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Repro/Endo FInal > midterm physio deck 3 > Flashcards

midterm physio deck 3 Flashcards

1
Q

myxedema

A

severe hypothyroidism

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2
Q

signs of hypothyroidism

A

bradycardiacoarse hairdelayed relaxation of DTRsdry cool pale skingoiternon-pitting edema (myxedema)puffy eyes faceslow movement and speechthinning lateral third of eyebrows

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3
Q

endemic iodide goiter

A

seaweed ingestion “kombu” in japan –> massive iodide ingestion –> hyperplasia/overactive thyroid

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4
Q

graves disease classic triad

A

goiterthyrotoxicosisophthalmopathy

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5
Q

antithyroid drugs

A

tapazole, PYU, lithiumreduced t4 synthesisblock of t4 to t3 conversiondepletion of introthyroid iodine – less t4 synthesis

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6
Q

anti TPO antibodies

A

suggest hashimoto disease

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7
Q

adrenal glands: short term and long term function

A

in acute stress = catecholamines mobilize glucose and free FA for fight or flight reactionlong term = glucocorticoids stimulate gluconeogenesis to maintain glucose supply and protect against over-reactions of the body to stress

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8
Q

dual embryonic origins of the adrenal glands

A

cortex from mesenchyme of the urogenital ridge –> forms a thick inner fetal cortex and a thin outer layer which becomes permanentmedulla is from neural crest cells

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9
Q

cortex steroid hormones are not stored but _____ are

A

their precursors

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10
Q

zona glomerulosa

A

outermost cortex layer; secretes aldosterone (mineralcorticoid)

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11
Q

aldosterone function

A

increases renal sodium retention and potassium/H excretioncontrolled by renin-angiotensin system

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12
Q

zona fasciculata

A

second adrenal cortex layersecretes glucocorticoids (cortisol)controlled by ACTH

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13
Q

CRH and ACTH

A

CRH from hypothalamus allows pituitary to release ACTH which causes z. fasciculata to release cortisol

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14
Q

zona reticularis

A

innermost cortex layer; secretes glucocorticoids and DHEAS (weak androgen)regulated by ACTH

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15
Q

fetal cortex

A

between medulla and permanent cortexsecretes DHEAS - a major source of estrogen during gestationeventually degenerates

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16
Q

adrenal medulla

A

part of sympathetic nervous systemmade of postganglionic nerveschromaffin cells secrete catecholamines (epi and norepi)

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17
Q

cortisol

A

a glucocorticoidmobilizes glucose and free FA for use

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18
Q

how specifically does cortisol work on the z fasciculata

A

accelerates the activity of rate limiting step in cortisol biosynthesis = the 20,22 desmolase enzyme

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19
Q

ACTH mechanism

A

membrane receptoradenylate cyclasecAMPprotein kinasesenzymes

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20
Q

chronic ACTH stimulation

A

(cushings disease) cortex mass increases and secretions rise 20x –> hypercortisolemia and skin bronzing

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21
Q

CRH

A

corticotropin releasing hormonestimulates the corticotrophs in the anterior pituitary to release ACTH, B endorphin, and B lipotrophin

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22
Q

4 secretory control mechanisms for pituitary ACTH and cortisol

A

1 - negative feedback by cortisol at pituitary and hypothalamus2 - episodic release (7-15x per day) = pulsatile and variable; more responsive to bursts of stimulation—-in pathologic states: constant stimulation causes downregulation and decreased sensitivity to it3 - diurnal/24 hr rhythm w relation to sleep wake cycle for both cortisol and ACTH—levels highest early in morning, lowest at night4 - stress - fever/surgery/emotions, etc - can be independent of negative feedback in severe stress

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23
Q

how does cortisol travel in blood?

A

CBG (transcortin) - alpha 2 binding globulin = 80%15% bound to albuminonly 5% is free (active fraction)

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24
Q

cortisol functions

A

-increase blood glucose-maintain metabolism and circulation in stress-anabolic in liver (gluconeogenesis and ketogenesis); catabolic in other tissues (breakdown of protein and fat)-can induce insulin resistance to keep glucose available for the brain

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25
Q

cortisol and fat distribution

A

leads to thinning of extremities and truncal fatness

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26
Q

effect of cortisol on circulation

A

maintains integrity and responsivenessin absence of cortisol, vasodilation occurs and blood pressure falls; glomerular filtration falls and water cant be excreted as fast

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27
Q

effect of cortisol on immune system

A

blocks inflammatory and immune reactions-stabilizes lysosomal membranes, decrease capillary permeability, and depressed WBCs

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28
Q

the distinguishing feature in cushings disease is….

