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Clin Med I > Adrenal Disorders (pt. 1, 2, 3) > Flashcards

Adrenal Disorders (pt. 1, 2, 3) Flashcards

Paulson lectures (50 cards)

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1
Q

Zona glomerulosa secretes ____, such as ____.

- Function?

A

mineralocorticoids, such as aldosterone

- regulates BP and electrolyte homeostasis

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2
Q

Zona fasciulata secretes ____, such as ____.

- Function?

A

glucocorticoids, such as cortisol

- regulate stress response, immune system, metabolism

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3
Q

Zona reticularis secretes ____, such as ____.

- Function?

A

gonadocorticoids, such as androgens, progesterone, testosterone

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4
Q

aldosterone is synthesized from ____

A

cholesterol

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5
Q

production of aldosterone is stimulated by ____ and _____

A
  • increase in K+

- angiotensin II secretion

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6
Q

aldosterone acts on convoluted tubules & collecting ducts to increase what?

A
  • increase reabsorption of Na+

- increase excretion of K+ and H+

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7
Q

cortisol is released in response to what?

A
  • stress

- low blood glucose

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8
Q

how does cortisol help increase blood glucose

A

stimulates gluconeogenesis

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9
Q

how does cortisol affect immune system

A
  • decrease absorption of Ca2+ in GI

- decrease osteoblast production of new bones tissue

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10
Q

Didehydroepiandrosterone (DHEA)

A
  • produced from cholesterol
  • precursor of sex steroid hormone synthesis
  • activates estrogen and testosterone
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11
Q

epinephrine is an agonist of ____ receptors

A

adrenergic

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12
Q

epinephrine effects

A
  • increase HR & RR
  • stimulates glycogenolysis & lipolysis
  • muscle contraction
  • vasoconstriction (vessels in GI, skin, kidneys)
  • vasodilation (lungs)
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13
Q

_____ is a neurotransmitter and hormone that activates ____ receptors and plays a role in fight-or-flight response

A

Norepinephrine

- noradrenergic receptors

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14
Q

norepinephrine effects

A
  • increase HR & BP
  • decrease GI motility and urination
  • triggers release of glucose from stores
  • increase arousal/alertness. memory formation and retrieval
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15
Q

what are the classic findings of hyperaldosteronism

A
  • difficult to control HTN
  • hypokalemia, hypernatremia
  • HA, vision impairment, muscle weakness, polyuria
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16
Q

some adrenal adenomas are nonfunctional, while other can secrete ____

A
  • aldosterone (conn’s syndrome)
  • cortisol (cushing’s)
  • androgens (hyperandrogenism)
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17
Q

what test would you order if you suspect hyperaldosteronism

A
  • PAC (plasma aldosterone conc)
  • PRA (plasma renin activity)

High PAC:PRA = primary hyperaldosteronism
Low PAC:PRA = secondary hyperaldosteronism

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18
Q

hyperaldosteronism Tx

A
  • adrenalectomy (unilat hyperplasia/carcinoma/adenoma)
  • spirinolactone
  • eplerenone
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19
Q

who is at higher risk of hypoaldosteronism

A

pts with DM, nephropathy, FHx, and NSAID/spirinolactone/heparin/beta-blocker use

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20
Q

clinical features of hypoaldosteronism

A
  • hyperkalemia (without source)
  • hypercloremic metabolic acidosis
  • often asymptomatic
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21
Q

what labs would you order for hypoaldosteronism

Study These Flashcards
A
  • BMP (ele K, ele Cl, ele BUN/Crt)

- PRA and serum aldosterone

22
Q

hypoaldosteron Tx

Study These Flashcards
A
  • primary = mineralocorticoid such as Fludrocortisone

- hyporen/hypoald = low K diet and diuretic (may use fludrocortison but can be bad for HTN)

