Flashcards in Endocrine Deck (73)
tyrosine kinase receptor that induces glucose uptake into insulin-dependent tissues via GLUT-4 receptors and affects gene transcription.
Regulation of insulin release
Glucose enters beta cell and is metabolized, increasing ATP. ATP closes K+ channels leading to depolarization. VG Ca++ channels open leading to Ca++ influx and exocytosis of insulin.
Effects of somatostatin
Decreases growth hormone and TSH release from the pitutiary. Analogues can thus be used to treat acromegaly.
Effects of TRH
increases TSH and prolactin
Two functions of growth hormone
Stimulates growth through IGF-1
Increases insulin resistance (diabetogenic)
Regulation of growth hormone
Released in pulses in response to GHRG. Secretion higher during exercise and sleep. Secretion inhibited by glucose and somatostatin.
Stimulates hunger and GH release. Produced by stomach
Satiety hormone produced by adipose tissue
Regulation of ADH
Osmoreceptors in hypothalamus
High mineralocorticoids; low cortisol and sex steroids. High BP, low K+, low androstenedione, non-virilizing. Males have ambiguous genitalia at birth, females lack secondary sex development.
Most common cause of CAH. high sex hormones; low mineralocorticoids and cortisol. Low BP and high K+. High 17-OH-progesterone and high renin activity.
Low aldosterone and cortisol but high 11-beta-deoxycorticosterone results in increased BP. High sex hormones. Virilization and salt wasting.
-increases insulin resistance
-decreases fibroblast activity which is what causes striae in cushings
-decreases inflammatory/immune response: inhibits leukotriene and PG production, inhibits WBC adhesion resulting in neutrophilia, blocks histamine release, reduces eosinophils, blocks IL-2 production
-decreases bone formation
functions of vitamin D
-increaes absorption of Ca++ and phosphorus in gut
-increases bone resorption, increasing Ca++ and phosphorus
regulation of vitamin D
Active levels increased by high PTH and low Ca++ and phosphorus
Functions of PTH
-increases bone resorption of Ca++ and phosphorus by increasing production of RANK-L which binds RANK receptor on osteoclasts to stimulate them
-increases kidney reabsorption of Ca++ in distal tubule
-decreases reabsorption of phosphorus in distal tubule
-increases active vitamin D production in kidney
Regulation of PTH
increased by low Ca++, high phos, low Mg++. Decreased by very low Mg++.
Hormones that signal through cAMP
FLAT ChAMP: FSH, LH, ACTH, TSH, CRH, hCG, ADH, MSH, PTH, calcitonin, GHRH
Pituitary hormones: FSH, LH, TSH, ADH (V2 receptor), ACTH, MSH (all but prolactin and oxytocin)
Hypothalamic hormones: CRH, GHRH
Others: hCG, PTH, calcitonin, glucagon
Hormones that signal through cGMP
ANP, BNP, NO
Hormones that signal through IP3
GOAT HAG: GnRH, oxytocin, ADH (V1 receptor), TRH, histamine (H1 receptor), angiotensin II, gastrin
Hormones that signal through intracellular receptor
Steroid hormones, thyroid hormone, vitamin D
Hormones that signal through intrinsic tyrosine kinase
Insulin, IGF-1, other growth factors
Hormones that signal through receptor-associated tyrosine kinase (JAK/STAT)
PIGG(L)ET: prolactin, immunomodulators, GH, G-CSF, EPO, thrombopoietin
Functions of T3
-increased basal metabolic rate
Symptoms of adrenal insufficiency
Weakness, fatigue, orthostatic hypotension, muscle aches, weight loss, GI disturbance, sugar/salt cravings
Primary vs secondary vs tertiary adrenal insufficiency
Primary: Def of aldo and cortisol. Hypotension, hyperkalemia, and metabolic acidosis. ACTH high resulting in hyperpigmentation. Can be acute due to massive hemorrhage or chronic due to Addison disease
Secondary: Decreased ACTH production. No hyperpigmentation or hyperkalemia
Tertiary: Abrupt withdrawal of chronic exogenous steroid use
Neuroblastoma of adrenal medulla
Most common tumor of adrenal medulla in kids. Usually seen in those less than 4. Neural crest derivative with overexpression of N-myc. Pathology includes Homer-Wright rosettes.
Presents with abdominal distension and firm, irregular mass (vs smooth Wilms tumor). May see dancing eyes-dancing feet.
Labs: elevated HVA, VMA in urine due to breakdown or dopamine and NE. Bombesin and neuron-specific enolase pos.
Genetic syndromes associated with pheo
NF1, VHL, MEN2A, MEN2B
treatment of pheo
1) irreversible alpha antag (before beta blocker to prevent hypertensive crisis)
2) beta blocker