Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
physiology
exam 4
| Question | Answer |
|---|---|
| Thyroid gland produces what hormones | T3 and T4 |
| T3 full name | Triiodothyronine. Active form |
| T4 full name | Thyroxine. Higher concentration in blood b/c converted to T3 in tissue |
| Overall functions of T3 and T4 | 1. increase rate of basal oxygen use 2. increase met 3. increase rate of heat prod 4.modulate delivery of substrates and O2 by cardiovascular and respiratory system. sustain metabolic rate |
| Thyroid hormone levels change based on what | every need, calorie supply, env temp |
| what do you need for thyroid syn | 2 tyrosines and iodine |
| When is reverse T3 produced | when less thyroid hormone action is needed |
| what enzyme converts T4 to T3 | 5'deiodinase enzyme |
| what is the cellular structure of single-layer circular follicles | cuboidal endocrine cells surrounded by basement mem |
| cellular structure of lumen of follicle | colloid material |
| what is colloid material | newly syn, stored hormones attached to thyroglobulin |
| what happens to colloidal thyroid hormone if understimulated | it is absorbed into follicular cells |
| Parafollicular cells (C cells) secrete what | calcitonin |
| where does the iodine come from to syn thyroid hormones | the diet. amount transported via Na/I symporter depends on dietary intake. if diet has low amount the symporter is activated |
| How is thyroglobulin syn | from tyrosine. syn on RER and golgi. put into follicular lumen. |
| How are thyroid hormones bound to thyroglobulin | peptide link |
| how is iodide transported from blood into follicular epithelial cells | via 2Na+/1 I- symporter. |
| How is Iodide transported across the apical mem into the colloid of follicles | pendrin where they are then oxidized to iodine via |
| what enzyme oxidizes iodide to iodine | thyroidperoxidase |
| wolff-chaikoff effect | transient reduction in thyroid hormone levels b/c ingestion of large amt of iodine. |
| how long does the wolff-chaikoff effect last | about 10 days |
| why (physiology) does the wolff-chaikoff effect happen | excess dietary iodide suppresses activity of 2Na/1 I pump. hyperthyroid in cats. |
| what enzyme incorporates iodine into tyrosine in thyroglobulin | thyroidperoxidase. results in MIT and DIT |
| what molecule combine to form T4 | 2 DIT |
| what molecules combine to form T3 | 1 DIT and 1 MIT |
| ratio of T4:T3 within gland | 10:1 |
| Thyroglobulin is stored as what until stim of release | stored as colloid in follicles |
| How is thyroglobumin retrieved from follicle when stimulated | endocytosis via pseudopods |
| How are T3, T4, MIT, and DIT released from thyroglobulin | lysosomes fuse with colloid droplet |
| when T3 and T4 are released into blood what happens to DIT and MIT | they are rapidly deiodinated by deiodinase enzyme. recycle iodine |
| Circulating T3 and T4 are higher in large or small breeds | small breeds |
| What happens to circulating T3 and T4 levels as animals age | decreases with age |
| What proteins are circulating T3 and T4 bound to | 1.TBG 2.Transthyretin 3.Albumin |
| why are T3 and T4 bound to proteins while circulating | to buffer against acute changes in thyroid gland function. helps with reg. so much can be bound at once what happens at tissue level may be unaffected even if thyroid stops working |
| TBG | Syn in liver. around 70% T4 and T3 bound |
| what are the effects of hepatic failure on circulating thyroid hormones | 1. decrease amt of binding protein 2. more free circulating therefore degraded more 3. buffering and control very affected! |
| Sick euthyroid syndrome | circulating levels of T3 and T4 abnormal, thyroid gland doesnt appear abnormal. dysreg of thyrotropic feedback control. set point of thyroid homeostasis has changed |
| what conditions cause sick euthyroid syndrome | fasting/starvation. stress (cortisol). catabolic diseases. hepatic diseases. renal disease. |
| in sick euthyroid syndrome what enzyme is not functioning properly | low levels of 5'deiodinase enzyme. not converting T4 to T3 |
