endocrine Flashcards
Linagstiptin, sitagliptin, -liptin
inhibit DPP4 enzyme tha tdeactivates GLP1, decreases glucagon release, uninary infection
Glitazones -zone
Activates PPAR-gamma, increases insulin sensitivity
Canagliflozin -flozin
SGLT2, blocks the reabsorption of glucose int the PCT, glucosuria, UTI, weight loss
miglitol, acarbose
inhits brush -border alpha-glucosidases, GI upset
chlorpromide, glimepiride -ide
sulfonylureas, close K+-channel in pancreatic beta cell—-> the insuline release (ca+), hyoglycemia and weight loss
Metformin
inhibit gluneogenisis and action of glucagon, lact. acidosid, GI, B12, weight loss
Rapid acting insulin
1 hr Lispro, Aspart
short acting
2-3 hrs, regular
intermediate acting
4-10hrs: NPH
Long acting
no peak: determine, glargine
PTU, methimazol
block thyroid peroxidase, inhibit oxidation of 5’deiodinase
MEN1
3 P’s Pituitory t. (prolactinoma), Panreas t. (Zollinger, insuloas, Vipoma, Glucanomas) parathyriod adenomas
Men 2A
Parathyroid hyperplasia: medullary thyroid carcinoma
Pheochromocytoma RET
Men 2b
Pheochromocytoma RET
Type diabetes is associated with?
HLA-DR4 and DR3 (4-3=1)
acromegali
GH increased, increased IGF-1 in the liver, octreotide
hypopituitarism
Sheehan: symptoms failure to lactate, absense of metruation, cold intalerance
emty sella s. : compression of the petuitotary, obese, intracranial bleading
pituitary poplexy: sudden hemorrhage -symp: bil. hemianopsia
treatment: replacement—corticosteroids
CAH
congenital adrenal hyperplasia
in deficiency in 17, 21 and 11
17 aplha hydroxylase def.
no cortisol, no cortisol causes increase in ACTH,
cortisol is low in all deficiencies, 17, 21, 11
17 alpha hydroxylase def. leads too?
lack of androgens
males may have genotypically normal female genitalia
increased ACTH (adrenocorticotropic hormone), decreseased androstenedion, low K+
Presents wit XY: abiguous genitalia, undescensed testes XX: lacks 2° sexual development
21 hydroxylase
increased androgens, males may look phenotypically norlmal
decreased ACTH, increased renin activity, increased 17 hydroxyprogesteron, high K+
Presentation: in infancy (salt wasting) or childhood ( in precocious puperty)
XX: virilization
11 beta-hydroxylase
increased androgens, but decreased ACTH (mineral corticoids), decreased renin activity, low K+
XX: virilization
alpha 5 -reductase
decreased conversion of dyhydrotestesteron to testosteron. leads to ambigious genitalia at birth
Which cells produce Cacitonin?
C for Cells are derived from endoderm, calcitonin increases calium
The 3 Zone of the Adrenal gland and hormone?
G.F.R
Glomerulosa= (SALT)Mineralcorticoid: Aldosteron
Fasciculata=(Sugar)Glucocorticoids:Cotisol
Reticularis= (Sex) Androgen: DHEA
Anterior pituitory
A for Adenohypophysis: FSH, LH, ACTH, TSH, prolactin
derivative: ectoderm rathke pouch
Posterior pituitory
neurohypophysis: ADH, oxytoxin (supraoptic and paraventricular nuclei) derivative of neuroectoderm
Glut1
RBS
GLUT2
2 for bidrectional beta-islet, GI
Glut3
brain
Glut4
adipose tissue
SGLT1/SGLT2
Na+-glucose transport of the kidney and intestine
what decreases inhibits prolaction secretion?
dopamine
what increases prolactin secretion?
TRH and GnRH
crushings syndome
increased cortisol levels
exogeneous corticosteroids decreased ACTH—–> adrenal athrophy
ACTH secreting adenoma= cushings disease
Screening: increased free cortisol on 24 hr urinalysis, dexamethasone supression test
Nelson sydrome
Removal of the feedback mech. after bil. andrelectomy for refractory cushings disease—->enlarged acth sec. pituitary adenoma. Symp: bil. hymianopsia, headages, hyperpigmentation
adrenal insuff.
inability of the adrenal gland to generalte enough glucorticoids or mineralcort.
symp: fatigue, arth. hypotension, muscle aches, weakness, weight loss, salt/sugar cravings
primary adrenal insuff.
Def. in aldosteron and cortisol—–> hypokalimia, met acidosis, hyperpimentation
Acute: hemorrhage
Chronic: Addisons: autoimmune d. causing distruction of the adrenal gland/ atrophy, other casue is TB
