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Physiology > Small Group > Flashcards

Small Group Flashcards

1
Q

what suppresses prolactin release in the anterior pituitary, and where does it come from?

A

dopamine produced in the arcuate nucleus of the hypothalamus

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2
Q

what does prolactin inhibit?

A

synthesis & release of GnRH

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3
Q

what key symptoms suggest excessive prolactin secretion?

A

amenorrhea & galactorrhea

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4
Q

If a patient had high prolactin levels and amenhorrhea, what would you expect to see if you gave them GnRH?

A

GnRH would increase the secretion of LH and FSH if the gonadotropes were unaffected by a tumor

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5
Q

What does Sudan III staining look for?

A

presence of fat in breast discharge

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6
Q

which is a common cause of hyperprolactinemia?

A

pituitary tumor

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7
Q

what is sheehan’s syndrome? what are the key symptoms?

A

postpartum hemorrhage results in ischemic pituitary

1) cannot lactate
2) amenorrhea (cycle doesn’t come back)

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8
Q

during sheehan’s syndrome, which hormone are compromised?

A

ACTH, TSH, LH, FSH, GH, prolactin

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9
Q

what are some hormone pairs that are affected by Sheehan’s?

A

ACTH- cortisol
GnRH- LH/FSH
TSH- T3/T4

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10
Q

what are the two categories of growth hormone excess?

A

acromegaly & gigantism

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11
Q

what are the tell-tale signs of acromegaly?

A
  • change in facial appearance (mandible)

- increased shoe size

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12
Q

If GH is elevated, what other peptide is likely elevated? where is it produced?

A

IGF-1; produced in liver

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13
Q

what are the effects of excess GH? excess IGF-1?

A

GH: muscle cell proliferation (large tongue)
IGF-1 : chondrocytes/osteocytes/connective tissue proliferation, widening of digits, thickening of skull bones/mandible/ribs

both: proliferation of cells in liver/kidney/organs

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14
Q

in acromegaly, which is the tingling and joint pain caused by?

A

compression of nerves against bones in joints; increased cartilage

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15
Q

what inhibits GH?

A

hyperglycemia; somatostatin

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16
Q

You’d expect fasting insulin to be high/low in a patient with acromegaly?

A

HIGH- GH inhibits insulin-stimulated glucose uptake, high circulating glucose, no negative feedback on insulin

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17
Q

what inhibits GH? under what conditions is GH not secreted?

A

somatostatin; hyperglycemia

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18
Q

what is the signature of Cushing’s syndrome? what are some symptoms?

A

excess cortisol

1) weakness- cort breaking down muscle
2) bruising- loss of subcu fat
3) purple striae - central obesity, fragile skin
4) increase in plasma glucose (role of glucocorticoids)

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19
Q

how could you tell if a tumor was a pituitary adenoma (2), adrenal adenoma (1), iatrogenic (exogenous) or ectopic?

A

1) adrenal- low ACTH, confirm with CT
2) pituitary- dexamethasone able to block high ACTH, use MRI
3) iatrogenic- ask about pharma, see atrophy of zona fasiculata
4) extopic- high ACTH, not responsive to dexamethasone

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20
Q

what is the signature of Addison’s? what are some symptoms?

A
  • no cortisol
    1) light headedness, low blood pressure- hypotension from lack of aldosterone
    2) high Ne/Epi ratio, high heart rate and low systolic pressure
    3) pigmentation
    4) electrolyte imbalance
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21
Q

what causes the skin pigmentation with Addisons?

A

ACTH transcribed with MSH (in POMC gene), high MSH results in hyperpigmentation

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22
Q

how can you tell the difference between primary and secondary/tertiary addisons?

A

primary- ACTH is high, cortisol doesn’t respond to exogenous ACTH

secondary/tertiary- ACTH is low, cortisol response to exogenous ACTH

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23
Q

what tests do you do for hypothyroidism? what would you expect to see?

A

measure TSH/free T4

- expect high TSH because T3 is probs low, lack negative feedback

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24
Q

how is T4 transported in blood?

A

75% bound to TBG
20% bound to TTR
5% bound to albumin

25
Q

what increases TBG?

A

estrogen during pregnancy

26
Q

what can cause hypothyroidism?

A

iodide deficiency, Hashimoto (autoimmune disorder)

27
Q

what causes the thick skin/deep voice/puffy face with hypothyroidism? yellow tint?

A
  • poor carb metabolism, excess polysaccharides accumulate and increase water retention
  • yellow tint caused by increased free lipids binding caratenoids
28
Q

what do you measure when considering hyperthyroidism?

