Endocrine Brandon Flashcards

1
Q

How does somatropin compare to GH?

A

identical 191 amino acid sequence as GH

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2
Q

What hormone does somatropin resemble?

A

Prolactin

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3
Q

When does IGF-1 become dependent on GH?

A

during first year of life

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4
Q

When is IGF-1 essential?

A

prenatal and postnatal growth

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5
Q

adverse effects of mecasermin

A

hypoglycemia
intracranial HTN
adenotonsilar hypertrophy
elevated liver enzymes

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6
Q

What is rhIGFBP-3?

A

Mecasermin Rinfabate

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7
Q

GnRH Agonists?

A

Gonadorelin
Goserelin
Histrelin
Leuprolide
Nafareline
Triptorelin

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8
Q

hcG bind what receptors?

A

LH receptors

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9
Q

When to use GnRH antagonists?

A

endometriosis
prostate cancer
central precious puberty (early puberty)
breast & Ovarian Cancer

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10
Q

Which hormones act directly on target tissues?

A

POV
prolactin
oxytocin
vasopressin

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11
Q

S/S hyperprolactinemia in males?

A

loss of libido
infertility

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12
Q

s.s of hyperprolactinemia in females?

A

amenorrhea (no menstration)
galactorrhea (random nipple discharge)

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13
Q

how do antipsychotics affect prolactin levels?

A

they increase prolactin

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14
Q

What are the GnRH antagonists?

A

“relix”
Ganirelix
Cetrorelix
degarelix
Abarelix

cause dose dependent decrease of FSH/LH

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15
Q

What are ganirelix and cetrorelix used for?

A

ovarian hyperstimulation procedures

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16
Q

what are degarelix and abarelix used for?

A

advanced prostate cancer

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17
Q

extrarenal V2 receptors do what?

A

regulate factor VIII and von willebrand factor

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18
Q

Vasopression toxicity / CI

A

headache, NV, abd cramps, agitation (al masked by anesthesia)

overdose = hyponatremia > seizure

careful in pts with CAD

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19
Q

Vasopressin antagonists

A

Conivaptan
tolvaptan

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20
Q

conivaptan receptor affinity?

A

1:1 for V1:V2

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21
Q

Tolvaptan receptor affinity?

A

30:1 V2:V1

22
Q

role in dexamethasone in pediatric patients undergoing tonsillectomy/adenoidectomy?

A

prevents inflammation, decrase risk of PONV,

23
Q

Effects of Chronic corticosteroid treatment

A
  1. insomnia, euphoria, depression, ^ICP
  2. suppression of ACtH, GH, TSH, LH,
  3. PUD (can happen quickly)
  4. fat redistribution to viscera, face, nape of neck, supraclavicular
  5. antagonize the effects of Vit D on Ca reabsorption
  6. ^ RBCs and platelets
24
Q

another name for ACTH?

A

corticotropin

25
Q

What hormones use g-protein mediated signal transduction?

A

FSH, LH, hCG

26
Q

what is hMG and what class?

A

humana menopaousal gonadotropin
menotropins

27
Q

three types of FSH?

A

urofollitropin (uFSH) off market in 2015
Follitropin alpha (rFSH)
Follitropin beta (rFSH)

last two are synthetic and expensive

28
Q

What is leutropin alpha?

A

recombinant LH

29
Q

When / with what do you use leutropin alpha?

A

can use with follitropin alpha

used in women with profound LH deficiency

30
Q

what is choriogonadotropin alpha?

A

rhCG

31
Q

SE of somatropin?

A

edema
hyperglycemia
pancreatitis
gynecomastia
^ CYP450 ENZYMES

32
Q

when do you want to supress gonadotropins?

A

controlled ovarian hperstimulation

endomedtriousus/uterine fibrosis

prostate cancer (anti-androgen is primary though)

central precioucous puberty

33
Q

short to medium acting glucocorticoids

A

hydrocortisone
prednisone
methylprednisolone

34
Q

long acting glucocorticoids

A

betamethasone (25-40)
dexamethasone (30)

35
Q

what primarily controls mineral corticoids?

A

circulating angiotensin and K

36
Q

three things that increase cortisol?

A

stress
hypothyroidism
liver dz

37
Q

how is cortisol metabolized and excreted?

A

liver metabolism

urinary excretion but 1% unchanged, 20% cortisone, 30% dihydroxyl ketone metabolites

38
Q

describe glucocorticoids mech of action?

A

cortico binding globulin present steroid to cell

steroid enters by itself

binds heat shock protein and becomes unstable

heat shock protein leaves

steroid receptor complex forms dimer and enters cell nucleus

bind glucocorticoid response element (GRE)

regulates gene transcription that regulate growth factors

can also bind other transcription factors in nucleus

39
Q

how many genes are regulated by glucocorticoids?

A

10-20%

40
Q

Effects of cortisol?

A

metabolic
catabolic/anti-anabolic
anti inflammatory
immunosupressive

41
Q

metabolic effects of cortisol?

A

All to maintain glucose supply to the brain

muscle catabolism (inhibit muscle uptake of glucose)
gluconeogenesis
^ glucose > ^ insulin > ^lipogenesis
^ lipase

dose related effects of carbs, protein, fat metabolism

42
Q

where does cortisol have anti-anabolic effects?

A

bone

i.e osteoporosis from cushing syndrome

43
Q

antiinflammatory effects of cortisol?

A

decrease distribution, function, concentration of peripheral leukocytes

decrease inflammatory cytokines, chemokine and other inflammatory mediators

44
Q

general immunosupressive effects of cortisol

A

inhibit phospholipase A

decrease COX2 > decrease prostaglandins

vasoconstrction

45
Q

immunosupresive effects of single dose short acting glucocorticoid

A

^neutrophils
decrease lymphocytes

46
Q

immunosupressive effects of large dose glucocorticoids (20mg/day of prednisone)

A

decrease antibody production

decrease phagocytosis

decrease TNF alpha, interleukins, metalloproteins plasminogen factor

47
Q

effects of cortisol deficency?

A

impair renal function
increase vasopressin secretion
issues with fetal lung development

48
Q

three types of adrenocorticohyperfunction

A

cushing syndrome
chrousos syndrome
aldosteronism

49
Q

how are synthetic corticosteroids absorbed?

A

rapidly and completely

50
Q

steroid stress dose for minor stress

A

2x dose for 23-48 hr

51
Q

steroid dose for major stress

A

10x dose for 48-72 hours