Drugs Flashcards

Question

25. Pentoxifylline

Answer 1

a. Methylxanthine of theobromine – minimal bronchodilator b. Hepatic metabolism - >7 metabolites c. MOA: i. Inhibits complement cascade ii. Inhibits neutrophil degranulation iii. Inhibits cytokine production (esp TNF alpha) iv.  inc collagenases,  dec collagen,  dec GAG fibronectin production d. Uses: variety of inflammatory conditions, ___? i. Shock to IBD

Answer 2

a. MOA: inhibits off A cascade b. PK: metabolized by liver, <2% excreted in urine, t ½ in plasma and tissues c. SE: dyscriasis, hepatopathy, nepropathy, chondrodestructive effects d. Toxicity: hemorrhage, biliary stasis, renal failure i. High toxicity in cats 1.  dec erythroblastic activity in bone marrow 2. GI drug, nephrotoxicity, hepatotoxicity

Answer 3

a. Usually COX-1 sparing, but not at higher concentrations b. Undergoes hepatic metabolism c. Once daily dosing d. SE: GI – esp with micronized material i. KCS – it’s a sulfonamide

Answer 4

a. Cholagogue: substances that cause contraction of GB i. Eg. CCK / pancreozymin ii. Insert tube with fat/MgSO4 into duodenum to stimulate contraction of GB b. Choleretic: substances that  inc secretion of bile by hepatocytes i. Eg. phenobarbital, ursodiol, turmeric c. Hydrocholeretic: stimulate liver to  inc output of bile of low specific gravity i. Eg. Dehydrocholic acid

Answer 5

a. A linear polydisaccharide component of synovial fluid linked to proteoglycans in articular cartilage b. Lubricant? Inhibits phagocytosis, lymphocyte migration, & synovial permeability

Answer 6

a. Oxicam family – oral approved US discontinued; inject only as single dose b. Favors COX-2 inhibition – wider margin of safety c. More potent than aspirin d. Time to peak concentration one of longest for NSAIDS in dogs (7-8 hr) e. Also one of longest t ½ - thus loading dose recommended f. SE: renal, GI, hepatic i. Dogs – V+, GI upset, renal toxicity; one report of cutaneous / ocular lesions ii. Cats – shorter t ½ than dogs, therapeutic margin very narrow

Answer 7

a. Salicylic acid ester b. MOA i. Inhibition of COX enzyme, inhibits formation & release of kinins, stabilize lysosomes, remove energy needed for inflammation via uncoupling oxidative phosphorylation ii. Acetylates TXA2; low doses stimulate formation of lipoxins c. PK: i. Rapid metabolism, distributes to ECF rapidly --> synovial, peritoneal, saliva, milk ii. Bioavailability 68-76% iii. Eliminated by liver & kidney (excretion rapid in alkaline) d. SE: i. GI effects, V+, anti-thrombotic effect, hepatotoxicity, renal toxicity, electrolyte imbalances, depression (toxicity) ii. Toxicity more likely in cats bc slow metabolism e. Note: glucuronidation deficient in cats – so t ½ longer

Answer 8

a. Proprionic acid-derivative NSAID b. MOA: [??]- selectively inhibited for COX-2 c. PK: highly protein bound, metabolized by liver, 70-80% excreted in feces (rest in urine) i. Enterohepatic for sisomer; COX-selectivity not as evident in cats ii. Also not as reported to have GI effects iii. Efficacy +/- in cats d. Adverse effects: i. GI (reported consesvray) – ulceration, gastritis, etc. ii. Hepatotoxicity (acute necrosis) – esp those on phenobarbital iii. Nephrotoxicity iv. Hemostasis -  dec platelet aggregation,  inc PT time v. Chondral drug -  inc PGAG synthesis (low concentration) – inhibits at high conc.

Answer 9

a. Synergistic action with anti-cancer drugs to  dec size of tumors b. T ½ much shorter in cats than dogs c. GI toxicity / effects possible, but not really reported

Answer 10

a. COX-2 selective “oxib” NSAID family b. Short t ½ , but still given once daily c. Oral bioavailability 38% d. Still not ideal for young dogs e. Higher therapeutic range for given weights f. SE: GI, hepatic, cartilage, renal?

Answer 11

a. Pyranocarboxylic acid – inhibits chondrocyte & synoviocyte PGE2 b. Food slows absorption & prolongs elimination c. Majority excreted in bile, 10% excreted in urine d. Enterohepatic circulation inc , so  inc risk of GI toxicity e. SE: GI disease, hepatotoxicity, KCS, cartilage damage f. Dosed once daily

Answer 12

a. MOA: interferes with endoperoxide intermediates (PEG1, PGH) of AA conversion (+/- inhibitor of “COX-3” really COX-1) b. PK: weak anti-inflammatory, maybe best in CNS i. Narrow safety margin in cats d/t glucuronide deficiency – toxic metabolites overwhelmed c. SE: methemoglobinemia (cats) +/- centrolobular hepatic necrosis i. SAFE IN DOGS! ii. Tx toxicity with N-acetylcysteine, Vit C, antioxidants

Answer 13

a. Zileuton, limited use due to hepatotoxicity b. Efficacy limited

Answer 14

a. Inhibit COX & LIPOX b. Tend to inhibit other redox-active enzyme systems so liver toxicity limits its use c. Both limit GI effects bc don’t inhibit lipox 12-15 d. Since both COX-1 / COX-2 inhibited, --> thromboembolic balance not disrupted e. Eg. Tepoxalin i. Hepatic metab, highly protein bound, leaves in feces ii. Cats – can get CNS side effects f. May have improved benefit over other NSAIDS against allergies

