Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Bloc E - GI & Metabolism > Feb1 M1,2-Adrenal Gland > Flashcards

Feb1 M1,2-Adrenal Gland Flashcards

1
Q

adrenals crucial fct

A

response to stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

adrenals embryo origin, parts and relative volume

A

cortex 10%

medulla 90%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

medulla vs cortex (adrenals) molecules made

A

cortex: steroids
medulla: catecholamines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

circulation to adrenals and word describing it

A

suprarenal arteries coming along cortex and then dive 90 degrees inside cortex to medulla. called centripetal circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

importance of centripetal circulation on adrenal fct

A

some steroid hormones produced in cortex released there and have enzymatic influence in adrenal medulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

part of adrenals that is in ANS and why

A

medulla. preganglionic synapse on it with Ach (medulla acts on ganglion). medulla releases NE and E directly in circulation rather than blood stream

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

name of nerves from which the medulla is derived and spinal origin

A

splanchnic nerves, coming from T8 to T11 form the medulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

precursor molecule to making NE and E and diff intermediate molecules

A

tyrosine. L-DOPA. dopamine. NE. E.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

2 important enzymes (rate limiting) in adrenaline biosynthesis and which rx they control

A
  • tyrosine hydroxylase (tyrosine to L-DOPA)

- PNMT (NE to E)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

example of steroid influence from cortex on medulla

A

in response to stress, cortisol from cortex goes to medulla and increases PNMT activity (more adrenaline made)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

4 NE and E receptorss

A

alpha 1, alpha 2, beta 1 and beta 2 adrenergic receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

beta 1 R location and effect and pharmaco principle

A

heart. chronotrope and inotrope effect.

for BP and angina, give beta 1 specific antagonist. otherwise get bronchoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

beta 2 R location and effect and pharmaco principle

A

SM dilation. in lungs, must give beta 2 specific agonists for asthma otherwise, tachycardia as side effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

rule of thumb on effect of alpha activation

A

vasconstriction and SM constriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

rule of thumb on effect of beta adrenergic activation

A

SM relaxation and vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

pheochromocytoma symptoms

A

pheochromocytoma spells: very high BP, lapitations, anxiety, headache, pallor and sweating

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

only adrenal medulla pathology that exists and specific definition

A

pheochromocytoma: tumor (growth) of chromafin cells in adrenal medulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

2 types of pheochromocytoma, % and definition

A

90% are in adrenal medulla

10% can happen in any SS ganglia along the aorta (called paraganglioma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

lab to dx pheochromocytoma

A

can measure metabolites of NE and E (metanephrines and vanilmandelic acid (VMA)) in 24h urine excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

steps in pheochromocytoma investigation

A
  • 24h urine collection: catecholamines and metanephrines

- MRI scan if elevated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

danger of pheochromocytoma in surgery

A

can release NE and E a lot and have hypertensive crisis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

special test used in paraganglioma (to scan it)

A

MIBG scan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

is pheochromocytoma indiv in vasodilation or vasoconstriction and why

A

vasoconstriction bc high NE and E causes a predominant alpha effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

in PCC surgery prep, 2 steps and why

A
  1. alpha blocker to vasodilate
  2. replenish plasma volume (high salt diet)
    Because otherwise, removing PCC will just vasodilate and will put in low volume state
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

mistake in PCC surgery prep and why + why would this happen

A

beta blocker. (beta adrenergic R have vasodilative effect so blocking them will cause constriction and oppose alpha-blocker effect.
could happen if had beta blocker for BP or wtv

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

when would give beta blocker in PCC surgery prep

A

might give it, after alpha blocker and fluid, for the tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

diseases of adrenal insufficiency

A

none. don’t exist bc SS system can do its work

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

3 layers of adrenal cortex

A

zona glomerulosa
zona fasciculata
zona reticularis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

zona glomerulosa fct and influences

A

make aldo (mineralocorticoids) in response to AT2 and K+ (and ACTH to a lesser extent)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

zona fasciculata fct

A

make cortisol (glucocorticoids) in response to ACTH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

zona reticularis fct

A

androgen pathway. make DHIAS (dehydroepoiandrosterone), a sex hormone precursor in males

