L5 Endocrine II Flashcards
Parathyroid composed mostly of
Secretion and regulation
Location
Chief cells
Parathyroid hormone for calcium levels
Posterior aspect of thyroid
Actions of pth
(Increase free Ca) Increase Ca reabsorption increase urine phosphate excretion Increase conversion of Vit D to active-->increase GI Ca absorption Increase osteoclast activity
Primary vs secondary hyperparathyroidism
Primary: spontaneous overproduction of PTH
Secondary: due to chronic renal failure
Features of primary hyperparathyroidism (6)
Painful bones, stones, abdominal groans, psychic moans
Ground glass appearance
Brown tumor
Secondary hyperparathyroidism mechanisms
Renal failure leads to Hyperphosphatemia (decreased excretion), lowers Ca levels, stimulates PTH
Unable to produce Vit D, lower Ca absorption in instestins, stimulates PTH
Ca levels in Secondary Hyperparathyroidism
Near normal
Endocrine function of pancreas is what type of cells
islets of langerhans Alpha: glucagon Beta: insulin Delta: somatostatin PP: VIP (polypeptide)
Normal blood glucose levels
70-120 mg/dL
Diabetes: >200 or fasting glucose of 126 on more than one occasion
Which prognosis is worse, DM I or II
DM I is worse, more likely to die of disease
Zollinger-Ellison syndrome
Pancreatic islet tumor
Hypersecretion of gastric acid
Peptic ulcers
Parts of adrenal gland and production
Cortex: homrones: cortisol, aldosterone, estrogen, progestronne
Medulla: catecholamines: epi, norepi, dopamine
Cushing’s syndrome
What is it
Features
Hypercortisolism
Weight gain
Moon face
Buffalo hump (fat in back of neck)
Hyperaldosteronism
Primary vs secondary
Primary: decreased plasma renin (kidney usually makes renin to then make aldosterone. Kid kidney is making too much aldo, so renin stops getting secreted)
Secondary: increased plasma renin
Addisons disease
Destruction of adrenal cortex (chronic adrenocortical insufficiency)
Addisons disease features (3)
Weakness
GI distubances
Hyperpigmentation