| TSH inhibition | 1. neg feed back on AP 2.cortisol and GH |
| TSH is tonically inhibited by | dopamine and somatostatin |
| which subunit allows TSH to be bioactive | Beta subunit |
| Is TRH a tripeptide or glycoprotein | tripeptide |
| is TSH a tripeptide or glycoprotein | glycoprotein with 2 subunits (alpha and beta) |
| Sustained exposure to TSH causes | hyperplasia, hypertrophy of follicular cells. increase in ER, ribosomes, etc |
| Absence of TSH causes | gland atrophy |
| How do the trophic effects of TSH occur | through IGF |
| effect of thyroid hormone when fasting | low metabolic rate. TSH response to TRH will diminish and T3 falls |
| effect of thyroid hormone after having meal or cold exposure | Increase T3 availability |
| function of 5'deiodinase | converts T4 to T3 inside cells |
| function of 5 deiodinase | converts T4 to rT3 |
| effects of starvation on activation of T4 to T3 in target tissues | inhibit 5'deiodinase. brain 5'deiodinase is not affected b/c brain has priority |
| what organs are major sites of degradation of thyroid hormones | liver, kidney, skeletal muscle. some T4 excreted in bile |
| if more thyroid hormone is needed is more T3 or rT3 expressed | more T3 relative to rT3 |
| what does T3 bind to on DNA to stim transcription | thyroid regulatory element |
| T3 stim generally leads to syn of what things | 1. making more Na/K ATPase therefore increase BMR and O2 consumption 2.Transport proteins 3.B1 adrenergic receptor (increase HR) 4.Proteolytic enzymes 5.structural proteins |
| cardiovascular effects of thyroid hormone | increase cardiac output and pulse pressure. increased syn of B-1 adrenergic receptors |
| thyroid effects on BMR | 1. increased O2 consumption and increased Na/K ATPase 2.cardiovascular effects 3.increase thermogenesis |
| thyroid effects on metabolism | 1. increase supply of substrates for prod of energy 2.increase appetite, gut absorption and motility 3. increase mobilization of carbs and fat |
| why does thyroid hormone increase supply of substrates for energy prod | needed for oxidation. increase glucose from liver and gut (increase absorption) |
| why does thyroid hormone increase appetite, gut absorption and motility | need for increase lipolysis and FFA ox |
| thyroid hormones at phys level promote protein syn or degradation | protein syn dominates |
| thyroid hormones at high level promote protein syn or degradation | protein degradation dominates |
| effects of thyroid hormone on growth | required for normal growth. Act with GH, IGF to promote growth of bone, cartilage, teeth, epidermis, hair |
| effects of thyroid hormone on CNS | essential for normal maturation of CNS. increase blood flow and glucose met of brain. enhance peripheral nerve reflexes. activating skeletal muscle and deep tendon reflexes. |
| effects of thyroid hormone on ANS | interact with sympathetic nervous system to have similar effects on increasing cardiac output, head prod, etc |
| symptoms of hyperthyroidism | increase metabolic rate, food intake, heat prod, heart rate, weight loss, muscle weakness, atrophy |
| if hyperthyroidism is caused by thyroid gland what is seen | TSH low. T3, T4 levels high. neg feedback needed to decrease TSH |
| if hyperthyroidism is causes by hypo or pit what is seen | TSH high. T3, T4 level high. |
| hyperthyroidism in cats is most likely caused by what | disruptors in env |
| hyperthyroidism in dogs and horses is most likely caused by what | thyroid adenocarcinoma |
| symptoms of hypothyroidism | decrease metabolic rate, cardiac output, cold intolerance, decreased sweating, weight gain |
| congenital cretinism | thyroid dwarf. lacking enzymes to make thyroid hormones. ex thyroid peroxidase |
| if hypothyroidism is causes by hypo or pit what is seen | TSH low. central hypothyroidism |
| if hypothyroidism is caused by thyroid gland what is seen | TSH high. overt primary hypothyroidism. T3 and T4 levels low. very little if any feedback. |
| where are the adrenal glands located | retroperitoneal cavity above each kidney |
