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MOD 1 Quiz 1 > Physiology: Adrenal Glands > Flashcards

Physiology: Adrenal Glands Flashcards

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1
Q

Primarily steroids in circulation are bound to what protein?

A

Corticosteroid-binding protein (CBP)

And/or other plasma proteins (albumin)

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2
Q

3 cellular layers of the adrenal cortex?

A

glomerulosa
fasiculata
reticularis

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3
Q

glomerulosa creates what steroids? what do they do?

A

mineralcorticoids (aldosterone)

promotes salt and water retention by the kidney

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4
Q

fasiculata makes what steroids? what do they do?

A

glucocorticoids (cortisol)

increase plasma glucose levels

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5
Q

reticularis makes what steroids?

A

androgens/ sex steroids

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6
Q

The adrenal medulla makes what steroids?

A

catecholamines (Epinephrine, Norepinephrine)

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7
Q

chromaffin cells?

A

produce epinephrine or adrenaline (catecholamine)

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8
Q

Amino acid needed to synthesize epinephrine?

A

tyrosine

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9
Q

definiceny in cortisol can lead to?

A

hypoglycemia

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10
Q

3 major classes of steroid hormones?

A

glucocorticoids
mineralcorticoids
sex steroids

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11
Q

how does cortisol increase plasma glucose?

A

enhances mobilization of amino acids from proteins in many tissues and to enhance the ability of the liver to convert these amino acids into glucose and glycogen by activating gluconeogenesis

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12
Q

Other actions of glucocorticoids

A

potent immunosupressive and anti-inflammatory activity, effects on protein and fat metabolism, behavioral effects on the CNS, and important effects on calcium and bone metabolism

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13
Q

Excess glucocorticoid secretion

A

Cushing syndrome

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14
Q

glucocorticoid deficiency

A

Addison disease

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15
Q

glucocorticoid excess is commonly seen because of?

A

individuals receiving treatment for a chronic inflammatory or neoplastic disorder

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16
Q

less common glucocorticoid excess?

A

cortisol producing adrenal tumor, secondary to a pituitary tumor

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17
Q

Symptoms of overproduction of glucocorticoid? aka?

A

truncal adiposity, hypertenstion, loss of subcutaneous adipose and CT in the extremities associated easy brusing, loss of bone mineral, muscle weakness and wasting and hyperglycemia

Cushing Syndrome

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18
Q

If pituitary gland is responsible for cushing syndrome it’s called?

A

Cushing disease

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19
Q

Common cause of glucocorticoid deficiency?

A

autoimmune adrenal disease

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20
Q

Etiology of glucocorticoid deficiency?

A

increase ACTH and other products of POMC

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21
Q

Cause hyperpigmentation of skin?

A

alpha MSH and gama MSH

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22
Q

lack of glucocorticoid predisposes patient to?

A

hypoglycemia

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23
Q

combined glucocorticoid and mineralcorticoid leads to?

A

hypotension

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24
Q

Aldosterone deficiency leads to?

