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29 Cards in this Set
- Front
- Back
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Hypothyroidism - Aet - Dx |
• Primarily a disease of dogs – Lymphocytic thyroiditis, idiopathic atrophy • Diagnosis based on clinical signs, serumhaematology and biochemistry • Measure bound and free T4 and alsocTSH |
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Treatment of hypothyroidism |
LEVOTHYROXINE SODIUM Liothyronine sodium |
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Lethothyroxine sodium MOA |
Levothyroxine sodium – drug of choice – Acts in the same way as endogenousthyroxine (T4) – Converted to T3 in peripheral tissues |
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Levothyroxine sodium pharmacokinetics and admin |
– Given orally usually once or twice daily • Start at maintenance dose but increase dose orfrequency depending on clinical signs and TDM • Necessary to tailor to individual animal5 • Generally good oral bioavailability – In individuals may have reduced absorption Available as tablets or liquid • T ½ of about 12-15 hours but individualanimal variation |
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Levothyroxine sodium side effects and CI |
• Thyrotoxicosis unusual – Vomiting, diarrhoea, tachycardia, PU, PD. • Care when administering to hypertensivepatients or those with pre-existing cardiacdisease • Care when administering to patients withconcurrent adrenal disease |
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Liothyronine sodium - MOA - PK's |
Liothyronine sodium – Acts like endogenous T3 (triiodothyronine) – Shorter duration of action and more rapidlymetabolised – Only used when there has been no, or poorresponse to levothyroxine sodium – May be used to do a T3 suppression test inthe diagnosis of equivocal hyperthyroidism inthe cat |
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Hyperthyroidism - signalment - aet |
• Generally a condition of elderly cats(>10yrs of age) • Usually associated with a benign adenomaof the thyroid gland leading tooverproduction of thyroid hormones |
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Hyperthyroidism - management and treatment options (3) |
• Management / treatment3 options – Surgical removal of the thyroid – Radioactive iodine treatment – Drug therapy pre-surgery or forlong term management |
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Hyperthyroidism management - Drugs > MOA |
• Most drugs used to treat/controlhyperthyroidism inhibit thyroid peroxidase – Act as a preferential substrate – Fail to get incorporation of iodine into thethyroglobulin molecule – Reduction in the production of T3 and T4 • A number of drugs have been used– Carbimazole, methimazole andpropylthiouracil |
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Methimazole/A.K.A. Thiamazole - MOA - license - admin |
• Methimazole is licensed in the UK for feline use(Felimazole® and Thiafeline®) • Blocks thyroid peroxidase activity thus reducinglevels of T3 and T4 • Effects reversible i.e. control not cure • Can be used long term or prior to surgery (2-3weeks) • BID administration – compliance? |
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Methimazole - side effects - CI |
• Animals should be monitored every three weeksin terms of biochemistry, haematology andserum T4 levels for the first 4-5 months andthereafter every 3 months – Care especially in renal disease since GFR will bereduced • Especially at higher doses side effects notuncommon – but reversible – Vomiting, jaundice, haematological abnormalities,anorexia, self mutilation |
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Methimazole PK's |
• After oral absorption t ½ only 4-6 hours butmay stay in the thyroid for about 20 hours • There is a great deal of variation in oralbioavailabilty and volume of distribution • It takes a period of 1-3 weeks to seereduction in T4 levels • Preliminary work in transdermal administration = ease problem of frequent oral dosing |
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Carbimazole - metabolism - MOA - license - t1/2 |
• Metabolised almost entirely to methimazole – Appears to have fewer side effects thanmethimazole but the reason for this is not clear• Licensed for feline use in the UK – Sustained release preparation for once dailydosing (Vidalta ®) – T ½ 9 hours versus 5 hours for methimazolestandard – Carbimazole less bitter than methimazole – DO NOT CRUSH OR BREAK TABLETS |
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Radioactive iodine - MOA - Draw backs |
• 131 I is selectively taken up by the thyroid to beincorporated into thyroid hormone precursors • It emits beta and gamma radiation and sodestroys the thyroid tissue • It is selective and not associated with damage tosurrounding tissue like the parathyroid • Draw backs: special facilities and hospitalisationof the cat post treatment since I-131 eliminated in faeces, urine and other secretions |
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Hyperadrenocorticalism –Cushing’s disease - aet |
Hyperadrenocorticalism –Cushing’sdisease • A relatively common endocrine abnormality inthe dog • Syndrome results from overproduction of cortisoland corticosterone from the adrenal gland • May be due to a pituitary adenoma or adrenalgland tumour • Leads to a large number of clinical signs andsymptoms due to the wide ranging effects ofglucocorticoids |
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Management of hyperadrenocorticism Trilostane - MOA |
