Endocrine review
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| 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
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| 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
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| 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
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| 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)
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| 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)
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| 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
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| Polyuria Polydipsia Very low BP C/O dizziness Fasting blood glucose normal No history of diabetes mellitus | diabetes insipidus
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| Polydipsia Polyphagia Polyuria Glucosuria High fasting and post prandial glucose No insulin noted in the blood after a glucose challenge. | diabetes mellitus - I
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| Polyuria Polydipsia Polyphagia Visual disturbances Neuropathy Patient is overweight and sedentary High fasting glucose High blood insulin levels | Diabetes mellitus - II
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| Peripheral edema is noted BP is high Blood potassium is low Pt. C/O water weight gain | hyperaldosteronism
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| 2 posterior pituitary hormones | oxytocin and ADH found here
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| anterior pituitary releases | releasing hormones released by this organ
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| LH, FSH, ACTH, PRL, GH, TSH | released by anterior pituitary (partial list)
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| vasopressin same as ADH? | yes vasopressin same as ADH
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| 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.
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| CRH--> ACTH-->adrenal cortext to make 3 hormones | *cortisol (primary)
*aldosterone
*androgens
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| 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
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| if adrenal cortex damaged, not enough cortisol, which inhibits CRH & ACTH called | adrenal cortical insufficiency
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| ADH=vasopressing has mult targets | kidney, sudoriferous glands, arterioles (constrict to increase bp)
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| RAA used when pt has: | decreased bp sensed by baroreceptors in KIDNEY afferent arteriole
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| JG cells in kidney secrete | renin
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| renin acts like enzyme to stim rxn of | angiotensinogen --> angiotensinI
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| Angio I --> Angio II where | in lungs, catalyzed by ACE (angiotensin converting enzyme)
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| 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
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| RAA also effects hypothalamus osmoreceptors as it responds to angio II and increased osmolarity (needs water)? | Yes hypothalamus activated by RAA
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| ACE enzyme -->angio II, so if give ACE inhib would have what effect on bp | lower bp (antihypertensive ACE inhib)
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| Aldosterone blocking drug - aldactone - it's action | sodium not reabsorbed, pt diuresing
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| vasopressin admin to pt effect on bp | would increase bp ('pressor drug')
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| effect of over production of renin | high bp, needs antihypertensive drugs
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| effect of lack of ADH disease state | diabetes insipidus tx with vasopressin/ADH
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| 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
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| 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
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| hyperthroidism | increased HR, BP, cell metab, heat production etc
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| hypothyroidism | s/s dec bp, hr, feeling cold, dry skin, lethargy, weight gain
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| cretinism (hypothyroidism) in babies causes | mental retardation
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| PTH | secreted in response to low blood CA.
*promotes increased CA by stim osteoclasts
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| hypocalcemia results in muscular | tetany (opens Na vgates)
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| 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
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| BNP is a marker for what disorder | heart failure
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| What ANP/BNP want to accomplish | relieving heart of xs fluid
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| how to treat Diabetes insipidus | give pressin drug
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| 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
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| Cushing's Disease | too much cortisol
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| symptoms of Cushings | *hyperglycemia, loss of muscle tone, bv integrity, osteoporosis, bruising, immunosuppression, moon face/buffalo hump
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| 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
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| Aldosteronism | too much aldosterone, usually due to cortical tumor
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| aldosteronism effects | edema, hypertension, hypokalemia resulting in nm weakness & paralysis
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| Addison's | decreased cortisol AND aldosterone AKA adrenal cortical insufficiency
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| s/s Addisons | hypoglycemia, hyponatremia, hyperkalemia, HTN
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| Tx for Addison's | give aldosterone and cortisol - dosing imp so don't induce Cushings
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| Epi/norep | chromaffin cells in symp secreted by adrenal medulla
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| Insulin targets all cells but mostly | liver, muscle
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| insulin promotes | cellular uptake of glucose, glycogenesis, pro synth, lipogenesis
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| glucagon (alpha cells) targets | hepatocytes
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| glucagon (beta cells) promotes | gluconeogenesis and glycogenolysis
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| promotes increased glucose | glucagon
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| promotes decreased glucose | insulin
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| Type 1 diabetes | B cells don't produce insulin
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| Type 2 diabetes | cells not receptive to insulin, but cell receptors downregulated (less sensitive due to overstimulation chronic)
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| Tx Type II diabetes to increase receptor sensitivity | *TZDs and Actos to increase receptor sensitivity
*give metformin to decrease gluconeogensis
*give incretin mimetics (Byeta)
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| 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
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