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USMLE Step 1: Endocrine > Endocrine Pathology > Flashcards

Endocrine Pathology Flashcards

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USMLE® Step 1 flashcards
1
Q

Patient presents to clinic with hypertension, weight gain, moon facies, truncal obesity, buffalo hump, hyperglycemia, striae. You suspect _____. What is the #1 exogenous cause?

A

Cushing’s syndrome; steroids

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2
Q

What are 3 endogenous causes of Cushing’s syndrome? State whether ACTH inc/dec for each.

A

Cushing’s disease (inc ACTH from pituitary adenoma), ectopic ACTH (inc ACTH from non-pituitary tissue), adrenal adenoma/carcinoma/nodular adrenal hyperplasia (dec ACTH)

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3
Q

What are some examples of nonpituitary tissue making ACTH?

A

Small cell lung cancer, bronchial carcinoids

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4
Q

Is cortisol elevated/suppressed during a dexamethasone suppression test for ACTH-pituitary tumor?

A

With low dose dex: remains elevated; with high dose dex: suppressed

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5
Q

Is cortisol elevated/suppressed during a dexamethasone suppression test for ectopic ACTH-pituitary tumor?

A

With low dose dex: remains elevated; with high dose dex: remains elevated

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6
Q

Is cortisol elevated/suppressed during a dexamethasone suppression test for cortisol-producing tumor?

A

With low dose dex: remains elevated; with high dose dex: remains elevated

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7
Q

Patient with adrenal hyperplasia who presents with HTN, hypokalemia, metabolic alkalosis, and low plasma renin. What is the treatment?

A

Patient has primary hyperaldosteronism. Surgery to remove the tumor and/or spironolactone

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8
Q

Secondary hyperaldosteronism is associated with high/low plasma renin. What is the treatment?

A

High; spironolactone

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9
Q

How does a patient with Addison’s disease clinically present?

A

Hypotension, hyperkalemia, acidosis, skin hyperpigmentation (due to MSH, a by-product of inc ACTH production from POMC)

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10
Q

T/F: Addison’s disease only affects the outer 2 cortical divisions.

A

FALSE: Involves all 3 cortical divisions (spares medulla)

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11
Q

What are 2 clinical features that distinguish primary from secondary adrenal insufficiency?

A

Unlike primary, secondary does not have skin hyperpigmentation and no hyperkalemia

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12
Q

What is Waterhouse-Friderichsen syndrome?

A

Acute primary adrenal insufficiency due to adrenal hemorrhage. Associated with Neisseria meningitidis septicemia, DIC, endotoxic shock

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13
Q

What is the Rule of 10’s for pheochromocytoma?

A

10% malignant, bilateral, extra-adrenal, calcify, kids

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14
Q

Most pheochromocytomas secrete which 3 hormones?

A

Epinephrine, NE, dopamine

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15
Q

How is pheochromocytoma diagnosed and treated?

A

Dx: Urinary VMA and plasma catecholamines are elevated; Treatment: Tumor surgically removed only after effective alpha and beta blockade

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16
Q

T/F: Pheochromocytoma is associated with neurofibromatosis type 1, MEN types 2A and 2B.

A

TRUE

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17
Q

T/F: When treating pheochromocytoma, beta blockers must be given first to avoid a hypertensive crisis.

A

FALSE: Irreversible alpha-antagonists must be given first to avoid a hypertensive crisis

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18
Q

What are the 5 P’s of pheochromocytoma (episodic hyperadrenergic symptoms)?

A

Pressure (elevated blood pressure), pain (headache), perspiration, palpitations (tachycardia), pallor

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19
Q

T/F: In neuroblastoma, HVA is elevated in urine.

A

TRUE

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20
Q

Patient presents with weight gain, constipation, cold intolerance, decreased appetite, lethargy and fatigue. On exam, some facial myxedema is noted and patient has decreased reflexes, bradycardia. You suspect hypothyroidism. What is the most sensitive test for primary hypothyroidism?

A

TSH (increased, also see decreased free T4)

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21
Q

Patient presents with heat intolerance, weight loss, diarrhea. Increased reflexes and pretibial myxedema seen on exam. Would you expect TSH, free or total T3 and T4 to be inc or dec?

