Physiology Final

anskorczewski12's version from 2016-05-18 19:53

endocrine (thyroid)

Question Answer
hypothalamus inputs hormone conc. peripheral receptors, high center (emotions), special senses (light), blood conditions (glucose con., osm, temp)
anterior pituitary derived from desmodermal cells (roof of mouth), adenohypophysis (glandular tissue), hypothalamo-pituitary portal vessels connect it
posterior pituitary neural extension of hypothalamus (neurohypophysis), supraoptic and paraventricular nucleu produce vasopressin and oxytocin for it (peptides)
tropic hormonecauses release of another hormone and growth of the receptor gland
thyroid glandcomposed of colloid-filled spheres surrounded by follicular cells
thyroid hormone made ofT4 (thyroxine, 90%, storage), T3 (triiodothyronine, active), lipophilic (stored with thyroglobulin to stay in cells)
TH production processtyrosine in thyroglobulin; iodide gets cotransported into follicular cells with Na+, gets modified, goes through channel into colloid, binds to thyroglobulin, gets endocytosed into follicular cell, clips off thyroglobulin when needed in blood
functions of TH1.affects about every cell (increase gene transcription and protein synthesis) 2.controls basal metabolic rate (high body temp by increase pump action) 3.needed for beta-adrenergic receptor expression) 4.needed for CNS development and activity (and overall growth and development)
pathway of TH controlthyrotopin-releasing hormone (TRH) to thyroid-stimulating hormone (TSH) to TH
hypothyroidismfrom low iodine, radiation, autoimmune destroy thyroid; high TRH/TSH, low BRM, fatigue, weight-gai, cold-intolerant, decreased sym (low heart rate and mental alertness); treat with more iodine and TH-imitator
cretinismhypothyroidism from birth (short)
hyperthyroidismtumors of thyroid or anterior pituitary (high TH or TSH); sleep troubles, heat production, weight loss, heart rate, mental alertness/anxiety; TH inhibitors, remove part of thyroid, radioactive iodine, beta blockers
primary hyposecretionproblem with hypothalamus
secondary hyposecretionproblem with anterior pituitary
Graves' disease(Hyperthyroidism) autoimmune, produces TSI which targets TSH (no feedback), always have goiter and exopthalmos (bulged eyes)

endocrine (adrenal)

Question Answer
adrenal cortex steroid types1.mineralocorticoids (aldosterone, mineral balance) 2.glucocorticoids (cortisol-glucose protein, lipid metabolism), sex hormone (similar to gonad hormones, most abundant DHEA) all are lipophilic, from cholesterol, not stored
pathway of cortisol1.corticotropin-releasing hormone (CRH) to adrenocorticotropic hormone (ACTH) to cortisol
cortisol functions1. create adrenergic receptors in cardiovascular system (for bp) 2.liver glucose production between meals after glycogen used up 3.decreases immune system 4.fetal development of brain, intestines, lungs, glands
effects of cortisol glucose sparing, bone resorption, support fight-or-flight, stimulates erythropoietin (replace RBC, thick blood, increase bp), immunosuppression, inhibit pain with endorphins, inhibit reproduction/growth
cortisol hyposecretionautoimmune destroy cortex, lowers bp (less water and beta receptor constriction), low blood sugar, anxiety, disturbed cardiac rhythm, fatigue, weight loss, muscle weakness/pain (low glucose), hyperpigmentation of skin
addisons diseaseprimary adrenocortical hyposeretion affecting all cortex layers (cortisol and aldosterone lowered)
secondary adrenocortical insufficiencyundersecreting pituitary or hypothalamus (low ACTH) aldosterone not affected, no pigment problem
cortisol hypersecretion(tumors of adrenal or pituitary); cushings
cushings syndrome/diseaseany hgh levels of cortisol/tumor in pituitary secreting ACTH; results in osteroporosis, thin skin, weak muscles,(steal protein from collagen) immunosupressin, increased blood sugar and bp, fat goes to neck/face
adrenal medullaconsidered a modified sympathetic ganglion that doesn't give rise to postganglionic fibers (right into blood), secretes catacholamines, releases epinephrine and norepinephrine (to adrenal receptors)
catacholamine functionreinforce SNS during stress response; dilate airways, low digestion, bladder emptying, mobilixe glucose/fatty acids, more renin (increased aldosterone), low insulin, high glucagon
major fuelscarbohydrates (run out fast, glucose stored as glycogen in liver and muscles), proteins (aa stored as proteins in muscles), fats (fatty acids of triglycerides in adipose tissues)

