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MLSCI 263 > LECTURE - Adrenal Hormones > Flashcards

LECTURE - Adrenal Hormones Flashcards

1
Q

mineralocorticoid hormones act on kidneys to:

A
  • increase Na+ reabsorption into blood
    > increase blood volume so increase blood pressure by synthesis of Na+ channels, Na+/K+-ATPase and ATP
  • increase K+ excretion into the urine
  • increase H+ excretion into urine
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2
Q

T or F. the hypothalamus and pituitary regulate aldosterone regulation

A

F! no role; the renin-angiotensin aldosterone system is what regulates this
renal baroreceptors detect decrease in BP and blood volume to turn on RAAS

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3
Q

adrenal primary disorder

A
  • autonomous aldosterone production by adrenal tumor

- Cohn’s disease

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4
Q

secondary adrenal disorder

A
  • renin-producing tumor
  • renal artery stenosis (impaired flow to the kidney)
  • drugs (some diuretics, laxatives)
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5
Q

consequences of aldosterone excess

A
  • Na+ retention: blood vol expansion and hypertension
  • K+ loss: muscle weakness and cardiac arrhythmias
  • H+ loss: increased blood pH
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6
Q

Addison’s disease

A
  • primary disorder
  • the destruction of the adrenal cortex; other adrenal cortex hormones are deficient in Adison’s
  • enzyme deficiency in aldosterone synthesis pathway
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7
Q

cause of aldosterone deficiency: secondary disorder

A
  • renin deficiency
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8
Q

physiological effects of cortisol

A
  • stress hormone
  • effects carbohydrate, protein, lipid metabolism
    > increase blood glucose (gluconeogenesis)
    > increase protein breakdown
    > increase lipolyis
  • facilitates catecholamine effects (increase BP)
  • suppresses immune system
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9
Q

insulin antagonist

A

cortisol

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10
Q

Cushing’s syndrome

A
  • diabetes; glucose cannot enter cells
  • skin thinning, easy bruising, poor wound healing, muscle weakness (increase protein breakdown)
  • abnormal fat distribution: moon face, buffalo hump, central obesity; glucose is stored as fat
  • hypertension
  • immune system suppression
  • osteoporosis
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11
Q

T or F. bound cortisol is the active form

A

F! it is the free cortisol that is the active form

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12
Q

consequence of cortisol deficiency

A
  • hypoglycemia
  • low BP- severe weakness + fatigue
  • weight loss and decreased appetite
  • +/- hyperpigmentation (only if ACTH high)
  • in Addison’s disease, can also see Na+ loss (dehydration); K+ retention (cardiac arrhythmias)
    > due to co-existing aldosterone deficiency
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13
Q

lab investigation of aldosterone excess

A
  • measure aldosterone => excess
  • measure renin and aldosterone/renin ratio to differentiate primary (adrenal) vs secondary (kidney)
  • deceased renin; increase in aldosterone/renin = primary
  • increased renin; aldosterone/renin not drastically increased = secondary
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14
Q

T or F. all labs measure renin and aldosterone

A

F

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15
Q

consequences of aldosterone deficiency

A
  • Na+ loss = dehydration, decreased BP, weakness
  • K+ retention = muscle weakness, cardiac arrhythmias
  • H+ retention = decreased blood pH
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16
Q

lab investigation of aldosterone deficiency

A
  • measure aldosterone = decreased
  • measure renin and aldosterone/renin ratio
    > increased renin; decreased aldosterone/renin = primary
    > decreased renin; aldosterone/renin not drastically decreased
17
Q

cortisol regulation

A
  • CRH = corticotropin-releasing hormone
  • ACTH = adrenocorticotropic hormone
  • undergoes diurnal variation = highest in morning and lowest at midnight
18
Q

causes of cortisol excess

A
  • adrenal/primary disorder = autonomous cortisol production by adrenal tumor
  • pituitary/secondary disorder = autonomous ACTH production by pit tumor = Cushing’s
  • ectopic ACTH-producing tumor (tumor somewhere else)
19
Q

in serum, cortisol is highly ….

A

protein-bound

- cortisol binding globulin and albumin

20
Q

lab tests for cortisol and their disadvanatges

A
  • serum (total) cortisol => does not measure active form, diurnal variation
  • 24 hr urinary free cortisol => difficult for patient
  • salivary cortisol => not widely available (but preferred), diurnal variation
21
Q

when is cortisol lowest?

A

midnight

22
Q

lab investigation for Cushing’s

A
  • excess cortisol? patient gives midnight saliva or 24 hr urinary free cortisol sample
  • if high = Dexamethasone suppression test
    > measure serum cortisol before and after administering DXM
  • if not cortisol not suppressed = TUMOR
  • ACTH measurement can help identify cause
    > adrenal 1ry if decreased ACTH
    > pituitary 2ry or ectopic if increased ACTH
23
Q

DXM

A
  • a potent glucocorticoid

- normally suppresses cortisol production

24
Q

lab investigation of cortisol deficiency

A
  • AM serum cortisol (when it should be highest)
  • can we stimulate the production of cortisol?
    > measure serum cortisol before and after giving synthetic ACTH
  • if healthy = large increase in cortisol
  • if primary def = no increase in cortisol
  • secondary def = small increase in cortisol
  • ACTH measurement can help distinguish primary and secondary
25
Q

this is the only thing that varies among catecholamines

A

the monoamine structure

26
Q

catecholamines

A

dopamine, norepi, epi

27
Q

catcholamine synthesis

A
  • amino acid = tyrosine
  • also produced in the nervous system
  • adrenal medulla = epi (80%), norepi (20%)
28
Q

fight or flight

A
  • increase in BP
  • increase rate/strength of heart contraction
  • bronchodilator
  • increase in blood glucose
29
Q

pheochromocytoma

A
  • catecholamine-secreting tumor

- adrenal medulla

30
Q

symptoms of pheochromocytoma

A

4 P’s

  • perspiration
  • palpitations (pounding/racing heart)
  • pain (headache, abdominal pain)
  • increased blood pressure
  • severe panic attack symptoms last few seconds to an hr; sporadic or persistent hypertension*
31
Q

why are epi and norepi not the preferred tests for pheochromocytoma?

A
  • SECRETED EPISODICALLY BY TUMOR (CHROMAFFIN CELLS)

- ALSO PRODUCED IN SIGNIFICANT AMOUNTS BY NERVOUS SYSTEM (NOT SPECIFIC TO ADRENAL MEDULLA)

32
Q

what do we measure when we want to investigate excess catecholamines (pheochromocytoma)?

A

metanephrine and normetanephrine
- methylated metabolites of epi and norepinephrine
- BEST tests for investigation
> produced continuously
> much more specific to the adrenal medulla

33
Q

when does pheochromocytoma occur?

A

any age

- most commonly between 30-50

34
Q

affected individuals (pheochromocytoma) should…

A
  • avoid foods with tyramine (tyrosine = natural derivative)
    > pickled foods, cured smoked or processed meats, fermented soy products, leftovers
  • avoid meds with monoamine oxidase inhibitors
    > antidepressants, antianxiety=, meds for Parkinson’s
35
Q

treatment for pheochromocytoma

A

surgery
chemotherapy
radiation therapy

MLSCI 263 (31 decks)

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