A

dec TSH, inc free or total T3 and T4

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22
Q

Patient presents with moderately enlarged, nontender thyroid. Histology shoes Hurthle cells and lymphocytic infiltrate with germinal centers. What are the antibodies associated with this disease?

A

Antithyroglobulin antibodies (this is Hashimoto’s thyroiditis)

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23
Q

What are the 5 P’s associated with cretinism?

A

Pot-bellied, Pale, Puffy-faced child with Protruding umbilicus and Protuberant tongue

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24
Q

Patient with recent flu-like illness presents with jaw pain and a very tender thyroid. Histology shows granulomatous inflammation. What is a lab finding associated with the disease and treatment?

A

Inc ESR; self limiting

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25
Q

T/F: Patients with subacute thyroiditis may be hyperthyroid early in course.

A

TRUE

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26
Q

T/F: Riedel’s thyroiditis presents as a fixed, hard, painful goiter.

A

FALSE: Painless

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27
Q

Fill in the blank: Toxic multinodular goiter is focal patches of hyperfunctioning follicular cells working independently of TSH due to a _____.

A

Mutation in TSH receptor

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28
Q

Hot nodules are rarely malignant/benign.

A

Malignant

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29
Q

What are some clinical findings associated with Graves’ disease?

A

Proptosis, pretibial myxedema, inc in connective tissue deposition, diffuse goiter

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30
Q

What is thyroid storm?

A

Stress-induced catecholamine surge leading to death by arrhythmia

31
Q

What type of thyroid cancer is associated with Orphan Annie’s eyes and psammoma bodies on histology?

A

Papillary carcinoma

32
Q

Calcitonin is produced in which type of thyroid cancer?

A

Medullary carcinoma

33
Q

What malignancy is associated with Hashimoto’s thyroiditis?

A

Lymphoma

34
Q

Which type of thyroid cancer is associated with the best prognosis: papillary, medullary, follicular, or medullary?

A

Papillary carcinoma

35
Q

T/F: Primary hyperparathyroidism is usually an adenoma.

A

TRUE

36
Q

Hypercalcemia is seen with primary/secondary hyperparathyroidism while hypocalcemia is seen with primary/secondary hyperparathyroidism.

A

Primary; secondary

37
Q

Urine cAMP is inc/dec in primary hyperparathyroidism.

A

Inc

38
Q

What is osteitis fibrosa cystica?

A

Cystic bone spaces filled with brown fibrous tissue, leads to bone pain

39
Q

What is renal osteodystrophy?

A

Bone lesions due to secondary or tertiary hyperparathyroidism due to renal disease

40
Q

What are some causes of hypoparathyroidism?

A

Accidental surgical excision (thyroid surgery), autoimmune destruction, DiGeorge syndrome

41
Q

Describe the 2 clinical signs associated with hypoparathyroidism.

A

Chvostek’s sign: tapping of facial nerve leads to contraction of facial muscles; Trousseau’s sign: occlusion of brachial artery with BP cuff leads to carpal spasm

42
Q

Patient presents with decreased PTH, hypocalcemia, shortened 4th/5th digits, and short stature. Name the genetic disease.

A

Pseudohypoparathyroidism (Albright’s hereditary osteodystrophy)

43
Q

Patient presents with amenorrhea, galactorrhea, low libido and has been undergoing treatment for infertility. Bitemporal hemianopia is observed on exam. What is the treatment?

A

Dopamine agonists (bromocriptine or cabergoline)

44
Q

Patient presents with large tongue, deep voice, large hands and feet, coarse facial features. Patient also with insulin resistance DM. What is the diagnosis and treatment for this disease?

A

Dx: increased serum IGF-1; Treatment: pituitary adenoma resection followed by somatostatin analog if not cured

45
Q

What is the difference between central and nephrogenic DI.

A

Central is due to lack of ADH while nephrogenic is due to lack of renal response to ADH

46
Q

Compare the different etiologies of central and nephrogenic DI.

A

Central: pituitary tumor, trauma, surgery, histiocytosis X; Nephrogenic: hereditary or secondary to hypercalcemia, lithium, demeclocycline

47
Q

What are the findings consistent with DI (urine specific gravity and serum osmolality)?

A

Urine specific gravity 290mOsm/L

48
Q

How is DI diagnosed? What is the test used to distinguish central from nephrogenic DI?