• UK licensed treatment for Cushing’s disease(Vetoryl ®) • Inhibits the enzyme 3 B-hydroxysteroiddehydrogenase – Inhibition is reversible • Reduces the production of cortisol andcorticosterone • Does not consistently reduce aldosterone |
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Trilostane - PK's - Use |
• Pharmacokinetics – Oral bioavailability improved with the presence offood – Has an active metabolite – ketotrilostane – Elimination in the dog is not known • Use – Close monitoring essential – Given once daily – Day 10, week 4, week 12 and every 3 months repeatACTH stimulation test 4-6 hours post pill – Adjust dose according to clinical signs and test results26 |
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Trilostane side effects |
– Care should be taken when given to dogs with heartdisease especially those on potassium sparingdiuretics and ACE inhibitors – Mild side effects resolve on discontinuation, othersmore severe – Vomiting, diarrhoea, pancreatitis, thromboembolism,adrenal necrosis, Addisonian crisis – Care handling the tablets, tablets should not be split |
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Mitotane |
Mitotane (o,p’DDD) • Not available in the UK so imported on a Special TreatmentCertificate (STC) by applying to the VMD • Was the standard treatment prior to licensing of trilostane • If treatment with trilostane unsuccessful, mitotane may be used • Related to DDT (dichloro diphenyl trichloroethane) • Kinetics and mechanism of action not that clear- in humansbioavailability about 40% • Causes a selective destruction of the adrenal cortex zonafasciculata and zona reticularis • As it is a cytotoxic agent extreme care should be taken whenhandling and administering the drug |
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Hypoadrenocorticism - what is it? - Treatment |
Hypoadrenocorticism – Addison’s • Deficiency of mineralocorticoid andglucocorticoid production by the adrenalgland • Treatment involves mineralocorticoid andto a lesser extent glucocorticoid therapy • Physiological replacement versuspharmacological effect ***FLUDROCORTISONE*** |
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Hypoadrenocorticism - Aet - Signalment - Clinical signs - Acute and long term management |
– deficiency of adrenocortical steroid production – mineralocorticoid and glucocorticoid deficiency – mostly in young female dogs (immune mediated ?) – animals generally present collapsed, bradycardic,hyperkalaemic, hyponatraemic and dehydrated – Treated acutely with hydrocortisone – Long term manage with fludrocortisone |
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Hypoadrenocorticism/Addisons management using DOCP |
• DOCP: desoxycorticosterone pivalate– Another option available in the U.S. andCanada – Long acting analogue of DOCA – Given i/m approximately once every 25 days tailordose to individual animal |
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Diabetes Mellitus - where is insulin produced? Prevelence of type I and type 2 DM |
• Insulin is produced by the beta cells in the pancreas • There is extremely high interspecies sequencehomology; with porcine and canine insulin beingidentical • Type 1, 2 and 3 Diabetes Mellitus all reflect anabnormality in glucose metabolism • Type 1 is most common in the dog • Type 2 may be more important in the cat (noparticular test to distinguish this) |
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Functions of insulin |
1. Facilitates cellular uptake andmetabolism of glucose 2. Promotes the synthesis of glycogenprotein and fat 3. Involved in the cellular uptake ofions such as K+ |
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Types of insulin |
• Short acting • Intermediate • Long acting • Insulin since it is a peptide hormone, must beadministered parenterally • All preparations need to be stored between 2 to8C • Specialised syringes should be used • Insulin usually of bovine or porcine origin*.Human preparations are recombinant products |
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Short acting insulin - admin - indications |
• Soluble insulin; Neutral Insulin • The only form of insulin that can be giveni/v (may also be given i/m or s/c) • Duration of activity when given i/v is about2-4 hours • Ideal for use in ketoacidotic emergencies – May be administered as a constant rateinfusion • Can also be used in hyperkalaemiaassociated with UT obstruction |
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Intermediate acting insulin - onset of activity - admin |
• Onset of activity 1-2 hours; peak activity 6-12hours; duration of effect 18-26 hours • Above guide only. Often these times are reducedin cats • Given s/c • Insulin Zinc Suspension – Mixture of 30% amorphous insulin zinc and 70%crystalline insulin zinc – Crystalline has a longer duration of action – Caninsulin ® is porcine origin (vet licensed) |
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Long acting insulin |
Long acting • Onset of activity 4-6 hours; peak activity 14-24hours; duration of effect 32-36 hours • Above is a guide only • Especially useful for cats where effect tends tobe shortened vs the dog • Protamine Zinc Insulin – A bovine insulin – Administered s/c • ProZinc® NEW – Cats – Human insulin |
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Long acting insulin - Insulin glargine |
• Insulin glargine – Relatively new recombinant insulin (last fewyears) – Engineered to alter pharmacokinetic profile – Acidic (pH 4) • Necessary for effect don t dilute or mix – Injected s/c get microprecipitates to giverelatively constant absorption profile – Good results in cats where it is given twicedaily in combination with a high protein lowcarbohydrate diet |
