pharmacology Flashcards
(34 cards)
What are glucocorticoids used for?
-respiratory disease-asthma
-dermatological disease- atopy/food allergy
-gastrointestinal disease-IBD
-ophthalmic disease-anterior uveitis
-musculoskeletal disease-immune-mediated myositis
-neurological disease- meningitis
-Immune-mediated and autoimmune disease
Species differences for prednisone
Cats and horses have low bioavailability of prednisone-low capacity to convert prednisone to prednisolone
Species differences-cats v dogs
-cats require higher doses
-cats have fewer glucocorticoid receptors
-cats have lower affinity glucocorticoid receptors
-cats are more resistant to adverse effects
Glucocorticoid effects
-increase the number of neutrophils and monocytes
-decreased lymphocytes, eosinophils, and basophils
-decrease function (release of inflammatory cytokines)
Glucocorticoid adverse effects
-immunosuppression at higher doses (TREATS OVERACTIVE IMMUNE RESPONSE)
-chronic low doses have effects on innate and cell-mediated immunity
-hyperglycemia
-increase triglycerides, cholesterol, glycerol
-muscle breakdown
-stabilize membranes and decrease vascular permeability
-stimulate ALP production in dogs
-hepatomegaly
-GI ulceration
-alterations in fluid and electrolyte balance
-polyuria/polydipsia
-accidents in the house within 5 days
-mood and behavior changes (polyphagia)
-laminitis (horses) (can’t be replicated in experiments)(fat horses with cresty necks (EMS) are predisposed)
How to prevent adverse effects of glucocorticoids?
-give drugs every other day
-taper dose when d/c treatment (not necessary with short term treatment)
-give dose in the morning to prevent alteration in sleep
-localize therapy (results in less systemic exposure)
What are the prostanoids you need to know and their effects?
-PGI2=anti-platelet; vasodilatory
-TXA2=pro-platelet; vasoconstriction
-PGE2=pro-inflammatory, pain; vasodilation; GI motility; fever
-PGF2alpha=vasoconstriction; SmM contraction (uterus, GIT); luteolysis
What do COX-2 inhibitors do?
-Block the bad (pro-inflammatory effects)
-Leave the good (cytoprotective to the GIT)
-no adverse effects
What are the clinical uses of NSAIDs?
-to treat endotoxemia
-anticoagulant
What are NSAIDs not appropriate for?
-Immune-mediated diseases (IMHA/IMTP)
-Autoimmune diseases
-Allergic diseases
-Inflammatory respiratory diseases (asthma, chronic bronchitis)
-Neurologic disease (meningitis)—-doesn’t cross BBB
Adverse effects of NSAIDs
-GI ulcers (stomach and SI in cat and dog) (stomach and right dorsal colon in horses)(abomasum in ruminants)
-PGE2 effects (necessary for healing with pre-existing damage)
-nephrotoxicity (inhibition of PGE2 and PGI2 causes vasoconstriction, decreased renal BF (blood flow), possible toxicity)
-Lesions in the kidneys (characterized by medullary crest or papillary necrosis)
-COX-1 inhibitor=inhibits platelet function
-hepatotoxicity (mainly in dogs)
-blood dyscrasias (phenylbutazone in dogs)
-Injection site reactions (heat, pain, swelling, abscess formation, tissue necrosis, clostridial myositis)
-PHENYLBUTAZONE=severe tissue necrosis when given peri-vascular
-IM FLUNIXIN MEGLUMINE= clostridial myositis (huge abscess)
How to minimize adverse effects of NSAIDs?
-Prevent injection site reactions by given drug another route (oral)
-dose appropriately (lowest effective dose at the longest effective dosing interval)
-choose COX-2 selective
-dedicated dosing syringe
-GI protection
-Avoid co-administration of other nephrotoxic drugs
-use EXTREME caution in animals with underlying disease
-client education
-monitor
What is MIC?
-Minimum Inhibitory Concentration=the lowest concentration of drug that inhibits visible bacterial growth
What is MBC?
-Minimal Bactericidal Concentration=the lowest concentration of a drug that kills 99.9% of bacteria
What is a bacteriostatic drug?
-A drug that stops the bacteria from multiplying but doesn’t kill the bacteria
-relies on the host immune system to kill bacteria
-not ideal for immunosuppressed patients
What is a bactericidal drug?
-A drug that kills bacteria directly
-preferred for immunosuppressed patients or severely ill patients
What is PAE?
-Post antibiotic effect
-occurs once MBC and MIC decline in plasma
-bacteria still around and evade host immunity
-persistent sites of infection
What are the antibiotic mechanisms of action?
-Inhibit cell wall synthesis
-inhibit cell wall function
-inhibit nucleic acid synthesis and function
-inhibits protein synthesis
What type of bacteria is penicillins effective against?
-active against streptococci NOT most staphylococci
-Not active against gm(-)
-active against some gm(-) and gm(+) anaerobes
What type of bacteria is amino-glycosides effective against?
-active against staphylococci NOT most streptococci
-active against respiratory and enteric gm(-)
-no activity against anaerobes
What type of bacteria are macrolides effective against?
-active against gm(+) anaerobes
-active against respiratory gm(-) but not enteric
-active against most gm(+) anaerobes
What are the routes of administration of antibiotics for systemic infection?
-IV=severe illness, fast effect
-IM=severe illness, when IV is not possible
-SubQ=avoid in dehydration
-Oral=bioavailability lower, variable absorption; avoid in GI diseases; drug interactions
What are the routes of administration of antibiotics for local infections?
-topical=eyes, skin, wounds
-inhaled=pneumonia
-intraarticular/regional limb perfusion=synovial infections
-transdermal=NEVER
What are the type of beta lactam antibiotics?
-penicillins
-cephalosporins
-carbapenems=imipenem and meropenem
-monobactams=aztreonam