A

that set point regulation does occur but it is an abnormal higher level

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29
Q

cushings disease

A

abnormally high set point –> ACTH is hypersecreted and plasma cortisol increases until it reaches that new set pointadrenal glands hypertrophy due to excess ACTH stimulation**still under regulation though

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30
Q

primary hypercortisolism

A

cushings syndrome due to adrenal tumorunregulated production of cortisol –> hypothalamic CRH and ACTH are maximally suppressed

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31
Q

ectopic ACTH hypercortisolism

A

ACTH from ectopic site no tunder regulationdrives a large cortisol production that causes CRH and ACTH from pituitary to be suppressedadrenal cortex hypertrophies**not responsive to usual diagnostic tests since ectopic production is not under control

32
Q

psychiatric hypercortisolism can be due to

A

excessive CRH secretion from hypothalamus

33
Q

iatrogenic cushings syndrome

A

consumption of excess glucocorticoids –> suppresses entire hypothalamic-pituitary adrenal axis

34
Q

secondary vs tertiary hypocortisolism

A

2 - due to pituitary failure3- hypothalamic failure

35
Q

ACTH stimulates what enzyme?

A

20,22 desmolase (cyp450)this enzyme converts cholesterol to pregnenolone = the rate limiting step in testosterone, cortisol, and aldosterone production

36
Q

atrial natriuretic peptide

A

released by muscle cells in the upper chambers (atria) of the heart (atrial myocytes) in response to high blood volume. ANP acts to reduce the water, sodium and adipose loads on the circulatory system, thereby reducing blood pressurepeptide hormone

37
Q

what is secreted in response to 1) ACTH2) FSH3)LH

A

1) aldosterone in z glomerulosa, cortisol in z. fasciculata, and androgens in z. reticularis2) estradiol in ovary/testes3) testosterone in the ovary (converted to estrogen) and testes

38
Q

ACTH/LH/FSH work through what mechanism

A

G-protein coupled receptors and cAMPGPCR –> GTP –> adenylyl cyclase –> cAMP –> protein kinase –> steroid synthesis

39
Q

angiotensin 2 works through what mechanism

A

GPCR + phospholipase ckidney secretes reninrenin converts angiotensinogen to angiotensin 1angiotensin 2 stimulates production of aldosterone (vasoconstriction)GPCR –> GTP –> phospholipase c –> PIP2 converted to DAG and IP3DAG stimulates protein kinase c –> aldosterone productionIP3 opens ca channels on ER and ca increases

40
Q

glomerulosa –>fasciculata –>reticularis –> medulla –>

A

g - aldosteronef - cortisol r - androgensm - catecholamines

41
Q

cortisol effects on1 -muscle glucose uptake2 glucose use3 protein synthesis4 glucose output5 ketogenesis6 glycogenolysis

A

1 - decreased2 - decreased3 - decreased4 - increased5 - increased6 - increased

42
Q

without cortisol there will be

A

hypoglycemiaweaknes/fatigueinfections

43
Q

how does lack of cortisol cause hypoglycemia

A

cortisol inhibits the release of insulin and stimulates glucagon –> makes glucose availablewithout cortisol, more is stored

44
Q

aldosterone does what?

A

increasing Na and water reuptake and excretion of K –> increases Blood volume and cardiac output!

45
Q

aldosterone is secreted in response to

A

low Naincreased blood Kangiotensin ACTH

46
Q

which is less potent? T or DHT

A

testosterone is less potent

47
Q

progesterone is stimulated by what? does what?

A

stimulated by FSHprepares uteral lining during ovulation and maintains pregnancysecreted by the corpus luteum and placenta

48
Q

estrogensE1E2E3

A

E1 - estrone - source of estrogen in post-menopausal women; made in adipose and ovaryE2 - estradiol - predominant in ovariesE3 - estriol - made in placentapotency: E2 > E1 >E3

49
Q

precursor for MC and GC synthesis?

A

progesterone(cholesterol –> pregnenolone –> progesterone)

50
Q

precursor for sex hormone synthesis

A

androstenedione(cholesterol –> pregnenolone –> 17ahydroxypregnenolone –> DHEA –> androstenedione)

51
Q

MC and GC both have 21 C…how are they structurally different?

A

aldosterone has an aldehyde at c18cortisol has an ancohol at c17

52
Q

main type of enzyme used in steroid synthesis? main rxn type?

A

cytochrome p450smonooxygenase reactions = insert one oxygen while the other oxygen atom is reduced to water

53
Q

fatty deposts, moon facies, buffalo hump, muscle weakness, infectionswhat condition?

