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Pharmacology Drgus10
Thyroid/Anithyroid-Equine Obesity
| Question | Answer |
|---|---|
| what are some treatment options for cats with hyperthyroidism? | surgery, radioactive iodine therapy, medical management |
| what are three main classes of antithyroid drugs? | thiourylene, cholecystographic contrast agent antithyroid drugs, stable iodine |
| what are three thiourylene drugs and which is the most commonly used one? | Propylthiouracil; Thiamazole (methimazole); Carbimazole; thiamazole most commonly used in US |
| what are the thiourylene drugs derived from and how do they work (MOA)? | derived from thiouricil; inhibit thyroid hormone synthesis by: 1.) Preventing the organification of iodide, 2.) Preventing the coupling of iodothyronines to form T4 and T3 in the thyroid, 3.) May inhibit thyroid peroxidase |
| which thiourylene drug prevents the conversion of T4 to T3? | propylthiouracil |
| which thiourylene drug has a transdermal preparation? | thiamazole |
| what are the two drugs that are classified as cholecystographic contrast agent antithyroid drugs? | Na/Ca ipodate; Iopanoic acid |
| what is the MOA of cholecystographic contrast agent antithyroid drugs? | Inhibits outer-ring 5’ deiodination of T4 to T3 |
| Do the cholecystographic contrast agent antithyroid drugs decrease T4 concentrations? | NO |
| would you monitor concentrations of T3 or T4 with administration of cholecystographic contrast agent antithyroid drugs? | T3 |
| what is the method of action of stable iodine? | Inhibits thyroid peroxidase and release of thyroid hormone from the thyroid. Transient decrease in thyroid hormone production |
| what are the side effects of thiourylene antithyroid drugs? | anorexia, lethargy, vomiting, facial and cervical excoriation, bone marrow suppression, IMHA, Coagulopathy, Hepatotoxicity, ANA (without signs of lupus), Myasthenia gravis, cold agglutinin-like disease, bleeding |
| when administering thiourylene antithyroid drugs, what do you measure to determine if the drug is working? | T4 concentrations |
| what are some treatment options for an animal with hypothyroidism? | Synthetic L-tri-iodothyronine; Synthetic Levothyroxine; Natural T4 |
| What is the most commonly used drug used to treat hypothyroidism? | Synthetic levothyroxine- aka- L-thyroxine, thyroxine, T4 |
| Synthetic levothyroxine is a synthetic T4. Should you monitor both T4 and T3 levels or just one or the other and why? | monitoring T4 levels should be sufficient b/c T4 can still be converted to T3; should see a normalization of both T4 and T3 after treatment |
| should synthetic levothyroine be given with a meal? | no |
| if you increase the dose of synthetic levothyroxine, what happens to the biological half life of the drug? | it decreases |
| why is Synthetic L-tri-iodothyronine not commonly used to treat hypothyroidism? | larger risk of thyroid toxicity b/c administering T3 |
| under what circumstances would you elect to use Synthetic L-tri-iodothyronine? | in a dog that cannot convert T4 to T3 |
| when treating a hypothryoid dog with sythetic levothyroxine, you monitor T4 levels. Where do you want T4 concentrations to be? | upper 50% but not higher |
| when do you begin evaluating T4 after administering synthetic levothyroixine to determine if treatment is working? how long should you monitor? | start 4wks after initiating therapy, 4-6 hrs post pill; then, every 6-12 mo after optimum dose is determined; this is a lifelong commitment |
| what is one finding that is consistent with t4 toxicity? | pu/pd |
| what is the basic structure of a glucocorticoid steroid? | 17 carbon atom with steroid nucleus |
| if you were to alter ther steroid nucleus of a glucocorticoid, what would you expect in return? | may suppress or enhance certain features of that glucocorticoid |
| what would you expect to see happen if you altered the esterification of a glucocorticoid? | change solubility or alter duration of action |
| what are two desired effects of glucocorticoid use? | anti-inflammatory; immunosuppressive |
| how do steroids work to alter the function of a cell? | altering gene transcription and protein production |
