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Endocrinology > H.P.A. Pharmacology > Flashcards

H.P.A. Pharmacology Flashcards

1
Q

Clinical presenation of acromegaly

A

excessive sweating, joint pain, headache, visual field loss, diplopia, carpel tunnel, sleep apnea, osteoarthropathy, menstrual irregularities or sexual dysfunction

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2
Q

What hormone will slow the production of GH from the anterior pituitary?

A

somatostatin

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3
Q

three etiologies of acromegaly

A

pituitary adenoma (>95%) hypothalamic tumor ectopic GH or GHRH secretion

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4
Q

Clinical diagnosis of acromegaly requires 2 or more of the following symptoms

A

new onset diabetes, arthralgia/fatigue, new onset HTN, biventricular myocardial hypertrophy, and systolic or diastolic dysfunction, headaches, carpal tunnel syndrome, sleep apnea, loss of vision, diaphoresis, colon polyps, progressive jaw malocclusion

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5
Q

Biochemical/Radiological diagnosis of acromegaly

A

elevated serum IGF-1 AND serum GH >1 two hours after OGTT

pituitary MRI → screen for adenoma

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6
Q

Primary treatment for acromegaly

A

surgical resection of tumor surgical RR > medical RR

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7
Q

Secondary treatment for acromegaly

A

GHR antagonist dopamine agonist somatostatin receptor ligand

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8
Q

Adjunctive therapy for acromegaly

A

radiation

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9
Q

GHR Antagonist for acromegaly

A

pegvisimant

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10
Q

Side effects of pegvisimant

A

hepatotoxicity, nausea, diarrhea

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11
Q

what needs to be monitored in a patient on pegvisimant?

A

IGF-1

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12
Q

Three somatostatin receptor ligands used in treating acromegaly

A

octreotide, ianoreotide, pasireotide

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13
Q

Side effects of somatostatin receptor ligands

A

GI upset, malabsorption, constipation, gallbladder disease, hair loss, bradycardia, glucose intolerance (mainly pasireotide)

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14
Q

Two dopamine agonists used in treating acromegaly

A

cabergoline and bromocriptine

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15
Q

Side effects of dopamine agonists

A

GI upset, orthostatic hypotension, headache, nasal congestions

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16
Q

Patient presents with severe short stature or less severe stature with growth failure, diagnosis?

A

GH Deficiency

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17
Q

Diagnosis of GH Deficiency

A

severe growth failure, delayed bone age, very low serum GH, and IGF ghrelin receptor agonist response

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18
Q

Treatment for GH deficiency

A

somatropin → genotropin omnitrope, humatrope, norditropin, saizen, zomacton

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19
Q

Side effects of somatotropins

A

edema, arthralgia, headache, paresthesia, dizziness, diaphoresis, GI upset

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20
Q

What do you monitor when treating a patient with somatropin?

A

growth curve, bone age, glucose levels, fundoscopic exam (retinopathy)

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21
Q

Three classes of hormones produced by the adrenal cortex

A

mineralocorticoids (aldosterone) glucocorticoids (cortisol) androgens (testosterone and estradiol)

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22
Q

What is produced by the adrenal medulla?

A

catecholamines → Epi and NE

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23
Q

When are cortisol levels the highest?

A

6 - 8 am

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24
Q

Excess cortisol causes the glucocorticoid disorder

A

Cushings Syndrome

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25
Q

Three etiologies of Cushings Syndrome

A

ACTH dependent ACTH independent iatrogenic

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26
Q

Excess aldosterone causes the mineralocorticoid disorder

A

primary or secondary aldosteronism

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27
Q

Inadequate cortisol causes the glucocorticoid disorders

A

Addisons Disease → primary HPA axis suppression → secondary

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28
Q

Inadequate aldosterone causes the mineralocorticoid disorder

A

hypoaldosteronism

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29
Q

clinical presentation of Cushings syndrome

A

central weight gain, facial rounding, hirsutism, hump on upper back, severe fatigue, muscle weakness, bone fractures, high BP, anxiety/irritable/depression, infections, diabetes, decreased concentration and memory

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30
Q

two etiologies of ACTH dependent Cushings syndrome

A

pituitary adenoma ectopic tumor outside of the pituitary secreting ACTH

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31
Q

where will you find the adenoma or carcinoma in ACTH independent Cushings Syndrome

A

adrenal cortex

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32
Q

What causes iatrogenic Cushings syndrome?

A

excessive pharmacologic glucocorticoid supplementations

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33
Q

what is the normal 24 hour secretion of cortisol?

A

~20 mg

34
Q

Which exogenous glucocorticoid is most equipotent to cortisol?

A

hydrocortisone

35
Q

Which drugs decrease glucocorticoid clearance and cause iatrogenic Cushings?

A

CYP 450 3A4 inhibitors

36
Q

Hepatic disease, renal disease, increased age, malnutrition, hypothyroidism, pregnancy are disease states that decrease what?

A

glucocorticoid clearance

37
Q

What pharmacologic agents can cause iatrogenic Cushings?

A

progestins

38
Q

Which tests are done to confirm elevated cortisol levels?

A

midnight plasma (cortisol)

24 hr urine free cortisol

late night salivary (cortisol)

dexamethasone suppression test

39
Q

Two ways to determine etiology of Cushings

A

plasma ACTH CT or MRI screen for tumors

40
Q

first line treatment for ACTH dependent Cushings

A

surgical resection of tumor

41
Q

Traditional approach to medical therapy in Cushings

A

ketoconazole + metyropone consider mitotane

42
Q

What pharmacologic agent is used to treat female with Cushings?