endocrine terms

Question Answer
anabolismbuilding up, dominant during absorptive state (fed)
catabolismbreaking down to get energy, post absorptive (4 hrs after meal)
glucose to glycogenglycogenesis
glycogen to glucoseglycogenolysis
aa/lactate to glucoseglyconeogenesis
aa to glucose and oppositeproteolysis vs. protein synthesis
fats to glucose and oppositelipogenesis vs. lipolysis
diabetes mellitus (type 1)autoimmune destroy pancreatic B cells, so no insulin, leads to extreme hyperglycemia (plugs vessels), extra mobilization and ketoacidosis, atherosclerosis, kidney failure
Diabetes mellitus (type 2)desensitized insulin receptors (from obesity/inactivity), milder, diet and exercise help
Cushing's syndromeany level of high cortisol (disease is a tumor in pituitary secreting ACTH), results in osteoporosis, thin skin, weak muscles, immunosupressin, high blood sugar, high bp, fat goes to neck and face
Grave's diseaseautoimmune, body produces TSI (targets TSH receptors, blocks from TSH, and imitates them), goiter, exopthalmos (treat with TH inhibitors, remove thyroid gland, radioactive iodine, B-blockers)
Addison's diseaseprimary adrenocortical hyposecretion affecting all cortex layers (so it affects cortisol and aldosterone)
celiac diseasedestroyed brush border (less absorption)
gallstonesout of control cholesterol secretion from liver
xerostomiadry mouth
pernicious anemialack of intrinsic factor (from parietal cells)

GI system

Question Answer
wall layersmucosa (muscous membrane-endo&exocrine cells, lamina propria-blood vessels, muscularis mucosa), submucosa (specialized immune cells, submucosal plexus), muscularis externa (circular, longitudinal, myenteric plexus), serosa (connects to mesentery to peritoneum to cavity wall)
sphinctersupper esophageal (skeletal); lower esophageal (smooth); pyloric; ileocecal (relaxes after meal); internal and external anal; ALSO sphnicter of Oddi (from liver & pancreas to SI)
regulation of processes1.local changes in tract (osmoreceptors/mechano/chemo) cause intrinsic nerve plexuses, extrinsic autonomic nerves, and gastrointestinal hormones from mucosa; 2.external influences trigger extrinsic autonomic nerves (which can then modify others); 3.smooth muscle can self-excite when food present
dry mouthxerostomia
stomach partsfundus; body (where mucus/hydrochloric acid/pepsinogen secreted); antrum (thick smooth muscle, controls movement through pyloric sphincter, some secretions)
secretion areas of stomach1.oxyntic mucosa (has mucus cells, chief cells-pepsinogen, and parietal cells-hydrocholic acid) 2.pyloric gland area (no acid secretion; G cells-stimulate acid production; D cells-inhibit acid; ECL cells-secrete histamine, an acid enhancer)
chymegastric juice and bolus
factors stimulating/inhibiting acid secretion in stomachstimulate (1.gastrin from G cells 2.histamine from ECL cells 3.Ach from parasympathetic input--all add more pumps to parietal cells); inhibit (somatostatin from D cells; and antihistamines)
pernicious anemialack of intrinsic factor from parietal cells (so you can't absorb vitamin B12, which is required for RBC production)
factors affecting stomach from digestion1.luminal membrane impermeable to HCL (no transporters) 2.tight junctions 3.mucus coating buffers pH 4.mucus is a physical barrier 5.high turnover when degradation happens
enterogastric reflexthe intrinsic plexus and autonomic nervous system
what does the stomach absorbalcohol (more slowly than SI) and aspirin (weak acids)

SI and LI

Question Answer
small intestine partsduodenum, jejunum, ileum, ileocecal sphincter
succus entericuswater, mucus, bicarbonate, and NaCl that move things along and neutralizes acid (high NaCl helps secondary active transport of glucose and amino acid)
celiac diseasedestroyed brush border, so less absorption in small intestine
migrating myoelectric complexafter a meal, intense peristaltic contractions begin in stomach and keep pushing food through (stops when eat again)
bilecontains bicarbonate to neutralize acid, phospholipids and bile salts to emulsify fats and help prevent fat globules from reassembling so they can be digested (forms Micelles), cholesterol, bile pigments (form RBC breakdown), organic waste
micellesbile salts form huddle with hydrophilic parts out, so can dissolve water-insoluble substances (like fats and cholesterol) and transport them through luminal contents
enterohepatic circulationbile salts enter duodenum (for digestion, absorption) go into blood, into hepatic portal system, into liver, and then into bile (gall bladder stores and concentrates bile)
CCKstimulates enzyme secretion from pancreas, gallbadder contraction to deliver more bile and sphincter of Oddi relaxes to deliver enzymes and bile salts (comes from duodenal mucosa)
haustracontractions of smooth muscle in LI
valsalva maneuverabdominal muscles contract, increasing pressure to push out feces