23
Q

primary adrenal insufficiency is also known as

Study These Flashcards
A

Addison’s disease

24
Q

causes for primary adrenal insufficiency

Study These Flashcards
A
  • autoimmune adrenalitis
  • FHx
  • infectious adrenalitis (TB, HIB, fungal)
  • medication use
  • metastases
  • abrupt withdrawal of steroid Tx (suppresses HPA axis)
25
clinical features of primary adrenal insufficiency (Addison's)
*both cortisol & aldosterone affected - hyponatremia, hyperkalemia = Hypotension - hyperpigmentation of skin & mm (d/t ele ACTH) - salt craving
26
clinical features of secondary/tertiary adrenal insufficiency
- Hypoglycemia | - NO: hyperpigmentation, hyperkalemia, dehydration
27
clinical features of Addisonian crisis
- hypovolemic shock (hypotension) - acute abdomen (abd TTP, N/V, fever) - AMS
28
Addisonian crisis Tx
- aggressive IV fluids - Hydrocortisone IV bolus (or Dexamethasone) - Tx underlying cause (sepsis, hemorrhage) DON'T DELAY TX WAITING FOR CORTISOL LVL
29
Primary adrenal insufficiency Tx
- Florinef + Hydrocortisone (MC & GC replacement) | GC given at different times to mimic nml endogenous cortisol levels
30
pheochromocytoma
- catecholamine producing tumor; commonly in adrenal medulla | - secretes mostly norepi, but also epi
31
pheochromocytoma pathophysiology
- arise from chromaffin cells (can also be from paragangliomas) - stimulate alpha & beta receptors
32
pheochromocytoma triad
- HA - sweating - tachycardia
33
pheochromocytoma spells
- spontaneous | - from meds, exercise, increase abd pressure, anxiety, postural change
34
pheochromocytoma crisis (complications)
- ARDS - acute HF - pulmonary edema - severe hypotension - kidney & liver failure - ICH
35
pheochromocytoma Tx
1. alpha blocker (phenoxybenzamine) 2. beta blocker 3. increase salt and fluid intake 4. surgical resection
36
how would you diagnose pheochromocytoma
1. 24hr urine catecholamine/meta --OR-- plasma fractionated metanephrines - if elevated = CT or MRI - if nml = repeat during a spell
37
how can multiple endocrine neoplasia be diagnosed
- clinical features (2+ of the associated tumors) - familial pattern (associated tumor in a patient who has a 1st degree relative with syndrome) - genetic testing
38
MEN1 (Wermer syndrome) affects what organs
- parathyroid - anterior pituitary - pancreas
39
MEN2a (Sipple syndrome) affects what
- parathyroid - pheochromocytoma - medullary thyroid carcinoma
40
MED2b affects what
- marfanoid body habitus - pheochromocytoma - medullary thyroid
41
MEN4 affects what
- parathyroid adenomas - pituitary adenomas - pancreatic neuroendocrine tumors in association with gonadal, adrenal, renal, and thyroid tumors
42
congenital adrenal hyperplasia (CAH)
- genetic defect that decreases production of cortisol from its precursors - AP secretes more ACTH to compensate - increased ACTH during developmental years causes hyperplasia (can lead to excess androgens and decreased aldosterone)
43
CAH clinical features
- skin hyperpigmentation - Salt wasting = hyponatremia, hyperkalemia, dehydration, arrhythmia, vomiting - short stature - females with ambiguous genitalia and masculinization
43
CAH clinical features
- skin hyperpigmentation - Salt wasting = hyponatremia, hyperkalemia, dehydration, arrhythmia, vomiting - short stature - females with ambiguous genitalia and masculinization
44
Chronic Tx for CAH
corticosteroids +/- mineralocorticoids (indefinitely) | to replace cortisol & aldosterone
45
CAH: Tx for salt-wasting crisis
- fluid rescusitation - immediate hydrocortisone - correct electrolyte imbalance - mineralocorticoids replacement ADMIT
46
clinical features of Cushing's
- moon facies - buffalo hump - central obesity - striae - bruise easily - hyperpigmentation
47
what is the first step in diagnosing Cushing's
Determine increased cortisol levels - Low-dose dexamethasone suppression test (overnight and 48 hour) - late night salivary cortisol (11pm, 12am) - 24hr urinary free cortisol excretion
48
what is the second step in diagnosing Cushing's
Determine cause of increased cortisol - Plasma ACTH (if low = adrenal tumor cause)
49
Tx of Cushing's for: - iatrogenic - 1* - cushing's disease - ectopic ACTH
- iatrogenic = taper off corticosteroid - 1* = surgery - cushing's disease = transsphenoidal resection - ectopic ACTH = surgery

Clin Med I (21 decks)

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