A

hypercortisolemia

54
Q

addisons disease

A

destruction of the adrenal cortexdue to autoimmune or adrenal tumor (less cortisol)hypoglycemia, dehydration, weightloss, bronzingADRENAL INSUFFICIENCY

55
Q

3 types of congenital adrenal hyperplasia

A

cyp21 deficiencycyp11b1 deficiencycyp17 deficiency

56
Q

cyp21 deficiency

A

conversion of progesterone to aldosterone and cortisol is blocked so precursors are funneled into sex steroid production–increased progesterone, androgens,and ACTH–> hyponatremia, hirsutism, menstual irregularity, enlarged adrenal glands due to excess ACTH; ambiguous genitalia in neonatesvirilization

57
Q

cyp 11b1 deficiency

A

increased DOC and 11deoxycortisol = hypertension due to activation of MC receptorupstream intermediates spill into androgensincreased ACTHvirilization

58
Q

cyp17 deficiency

A

hydroxylase and lyase activity inhibited –> those are needed for sex steroid productionincreased aldosterone, DOC, and ACTHdecreased cortisol and no sex steroidsNO virilization

59
Q

which CAH condition does NOT allow virilization

A

cyp17 deficiency –> no sex steroid production!

60
Q

how to treat CAH?

A

administer prednisone (glucocortiocids) to suppress the ACTH overproduction

61
Q

what steroid controls body fluid volume?

A

aldosterone - by increasing Na reabsorption and equal water reabsorption and increased K excretion

62
Q

where does aldosterone exert effects?

A

nephron distal tubules, as well as sweat glands, intestines, and salivary glands to decrease Na loss

63
Q

what treats aldosterone excess?

A

spironolactoneblocks aldosterone receptors

64
Q

mechanism of aldosterone

A

steroid hormone so it binds to intracellular receptorstranslocates to the nucleus –> induces formation of mRNA –> protein synthesis forms anzymes and sodium transporters

65
Q

is the excretion of K by aldosterone a direct Na/ K exchange?

A

NO

66
Q

juxtaglomerular apparatus

A

in the nephron = a chemo and baro receptor, and a neuroendocrine transducerif perfusion pressure or ion concentration is low, JGA secretes renin which cleaves angiotensinogen to angiotensin 1 (inactive) –> converted to angiotensin 2 by ACE –> angiotensin 2 works on the adrenal cortex and causes increased aldosterone

67
Q

ACE inhibitors

A

inhibit ACE from activating angiotensin 1 –>2Anti-HTN drugs

68
Q

potassium (K) ions act directly on the _________ to stimulate _____

A

z. glomerulosa; aldosterone

69
Q

aldosterone excess causes

A

hypokalemia and hypertensonhypokalemia results in polyuria and weakness/paralysis

70
Q

chronic edema leads to shrunken blood volumepersistent leak of effective blood volume into the abdomen results in…

A

increased levels of renin-angiotensin and increased aldosterone (excess) –> stimulus for aldosterone secretion never turns offdespite high aldosterone, fluid volume stays low and BP is low/normal due to continuous leak

71
Q

PNMT

A

phenyl M methyl transferasemade by chromaffin cells in the adrenal medullaconverts norepi to epinephrine

72
Q

blood supply of medulla

A

arterioles carry fresh blood to medulla, bypassing cortexmixes with blood from cortical sinuses

73
Q

circulating norepi reflects ____?circulating epi reflects ____?

A

vascular sympathetic toneadrenal meduallary secretion

74
Q

catecholamines on alpha receptor

A

norepi >epiincreased gluconeogenesisdecreased insulinincreased artery constriction in renal, genital and splanchnic circulationincreased sweating and pupil dilation

75
Q

catecholamines on B receptor

A

epi>norepiincreased glycogenolysis, lipolysis and ketosisincreased insulin and glucagon secretionincreased muscle K uptakearteriolar dilation in muscleincreased heart contractility and heart raterenin secretion Thyroid and parathyroid hormone secretion

76
Q

catecholamine biosynthesisrate limiting step?last step?

A

rls = tyrosine hydroxylase (1st step)last = PNMT (induced by cortisol) = why medulla needs to be within the cortex

77
Q

catecholamine excess

A

pheochromocytomacatechlamine secreting tumor of the adrenal medullaexcess epi and norepi signs: headache, sweating, forceful heartbeat, anxiety, tremor, fatigue, nausea, chest pain, visual disturbances

Repro/Endo FInal (23 decks)

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