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Step 1 > Endocrine Pathoma > Flashcards

Endocrine Pathoma Flashcards

1
Q

What is t he most comon typ eof pituitary adenoma?

A

prolactinoma

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2
Q

What are the sxs of prolactinoma in males?

A

Headache and decreased libido (dec GnRH and mass effect)

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3
Q

What are the sxs of prolactinoma in females?

A

amenorrhea and galactorrhea

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4
Q

How do you treat prolactinoma?

A

dopamine analog like bromocriptine -r cabergoline to suppress prolactin production

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5
Q

What mediates growth in people with GH adenoma?

A

GH triggers liver to release IGF-1 which mediates growth

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6
Q

What is GH excess in adults called and what are the sxs?

A

Acromegaly. will have enlarged bones of hands, feet, jaw, growth of bisceral organs leading to dysfunction like cardiac failure, enlarged tonue, secondary diabetes.

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7
Q

Why does GH excess lead to secondary diabetes?

A

GH decreases glucose uptake into cells and induces gluconeogenesis in the liver

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8
Q

What is the treatment for acromegaly?

A

Octreatide (somatostatin analog)

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9
Q
A
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10
Q

What is apoplexy?

A

bleeding into and adenoma, common cause of hypopituitarism

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11
Q

What is the common cause of hypopituitarism in children?

A

craniopharyngioma

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12
Q

What is Sheehan Syndrome?

A

During pregnancy, anterior pituitary doubles in size but the blood supply stays the same. If during delivery there is a lot of blood loss, then the pituitary will not revcieve enough blood and precipitates infarction

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13
Q

Sxs of Sheehan syndrome?

A

loss of pubic hair, poor lactation, and fatigue (loss of LH which stimulates androgens)

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14
Q

How do you treat central diabetes insipidus?

A

desmopressin (ADH analog)

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15
Q

What are common causes of nephrogenic diabetes insipidus?

A

lithium, demeclocycline (used for treated of SIADH, which can then lead to the opposite problem of nephrogenic DI)

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16
Q

Common causes of SIADH?

A

Small cell carinoma of the lung, paraneoplastic syndrome producing excess ADH. Also due to CNS trauma, pulmonary infection like COPD, and cyclophosphamide (alkylating agent used to treat cancer)

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17
Q

Treatment for SIADH?

A

demeclocycline (blocks the effects of ADH, can lead to Nephrogenic DI)

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18
Q

Why is there a mental status change and seizures associated with SIADH?

A

Hyponatremia leads to neuronal swelling and cerebral edema causeing mental status changes

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19
Q

What presents as an anterior neck mass?

A

thyroglossal duct cyst

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20
Q

What presents as a base of the tongue mass?

A

lingual thyroid

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21
Q

What is the case of increased basal metabolic rate in hyperthyroidism?

A

increased synthesis of Na+/K+ ATPase

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22
Q

What is the cause of increased sympathetic nerbous system activity in hyperthyroidism?

A

increased expression of B1-adrenergic receptors

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23
Q

What are two high yield clinical assocaitions to hyperthyroidism?

A
  1. Hypocholesterolemia (inc LDL receptor synthesis)
  2. Hyperglycemia (inc gluconeogenesis and glycogenolysis)
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24
Q

What type of hypersensitivity reaction is Graves’ disease?

A

type II hypersensitivity, autoantibvody IgG that stimulates TSH receptors leading to increased production and release of thyroid hormone

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25
Q

What causes the exophthalmos and pretibial myxedema in Graves’?

A

fibroblasts behind the orbit and overylying the shin express the TSH receptor, gets activated by autoantibody which leads to glycosaminoglycan (chonroitin sulfate and hyaluronic acid) buildup, inflammation, fibrosis and edema

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26
Q

How is myxedema commonly described?

A

doughy appearance due to glycosaminoglycans

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27
Q

What is the histological defining feature of Graves’?

A

scalloped colloid appearance, white stuff inbetween the coloid and the endothelial cells.

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28
Q

What is the rare complication of multinodular goiter?

A

Toxic goiter– TSH-independent regions leading to T4 release and hyperthyroidism

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29
Q

What is the most common defect associated with dyshormonogenetic goiter, a form of congenital hypothyroidism (cretinism)?

A

congenital defect in thyroid peroxidase (involved in organification, coupling and oxidation)

30
Q

What causes voice deepening in hypothyroidism?

A

accumulation of glycosaminoglycans in the skin and soft tisses, especially the larynx leading to deepening of the voice and a large tongue

31
Q

What lab values are typically affected by myxedema?

A

Hypercholesterolemia (downregulation of LDL receptors)

32
Q

What HLA class is associated with hashimoto thyroiditis?

A

HLA-DR5

33
Q

What is the histo appearance of hashimoto thyroiditis?

A

chronic inflammation with germinal centers and Hurthle cells (eosinophilic metaplasia of cells that line follicles)

34
Q

What cancer are people with hashimoto thyroiditis prone to?

A

marginal zone B-cell lymphoma (presents as an enlarging thyroid gland late in disease course)

35
Q

What type of thyroiditis presents with a tender thyroid usually after a viral illness?

