Adrenal Physiology Flashcards

1
Q

outline the regulation of adrenal cortisol secretion

A
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2
Q

outline the affect of cortisol on ADH

A

cortisol inhibits ADH

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3
Q

why is hyponatremia seen in adrenal insufficiency

A
  1. hypovolemia
  2. when cortisol lowers, it causes an absence of cortisol inhibitory effects on ADH. Relative excess of ADH causes reabsorption of water and the dilution of Na+–> hyponatremia
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4
Q

• In primary adrenal insufficiency, what is the
expected level of ACTH?

A

high

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5
Q

In central adrenal insufficiency, what is the
expected level of ACTH?

A

low

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6
Q

• If you have adrenal insufficiency and a normal
ACTH, what can potentially be causing the AI?

A

normal ACTH= inappropriately low, hsould be high if your cortisol is low. this is a central problem:

hypothalamic issue; mass, infarct/stroke, trauma

pituitary; stalk severing/damage to the axis, mass

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7
Q

Using this diagram, outline where each adrenal gland chemical is released from and what regulates it.

A
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8
Q

which areas of the adrenal gland is affected with PAI

A

GFR– the whole cortex. therefore there is a deficiency in aldosterone, cortisol, and sex hormones (testosterone, mainly in women)

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9
Q

which areas of the adrenal gland is affected in CAS

A

ONLY FR– cortisol and sex hormones. Aldosterone is not afected because its main driver/regulator is the RAAS system of the kidneys. The FR region is regulated by ACTH from the pituitary, so its more affected when the pitutiary or hypothalamus is diseased.

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10
Q

Do you expect hyperkalemia in primary vs.
central adrenal insufficiency?

A

hyperkalmiea= inability to get excreted. The ENAC- collecting tubule system is not working properly. therefore the glomerulosa area of the adrenal gland not working–PAI.

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11
Q

• In a patient with primary AI, your long term
management would include:

A. GC replacement

B. Mineralocorticoid replacement

C. Medic alert bracelet

D. A & C only

E. All of the above

A

E

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12
Q

• In a patient with primary AI, your long term
management would include:

A. GC replacement

B. Mineralocorticoid replacement

C. Medic alert bracelet

D. A & C only

E. All of the above

A

D. dont need glomerulosa (aldosterone) replacement

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13
Q

Do you expect to see skin hyperpigmentation in primary or central adrenal insufficiency?

A

PRIMARY– primary because ACTH would be really high. ACTH production also produces melanin precursors.

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14
Q

features suggesting corticosteorid insufficiency

A
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15
Q

glucocorticoid CVS effects

A

increases contractility of the heart muscle

  • increases peripheral vascular tone by augmenting other vasoconstrictor actions
  • facilitates catecholamine production and modulation of beta adrenergic receptor synthesis
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16
Q

what kind of shock do you expect in acute adrenal insuffieicny

A

hypovolemic because of no mineralocorticoids

cardiogenic because of GCs direct effect on heart muscle contractility.

distributive shock due to the decrease in systemic vascular resistance.

17
Q

main clinical featurse that facor primary over central AI

A

primary: GFR affected.
- salt craving
- weakness and fatigue because of hyperkalemia
- thin skin
- increase in pigmentation because ACTH is high
- vitiligo

18
Q

In addition to the GC deficiency symptoms, what other symptoms might make you think of central hypocortisolism?

A

decrease in sex hormones because ACTH is not present.

  • hair thinning, hypogonadism, decreased libido. Not so much the electrolyte disturbances because the MC is still there.
  • other symptoms that are cuased by mass affects/hypothalamic disease
19
Q

A very sick, septic patient in the ICU has a cortisol level of >1000, is this Cushing’s?

A

no. the person is natrually increased in cortisol because of the acute phase reactanct-ness of it.

20
Q

best time to measure cortisol if suspecting excess

A

at night, whne it should be low

21
Q

best time to measure cortisol if it is suspected to be low

A

in the morning, when it should be high.

22
Q

stress that can cause cortisol increase

A

• Increased ACTH secretagogues: CRH & AVP • Cortisol levels increase at inflammation sites • IL-6 enhances HPA axis response to inflammation • Diurnal variation is lost

23
Q

• In addition to the 8am cortisol, can you think
of a dynamic way to test the HPA axis to rule out deficiency?

A

ACTh stimulation test; ACTH infusion should cause cortisol to rise. If it rises, the adrenal galnds are fine but the pit/hypothalamus is the problem. if the cortisol is low, might be primary adrenal insufficiency.

Insulin tolerance test; make the person hypoglycemic– the HPA axis should activate and ACTH levels should be elevated. If not, might be central.

24
Q

cortisol excess

A

cushings

25
Q

aldosterone excess

A

conns

26
Q

metanephrine excess

A

pheochromocytoma

27
Q
A