A

hyperkalemia

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25
2 sources of cholesterol for steroid hormone synthesis?
1. LDL receptor-mediated endocytosis | 2. synthesize cholesterol de novo from acetate
26
Which pathway for cholesterol to synthesize hormone is more important?
LDL cholesterol circulating
27
Except for 3B-HSD all enzymes are found where for steroid synthesis?
mitochondria or smooth endoplasmic reticulum
28
Adrenal adnrogens?
dehyroepiandrosterone and androstenedione
29
21alpha Hydroxylase deficiency?
inadequate production of glucocorticoid and mineralcorticoid hypotension, dehydration, hypoglycemia excess ACTH
30
Excess ACTH will cause? (21alpha Hydroxylase deficiency?)
enhanced growth of adrenal gland excessive production of androgens females- ambiguous genitalia at birth
31
effect of glucocorticoid use on the body?
Moon facies- increase in supraclvaicular and dorsal interscapular fat, rounding of the face wasting of fat in extremities produces thining of skin and fragility of cutaneous blood vessels osteopenia, osteoporosis glucose intolerant
32
CRH?
corticotropin-releasing hormone | travels via hypophyseal portal venous plexus to the anterior pituitary
33
CRH receptor
G protein coupled receprot on corticotroph cells | Galphas- adenylyl cyclase,cAMP, protein kinase A, increase Ca2+
34
arginine vasopressin
role in cortisol production under stress
35
ACTH
secreted by corticotroph cells of the anterior pituitary | melanocortin (as well as a, b, gamma MSH)
36
ACTH receptor
ACTH binds to MC2R in the fasculata cells of the adrenal cortex
37
Only source of CYP11b2
glomerulosa layer of cortex
38
Neg feedback for ACTH?
glucocorticoids neg regulate corticotrophs (release ACTH) and hypothalamus (release CRH)
39
stAR?
steroidogenic acute regulatory protein | mediates the transfer of cholesterol into the mitochondria for steroidogenesis
40
cortisol at the pituitary?
decrease synthesis of CRH receptor | decrease synthesis of ACTH
41
cortisol at the hypothalamus?
decrease synthesis and release of CRH
42
Glucorticoid receptors?
intracellular, nuclear receptors | heat shock proteins, influence gene transcription
43
Inhibited by ANP?
stAR | stop cholesterol from making steroids
44
Congential adrenal hyperplasia
hyposecretion of glucocorticoids defect/ deletion in genes encoding stAR or steroidogenic enzymes defects include CYP21A1, CYP11B1, CYP17, stAR
45
Overall effect of glucocorticoids?
``` increase appetite increase fetal maturation through synthesis of surfactant in the lung omental adipose exrpession of GR decrease osteoblast function increase renal Ca expression decrease intestinal Ca uptake decrease Ca absorption increase secretion into aqueous humor decrease GnRH release decrease TSH, deiodinase conversion of T4 to T3 ```
46
Most common defect with congenital adrenal hyperplasia?
CYP21A2
47
defect of CYP21A2 causes?
build up of precursors and a shunting to make androgens
48
Defect of CYP11B1?
not as common, reduce final conversions | again shunt to androgens
49
defect of CYP17?
very rare, no glucocorticoids and androgens | still make mineralcorticoids
50
defect of stAR?
no steroids made
51
Primary cause of hyposecretion of glucocorticoids?
adrenal disease, addison's disease
52
Addison's disease?
autoimmune infectious (TB) congenital adrenal hyperplasia
53
Can adrenal disease also affect mineralcorticoids and androgen production?
yes (congential adrenal hyperplasia for ex)
54
hirsuitism?
abnormal hair growth in women
55
Simulate mineralcorticoid release?
Angiotensin II extracellular K ACTH
56
angiotensin II?
AT1 receptor, Gq, activation of calmodulin kinases, increase of CYP11B2
57
extracellular k?
depolarize plasma membrane, open Ca channels, activate calmodulin kinases, increase CYP11B2
58
renin-angiotensin-aldosteone and potassium-aldosterone negative feedback loops?
Decreased Na activates the acis, angiotensin II promotes renal retention of Na decrease renal perfusion, aldosterone increases the expression of Na channel in apical membrane of cells in the the distal tubule of the kidneyand also a NA/K ATPase in the BM (promote Na reabsorption) Aldosterone increases membrane permeabilty to K in the kidney tubule, facilitating the secretion of K into the tubule lumen
59
Aldosterone elicits effects via
``` mineralcorticoid receptor (type 1 GR) conservation of sodium, secretion of potassium, increased water retention, and increased blood pressure. ```
60
11bHSD on mineralcorticoids?
limits cortisol in kidney thereby reserving activation of type 1 GR for mineralcorticoids aka aldosterone why aldosterone works in kidney vs cortisol
61
Role of mineralcorticoids?
``` salt and water retention maintain K blood pressure elicit effects via mineralcorticoids receptor (type 1 GR) excess aldosterone leads to hypertension ```
62
Adrenal Androgens?
stimulated by ACTH important contributor of circulating androgens in women, not in men (testes) reticularis layer
63
Catecholamines?
chromaffin cells in the adrenal medulla Epi primary product, NE secondary stored bound to granular proteins, chromogranins
64
rate limit step in catecholamine production?
tyrosine hydroxylase
65
catecholamines?
epi, ne, dopamine, L-DOPA
66
Stim release of Epi?
preganglionic sympathetic axons terminate on chromaffin cells
67
Catecholamine regulation: ACTH?
increase tyrosine hydroxylase, N-methyltransferase
68
Catecholamine regulation: Cortisol?
increase N-methyltransferase
69
Catecholamine regulation: Sympathetic stimulation?
increase tyrosine hydroxylase | chronic: increase N-methyltransferase
70
Catecholamine regulation: Chromogranins?
vasostatin- vasoinhibitory effects on bv catestatin- inhibit nicotinic actylcholine receptor, limit catecholamine secretion, suppressive on cardiomyocytes used to eval tumors, hypertension, organ failure
71
receptors for catecholamines: alpha 1?
Gq | vasconstriction, gluconeogenesis, glycogenolysis
72
receptors for catecholamines: alpha 2?
Gi | vasoconstriction, decrease sympathetic outflow, simulate vagal outflow, decrease insulin secreation
73
receptors for catecholamines: beta 1?
Gs | increase hear rate, myocardial contractilility, lipolysis, increase renin secretion
74
receptors for catecholamines: beta 2?
Gs | vasodilate, bronchial relax, GI relax, stim renin secretion, gluyconenolysis, gluconeogeneis
75
receptors for catecholamines: beta 3?
Gs | lipolysis

MOD 1 Quiz 1 (15 decks)

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