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EndoRepro > Endocrine Week 2 > Flashcards

Endocrine Week 2 Flashcards

0
Q

Aldosterone actions

A

increased reabsorption of Na (and water), hypokalemia

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1
Q

Substances that promote aldosterone excretion

A

potassium/hyperkalemia, ACTH

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2
Q 
What happens to renin concentration and activity in these drugs:
A) Aliskiren
B) ACE inhibitors
C) ARBS
D) Mineralcorticoid receptor antagonists
A

A) renin concentration increased, activity decreased
B) renin concentration and activity increased (+ hyperkalemia)
C) renin activity increase (+hyperkalemia)
D) renin levels increase (+hyperkalemia)

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3
Q

Clinical presentation of primary hyperaldosteronism

A

hypertension and hypokalemia, age of onset <30 years

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4
Q

What is the plasma aldosterone:renin ratio in patients with primary hyperaldosteronism?

A

Aldosterone level is increase (>12) and renin activity is suppressed (<1) and so the ratio is elevated

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5
Q

In unilateral aldosterone secretion, what are the levels of the contralateral adrenal venous blood like?

A

very low

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6
Q

What is the difference between primary and secondary hyperaldosteronism?

A

Renin levels are increased in secondary while the levels are decreased in primary

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7
Q

Patient presents with hypertension, hypokalemia, metabolic alkalosis, low renin activity, low aldosterone, normal plasma cortisol levels. What condition?

A

Apparent mineralocorticoid excess

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8
Q

Deficiency in AME?

A

11-B HSD2 enzyme, converts cortisol to cortisone in kidney

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9
Q

AME causes

A

hereditary, glycyrrhizic acid (licorice)

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10
Q

Patient appears with hypertension, hypokalemia, low renin and aldosteronism. Appears like primary hyperaldosteronism.

A

Liddle Syndrome (treat with triamterene and amiloride)

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11
Q

Common alpha agonist used in ICE, vasoconstriction and raises BP

A

phenylephrine

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12
Q

What physiological response should you be wary of when combining alpha and beta blockers?

A

Alpha blockers cause reflex tachycardia–use together leads to large BP lowering

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13
Q

What neurotransmitter do adrenal medullary (chromaffin) cells mainly secrete?

A

epinephrine

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14
Q

Pheochromocytomas (tumors of chromaffin cells) mainly secrete what? Paragangliomas (extra adrenal SNS ganglia) & metastases of pheos mainly secrete what?

A

epinephrine and norepinephrine

norepinephrine

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15
Q

Classic symptoms of pheochromocytomas

A

hypertension, headaches, diaphoresis, palpitation, orthostatic BP changes

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16
Q

What to test for to diagnose pheochromocytoma?

A

urinary catecholamines, plasma free metanephrines

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17
Q

What can the secretion of large amounts of catecholamines from vesicles cause?

A

hypertensive crisis

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18
Q

Best imaging test for pheochromocytomas?

A

CT scan of abdomen/adrenal glands

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19
Q

Treatment for pheochromo?

A

A) alpha blocker (phenoxybenzamine)
B) then a beta blocker
C) hydration
D) adrenalectomy

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20
Q

What mediates energy-dependent calcium absorption?

A

1,25(OH)2D

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21
Q

Used to treat severe hyperparathyroidism

A

calcimimetic (cinacalcet)

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22
Q

How are PTH and hypercalcemia related?

A

hypercalcemia is caused by increased PTH secretion and in turn suppresses PTH secretion

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23
Q

PTH dependent hypercalcemia cause

A

primary hyperparathyroidism, familial hypocalciuric hypercalcemia

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24
Q

Primary hyperparathyroidism findings

A

increased/normal PTH, hypercalcemia, hypophosphatemia

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25
Q

FHH symptoms

A

most asymptomatic, PTH not suppressed, CaSR mutation

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26
Q

Causes for PTH-independent hypercalcemia

A

malignancy, calcitriol-mediated, hyperthyroidism

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27
Q

First measure what in hypercalcemia?

A

PTH, if elevated, most likely primary hyperparathyroidism

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28
Q

treatment of hypercalcemia

A

saline, furosemide, calcitonin, bisphosphonates

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29
Q

Clinical exams for hypocalcemia

A

Chvostek’s, Trousseau’s

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30
Q

Treatment hypocalcemia

A

calcium supplements, vitamin D2/D3/calcitriol

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31
Q

FGF23 and phosphate in the body

A

excess cause hypophosphatemia, decrease causes hyperphosphatemia

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32
Q

What is the primary function of cortical bone? trabecular?

A

cortical: structural function
trabecular: metabolic

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33
Q

Activators of osteoclast activity

A

PTH

1, 25 di-OH vitamin D

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34
Q

What part of the bone is good for resisting compressive loads? Tensile?

A

Compressive: mineral
Tensile: protein

35
Q

Primary protein component of bone

A

type 1 collagen

36
Q

Most common sites of low trauma fractures

A

spine, distal radius (Colles’ or wrist fractures), and hip

pelvis, proximal humerus

37
Q

What DXA T-score suggest that a patient might have osteoporosis?

A

T<-2.5

38
Q

What is the single most powerful predictor of future fracture?

A

past fracture

39
Q

Fracture risk factors

A

age, sex, glucocorticoid use

40
Q

Differentiate between osteomalacia and osteoporosis

A

in the latter, quantity of bone matrix insufficient, architecture impaired

41
Q

What is elevated in serum in osteomalacia?

