E4: ADRENAL and DI Flashcards

1
Q

addison’s disease

A

adrenal hormone deficit

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2
Q

cause of addison’s

A
  • tumors
  • autoimmune
  • immediate withdrawal of glucocorticoid meds
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3
Q

pathway of addisons

A

hypothalamus–> CRF–> ant pit–> ACTH–> adrenal gland–> decreased corticosteroids (mineralocorticoids, glucocorticoids, sex steroids)

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4
Q

what is the main feedback loop with addison’s

A

decreased corticosteroids –> ant pituitary to release ACTH

something causes less adrenal hormones to be released

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5
Q

clinical mani of addisons R/T decreased glucocortiocoids

A
  • decreased liver gluconeogenesis

- hypoglycemia

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6
Q

what are the corticosteroids

A
  • mineralocorticoid (aldosterone)
  • glucocorticoids (cortisol)
  • sex steroids (androgens, estrogens, progesterone)
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7
Q

what is adrenal crisis

A

sudden decrease or absence of adrenocortical hormones

-often from suddenly stopping of prednisone

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8
Q

cause of adrenal crisis

A
  • stress/illness

- sudden withdrawal of corticosteroid meds

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9
Q

clinical mani of addisons R/T decreased mineralocorticoids

A
  • fluid and electrolyte imbalances (Na and H2O out, not enough reabsorption)
  • –hypotension (loss of water)
  • –hyponatremia (loss of salt)
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10
Q

clinical mani of addisons R/T decreased adrenal androgens

A

mostly in females:

-loss of secondary sex characteristics

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11
Q

cushing’s syndrome

A

overactivity of adrenal gland with hypersecretion of corticosteroids

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12
Q

cause of cushing’s

A
  • tumor of the adrenal gland

- hyperplasia

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13
Q

patho chain of cushing

A

hypothal–> CRF–> ant pit–> ATCH–> adrenal gland–> increased secretion of corticosteroids

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14
Q

clinical mani of cushings RT increased glucocorticoid

A
  • hyperglycemia/insulin resistance (cortisol induced insulin resistance with increased gluconeogenesis)
  • wt gain and abnormal fat distributionDrug and food interactions
  • protein wasting
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15
Q

diabetes incipidus

A

deficiency of ADH resulting in H2O imbalance

too much diuresis

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16
Q

cause of diabetes incipidus

A
  • genetic
  • neurogenic/trauma
  • infections
  • medications
  • nephrogenic
  • feedback mechanisms hyperactive
17
Q

clinical mani of cushing RT increased aldosteroine

A

increased Na and H2O (excessive reabsorption):

  • HTN
  • hypernatremia
18
Q

clinical mani of cushing RT increased androgens

A
  • hirsutism (increase hair on face, chest and back)
  • thinning hair on head
  • acne
19
Q

what is the abnormal fat distribution with cushings

A

wt gain from accumulation of adipose tissue in the trunk (truncal obesity), face (moon face) and cervical areas (buffalo hump)

20
Q

what does protein wasting, collagen and osteoporosis have to do with cushings

A
  • lose protein matrix from the bone which leads to osteoporosis
  • thin skin with visible capps, purple striae in drunk, bruising from loss of collagen
21
Q

patho chain of diabetes incipidus

A

hypothal–> post. pit–> decreased ADH secretion–> decreased H2O reabsorption–> increased urine output

22
Q

clinical mani of DI RT failure of the nephrons to reabsorb H2O

A
  • large, dilute output
  • hypernatremia (hyperosmotic serum)
  • polyuria
  • polydipsia
23
Q

ADH target and role

A
  • target organ is kidney

- role increases or decreases the amount of fluid that is excreted