A

ketoconazole

43
Q

What pharmacologic agent is used to treat males with Cushings?

A

metyrapone

44
Q

Why is keotconazole not first line in men?

A

reduced testosterone → hypogonadism and impotence

45
Q

Why is metyrapone not first line in women?

A

increase production of androgens → hirsutism

46
Q

what needs to be monitored in a patient on ketoconazole?

A

LFTs

47
Q

What can decrease the bioavailability of ketoconazole?

A

PPI therapy → need acidic environment for absorption

48
Q

this drug affects mitochondria in adrenal cortex cells and causes adrenal cortical atrophy

A

mitotane

49
Q

this drug is a dopamine agonist that binds to D2 receptors on corticotroph tumor cells → reduces tumor cell secretion of ACTH → reduction in cortisol production

A

cabergoline

50
Q

somatostatin analog that binds somatostatin receptors on corticotroph tumor cells to reduce their secretion of ACTH → results in less cortisol production

A

pasireotide

51
Q

Biggest side effect of pasireotide

A

hyperglycemia

52
Q

durg that is approved for treating Cushings disease with acute complications who have failed or can’t have surgery

A

mifepristone

53
Q

who is mifepristone contraindicated in?

A

pregnancy

54
Q

side effects of mifepristone

A

hypokalemia, elevated BP, endometrial hyperplasia

55
Q

first line treatment in ACTH independent Cushings

A

surgical resection of adrenal or other tumor causing excessive cortisol production

56
Q

what is the goal of tapering glucocorticoid therapy?

A

prevent hypothalamic pituitary adrenal axis suppresion with glucocorticoid withdrawal

57
Q

signs of hyperaldosteronism

A

HTN, muscle tetany, excessive thirst, increased aldosterone to renin ratio, excessive urination, hypernatremia, glucose intolerance, hypomagnesemia, hypokalemia

58
Q

Treatment for bilateral adrenal hyperplasia

A

aldosterone receptor antagonist → spironolactone

potassium sparing diuretic → amiloride

59
Q

Treatment for aldosterone producing adenoma

A

surgical removal

60
Q

Term for decreased glucocorticoid (cortisol) production

A

adrenal insufficiency

61
Q

Hypotension and shock in a patient with adrenal insufficiency is called

A

acute adrenal crisis

62
Q

Most common etiology of acute adrenal crisis

A

abrupt glucocorticoid discontinuation with underlying HPA axis suppression

63
Q

clinical presentation of Addisons Disease

A

hypotension hyperpigmentation of skin exposed to friction fatigue and malaise N/V/D anorexia and weight loss dehydration hyponatremia hyperkalemia

64
Q

Clinical presentation of HPA axis suppression

A

normo or hypotensive no hyperpigmentation weight loss hypoglygemia hyponatremia eukalemia

65
Q

Test to diagnose adrenal hypofunction

A

corticotropin stimulation test → administer ACTH to assess adrenal cortisol production response

66
Q

two etiologies of Addisons Disease

A

autoimmune destruction of adrenal cortex

TB

67
Q

clinical signs of primary adrenal insufficiency

A

low cortisol, aldosterone, androgen levels

high levels of CRH and ACTH hypotension

68
Q

Treatment for Addisons Disease

A

glucocorticoid and mineralocorticoid supplementation

69
Q

Adverse effects of glucocorticoid therapy will mimic

A

symptoms of overproduction of cortisol

70
Q

What are some criteria that may make a patient more susceptible to glucocorticoid related osteoporosis?

A

low BMI hx of hip fracture smoker > drinks/day higher glucocorticoid dose

71
Q

How can you prevent glucocorticoid related osteoporosis?

A

supplement with calcium and vitamin D

72
Q

Which patient populations are at highest risk for opportunistic infections?

A

chemotherapy and organ transplant

73
Q

Steroids should be tapered if they have been taken ____

A

> 3 weeks

74
Q

Secondary adrenal insufficiency is caused my abrupt withdrawal of what two agents?

A

glucocorticoid supplementation

progestins

75
Q

elevated levels of circulating inflammatory cytokines leads to an increased in __ and ___ secretion → normal physiologic adrenal “stress response”

A

CRH

ACTH

76
Q

three ways the adrenal “stress response” can be imparied and lead to secondary insufficiency

A

50% decrease in corticosteroid bind globulin → tissue resistance to cortisol and higher serum free cortisol

decreased downregulation of cytokines in tissues (proinflammtory state)

excess serum free cortisol → decrease in CRH, ACTH, and cortisol production

77
Q

three instances that require “stress donse” glucocorticoid therapy

A

acute illness or minor outpatient procedure septic shock ARDS

78
Q

mirtazapine, ketoconazole, phenytoin, rifampin are pharmacologic agents that can cause

A

secondary adrenal insufficiency

79
Q

signs of hypoaldosteronism

A

severe postural hypotension, hyponatremia, hyperkalemia, hyperchloremic metabolic acidosis

80
Q

two possible etiologies of hypoaldosteronism

A

Addisons Disease adrenal tumor removal

81
Q

Treatment for hypoaldosteronism

A

mineralocorticoid supplementation → fludrocortisone

Endocrinology (7 decks)

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