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endocrine system > disorder of adrenal glands > Flashcards

disorder of adrenal glands Flashcards

1
Q

ACTH level is high and low when

A

high early in the morning and low in the night

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2
Q

causes of cushing syndrome

A
  1. iatrogenic–the most common cause (exogenous)
  2. endogenous is hypothalamic —–pituitary disease ACTH
    - non pit- ectopic
    - adrenal cortex adenoma/ca
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3
Q

cushing disease leading to adrenal hyperplasia

A

due to high ACTH produced by tumors in the anterior pituitary

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4
Q

iaterogenic causing cushing syndrome leads to

A

adrenal atrophy

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5
Q

paraneoplastic ACTH cushing syndrome can cause

A

adrenal hyperplasia– same as cushing disease

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6
Q

adrenal neoplasia cushing syndrome leades to

A

unilateral nodular hyperplasia

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7
Q

morphology of cushing disease

A

bilateral nodular cortical hyperplasia secondary to elevated levels of ACTH

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8
Q

common causes of paraneoplastic ACTH

A
  1. small cell carcinoma of the lungs
  2. carcinoids
  3. medullary carcinomas thyroid
  4. Pancreatic NETs
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9
Q

morphology of paraneoplastic ACTH

A

bilater cortical hyperplasia – same as cushing disease

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10
Q

paraneoplastic vs pitutary microademoa

A

CRH administration results in an excessive rise in plasma ACTH and serum cortisol in patients with pituitary

Cushing’s disease, whilst this is rarely seen in patients with ectopic ACTH secretion.

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11
Q

adrenal neoplam/hyperplasia

A

high cortisol but low serum ACTH
the tumors are functional unlike thyroid.

  • the adjacent adrenal cortex and adrenal glads are atropic
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12
Q

zona medulla

A

catecholamines
derived from neural crest cells

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13
Q

1.zona Glomerulosa
2. zona fasciculata
3. zona reticularis

A
  1. mineralocorticoid (aldo)- stimulated by ang II and K+
  2. glucorticoid- cortisol- stimulated by ACTH
  3. androgens (DHEA and androstenodione)
    cells of the adrenal cortex are derived from mesoderm
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14
Q

effects of cortisol on metabolism
and on the CVS

A

1.gluconeogeneis
2.glyconeolysis
3.proteolysis
4.lipolysis

  1. increase myocardial contraction
  2. increase CO
  3. increase catacholamine
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15
Q

when you take in IATROGENIC ACTH what will happen in causes of ZONA G, Z F and ZR

A

it will decrease ACTH as feedback then that causes
ZG- no effect because it is stimulated by ang II and K+
ZF and ZR will be atrophied

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16
Q

clinical features of cushing syndrome

A
  1. obesity/weight gain
  2. depression
  3. hypertension
  4. infection
  5. Nephrolithiasia
  6. decreased libido
  7. menstural irregularity
  8. hirsutism
  9. skin is thin and easily bruised and show striae
  10. muscle weakness
  11. osteoporosis
17
Q

pseudo-cushing syndrome is associated with

A

excessive alcohol consumption
it can also be due to elevated levels of total cortisol and can also be due to estrogen found in oral contraceptive– which contains a mix of estrogen and progeterone– causes and increase in cortisol binding globulin and thereby causes the total cortisol level to be elevated

18
Q

serum cortisol level greater than 5ug/dL

A

cushing

19
Q

actions of aldo on
1.HCO3-
2. H+
3. K+

A
  1. production
  2. excreted
  3. excreted
    ** aldo causes: hypertension, hypokalaemia and metabolic alkalosis
20
Q

what are the causes of hyperaldosteronism

A
  1. primary-
    -idopathic: bilateral nodular adrenal gland hyperplasia
    -adrenocortical neoplasm: adenoma (CONN syndrome) KCNJ5 gene- encodes postassium channel protien
  2. secondary extra renal cause-
    activation of RENIN angiotensin
21
Q

morphology of bilateral idopathic hyperplasia casuing hyperaldo

A

diffuse or focal hyperplasia of cells resembling those of the normal zona glomerulosa

22
Q

morphology of adenoma causing hyperaldo (CONNS)

A

small solitary
c/s- bright yello
composed of lipid-laden cortical cells more closely resembling fasicilata cells than the ZG cells

*spironolactone bodies - eosinophilic, laminated cytoplasmic inclusions, found after treatment with anti-hypertensive agent spironolactone ( drug of choice in primary hyperaldosteronism

23
Q

primary hyperaldosteronism clinical features

A
  1. hypertension- complications- in LVH, reducted diastolic volume
  2. hypokalemia- severe muscle weakness, paresthesia
  3. metabolic alkolosis- low calcium levles-postive chvostek or trousseaus sign

*no edema because of aldo escape

Elevated aldosterone & Low plasma renin activity
ELEVATED aldosterone and renin RATIO
24-hour URINE potassium - always increased

24
Q

features of secondary hyperaldosteronism syndrome

A

high plasma renin edema often present
there is decreased aldosterone and renin RATIO (because the renin levels are way higher)

hypernatreia–hence edema

hypokalemia
and here also high urine K+

25
Q

congenital adrenal hyperplasia

A

you have low cortisol and then that resuts in feedback increase in ACTH but that get shunted so you have high angrogens

26
Q

features of 21- hydroxylase deficiency

A
  • there will be decreased glucocorticodis and mineralocorticods but increase in sex hormones
    -male has normal genitalaia its just his puberty is early
    but female has ambiguoss genitalia and oligomenorrhea, hirsutism and acne
27
Q

21-hydro def types
1. classic salt wasting
2. classic non-salt wasting
3. non-classic or late-onset adrenal virilism

A
  1. low aldo: present at birth causes a failure to thrive: hyponatremia, hyperkalemia, acidosis, hypotension and CVS collapse
  2. classic non-salt wasting: sufficient mineralocorticoid to prevent salt-wasting crisis. more so issue with the genitalia
  3. partial deficienty so- so just hirsutism, acne and menstural irregularities seen in females
28
Q

11- beta hydro def fetures:

A
  • increase in sex
  • increase in deoxycorticosterone levels– so can compensatate fro mininarcorticoids
  • only a corsitoal def.

females- ambigous genitalis
males- just prepuberty
Renin is low becasue aldo no problem

29
Q

17-alpha hydro def. CF

A
  • decrease glucocorticods and sex steriods but excessive hypertension due to excessive aldo synthesis.
  • female- normal
    -males- low andogrens so look for female
30
Q

what are the primary causes of adrenal insufficeincy– deif of adrenal cortex

A
  1. acute
  2. chronic (addision disease)
31
Q

what are the secondary causes of adrenal insuficancy

A

decreased stimulation of adrenal d/t ACTH deficiency

32
Q

primary acute adrenal insufficiency seen in

A
  1. chronic adrenocortical insufficieny- d/t stress that required an immediate increase in steroid output from the glands that burdens the limited reserve
  2. PT maintained on exogenous corticosteroid–so with rapid withdrawal
  3. massive adrenal hemorrahge
  4. waterhouse–hypotensive shcok–causes bilateral adrenal hemorrhage
33
Q

CF of acute adrenal crisis

A

vomit, abdominal pain, hypotension, coma, vasular collapse

34
Q

chronic adrenocortical insufficancy cause

A

autoimmune- APSI APSI2 AIRE

endocrine system (5 decks)

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