| what are the metabolic effects of glucocorticoids? | Gluconeogenesis; Increase glycogen storage; Blunt the effect of insulin; Induce protein catabolism; Lipolysis leads to release of FFA |
| which hormones will have decreased release with glucocorticoid administration? | TSH, ACTH, LH, Prolactin, FSH |
| why does an animal often have PU/PD with glucocorticoid administartioN? | the secretion and sensivity of ADH is decreased |
| is it wise to vaccinate an animal when its on a glucocorticoid regimen? Why/Why not? | Yes; glucocorticoids only suppress T-cell activity (cell-mediate), not B-cell activity. Since B-cell (humoral) function isn't altered, an animal can still respond to the vaccination protocol. |
| when administering glucocorticoids, what leukogram would you expect to see? | stress leukogram |
| when would we elect to use glucocorticoids? | Immune mediated disease; Inflammatory disease; Hypoadrenocorticism; Some forms of neoplasia; Dynamic testing for endocrine disease |
| which has a longer half life: biological or synthetic glucocorticoids? | synthetic |
| what are two glucocorticoids used frequently with the longest half-lives? | dexamethasone, betamethasone |
| what are two glucocorticoids that require liver metabolism to be active and what are the active forms? | cortisone--> cortisol; prednisone--> prednisolone |
| what determines the bioavailability of glucocorticoid moieties? | esters |
| what ester side would a fast release glucocorticoid contain? | succinate or hemisuccinate or phosphate |
| what ester side would a moderate release glucocorticoid contain? | acetate, diacetate, tebutate |
| when making a formulation, would you want a fast acting or slow acting glucocorticoid? | Use the shortest release preparation possible |
| what do you have to consider when deciding to use a a fast vs slow release glucocorticoid preparation? | bioavailability; it will begin to vary with a longer release preparation |
| what is the physiologic dose of prednisone in dogs and cats? | 0.1-0.25mg/kg/d |
| what is the anti-inflammatory dose of prednisone in dogs? | 0.5-1.0mg/kg/d |
| WHAT is the anti-inflammatory dose of prednisone in cats? | 0.5-1.5mg/kg/d |
| what is the immunosuppressive dose of prednisone in dogs? | 2.0mg/kg/d |
| what is the immunosuppressive dose of prednisone in cats? | 10mg/cat/d or 2-4mg/kg/d |
| if you wanted to give dexamethasone instead of prednisone, what do you have to keep in mind? | dexamethasone is 8X stronger than prednisone. If you want to dive dexamethasone, divide the prednisone dose by 8 |
| why would you not want to give corticosteroids for more than 2 weeks? | concern of adrenal gland atrophy |
| why would you not give glucocorticoids with NSAIDS? | increase in GI ulcers |
| why would you not give glucocorticoids to a diabetic patient? | glucocorticoids antagonize insulin |
| what are some adverse effects of using glucocorticoids in dogs? | PU/PD, polyphagia--> weight gain, steroid hepatopathy, calcinosis cutis, alopecia, GI ulceration, hypertension, thromboembolism, peripheral edema, behavioral changes, neuropathy |
| what are the more common adverse effects seen in cats when administering glucocorticoids? | PU/PD/PP, weight gain, Hyperglycemia--> induction of diabetes mellitus, Possible risk of heart failure |
| is heart failure an adverse effect seen more often in cats or dogs when administering glucocorticoids? | dogs |
| where is insulin produced? | Beta cells of islets of langerhans of pancreas |
| the insulin of dogs is most similar to what other species? | pigs and humans |
| the insulin of cats is most similar to what other species? | cattle |
| what are some clinical signs that an animal has diabetes mellitus? | pu/pd; weight loss; polyphagia; dandruff; cataracts in dogs; plantegrade in cats |
| what are clinical sigsn that an animal has diabetic ketoacidosis? | dehydrated, weak, mentally dull, vomitting, anorexia, collapsed, ketone breath, "sick" diabetic |
| You diagnose a dog with diabetes mellitus based upon clinical signs, hyperglycemia, and glucosuria. What kind of insulin do you want to start, and how frequently do you want to administer? | NPH 2x/d |
