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Bio 203 endocrine

Endocrine review

This Disease is associated with very tall, yet normally proportioned people. They may be 8 ft tall due to lack of closure of epiphyseal plates on time. Usually occurs due to a pituitary gland tumor Giantism - hypersecretion of GH Acromegally happens in adulthood. Eipyseal plates close though
Results in a short person (4 ft tall) who is normally proportioned Hand x rays show unusually large epiphyseal plates for child’s age Insulin like growth factor levels in the blood are low hyposecretion of HGH = pituitary dwarfism
Rapid heart rate High BP Agitation and anxiety H/O weight loss Blood TSH levels are low T3 and T4 levels are high hyperthoroidism, like Grave's
High BP Agitation and anxiety C/O heart palpitations Metanephrines (metabolites of epi and NE) are found in the urine. This is an abnormal finding. adrenal medulla tumor (pheochromocytoma)
C/O fatigue, malaise, and dry skin Pt. feels cold all the time H/O recent weight gain BP is low for this person Blood TSH levels are high Blood T3 and T4 are low hypothyroidsims, ex myxedema (infant version is cretinism)
Recent water weight gain noted Fat deposition between shoulder blades Face appears round and puffy CT scan of the abdomen reveals an adrenal mass Blood ACTH levels are low adrenal cortex hypersecretion of cortisol, Cushing's syndrome
Polyuria Polydipsia Very low BP C/O dizziness Fasting blood glucose normal No history of diabetes mellitus diabetes insipidus
Polydipsia Polyphagia Polyuria Glucosuria High fasting and post prandial glucose No insulin noted in the blood after a glucose challenge. diabetes mellitus - I
Polyuria Polydipsia Polyphagia Visual disturbances Neuropathy Patient is overweight and sedentary High fasting glucose High blood insulin levels Diabetes mellitus - II
Peripheral edema is noted BP is high Blood potassium is low Pt. C/O water weight gain hyperaldosteronism
2 posterior pituitary hormones oxytocin and ADH found here
anterior pituitary releases releasing hormones released by this organ
LH, FSH, ACTH, PRL, GH, TSH released by anterior pituitary (partial list)
vasopressin same as ADH? yes vasopressin same as ADH
Human growth hormone functions insulin-like growth hormones. stimulates the building of proteins, to maintain blood glucose levels and tissue repair. At liver it promotes conversion of glycogen to glucose.
CRH--> ACTH-->adrenal cortext to make 3 hormones *cortisol (primary) *aldosterone *androgens
TRH-->TSH-->thyroid T3/T4 if T3/T4 present, neg feedback to stop TRH. If thyroid damaged, not enough T3/T4, losts more TRH and TSH. Therefore if those levels are high and T3/T4 low, you know thyroid damaged
if adrenal cortex damaged, not enough cortisol, which inhibits CRH & ACTH called adrenal cortical insufficiency
ADH=vasopressing has mult targets kidney, sudoriferous glands, arterioles (constrict to increase bp)
RAA used when pt has: decreased bp sensed by baroreceptors in KIDNEY afferent arteriole
JG cells in kidney secrete renin
renin acts like enzyme to stim rxn of angiotensinogen --> angiotensinI
Angio I --> Angio II where in lungs, catalyzed by ACE (angiotensin converting enzyme)
Angio II acts like hormone when it binds to its multiple targets . . . *adrenal cortex to yield aldosterone to reabsorb sodium in cduct *anterior pituitary --> ADH/vasopressin-->kidney cduct --> reabsorb water *sweat glands --> decrease sweat *bvessels -->vasoconstrict
RAA also effects hypothalamus osmoreceptors as it responds to angio II and increased osmolarity (needs water)? Yes hypothalamus activated by RAA
ACE enzyme -->angio II, so if give ACE inhib would have what effect on bp lower bp (antihypertensive ACE inhib)
Aldosterone blocking drug - aldactone - it's action sodium not reabsorbed, pt diuresing
vasopressin admin to pt effect on bp would increase bp ('pressor drug')
effect of over production of renin high bp, needs antihypertensive drugs
effect of lack of ADH disease state diabetes insipidus tx with vasopressin/ADH
effect angio II on bvessels vasoconstriction bwo of binding to AngioII receptors NOT alpha receptors, which increases bp. Therefore, ATII receptor-blocker drug class = ARBS
T3/T4 targets almost all body cells, stim metab enz, increase metab, NS maturation, GI motility, skin hydration, cardiac muscle fxn, upregulates (makes more sensitive) B receptors in myocardium
hyperthroidism increased HR, BP, cell metab, heat production etc
hypothyroidism s/s dec bp, hr, feeling cold, dry skin, lethargy, weight gain
cretinism (hypothyroidism) in babies causes mental retardation
PTH secreted in response to low blood CA. *promotes increased CA by stim osteoclasts
hypocalcemia results in muscular tetany (opens Na vgates)
ANP/BNP secreted by atria/ventricles respectively in response to stretch on walls of heart (too much fluid in heart) *diminishes activity of ADH/aldosterone *increases GFR *result is diuretic effect
BNP is a marker for what disorder heart failure
What ANP/BNP want to accomplish relieving heart of xs fluid
how to treat Diabetes insipidus give pressin drug
cortisol - metabolic hormone *promotes gluconeogensis in liver (big player) *promotes lipolysis/lypogenesis, pro catab to make metab enzymes *inhibits inflammation by decreasing activity of immune cells *immunosuppressant
Cushing's Disease too much cortisol
symptoms of Cushings *hyperglycemia, loss of muscle tone, bv integrity, osteoporosis, bruising, immunosuppression, moon face/buffalo hump
Aldosterone from adrenal cortex in response to low bp and ATII, or high K levels *targets principal cells of reabsorb Na, secrete K *major regulator of fluid volume/bp
Aldosteronism too much aldosterone, usually due to cortical tumor
aldosteronism effects edema, hypertension, hypokalemia resulting in nm weakness & paralysis
Addison's decreased cortisol AND aldosterone AKA adrenal cortical insufficiency
s/s Addisons hypoglycemia, hyponatremia, hyperkalemia, HTN
Tx for Addison's give aldosterone and cortisol - dosing imp so don't induce Cushings
Epi/norep chromaffin cells in symp secreted by adrenal medulla
Insulin targets all cells but mostly liver, muscle
insulin promotes cellular uptake of glucose, glycogenesis, pro synth, lipogenesis
glucagon (alpha cells) targets hepatocytes
glucagon (beta cells) promotes gluconeogenesis and glycogenolysis
promotes increased glucose glucagon
promotes decreased glucose insulin
Type 1 diabetes B cells don't produce insulin
Type 2 diabetes cells not receptive to insulin, but cell receptors downregulated (less sensitive due to overstimulation chronic)
Tx Type II diabetes to increase receptor sensitivity *TZDs and Actos to increase receptor sensitivity *give metformin to decrease gluconeogensis *give incretin mimetics (Byeta)
incretin mimetics are drugs that act like a hormone to *incretin = GIP = glucose dependent insulinotropic (move glucose) peptide *secreted by int cell when glucose passes through *Glu-GIP leaves blood, to pancreas, which secretes insulin
Created by: lorrelaws