A

Water deprivation test: urine osmolality does not increase; response to desmopressin distinguishes central vs. nephrogenic

49
Q

What is the treatment for central DI?

A

Adequate fluid intake; intranasal desmopressin

50
Q

What is the treatment for nephrogenic DI?

A

Adequate fluid intake; hydrochlorothiazide, indomethacin, amiloride

51
Q

T/F: In SIADH, serum osmolarity > urine osmolarity

A

FALSE: Urine osmolarity > serum osmolarity

52
Q

What are some causes of SIADH?

A

Ectopic ADH (small cell lung cancer), CNS disorders/head trauma, pulmonary disease, drugs (eg. cyclophosphamide)

53
Q

How is SIADH treated?

A

Fluid restriction, IV saline, conivaptan, tolvaptan, demeclocycline

54
Q

Patient with significant postpartum bleeding presents with failure to lactate. What is the diagnosis?

A

Sheehan’s syndrome: Ischemic infarct of pituitary following postpartum bleeding

55
Q

What is empty sella syndrome?

A

Atrophy or compression of pituitary, often idiopathic, common in obese women

56
Q

Patient presents with polydipsia, polyuria, polyphagia, weight gain. What tests would you consider ordering to diagnose this patient?

A

Fasting serum glucose, oral glucose tolerance test, HbA1c

57
Q

What are some small vessel disease manifestations of DM?

A

Retinopathy, glaucoma, nephropathy

58
Q

What are some large vessel disease manifestations of DM?

A

Large vessel atherosclerosis, CAD, peripheral vascular occlusive disease, gangrene

59
Q

How does osmotic damage occur in diabetics? What are 2 clinical manifestations?

A

Sorbitol accumulation in organs with aldose reductase; neuropathy and cataracts

60
Q

State whether the following is more commonly associated with type 1 or type 2 DM: autoimmune destruction of beta cells; insulin treatment is always necessary; associated with obesity; low insulin sensitivity; low beta cell numbers in the islets; islet amyloid deposit.

A

Type 1; 1; 2; 2; 1; 2

61
Q

Patient with DM1 presents with deep, rapid breathing, nausea, vomiting, abdominal pain, fruity breath odor. How do you treat this patient?

A

IV fluids, IV insulin, K+ (to replete intracellular stores); glucose if necessary to prevent hypoglycemia

62
Q

What would you see on the labs for a patient in DKA?

A

Hyperglycemia, inc H+, dec HCO3- (anion gap metabolic acidosis), inc blood ketone levels, leukocytosis, hyperkalemia

63
Q

Explain how a patient in DKA would have hyperkalemia on labs but depleted intracellular K+.

A

This is due to transcellular shift from decreased insulin

64
Q

What are some complications of DKA?

A

Mucormycosis (life-threatening), Rhizopus infection, cerebral edema, cardiac arrhythmias, heart failure

65
Q

Patient presents with recurrent diarrhea, cutaneous flushing, asthmatic wheezing, and right-sided valvular disease. Increased 5-HIAA is seen in urine. How should you treat the patient?

A

Somatostatin analog (eg. octreotide) (patient has carcinoid syndrome)

66
Q

What is the Rule of 1/3’s associated with carcinoid syndrome?

A

1/3 metastasize, 1/3 present with 2nd malignancy, 1/3 multiple

67
Q

What is the most common tumor of the appendix?

A

Carcinoid syndrome

68
Q

Patient presents with recurrent ulcers. On upper endoscopy, stomach shows rugal thickening with acid hypersecretion. What is the most likely diagnosis?

A

Zollinger-Ellison syndrome

69
Q

Name the tumors associated with MEN1 (Wermer’s syndrome).

A

Pituitary, Parathyroid, Pancreas

70
Q

Name the tumors associated with MEN2A (Sipple’s syndrome).

A

Parathyroid, Pheochromocytoma, medullary thyroid carcinoma

71
Q

Name the tumors associated with MEN2B.

A

Pheochromocytoma, medullary thyroid carcinoma, oral/intestinal ganglioneuromatosis (associated with marfanoid habitus)

72
Q

What is the inheritance pattern of all MEN syndromes?

A

Autosomal dominant

73
Q

MEN2A and 2B are associated with what gene mutation?

A

Ret gene mutation

USMLE Step 1: Endocrine (5 decks)

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