A

PTH, TNSALP, P1NP

42
Q

Drugs to treat osteoporosis

A

Estrogen/receptor: tomxifen, raloxifene
Bisphosphonates: -dronate
RANKL decoy receptor: Denosumab
Anabolic: Teriparatide (PTH fragment)

43
Q

What substrate in phostphate metabolism is associated with osteomalacia?

A

FGF23

44
Q

Most common pituitary tumor

A

prolactin

45
Q

postpartum pituitary necrosis cause by ischemia of pituitary gland

A

Sheehan syndrome

46
Q

Cells in the adrenal medulla? What is secreted there?

A

chromaffin cells

secrete cathecholamines

47
Q

Inherited causes of adrenocortical carcinoma

A

Li-Fraumeni syndrome (p53), Beckwith-Wiedmann syndrome (ch11 at WT2 locus)

48
Q

Pheochromocytoma rule of 10s

A

10% associated with familial syndromes, 10% extraadrenal, 10% bilateral, 10% malignant

49
Q

Adrenal cortical atrophy is most likely caused by ___(A)____? Bilateral hyperplasia is most commonly associated with ____(B)___?

A

A) exogenous steroids

B) endogenous Cushings’

50
Q

Most common cause of primary hyperparathyroidism

A

parathyroid adenoma

51
Q

Name the organ that is experiencing dysfunction:
(A) Primary hypothyroidism
(B) Secondary hypothyroidism
(C) Tertiary hypothyroidism

A

(A) thyroid gland (T4/T3)
(B) pituitary gland (TSH)
(c) hypothalamus (TRH)

52
Q

Most common cause of primary hypothyroidism

A

Hashimoto’s thyroiditis (chronic lymphocytic thyroiditis)

53
Q

Drugs that cause secondary hypothyroidism

A

dopamine, glucorticoids

54
Q

Drugs that cause primary hypothryoidism

A

antithyroid agents, lithium

55
Q

Most common thyroid hormone supplement provided?

A

Levothyroxine (T4)

Liothyronine (T3) available but not widely given

56
Q

How long to wait before adjusting thyroid hormone dose?

A

5-6 half lives

1 half life is 7 days

57
Q

Most common cause of primary hyperthyroidism?

A

Graves’ disease

Secondary is very rare–TSH secreting pituitary adenoma

58
Q

Driving force for thyrotoxicosis in primary hyperthyroidism?

A

thyroid stimulating immunoglobin

59
Q

What step should be taken after a TSH in order to diagnose betweeb different causes of hyperthyroidism?

A

radioactive iodine

60
Q

Main treatments of Graves’ disease

A

methimazole and propylthiouracil (inhibitors of thyroidal organification)
radioactive iodine
surgery

61
Q

Other meds to treat hyperthyroidism

A

Logul’s solution (oral iodine)
propanolol
cholestyramine

62
Q

Most common reason for congenital hypothyroidism in the world?

A

iodine deficiency

63
Q

Most common reason for congenital hypothyroidism

A

dysgenesis

64
Q

Most states test what in order to screen for congenital hypothyroidism?

A

high values TSH

65
Q

By what age does having hypothyroidism not affect mental function?

A

3 years

66
Q

Most common thyroid lesion-variable sized nodules with increased colloid, unencapsulated

A

nodular goiter

67
Q

Massive infiltration of lymphocytes with germinal center formation, Hurthle cell change (abundant cytoplasm)

A

Hashimoto’s Thyroiditis

68
Q

Granulomatous (giant cell) inflammation

A

Subeacutethyroiditis

69
Q

Follicular cells with scalloped colloid

A

Graves’ disease

70
Q

Uniform follicle pattern, capsule present

A

follicular adenoma

71
Q

Follicles but with capsular invasion

A

follicular carcinoma

72
Q

Orphan Annie clearing, psuedoinclusion

A

papillary carcinoma

73
Q

Nests and cords of cell in amorphous pink amyloid stroma

A

medullary carcinoma

74
Q

Pleiomorphic giant tumor cells, spindle cells

A

anaplastic carcinoma

75
Q

Fine needle aspirates are diagnostic for which diseases?

A

papillary carcinoma, medullary carcinoma

76
Q

Which transporter is the major insulin responsive glucose transporter found mostly in skeletal/cardiac muscle and fat?

A

GLUT4

77
Q

What substances stimulate glucose secretion?

A

glucose, amino acids, fatty acids, indirectly GH/cortisol

78
Q

What substance amplifies insulin?

A

GI hormones

79
Q

What inhibits insulin secretion?

A

somatostatin (paracrine)

80
Q

Which has a longer time course-regular or NPH insulin?

A

NPH (cloudy suspension)

81
Q

What is the longest acting insulin analog?

A

insulin glargine

82
Q

Why should metformin not be prescribed to patients with renal insufficiency?

A

side effect of lactic acidosis

83
Q

What target does metformin make more sensitive to insulin? Thiazolidinediones (-glitazone)?

A

Liver

Fat and Muscle (PPAR)

84
Q

What transporter leads glucose to enter the pancreatic beta cell?

A

GLUT2

85
Q

What are the microvascular long term complications of diabetes mellitus?

A

retinopathy, nephropathy, neuropathy

86
Q

What are the macrovascular complications of diabetes mellitus?

A

coronary artery disease, peripheral vascular disease

EndoRepro (4 decks)

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