| what does the adrenal cortex of the adrenal gland produce | mineralcorticoids, glucocorticoids, androgens |
| what does the adrenal medulla of the adrenal gland produce | epinephrine and norepinephrine |
| where are chromaffin cells found | adrenal medulla |
| what do chromaffin cell secrete | catacholamines (epi and norepi) |
| where does the adrenal medulla receive input from | sympathetic nervous system via preganglionic fibers originating in the thoracic spinal cord |
| what receptors does epi act on | all alpha (1 and 2) and beta (1 and 2) adrenergic receptors |
| what receptors does nor epi act on | alpha (1 and 2) and beta (1 |
| what is the predominant catechlamine syn in adrenal medulla | epi (80%). nor epi (20%) |
| what enzyme converts Nor epi to epi under the influence of cortisol | PNMT. |
| all epi originates from where | adrenal medulla |
| Most NE originates from where | sympathetic nerve terminals and brain |
| target tissues of catecholamines | muscle cells and liver (increase gluconeogenesis). fight or flight need glucose |
| catecholamines are primarily metabolized where | in liver and kidneys |
| effects of catecholamines | 1. incresaed heart rate, cardiac output, and blood pressure 2. redistribution of blood towards skeletal muscle 3.increased respiration 4. increased blood glucose |
| adrenal cortex physiological functions | 1. blood glucose regulation 2.protein turnover 3.fat metabolism 4.Na/K/Ca balance 5.cardiovascular maintenance 6.modulate tissue response to injury/infection |
| zona fasciculata is responsible for | where cortisol and corticosteron produced |
| what occurs in the zona reticularis | androgen precursors (DHEA and androstendione) are converted to testosterone and estrogen in peripheral tissue |
| what is the common precursor for all steriods | cholesterol |
| the reaction to produce steroid hormones uses what enzyme | cytochrome P450 in mitochondria and endoplasmic reticulum |
| what is the first step (rate limiting) in steroid hormone production | conversion of cholesterol to pregnenolone. |
| what enzyme is needed for the rate limiting step of steroid hormone production | cholesterol desmolase |
| what occurs in the zona glomerulosa | production of mieralcorticoids (aldosterone) |
| what is required for aldosterone production | ACTH to sim cholesterol desmolase. requires aldosterone synthase |
| aldosterone does what | long term regulation of blood pressure. diurnal pattern |
| Aldosterone primary regulation | changes in ECF volume via renin-angiotensin II aldosterone system. changes in blood K |
| Aldosterone is transported via | in blood via aldosterone binding globulin, transcortin, albumin |
| what happens if you don't have aldosterone | will die b/c can't regulate ECF |
| what happens if you have too much aldosteron | hypertension and increase BP |
| how does aldosterone change ECF volume | NA reabsorption by kidney, H2O follows. increase in blood K |
| first step of glucocorticoid syn needs what enzyme | 17a hydroxylase |
| the last step of glucocorticoid syn needs what enzyme | 11B-hydroxylase |
| what does 11B-hydroxylase do | converts 11 deoxycortisol to cortisol |
| cortisol is transported in blood via what | transcortin |
| where is cortisol metabolized | liver and excreted in urine as glucuronides |
| stim ACTH secretion | stress, low cortisol, ADH, hypoglycemia, infection, fever |
| inhibit ACTH secretion | high cortisol, exogenous sterioids, somatostatin, dopamine |
| long term administration of exogenous corticosteroids does what | creates artificial negative feedback resulting in adrenal gland atrophy |
| cortisol binds what type of receptor | Type II glucocorticoid receptor in cortisol |
| general effects of cortisol | "premissive". only free cortisol is biologically active |
| what is a permissive hormone | doesn't directly initiate actions but allows critical processes to occur. amplifies action of other hormones |
| the net effects of cortisol are anabolic or catabolic | catabolic. break down stored compounds for energy |