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

common precursor to all cortex steroid hormones and why

A

cholesterol. from it, can produce any of 3 hormone types in adrenal cortex via enzyme pathways

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

clinically relevant enzyme in cortex and what pathway

A

21-OH (21-hydroxylase)

In cortisol pathway AND aldosterone pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

mechanism of action of steroid hormones

A

bind receptor in cytoplasm or nucleus and this R acts as TF, affecting gene transcription
(no membrane R)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

feedback effect of cortisol

A
  • inhibits anterior pituitary (less ACTH)

- (to lesser extent), inhibits hypothalamus (less CRF)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

precursor molecule of ACTH and how it is processed in pituitary gland vs in neurons

A

POMC (pro-opio-melanocortin)

pit: broken in many parts, one of which is ACTH
neurons: broken in many parts, one of which is MSH (melanocyte stimulating hormone)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

symptom visible in any condition where ACTH is elevated and why

A

skin pigmentation. bc POMC needed to make the high ACTH also made MSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

3 functions of ACTH on adrenal gland

A
  • more steroid secretion
  • increased blood flow through adrenal
  • trophic effect (increase size of adrenal)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

consequence of low ACTH for weeks

A

adrenals are deprived of ACTH = become atrophic and no longer make cortisol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

can you reverse adrenal atrophy due to ACTH deprivation

A

reversible but no ACTH for weeks so will have cortisol prod defect for a moment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

pattern of cortisol secretion during the day + importance

A

low at night, rises a lot at 8 am. peak at 9 am. low in the afternoon.
Important clinically for how blood test done

42
Q

cortisol in the blood + importance

A

95% bound to transcortin (glucocorticoid-binding protein) inactive
5% unbound (free) = active

43
Q

2 main effects of cortisol (of glucocorticoids)

A
  • catabolic effect

- anti-inflammatory

44
Q

effect of cortisol on catabolism (think macromolecules categories)

A
  • higher gluconeogenesis in the liver (glucose creation from other nutrients)
  • fat redistribution
  • prot breakdown in muscle
  • increased gastric acid and pepsin (gastric ulcers)
45
Q

cortisol effect on gonads

A

amenorrhea (absence of menstrual period)

46
Q

cortisol effect on CNS

A

many effects
too much = euphoria
lacking = depression and fatigue

47
Q

pathologies of cortisol secretion

A

Cushing’s syndrome: hypersecretion

Addison’s disease: lack of cortisol

48
Q

Cushing’s syndrome on physical

A

think skin, thin arms, cushinoid fat distribution (abdomen and central), bruising in arm, muscle weakness, fleshoplethora (redness on cheeks), obesity, immunosuppresion

49
Q

Cushing’s physical in children main feature

A

growth stops

50
Q

abdominal features on Cushing’s physical and reason

A

violacious stretch marks because of rapid weight gain + protein catabolism so skin near viscera

51
Q

very important category of symptoms of Cushing’s syndrome

A

neuropsychiatric manifestations (insomnia, depression, psychosis, impaired cognition and memory)

52
Q

Cushing’s dx and management approach (3 steps)

A
  • dx CS
  • find cause (ACTH dependent vs independent + find source of ACTH dependent)
  • imaging of adrenal or pituitary (after source is known)
53
Q

cortisol rhythm in the day in CS patients

A

constantly elevated cortisol levels (loss of diurnal rhythm)

54
Q

pituitary tumor vs adrenal and ectopic tumor in CS

A

pituitary tumors are partially autonomous bc can still have feedback inhibition at higher than normal cortisol level
adrenal and ectopic = no feedback

55
Q

4 investigations (screening tests) (where any 1 positive of the 4 = CS)