| You diagnose a dog with diabetes mellitus based upon clinical signs, hyperglycemia, and glucosuria. How will you monitor this dog? | Monitor blood urine, and glucose concentrations A diabetic dog should have at least a trace amount of glucose in their urine. If they are getting negative dipsticks over and over then you should probably have them come in |
| You diagnose a cat with diabetic ketoacidosis. The cat is dehydrated and has been vomiting at home. Should this cat be hospitalized? What kind of insulin do you want to start, and how frequently do you want to administer? why not sub Q for this cat? | Yes; Regular insulin via IV; Because the cat is dehydrated. Vet insulin lasts 3-6 hours but redose every 3-4 hours |
| You diagnose a 19yo cat with hyperthyroidism based on clinical signs and an elevated total T4. What treatment options do you discuss with the client? How do you decide which treatment to use? | surgery, i131 therapy, or medical management; think about cost, think about goals; look at the side effects associated with each of the treatment modalities |
| You diagnose a 19yo cat with hyperthyroidism based on clinical signs and an elevated total T4. What complications of methimazole therapy do you discuss with the owner, and what do you do if complications develop? | Facial excoriations, bone marrow suppression, anorexia, lethargy, vomiting, toxicity, IMHA; stop or decrease dose depending on severity and change the formulation |
| You diagnose a dog with hypothyroidism based on clinical signs and low total T4 and elevated TSH level. What is the drug of choice for this condition? What testing do you recommend to monitor treatment? | T4; Look at serum total t4 concentrations, clinical signs |
| You diagnose a dog with hypoadrenocorticism (causes failure of production of the adrenal hormones cortisol and aldosterone). What is the appropriate method of cortisol replacement therapy in this dog? Clinical signs are assoc w/giving too much? little? | We are going to use a short acting oral. (we need some thing they can take home); PU/PD, increased appetite, Pendulous abdomen, hepatomegaly; glucocorticoid deficiency, Decrease in appetite, lethargy, anorexia, vomiting, or diarrhea |
| In which conditions is it appropriate to administer an intermediate dose of glucocorticoid? | Nonlife threatening conditions, allergic dermatitis, in a patient where administration of glucocorticoids is not going to be harmful |
| In what conditions is it appropriate to administer a high dose of glucocorticoid? | Patieitns with immune mediated disease |
| why is obesity such a problem in older horses? | they become physically inactive and are fed energy rich diets that exceed nutritional requirements |
| what are the four parts that comprise equine metabolic syndrome? | obesity, insulin resistance, pro-inflammatory phenotype, hypertension |
| what are four diseases that horses are at risk for contracting with equine metabolic syndrome? | laminitis, hyperlipemia syndrome, cushing's, diabetes mellitus |
| why are horses with the "thrifty" gene more prone to obesity? | the "thrifty" gene was a survival mechanism for when food was scarce, the horse could live; now, when food is plentiful, the gene is counter-productive |
| Even if horses are kept on pasture year round, why are more horses obese? | humans have changed the nature of grass to fit the needs of the beef industry; humans have planted grasses that are high in starch and sugar in order to fat on cattle and this is what horses are exposed to |
| adipose tissue acts as a gland to secrete what hormone? | leptin or adipocytokine |
| what are the three main structures that insulin targets? | skeletal muscle, adipose tissue, hepatocytes |
| how does obesity drive insulin resistance? | intramyocellular lipid inhibits action of insulin on pre-formed GLUT4 receptors which can increase the insulin uptake of a cell |
| how does obesity worsen insulin resistance | Excessive secretion of adipocytokines; Excessive fat stored within skeletal muscle fibers; Excessive fat stored within hepatocytes |
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