Adrenals Flashcards
Synthetized by the zona glomerulosa cells in the adrenal cortex: dehydroepiandrosterone 11-deoxycortizol cortisol aldosterone androgens
aldosterone
Synthetized by the zona fasciculata cells in the adrenal cortex: dehydroepiandrosterone corticosterone cortisol aldosterone androgens
cortisol
Synthetized by the zona reticularis cells in the adrenal cortex: dehydroepiandrosterone corticosterone cortisol aldosterone 11-deoxycortizol
dehydroepiandrosterone
17-OH-corticosteroids are the metabolite of: glucocorticoids androgens mineralocorticoids estrogens none of them
?glucocorticoids
mineralocorticoids
17-ketosteroids in urine are the metabolite of: glucocorticoid androgens mineralocorticoids estrogens none of them
androgens
Effects of glucocorticoids, except: gluconeogenesis se glucose↑ eosinopenia GFR↑ collagen synthesis ↑
gluconeogenesis se glucose↑ eosinopenia GFR↑ collagen synthesis ↑
Clinical signs of acute adrenocortical insufficiency, except: hypotension hypernatremia dehydration hypoglycemia nausea
hypernatremia
Clinical signs of chronic primary adrenocortical insufficiency, except: hypernatremia hypotension GI disturbances muscle weakness hyperpigmentation
hypernatremia
The most common cause of chronic primary adrenocortical insufficiency:
fungal infection
Tuberculosis most common = autoimmune 90%, but TB and tumor is also mentioned in the lecture so they can be right as well.
tumor metastasis
autoimmune
hemorrhagic necrosis
autoimmune
Clinical signs of chronic adrenocortical insufficiency, except: orthostatic hypotension abdominal pain hyperglycemia weight loss hyponatremia
hyperglycemia
Clinical signs of the secondary adrenocortical insufficiency, except: lymphocytosis dehydration ACTH ¯ eosinophilia anemia
dehydration
Clinical signs of Cushing-syndrome, except: central obesity livid striae virilization depression amenorrhea
virilization
Clinical signs of Cushing-syndrome, except: hirsutisms osteoporosis dysmenorrhea depression amenorrhea
dysmenorrhea
Conn-syndrome is not associated with: 17α-hydroxylase deficiency 11ß-hydroxylase deficiency hyperplasia 21-hydroxylase deficiency adenoma
?21-hydroxylase deficiency
adenoma
True statement for secondary mineralocorticoid-excess:
can be due to SIADH
can be due to 11β-hydroxylase deficiency
se renin level is low
can occur in liver-cirrhosis
all of them
?can occur in liver-cirrhosis
Cause of secondary mineralocorticoid excess with hypertension, except: Bartter-syndrome reninoma estrogen therapy accelerated hypertension renovascular disease
reninoma
estrogen therapy
accelerated hypertension
renovascular disease
Typical sign of pheochromocytoma, except: hypertension developed in paroxysm constipation nausea, vomiting, hyperhidrosis 24 hours urine VMA↑
constipation
True statements:
mineralocorticoids are synthetized in zona glomerulosa
mineralocorticoids are synthetized in zona fasciculata
glucocorticoids are synthetized in zona fasciculata
glucocorticoids are synthetized in zona glomerulosa
mineralocorticoids are synthetized in zona glomerulosa
glucocorticoids are synthetized in zona fasciculata