A
  • elevated 24h cortisol
  • non suppressed morning cortisol after night low dose dexamethasone
  • plasma cortisol in morning and evening (loss of circadian rhythm)
  • late-night salivary cortisol evelated
56
Q

principle of dexamethasone test for CS screening

A

it inhibits cortisol in the morning (puts it to less 50 normally), given at night and cortisol low in the morning

57
Q

3 etiologies (categories) of CS

A

pituitary ACTH, ectopic ACTH or ACTH independent

58
Q

most common cause of CS and % + distribution of pathologies

A

70% are pituitary ACTH dep
microadenomas 95%
macroadenomas 5%

59
Q

other cause of ACTH dependent CS + pathologies

A

ectopic ACTH or CRH

  • small cell lung CA
  • carcinoids (neuroendocrine tumors): lungs, pancreas, thymus
60
Q

ACTH independent CS: pathologies

A
  • exogenous (taking cortisol)
  • bilateral hyperplasia
  • unilateral (adrenal adenoma. adrenal CA is very rare)
61
Q

how to check if CS is ACTH dependent or independent and interpretation (2)

A

-ACTH assay
low ACTH = ACTH indep (tumor or exogenous)
-high dose dexamethasone suppression. if cortisol suppressed = pituitary tumor

62
Q

when to use high dose dexamethasone suppression test and interpretation

A
  1. dx CS bc pit not suppressed by low dose dex
  2. assay gave high ACTH
  3. high dose dex to check if pituitary or ectopic. ACTH suppressed by high dose dex = pituitary
63
Q

assay giving low ACTH (suppressed ACTH) points to what generally

A

to adrenal prob (adenoma or CA)

NO NEED to do high dose dex. we know it’s not ACTH dependent

64
Q

imaging to do it find out ACTH is suppressed for ex (low plasma ACTH)

A

CT of the abdomen

65
Q

dexamethasone and prednisone: type of molecule and why high dose dexamethasone test when high ACTH

A

glucocorticoids. high dose dex test checks if this glucocort. can suppress prof of ACTH (it can if ACTH comes from pit)

66
Q

pharmaco use of glucocorticoids

A
  • inflam and autoimmune conditions
  • rheumatoid arthritis
  • severe asthma
  • certain lymphatic system cancers
67
Q

how to stop a high dose long course of glucocorticoids (ex 15 mg prednisone daily)

A

lower dose over 9 months. bc adrenals atrophied due to no ACTH all the time. (exogenous glucocort suppresses pituitary) so have to avoid adrenal crisis

68
Q

adrenal crisis def and when it can happen

A

lack of endogenous cortisol. if stop and exogenous glucocorticoid immediately

69
Q

Addison’s disease main symptoms

A
  • fatigue
  • nausea
  • anorexia
  • low BP
  • hyperpigmentation
70
Q

Addison’s main cause

A

autoimmune destruction of the adrenal cortex: adrenal insufficiency, lack of adrenal steroids

71
Q

Addison’s pts risk in surgery

A

can get severe hypotension (hypotn crisis) bc can’t mount stress response needed in surgery

72
Q

ACTH level in Addison’s and why

A

high bc no cortisol and glucocorticoids to suppress it

73
Q

why hyperpigmentation scars in Addison’s

A

high ACTH production (so MSH came with it too)

74
Q

2 categories of adrenal insufficiencies and Addison’s in which

A

primary and secondary

Addison’s is primary

75
Q

cause of disease in secondary adrenal insufficiency and ACTH and cortisol levels

A

destruction of pituitary (or also hypoth problem). low ACTH, low cortisol

76
Q

dx test for adrenal insufficiency and can it differentiate primary from secondary?

A

ACTH stimulation test. (give ACTH) if no cortisol response, primary insufficiency
if weak cortisol response, secondary. (shows it’s due to adrenal atrophy) bc there is some response. If NO cortisol response, primary.