| cortisol increases BG by | 1.increasing gluconeogenesis 2.increasing glucagon release from pancreas to allow glycogenolysis 3.temporary causing insulin resistance in tissues |
| how does cortisol temporarily cause insulin resistance | tissues don't take up as much glucose. decrease translocation of glc transporters into cell mem |
| what are the effects of cortisol on energy met | 1.increase BG 2.increase glycogenesis 3.increase lipolysis and protein catabolism 4.increase appetite, visceral obesity |
| what are the effects of cortisol on muscloskeletal system | 1. increase protein catabolism 2.bone 3.connective tissue |
| what are the effects of cortisol on bone | 1.inhibits bone formation 2.increases bone resorption 3.causes osteoporosis |
| what are the effects of cortisol on connective tissue | 1.inhibits collagen syn 2.causes thin skin and fragile capillaries |
| effects of cortisol on kidneys and cardiovascular system | 1.water balance 2.maintain normal BP and volme 3.upreg a-1 adrenergic receptors |
| how does cortisol regulate water balance | increase golmerular filtration rate in kidney. decrease ADH (more dilute urine) |
| why is the upreg of a-1 adrenergic receptors via cortisol regulate kidneys and cardiovascular | necessary for vasoconstrictive response of arterioles to NE and epi |
| effects of cortisol on the immune system | 1.suppresses immune response 2.decrease neutrophil activity, formation of cytokines, T cells, AB formation |
| how does cortisol suppress immune responses | 1. suppresses prostaglandins, thromboxanes, leukotrienes 2.induce lipocortin 2.inhibit production of IL2 3.inhibit release of histamine |
| what enzyme is needed for androgen formation | 17,20 lyase |
| what are the causes of cushings | 1.PDH with bilateral adrenal hyperplasia 2.pars intermedia dysfunction 3.adrenal tumors 4.latrogenic hyperadrenocorticism resulting from chronic excessive exogenous steroid administration |
| PDH | Pituitary dependent hyperadrenocorticism. excess cortisol. pit adenoma secreting excess ACTH. middle age-older dogs |
| cushings symptoms in dogs | polydipsia, polyuria, panting, obesity, muscle weakness, alopecia, thin skin |
| causes of addisons disease | auto immune, infiltrative disease, idiopathic, iatrogenic steroids |
| addisons disease clinical | loss of aldosterone, increase K, decrease blood volume, decrease Na, bradycardia, irregular heart beat, circulatory collapse. loss of cortisol (decrease gluconeogenesis and BG) |
| primary hyperaldosteronism | idiopathic adrenal hyperplasia (usually bilateral). tumor |
| secondary hyperaldosteronism | the result of something else. liver or kidney disease. end in heart failure. |
| hyperaldosteronism symptoms | more common in cats. increase ECF volume, increase renal perfusion pressure therefore inhibits renin secretion |
| hyperaldosteronism treatment | spironolactone (aldosterone antagonist) |
| Alopecia X | atypical hyperadrenocorticism. elevation in androgens and/or sex sterioids. |
| breeds most commonly affected with alopecia X | pomeranians, poodles, yorkies, nordic breeds. affects both sexes, may start as early as 1 yo |
| endocrine pancreas is what percent of pancreatic mass | 1-2%. other 98% have exocrine function. |
| Beta cells | 65%. insulin. take up glucose in fat and muscle |
| alpha cells | 20%. glucagon. increase BG |
| delta cells | 10%. somatostatin. inhibit insulin and glucagon release |
| central core of islet is composed of what cell type | B cells |
| gap junctions in islet cells | connect alpha cells to each other, beta cells to each other, and alpha to beta cells |
| blood supply to pancreas | arranged so that venous blood from each cell type bathes other cell types |
| what innervates pancreatic islets | adrenergic, cholinergic and peptidergic neurons |
| insulin syn | 1.preprohormone with 4 peptides 2. proinsulin sent to ER, insulin folds, disulfide bridges form 3.golgi packages into granules, protease cut C peptide |
| glucose is transported into beta cells with what transporter | GLUT2. does not need insulin to work. allows glucose to enter cell via facilitated diffusion |
| what is the product of glucose phosphorylation by glucokinase | ATP that closes ATP sensitive K channels that depolarizes membrane. |
| why is the increasing intracellular Ca important with insulin secretion | signal needed to cause exocytosis of glucose granules into venous blood |
| why does oral glucose cause the greatest insulin response | incretin effect. substances that are generally other hormones |
| stimulate insulin secretion | AA, ketoacids, FFA, K, Ca, GIP, vagal stim, sulfonylurea drugs, glucagon |
| inhibits insulin secretion | fasting, exercise, somatostatin, leptin |
| insulin receptor is what receptor type | tyrosine kinase |
| when nutrients are available what is the effect of insulin | makes sure those nutrients are stores. glucose stored as glycogen in muscle and liver, FFA stored as adipose tissue, protein stored in muscle |
| insulin directly stim glucose uptake where | in muscle and fat |
| insulin independent transporters | GLUT1, GLUT2 |
| Where is GLUT1 found | brain and RBC |
| Where is GLUT2 found | liver, B cells of pancreas |
| insulin dependent transporters | GLUT4 |
| Where is GLUT4 found | fat, muscle, heart |
| where is GLUT5 found | intestine |
| actions of insulin | 1.decrease blood glucose 2.increases glucose transport into muscle and adipose 3.promotes glycogen formation in liver and muscle 4.inhibits gluconeogenesis and glycogenolysis |
| effects of insulin on lipid metabolism | 1.inhibits mobilization and oxidation of FA 2.inhibits ketogenesis in liver 3.promotes FFA storage as triglycerides 4.inhibits FFA uptake in muscle 5.inhibits lipolysis |
| effects of insulin on protein metabolism | 1.decrease blood AA 2.increase AA and protein uptake by tissues 3. increase protein synthesis 4.inhibits protein degradation |
| action of insulin with K | promotes K uptake into cells by increasing activity of Na/K ATPase |
| action of insulin with phosphate and Mg | promotes uptake into cells |
| action of insulin on appetite | decreases appetite via satiety center of hyo |
| excess insulin causes | hypoglycemia, that stim cortisol release to increase appetite |
| insulinoma | excessive insulin production by Beta cell tumor |
| hyperglycemia result as lack of insulin | cells starve, blood hyperosmolality, osmotic diuresis in kidneys. |
| why does hyperglycemia occur as lack of insulin | b/c cells don't take up glucose and hepatic output of glc increases. not getting normal cell response to existing glc. |
| why does blood hyperosmolality occur as lack of insulin | glc doesn't leave. water increase BP |
| hyperlipidemia result as lack of insulin | increased oxidation of fat, fat accumulation in liver. increase lipolysis and decrease lipid uptake |
| why does osmotic diuresis in kidneys occur as lack of insulin | all this glucose filtered in nephron. glc spills into urine, followed by water |
| peripheral tissue protein catabolism occur as lack of insulin | peripheral tissue protein catabolism. muscle wasting and weight loss. |
| why does peripheral tissue protein catabolism occur as lack of insulin occur | increase in gluconeogenesis and decrease AA uptake by cells. some AA are glucogenic therefore muscle wasting |
| inhibits glucagon | glc, insulin, somatostatin |
| glucagon is secreted where | alpha cells of pancreas |
| glucagon is synthesized as | preproglucagon. stored as glucagon in granules until release |
| stim glucagon | hypoglycemia, protein/AA (ala, arg), fasting, stress, intense exercise, cholecystokinin |
| when is cholecystokinin releases | in response to protein and fat ingestion |
| glucagon works through what receptor type | G-protein/cAMP |
| effects of glucagon | increase glycogenolysis, gluconeogenesis, lipolysis, ketoacid formation |
| glucagonoma | tumor of alpha cells in pancreas. low blood AA, increased glucagon, anemia, diarrhea, wt loss. |
| result of glucagonoma | diabetes mellitis and necrolytic migratory erythema |
| hyperglucagonemia/diabetes mellitis associated with infection | glucagon:insulin ratio increased |
| somatostatin | secreted by delta cells of pancreas and the hypo. stim by all nutrients, inhibited by insulin |
| somatostatin inhibits | insulin and glucagon, GI hormones, GI motility, enzymes, gastric acid secretion |
| leptin | inhibits appetite by binding neuropeptide Y. increases BMR. leptin resistance may contribute to obesity. |
| adiponectin | improves insulin sensitivity. |
| high adiponectin | low risk of type II diabetes |
| low adiponectin | obesity and diabetes |
| what are the regulatory systems that maintain extracellular fluid levels of Ca and P | vitamin D, parathyroid hormone, calcitonin |
| processes that involve Ca | neutrotransmission, learning and memory, muscle contraction, mitosis, mobility, secretion, fertilization, blood clotting, structure of bones and teeth |
| extracellular Ca | higher Ca concentration via CaATPase pump and Ca/Na exchange. 50% ionized and bio active. 40% bound protein, 10% complexed |
| intracellular Ca | lower Ca concenration. bound to proteins. cytosolic Ca can be increased as needed (fine control) |
| how is Ca balance maintained | if Ca intake goes down, body adjusts by increasing percentage of Ca absorbed |
| Hypocalcemia | decreases in plasma Ca. |
| causes of hypocalcemia | lactation, parathyroid, vit D disorders, gut malabsorption of Ca, renal failure, ethylene glycol toxicity |
| hypocalcemia causes what | twitching/cramping of skeletal muscle, numbness/tingling (paresthesia), seizures |
| hypercalcemia | increase in plasma Ca |
| causes of hypercalcemia | parathyroid disorders, Vit D toxicity, renal failure |
| hypercalcemia causes what | constipation, polyuria, polydipsia, lethargy, coma, death |
| how is the amount of Ca in plasma regulated | 1.changes in plasma protein concentration 2.changes in complexing anion concentration 3.acid-base disturbances |
| effects of acid-base disturbances on ionized Ca concentration | change the fraction of Ca bound to plasma albumin. |
| what does albumin bind | either H or Ca ions |
| Acidemia | more H ions in blood, more H ions bind to albumin, free ionized Ca increases |
| Alkalemia | less H ions in blood, more Ca blinds to albumin, ionized Ca in blood decreases |
| where does phosphate come from | absorbed form diet |
| how is P regulated | urinary excretion changes |
| where is P stored | in muscle and bone |
| when is Mg necessary | neuromuscular transmission |
| where is Mg secreted | in urine |
| dietary Mg absorption | absorbed by gut is enhanced by Vit D |
| what cells secrete PTH | chief cells |
| parathyroid hormone is syn as | preproparathyroid hormone |
| role of PTH | regulates plasma Ca and P. sustain/increase plasma Ca, decrease/prevent increase in plasma P. stim bone resorption, stim reabsorption of Ca from kidney, increase P excretion in urine |
| when is the Ca receptor on parathyroid cells activated | when plasma Ca falls, PTH containing granules exocytosed. inhibited with high plasma Ca |
| increased blood phosphate increases PTH secreions via what receptor | P receptor |
| stim of PTH release | 1.decrease blood Ca 2.increase blood phos 3.decrease Mg |
| PTH stim what | Vit D, which ultimately feeds back and decreases PTH secretion. |
| inhibition of PTH release | increases blood Ca |
| PTH uses what receptor type | G protein/cAMP |
| primary Hyperparathyroidism is causes by | benign tumor or hyperplasia of one or both parathyroid glands. |
| symptoms of primary hyperparathyroidism | increase PTH, increase Ca, decrease P, renal calculi, bone weakness, and susceptible to fractures |
| secondary Hyperparathyroidism is causes by | caused by increased phos in blood, which precipitates Ca and results in hypocalcemia. secondary increase in PTH. renal failure or increase dietary phos |
| hypoparathyroidism is caused by | accidental surgical removal, autoimmune destruction, idiopathic |
| hypoparathyroidism results in | decreased PTH, hypocalcemia, hyperphosphatemia |
| what cell type secreted calcitonin | parafollicular cells of thyroid gland |
