Busy. Please wait.

show password
Forgot Password?

Don't have an account?  Sign up 

Username is available taken
show password


Make sure to remember your password. If you forget it there is no way for StudyStack to send you a reset link. You would need to create a new account.
We do not share your email address with others. It is only used to allow you to reset your password. For details read our Privacy Policy and Terms of Service.

Already a StudyStack user? Log In

Reset Password
Enter the associated with your account, and we'll email you a link to reset your password.
Didn't know it?
click below
Knew it?
click below
Don't know
Remaining cards (0)
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


exam 4

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 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



Use these flashcards to help memorize information. Look at the large card and try to recall what is on the other side. Then click the card to flip it. If you knew the answer, click the green Know box. Otherwise, click the red Don't know box.

When you've placed seven or more cards in the Don't know box, click "retry" to try those cards again.

If you've accidentally put the card in the wrong box, just click on the card to take it out of the box.

You can also use your keyboard to move the cards as follows:

If you are logged in to your account, this website will remember which cards you know and don't know so that they are in the same box the next time you log in.

When you need a break, try one of the other activities listed below the flashcards like Matching, Snowman, or Hungry Bug. Although it may feel like you're playing a game, your brain is still making more connections with the information to help you out.

To see how well you know the information, try the Quiz or Test activity.

Pass complete!

"Know" box contains:
Time elapsed:
restart all cards