undergone rapid enlargement of gland presenting with dyspnea.
What should be done first?
 Endotracheal intubation
 Tracheostomy
 Exploration in ward
 OT
 Laryngeal mask airway
18. A pt. presented with mucosal pigmentation, orthostatic hypotension (as from supine and standing BP
given in qtn), Dx? Addison disease
19. A patient with obesity, hypertension, abdominal striae and other features of Cushing
 A hot nodule in thyroid

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  An adrenal mass of > 2 cm
20. Effect of dexamethasone supp test on ectopic ACTH
 Inc
 Dec
 Insensitive to low or high doses of dexamethasone
21. Most common site for ectopic ACTH production? Small cell lung carcinoma, Bronchial carcinoid
22. A pt. with Cushing syndrome presents most commonly with? Obesity, HTN, Bruising, Osteoporosis,
Glucose intolerance
23. One question with middle aged male. Bone pain, mild anemia, alkaline phosphatase and calcium was
increased, albumin:4.2. Don’t remember clearly
 Sarcoidosis
 Primary hyperparathyroidism
 Multiple myeloma
 Osteomalacia
 Chronic renal disease
24. A patient with numbness in lower limbs having Ca Dec, urea 7 inc phosphate inc, PTH 14 Dec
 Hypoparathyroidism
 Renal impairment
 Vit D def
 Familial hypocalciuric Hypocalcemia
25. A woman which type 2 diabetes comes to a clinic which increased glucose and polyuria and she was
diagnosed five years ago and taking metformin 500mg for 3 years. How will u proceed next?
 Increased the dose of metformin
 Add sitagliptin 50mg OD
 Stop metformin and start sulphonyureas
 Give sitagliptin plus sulphonyurea
 Stop metformin start Insulin
26. Treatment for young female patient diagnosed with DM 1? Multiple doses of SC insulin
27. Marked macrovascular complication of DM 2? Accelerating atherosclerosis
28. Neovascularization around the optic nerve head is due to
 Proliferative diabetic retinopathy
 Retinal vein occlusion
 Pre-proliferative diabetic retinopathy
29. Diagnostic value for diabetes (on two occasions)? FBS > 7 mmol/L
30. A child presented with dehydration, unconsciousness? DKA
31. Amine hormones are derived from? Tyrosine
32. Somatotrophs are? GH producing acidophilic cells
33. Untrue about pituitary? Lies in fossa of zygomatic bone
34. Defect of the diencephalon causing reduction of which hormone? Oxytocin
35. GH excess in adults? Acromegaly
36. A case of prolactinoma, Rx? Dopamine agonist
37. Why Betamethasone given in cerebral edema due to brain tumors? More potent, prevents retention of
Na/H2O
38. A patient having a mass in pituitary fossa, hyperglycemia, renal calculi. Dx? MEN 1
39. Which drug inhibits GH? Octreotide
40. Which drug inhibits GH? Beta adrenergic agonists
41. Long acting analogue of somatostatin? Octreotide
42. Mechanism of action of PTU? Inhibits iodination and coupling
43. Which oral diabetic drug inhibits hepatic gluconeogenesis? Metformin
44. 1st generation sulphonyurea? Chlorpropamide
45. Incorrect statement about insulin? Orally active
46. 1st line sulphonyl urea? Chlorpropamide
47. Ultra-short acting insulin

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  Insulin lispro
 Protamine zinc insulin
 NPH
 Insulin Lente
48. Mechanism of action of carbamate poisoning? Reversible inhibition of acetylcholinesterase, inhibiting
ferro chelatase causing porphyria, Inhibition of the cytochrome oxidation pathway
49. Defect in strychnine poisoning? Affects the anterior horn of the spinal cord
50. Child drinks liquid poison. Loin pain dark colored urine, nausea and vomiting and salivation.
 Organophosphate poisoning
 Organochlorine poisoning
51. A patient presents with nausea, vomiting, diarrhea, ate sausages in dinner. Cause?
 Clostridium Welchi
 Clostridium Botulinum
 Exotoxin sec. By botulinum
52. 20 years old with high fever, food poisoning, nausea, anorexia, constipation & abdominal discomfort after
a meal from a restaurant. What organism is responsible? Salmonella, shigella, E. coli, B. cereus
53. Which snake venom causes rhabdomyolysis? Sea snake venom
54. GI irritation, black colored urine, loin pain? Naphthalene poisoning
55. Child came in emergency which history of ‘alleged’ snake bite. no swelling or bite mark was seen on
examination He was anxiety, dyspnea, can’t open eyes. Blood clotting something for 20 minutes was
normal. What will you do?
 Don’t give anti snake venom (ASV) and observe the patient
 Give ASV and observe the patient
 Give anxiolytic and reassure
 Give antihistamines
 Give ASV and neostigmine
56. MOA of strychnine? Depression of inhibitory Pathways (GABA)
57. False perception of something with is not a fact? Delusion
58. False perception of external stimuli which indeed exists? Illusion
59. Patient comes with fear that someone is trying to kill him? Paranoid delusion
60. Boy below or at 3rd percentile. Shorter than his peers. Bone age 4 years height years 5 years. No chronic
diseases in family.
 Constitutional growth delay
 Familial short stature
61. Boy 7-year-old, healthy school going comes with complaint of short stature. His bone age 5 years, height
5 years. What to check? Thyroxine, GH
Case: 45-year female with neck mass for 2 years. Renal calculi, epigastric pain radiating to the back and bone
pain.
62. Most likely diagnosis? Hyperparathyroidism
63. Most likely cause? Parathyroid adenoma
64. Localizing test: Tc 99 sestamibi
65. What to do? Parathyroidectomy
66. Also most likely cause of epigastric pain? Pancreatitis, gall stones
Case:
67. Diagnosis? DKA
68. treat: 0.9% saline solution
69. Further test to confirm: urine and serum ketones

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OSPE
70. Diagnosis? Hashimoto
71. Cause: autoimmune
72. Morphology: mixed leukocytic infiltration with hurtle cells
73. Associated lymphoma: MALT lymphoma
74. Associates carcinoma: papillary cell carcinoma

OSPE
75. Diagnosis: Cushing’s
76. Least likely to be found?
 Increased cortisol
 Increased glucose
 Increased sodium
 Reduced potassium
 Increased potassium
77. Least likely symptom: thick skin
78. Least likely course: thick skin
79. Least likely causes
 Iatrogenic
 TB
 ACTH secreting Adenoma

Compiled by: Shabir Ahmed D22

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