| how does calcitonin decrease Ca and P | 1.inhibiting bone resportion 2. increasing urinary P excretion 3.inhibiting renal reabsorption of Ca |
| stim calcitonin | 1.increase blood Ca 2. Vit D 3. ingested food. absorbing Ca therefore no need to release from bone or reabsorbed in kidney |
| what is Vit D needed for | bone formation and increases in Ca absorption from GI tract |
| Vit D3 comes from where | hormone, syn in body |
| Vit D2 or D3 comes from where | vitamin, diet |
| where in the body is Vit D syn | skin |
| what is Vit D converted to in kidney | 1,25 dihydroxyvitamin D (bioactive) |
| where can Vit D be stored | adipose and liver |
| Vit D toxicity result | hypercalcemia, renal failure, elevated phos |
| actions of Vit D | stim Ca absorption via calbindin, stim absorption of phos and Mg |
| Vit D interaction with Ca and P | weakly stim Ca and P reabsorption in kidney |
| active Ca absorption | Ca intake low, transcellular process dominates. duodenum. need Vit D |
| passive Ca absorption | Ca intake high, paracellular process dominates |
| transcellular Ca absorption | vit D acts through cytosolic receptor and increases prod of calbindin |
| calbindin | binds Ca inside cells and facilitates transport to basolateral mem |
| effect of Vit D in presence of PTH | stim bone resorption |
| effect of Vit D in skeletal muscle | increases Ca transport and uptake by SR |
| effects of vit D deficiency | like Ca deficiency. muscle weakness, rickets, bone fractures, cardiac dysfunction |
| where is melatonin produced | pineal gland located behind 3rd ventricle. |
| melatonin is syn from | tryptophan, serotonin as intermediate |
| melatonin stim | darkness. retinal photoreceptors release nor epi, activates beta-adrenergic receptors in pineal gland. serotonin converted to melatonin |
| melatonin inhibition | retinal photoreceptor cells become hyperpolarized, inhibits release of nor epi |
| circadian rhythm of melatonin secretion is controlled by what | pace maker in the supra-chiasmatic nucleus |
| melatonin secretion peak | 2-4am |
| melatonin receptor | MT1 and MT2. G protein coupled |
| melatonin regulates/affects | sleep, circadian rhythm, mood, sexual maturation and reproduction, may have anti-inflammatory effects on immune system, may have beneficial effects on cancer, aging |
| what happens to melatonin amount as we age | decreases. may decreases cell damage from free radicals |
| melatonin as a treatment for Alopecia X in dogs | may decrease GnRH, decreases LH/FSH effects on adrenal androgen precursors. |
| omega 3 EFAs | derived from eicosapentaenoic acids. less inflammatory |
| omega 6 EFAs | derived from arachidonic acid. pro inflammatory |
| omegs 3 derivatives | prostanoids, leukotrienes. odd number double bonds |
| omega 6 derivatives | prostanoids, leukotrienes. even number double bonds |
| eicosapentaenoic acid | formed from omega 3. forms mostly prostanoids |
| eicosapentaenoic acid major function | dampen inflammatory effects of arachidonic acid prostanoids |
| arachidonic acid | formed from omega 6. prostanoids, leukotrienes, lipoxins |
| arachidonic acid major function | inflammatory response, modulate pain and fever, repro function, inhibiting gastric acid secretions, BP reg, platelet activation/inhibition |
| dietary precursors of arachidonic acid | linoleic acid, gamma linolenic acid. |
| why can't cats convert linoleci acid to arachidonic acid | low 6-desaturase enzyme |
| what enzyme releases arachidonic acid from phospholipids in cell mem | phospholipase A |
| arachidonic acid is oxygenated by | cyclooxygenase (COX1/2) to make prostanoids. Lipooxygenase (5LOX) to make leukotrienes |
| PGE2 | Smooth muscle contraction, pain, heat, fever, bronchoconstriction |
| PGI2 | Vasodilation, inhibits platelet aggregation |
| TXA2 | vasoconstriction, stim platelet aggregation |
| NSAIDs that inhibit COX1/2 | aspirin, carprofen, flunixin, phenylbutazone, ibuprogen, naproxen |
| NSAIDs that inhibit only COX2 | less side effects. firocoxib, deracoxib, meloxicam, piroxicam, celecoxib |
Created by:
ejohnson17
Popular Veterinary sets