77
Q

why ACTH stim test is not the best for adrenal insufficiency dx + primary vs secondary

A

if problem in axis hasn’t been going for long enough, adrenals not atrophied and will respond normally to ACTH (we’ll think they’re normal)

78
Q

what test + its steps used to diff primary vs secondary adrenal insufficiency with precision (gold standard but rarely done)

A

insulin stimulation test.

  • make sugar very low by giving enough insulin
  • at same time, measure cortisol and ACTH
79
Q

interpretation of insulin stimulation test (normal vs abnormal results)

A

normal result = rise in ACTH and cortisol in response to stress
abnormal = no rise in ACTH = hypopituitarism caused 2ndary insufficiency

80
Q

adrenal insufficiency: summary of dx tests (3)

A
  • ACTH level (low in 2ndary, high primary)
  • ACTH stim test (weak cortisol = 2ndary, 0 cortisol = primary)
  • insulin stim test (no ACTH rise = pit problem, 2ndary)
81
Q

treatment of primary adrenal insufficiency (2)

A
  • cortisol (hydrocortisone or prednisone or wtv) for life

- fluorinef (aldo pill)

82
Q

central adrenal insufficiency treatment

A
  • cortisol

- NO fluorinef (RAAS still functioning)

83
Q

cause of 2ndary adrenal insufficiency other than HP axis and ACTH and cortisol levels

A

exogenous corticosteroids.
ACTH is low (suppressed)
cortisol LOW (not high enough bc have adrenal insufficiency)

84
Q

treatment of central adrenal insufficiency due to HP axis being suppressed by exogenous corticosteroid

A

give only glucocorticoids (to reach good lvl)

85
Q

acute primary adrenal insufficiency treatment (how compares to chronic)

A

IV hydrocortisone and fluid replacement (no need for fluorinef)

86
Q

what to check regularly in patients on glucocorticoids

A

diabetes, bone health

87
Q

what stimulates aldo secretion

A
  • AT2 mainly
  • rise in K+
  • ACTH (to lesser extent)
88
Q

actions of AT2 in the body

A
  • aldo secretion

- arteriolar vasoconstriction

89
Q

2 types of hyperaldosteronism and how to differentiate

A

primary: low renin
secondary: high renin

90
Q

causes of primary hyperaldo

A
  • adrenal adenoma

- bilateral adrenal hyperplasia

91
Q

primary hyperaldo clinical presentation

A

htn, hypokalemia

92
Q

secondary hyperaldo causes

A

low flow to kidneys (CHF, RAS, cirrhosis, nephrotic syndrome)
rarely renin prod tumor

93
Q

3 main endocrine causes of resistant htn to check in young htn pts

A
  • primary hyperaldo
  • Cushing’s syndrome
  • PCC
94
Q

cause of 21-hydroxylase deficiency

A

2 mutations in the gene (autosomal recessive condition)

95
Q

primary consequence of 21-hydroxylase deficiency

A

adrenal pathology and no more cortisol and aldosterone produced

96
Q

labs in 21-hydroxylase deficiency

A

hyponatremia

hyperkalemia

97
Q

treatment of 21-hydroxylase deficiency

A

hydrocortisone, fludrocortisone (aldo and cortisol effect), NaCl

98
Q

reason for weird looking genitalia in newborn with 21-hydroxylase deficiency

A

blockage due to 21-hydroxylase deficiency leads to accum of precursors (17 hydroxy progesterone) so increase of androgen pathway

99
Q

general category of diseases in which 21-hydroxylase deficiency is included

A

congenital adrenal hyperplasia

100
Q

ACTH levels in congenital adrenal hyperplasia and why + consequence

A

very high bc low cortisol. lot of precursors made, shuttled to androgen pathway

101
Q

treatment of congenital adrenal hyperplasia

A

long term glucocorticoid and mineralocorticoid replacement

102
Q

what are the hormones lacking in primary vs secondary or central adrenal insufficiency

A

primary: cortisol and aldo
secondary: ONLY glucocorticoids are lacking (same for acute primary)

Bloc E - GI & Metabolism (58 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions