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

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

Paulson lectures

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

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

- PRA and serum aldosterone

22
Q

hypoaldosteron Tx

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

A

Addison’s disease

24
Q

causes for primary adrenal insufficiency

A
  • autoimmune adrenalitis
  • FHx
  • infectious adrenalitis (TB, HIB, fungal)
  • medication use
  • metastases
  • abrupt withdrawal of steroid Tx (suppresses HPA axis)
25
Q

clinical features of primary adrenal insufficiency (Addison’s)

A

*both cortisol & aldosterone affected

  • hyponatremia, hyperkalemia = Hypotension
  • hyperpigmentation of skin & mm (d/t ele ACTH)
  • salt craving
26
Q

clinical features of secondary/tertiary adrenal insufficiency

A
  • Hypoglycemia

- NO: hyperpigmentation, hyperkalemia, dehydration

27
Q

clinical features of Addisonian crisis

A
  • hypovolemic shock (hypotension)
  • acute abdomen (abd TTP, N/V, fever)
  • AMS
28
Q

Addisonian crisis Tx

A
  • aggressive IV fluids
  • Hydrocortisone IV bolus (or Dexamethasone)
  • Tx underlying cause (sepsis, hemorrhage)

DON’T DELAY TX WAITING FOR CORTISOL LVL

29
Q

Primary adrenal insufficiency Tx

A
  • Florinef + Hydrocortisone (MC & GC replacement)

GC given at different times to mimic nml endogenous cortisol levels

30
Q

pheochromocytoma

A
  • catecholamine producing tumor; commonly in adrenal medulla

- secretes mostly norepi, but also epi

31
Q

pheochromocytoma pathophysiology

A
  • arise from chromaffin cells (can also be from paragangliomas)
  • stimulate alpha & beta receptors
32
Q

pheochromocytoma triad

A
  • HA
  • sweating
  • tachycardia
33
Q

pheochromocytoma spells

A
  • spontaneous

- from meds, exercise, increase abd pressure, anxiety, postural change

34
Q

pheochromocytoma crisis (complications)

A
  • ARDS
  • acute HF
  • pulmonary edema
  • severe hypotension
  • kidney & liver failure
  • ICH
35
Q

pheochromocytoma Tx

A
  1. alpha blocker (phenoxybenzamine)
  2. beta blocker
  3. increase salt and fluid intake
  4. surgical resection
36
Q

how would you diagnose pheochromocytoma

A
  1. 24hr urine catecholamine/meta –OR– plasma fractionated metanephrines
  • if elevated = CT or MRI
  • if nml = repeat during a spell
37
Q

how can multiple endocrine neoplasia be diagnosed

A
  • 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
Q

MEN1 (Wermer syndrome) affects what organs

A
  • parathyroid
  • anterior pituitary
  • pancreas
39
Q

MEN2a (Sipple syndrome) affects what

A
  • parathyroid
  • pheochromocytoma
  • medullary thyroid carcinoma
40
Q

MED2b affects what

A
  • marfanoid body habitus
  • pheochromocytoma
  • medullary thyroid
41
Q

MEN4 affects what

A
  • parathyroid adenomas
  • pituitary adenomas
  • pancreatic neuroendocrine tumors
    in association with gonadal, adrenal, renal, and thyroid tumors
42
Q

congenital adrenal hyperplasia (CAH)

A
  • 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
Q

CAH clinical features

A
  • skin hyperpigmentation
  • Salt wasting = hyponatremia, hyperkalemia, dehydration, arrhythmia, vomiting
  • short stature
  • females with ambiguous genitalia and masculinization
43
Q

CAH clinical features

A
  • skin hyperpigmentation
  • Salt wasting = hyponatremia, hyperkalemia, dehydration, arrhythmia, vomiting
  • short stature
  • females with ambiguous genitalia and masculinization
44
Q

Chronic Tx for CAH

A

corticosteroids +/- mineralocorticoids (indefinitely)

to replace cortisol & aldosterone

45
Q

CAH: Tx for salt-wasting crisis

A
  • fluid rescusitation
  • immediate hydrocortisone
  • correct electrolyte imbalance
  • mineralocorticoids replacement

ADMIT

46
Q

clinical features of Cushing’s

A
  • moon facies
  • buffalo hump
  • central obesity
  • striae
  • bruise easily
  • hyperpigmentation
47
Q

what is the first step in diagnosing Cushing’s

A

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
Q

what is the second step in diagnosing Cushing’s

A

Determine cause of increased cortisol

  • Plasma ACTH (if low = adrenal tumor cause)
49
Q

Tx of Cushing’s for:

  • iatrogenic
  • 1*
  • cushing’s disease
  • ectopic ACTH
A
  • iatrogenic = taper off corticosteroid
  • 1* = surgery
  • cushing’s disease = transsphenoidal resection
  • ectopic ACTH = surgery

Clin Med I (21 decks)

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