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Bio 203 endocrine
Endocrine review
| Question | Answer |
|---|---|
| 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
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