A

Subacute granulomatous (De Quervain) Thyroiditis

36
Q

What is the disease course of Subacute granulomatous de quervain thyroiditis?

A

transient hyperthyroidism, usually self limited, rarely progresses to hypothyroidims.

37
Q

Buzzwords for Riedel Fibrosing Thyroiditis?

A

classically in a young female with hard as wood, non-tender thyroid gland that can invade local structures like the airway

38
Q

Differences between Riedel fibrosing thyroiditis and anaplastic carcinoma of the thyroid?

A

anaplastic presents in really old people, Riedels’ in young females

39
Q

Hot or cold nodule in a adenoma and carcinoma?

A

decreased uptake, cold nodule

40
Q

What are the defining features of follicular adenoma?

A

contained by a fibrous capsule

41
Q

Defining features of Papillary Carcinoma?

A

risk factors of ionizing radiation in childhood and psammoma bodies, orphan Annie eye nuclei and nuclear groves

42
Q

Defining features of follicular carcinoma?

A

invasion through the capsule, otherwise just like adenoma

43
Q

Defining features of medullary carcinoma of the thyroid?

A

malignant cells in an amyloid stroma, MEN 2 A/B

44
Q

What is the next step if diagnosed with RET mutation?

A

prophylactic thyroidectomy

45
Q

Common complication of primary hyperparathyroidism?

A

acute pancreatitis (Ca2+ activates pancreatic enzymes, and in this situation there is increased Ca)

46
Q

What are key laboratory findings in primary hyperparathyroidism?

A

Inc urinary cAMP and inc serum alkaline phsophatase. PTH binds to Gs and increases cAMP. PTH activated osteoblasts= inc ALP

47
Q

What is the most common cause of secondary hyperparathyroidism?

A

Chronic Renal Failure (dec phosphate secretion, phosphate binds free Ca, low free Ca, inc PTH)

48
Q

What is a common complication of secondary hyperparathyroidism?

A

renal osteodystrophy due to inc PTH activating the osteoblasts and then clasts.

49
Q

What are common causes of primary hyperparathyroidism?

A

parathyroid adenoma, sporadic parathyroid hyperplasia, and parathyroid carcinoma.

50
Q

What causes pseudohyperparathyroidism?

A

end-organ resistance to PTH due to Gs mutation

51
Q

What is the inheritance and sxs of pseudohyperparathyroidism?

A

AD, short stature and short 4th and 5th digits

52
Q

What is the characteristic histology of type I diabetes?

A

inflammation of the iselts

53
Q

How does obesity lead to Type 2 Diabetes?

A

decreased numvers of insulin receptors on skeletal and adipose tissues

54
Q

Characteristic histology of type 2 DM?

A

amyloid deposition in the islets

55
Q

What is hyperosmolar non-ketotic coma?

A

GLucose gets so high and leads to life-threatening diuresis with hypotension and coma, no ketones

56
Q

What are the major long-term consequences of diabetes?

A

Non-enzymatic glycosylation of vascular basement membranes

57
Q

What is a result of NEG of medium-large sized vessels?

A

atherosclerosis – CVD and peripheral vascular disease.

58
Q

What is the result of NEG of small vessels?

A

hyaline arteriolosclerosis involving renal arterioles, commonly affects the efferent arteriole

59
Q

Sxs of VIPoma?

A

increased BIP leading to watery diarrhea, hypokalemia and achlorhydria (inhibits gastrin secretion)

60
Q

sxs of somatostatinoma?

A

achlorhydria (inhibits gastrin) and cholelithiasis with steatorrhea (CCK inhibition)

61
Q

Gastrinoma sxs?

A

treatment-resistant peptic ulcers (Zollinger-Ellison syndrome)

62
Q

Is there edema in hyperaldosteronism?

A

no, due to aldosterone escape

63
Q

Aldosterone and renin values in primary hyperadlosteronism?

A

inc aldosterone, low renin due to increased renal perfusion pressure which downregulates renin

64
Q

What are the common casues of secondary hyepradlosteronism?

A

fibromuscular dysplasia in young women and atherosclerosis in old men. Dec blood flow to the kindey activates RAS leading to inc aldosterone

65
Q

What is the treatment for primary hyperaldosteronism?

A

spironolactone or eplereonone (aldosterone receptor antagonists)

66
Q

Why does cortisol increase BP?

A

cortisol upregulates alpha-1 receptors on arterioles, increasing the effect of NE and helps maintain vascular tone

67
Q

What are the 3 ways that cortisol inhibits the immune response?

A
  1. inhibits phospholipase A2
  2. inhibits IL-2
  3. inhibits histamine release from mast cells
68
Q

Where does lung cancer love to metastasize to?

A

the adrenal glands

69
Q

What do you treat a patient with before removing a pheochromocytoma?

A

phenozybenzamine (irreversible non-selective alpha blockers)

70
Q

What are the sxs if someone has a pheo in the bladder wall?

A

HTN after peeing

71
Q

What syndromes are pheos associated with?

A

MEN 2A/B, von Hippel-Lindau disease, and neurofibromatosis type 1.

72
Q

Is Hashimoto’s painful or painless?

A

Painless- nontender

Step 1 (17 decks)

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