disorder of adrenal glands Flashcards
ACTH level is high and low when
high early in the morning and low in the night
causes of cushing syndrome
- iatrogenic–the most common cause (exogenous)
- endogenous is hypothalamic —–pituitary disease ACTH
- non pit- ectopic
- adrenal cortex adenoma/ca
cushing disease leading to adrenal hyperplasia
due to high ACTH produced by tumors in the anterior pituitary
iaterogenic causing cushing syndrome leads to
adrenal atrophy
paraneoplastic ACTH cushing syndrome can cause
adrenal hyperplasia– same as cushing disease
adrenal neoplasia cushing syndrome leades to
unilateral nodular hyperplasia
morphology of cushing disease
bilateral nodular cortical hyperplasia secondary to elevated levels of ACTH
common causes of paraneoplastic ACTH
- small cell carcinoma of the lungs
- carcinoids
- medullary carcinomas thyroid
- Pancreatic NETs
morphology of paraneoplastic ACTH
bilater cortical hyperplasia – same as cushing disease
paraneoplastic vs pitutary microademoa
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.
adrenal neoplam/hyperplasia
high cortisol but low serum ACTH
the tumors are functional unlike thyroid.
- the adjacent adrenal cortex and adrenal glads are atropic
zona medulla
catecholamines
derived from neural crest cells
1.zona Glomerulosa
2. zona fasciculata
3. zona reticularis
- mineralocorticoid (aldo)- stimulated by ang II and K+
- glucorticoid- cortisol- stimulated by ACTH
- androgens (DHEA and androstenodione)
cells of the adrenal cortex are derived from mesoderm
effects of cortisol on metabolism
and on the CVS
1.gluconeogeneis
2.glyconeolysis
3.proteolysis
4.lipolysis
- increase myocardial contraction
- increase CO
- increase catacholamine
when you take in IATROGENIC ACTH what will happen in causes of ZONA G, Z F and ZR
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
clinical features of cushing syndrome
- obesity/weight gain
- depression
- hypertension
- infection
- Nephrolithiasia
- decreased libido
- menstural irregularity
- hirsutism
- skin is thin and easily bruised and show striae
- muscle weakness
- osteoporosis
pseudo-cushing syndrome is associated with
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
serum cortisol level greater than 5ug/dL
cushing
actions of aldo on
1.HCO3-
2. H+
3. K+
- production
- excreted
- excreted
** aldo causes: hypertension, hypokalaemia and metabolic alkalosis
what are the causes of hyperaldosteronism
- primary-
-idopathic: bilateral nodular adrenal gland hyperplasia
-adrenocortical neoplasm: adenoma (CONN syndrome) KCNJ5 gene- encodes postassium channel protien - secondary extra renal cause-
activation of RENIN angiotensin
morphology of bilateral idopathic hyperplasia casuing hyperaldo
diffuse or focal hyperplasia of cells resembling those of the normal zona glomerulosa
morphology of adenoma causing hyperaldo (CONNS)
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
primary hyperaldosteronism clinical features
- hypertension- complications- in LVH, reducted diastolic volume
- hypokalemia- severe muscle weakness, paresthesia
- 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
features of secondary hyperaldosteronism syndrome
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+
congenital adrenal hyperplasia
you have low cortisol and then that resuts in feedback increase in ACTH but that get shunted so you have high angrogens
features of 21- hydroxylase deficiency
- 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
21-hydro def types
1. classic salt wasting
2. classic non-salt wasting
3. non-classic or late-onset adrenal virilism
- low aldo: present at birth causes a failure to thrive: hyponatremia, hyperkalemia, acidosis, hypotension and CVS collapse
- classic non-salt wasting: sufficient mineralocorticoid to prevent salt-wasting crisis. more so issue with the genitalia
- partial deficienty so- so just hirsutism, acne and menstural irregularities seen in females
11- beta hydro def fetures:
- 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
17-alpha hydro def. CF
- decrease glucocorticods and sex steriods but excessive hypertension due to excessive aldo synthesis.
- female- normal
-males- low andogrens so look for female
what are the primary causes of adrenal insufficeincy– deif of adrenal cortex
- acute
- chronic (addision disease)
what are the secondary causes of adrenal insuficancy
decreased stimulation of adrenal d/t ACTH deficiency
primary acute adrenal insufficiency seen in
- chronic adrenocortical insufficieny- d/t stress that required an immediate increase in steroid output from the glands that burdens the limited reserve
- PT maintained on exogenous corticosteroid–so with rapid withdrawal
- massive adrenal hemorrahge
- waterhouse–hypotensive shcok–causes bilateral adrenal hemorrhage
CF of acute adrenal crisis
vomit, abdominal pain, hypotension, coma, vasular collapse
chronic adrenocortical insufficancy cause
autoimmune- APSI APSI2 AIRE