A

TSH (expect to be low), T4/T3 (high)

29
Q

what are primary causes of hyperthyroidism?

A
  • Graves disease (autoimmune stimulation of TSH receptors)

- pituitary/thyroid tumor

30
Q

why does Graves cause an enlarged thyroid?

A

increased TSH receptor stimulation results in excess thyroid hormone/TG stored in colloid

31
Q

how would you inspect the thyroid?

A
  • RIU- pertechnetate, 131I, etc.

looking for equal, symmetrical uptake or hot/cold nodules

32
Q

what are some key symptoms of hyperthyroidism?

A

increased sweating- vasodilation b/c of increased BMR producing heat; weight loss; increased pulse pressure because of increased cardiac output/stroke volume

33
Q

what can cause hypercalcemia?

A
  • overactive parathyroid gland
  • tumors
  • too much thyroid hormone
  • excessive Ca2+, vitamin D and A supplementation
34
Q

treatment for hypercalcemia?

A
  • reduce calcium intake
  • surgery to remove tumor
  • calcitonin or bisphosphonate therapy
35
Q

symptoms of hypercalcemia

A 
stones (kidney)
bones (pain)
groans (upset stomach)
thrones (polyuria)
psychiatric overtones (confusion, depression)
36
Q

tests to confirm diagnosis of hyperparathyroidism

A
  • intact PTH
  • PTHrP (longer half-life)
  • ionized (free) Ca2+ (rule out albumin)
37
Q

diagnosis of hypocalcemia- what tests do you need?

A
  • albumin levels
  • intact PTH levels
  • ionized calcium
  • phosphate (should be high)
  • Mg2+ and K+ to evaluate kidney function
38
Q

what is the treatment for hypocalcemia?

A

oral calcium and calcitriol (vitamin D)

39
Q

what is psedohypoparathyroidism? what are 2 symptoms?

A

congenital defect in g-protein used for PTH signaling (short statute, short fingers)
- cataracts and hand spasms Chvostek sign

40
Q

what would you test to diagnose psedohypoparathyroidism?

A

intact PTH levels (expect to be high), Ca2+, phosphate, kidney function

41
Q

treatment for hypercalcemia

A
  • surgery to remove parathyroid adenoma

- calcitonin or bisphosphonate therapy

42
Q

what reproductive disorder has key symptoms of anosmia and cleft palate?

A

Kallmann’s Syndrome

43
Q

what abnormalities would you expect to see in Kallmann’s syndrome with hormones?

A
  • 0 GH
  • low FSH/LH
  • low testosterone
44
Q

what tests confirms the diagnosis of Kallmann’s?

A

GnRH stimulation test

45
Q

how is testosterone distributed in plasma?

A

2% free
45% ShBG
55% albumin

46
Q

what reproductive disorder has key symptoms small firm testes, gynecomastia (enlarged breasts), long legs?

A

Klinefelter’s syndrome (XXY karyotype)

47
Q

hormone levels in Klinefelters

A

high FSH/LH

low testosterone

48
Q

what causes gynecomastia?

A

elevated estradiol/testosterone ratio

49
Q

what causes the E2/T imbalance in Klinefelters patients?

A
  • increased conversion of peripheral T-E2
  • leydig cells overdriven by high LH, start to make E2
  • E2 stimulates more SHBG which binds up free T
50
Q

what reproductive disorder has a female patient presenting with amenorrhea, no pubic hair, shallow vagina?

A

androgen resistance (defective receptor)

51
Q

hormone levels in androgen resistance

A

high LH/FSH, high testosterone/estradiol

52
Q

where does the estradiol come from with androgen resistance

A

peripheral conversion of testosterone

direct secretion by testes

53
Q

most common form of premature ovarian failure & common symptoms & fundamental genetic defect

A

Turner’s Syndrome
short stature, web neck, shield chest
lack of X chromosome

54
Q

turner syndrome expected hormone levels

A

elevated GnRH and FSH/LH (no ovary feedback)

55
Q

internal reproductive structures of someone with Turner’s

A

complete development of the Mullerian structures, external genitalia are female

56
Q

effect of estrogen and/or progesterone therapy on skeletal growth

A

stimulate closure of the epipheseal plates and terminate long bone growth

57
Q

34 year old obese woman presents to the clinic with complaints of irregular periods and new hair growth- what does she have?

A

polycystic ovarian syndrome- follicles degenerate into cysts that produce androgens

58
Q

way of restoring fertility in PCOS?

A

metformin to treat insulin resistance

Physiology (22 decks)

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