Answer 15

a. CLASS: Opioid b. MOA: mu-full agonist i. High doses – K receptor agonist ii. Activation causes influx K+ and  dec intracellular Ca ++ iii. Releases NT like substance P + glutamate --> hyperpolarize --> dec  pain c. PK: onset ~5-15 minutes; duration ~2-4 hrs i. 50% hepatic metabolism (vs 100 in others) --> so best for liver patients ii. Low lipophilicity so great for epidurals iii. Dose-dependent incident of GER d. SE: nausea, V+, defecation, constipation (long term), sedation, panting, hypothermia, bradycardia,  dec urine void / production, resp depression, excitement in cats, Histamine release IV e. Avoid in: animals with head trauma or increased ICP (risk of emesis)

Answer 16

a. CLASS: Opioids b. MOA: mu agonist to partial mu agonist + K agonist c. PK: has ceiling effect i. Duration 30 min-2 hrs ii. Prolonged sedation in dogs with MDR-1 mutation – substrate for P-glycoprotein d. SE: sedation, anti-emetic properties, less nausea/V+, less excitement in cats, less dysphoria, otherwise can get e. Useful as anti-tussive

Answer 17

a. CLASS: “Opioid-like” / analogue of codeine b. MOA: metabolizes to (M1) --> full mu agonist c. PK (M1) = O-desmethyltramadol --> need that formed to have any analgesia i. Cats produce M1> dogs ii. Duration ~6 hours d. SE: restlessness, V+, tremors, salivation, convulsions, unsteady gait e. DON’T GIVEN WITH SSRI, monoamine oxidase inhibitors, or tricyclic antidepressants --> serotonin syndrome

Answer 18

a. CLASS: Opioids b. MOA: Partial mu agonist i. Can antagonize full mu agonists ii. Greater affinity for receptors than morphine c. PK: 25x potent (L/J) than morning (Tobias says 40x) i. Duration 4-6 hrs & up to 12 depending dose ii. Maybe some promise with cat patches (definitely not dogs) d. SE: has ceiling effect! – really high doses doesn’t change analgesia i. Less ileus, V+, nausea than morphine ii. Mild resp / CV effects if any e. Can give transmucosally to cats

Answer 19

a. CLASS: NMBA b. MOA: Non-depolarizing NMBA – bind but do NOT activate acetylcholine receptors c. PK: 5 min onset for both; duration of action 30 min i. Atracurium degrades independent of hepatic / renal paths ii. Vec – significant renal elimination / slightly >50% hepatic iii. Smooth onset d. SE: Vec – devoid of CV effects e. Atra – way less likely to cause CV histamon?? effects than other NMBA f. Indications: Neuro, advanced CV, or ophtho sx

Answer 20

a. CLASS: alpha-2 agonist – tranquilizers b. MOA: bind to alpha 2 G-coupled protein receptors -  dec NorEpi release in CNS i. Some bind alpha-1 peripherally – vasoconstriction etc (see SE below) c. ONSET: quick, duration – 15-20 min d. PK: alpha 2: alpha 1 selectivity 160:1 e. SE: bradycardia (hypertension then hypo) – thus  dec CO but SV says the same i. Arrhythmias – sinus brady, 2 deg AV block ii.  dec RR (more often when combined with opioid) (but at appropriate doses M.V. still same) (thus blood gas normal) iii. Salivation, emesis (cats),  dec GI motility iv.  dec uterine flow, impacts neonatal survival?? f. Indications: sedation / analgesia, pre-med i. Reverse with yohimbine g. Contraindicated in dogs d/t increased anesthetic risk

Answer 21

a. CLASS: Benzodiazepine – tranquilizers b. MOA: enhance GABA effects - inc Cl- conductance & hyperpolarizes cell – prevent propagation of APs c. Duration of action: 2 hrs d. PK: Formulated in propylene glycol, absorbs into plastic, light sensitive i. Metabolized in liver (nordiazepam, oxazepam); breed differences in t ½ / poor water soluble ii. Give nasal, rectal, IV (IM very painful) e. SE: sedation, anxiolysis, muscle relaxation, anticonvulsant i. NO SIG CV effects or resp depression f. Indications: sedative (not strongly), anti-convulsant, give with ketamine to relax muscles, combine with opioid for neuroleptanalgesia

Answer 22

a. CLASS: Opioids b. MOA: full mu agonist – influx K,  dec intracell Ca++ --> hyperpolarize -->  dec pain c. PK: 10x potent than morphine i. Metabolized by conjugate formation ii. +/- some metabolized elsewhere and +/- excreted unchanged d. Duration of action: 2-4 hrs e. Effects: similar to morphine except – i. Less V+, less nausea ii. Doesn’t product histamine when IV iii. Less excitement than morphine f. $$$ g. Dose 0.05-0.2 mg/kg

Answer 23

a. CLASS: Anticholinergic b. MOA: competitively antagonize acetylcholine at post-gang muscarinic receptors c. ONSET: rapid d. Duration ~30 min in heart, other systems within few hrs e. PK: Eliminated in liver via enzymatic hydrolysis i. Eliminated in renal as well for cats ii. Crosses BBB f. SE: can have paradoxical bradycardia at low doses i.  dec salivation in cats on ketamine ii. Tachycardia, bronchodilation,  dec airway secretions iii. Mydriasis and cycloplegia iv.  dec lower esophageal stricture fxn v. AVOID IN HCM or restrictive cardiomyopathy g. Indications: to treat/prevent severe bradycardia, young

Answer 24

a. CLASS: anticholinergics b. MOA: competitive antagonist to acetylcholine at post-gang muscarinic R c. ONSET: few minutes (> atropine) d. Duration: > atropine (~1 hr at heart) e. Excretion: urine unchanged; 4x potency > atropine f. PK: very difficult to cross BBB or blood-placental barrier g. SE: paradoxical bradycardia i.  dec salivation in cats on ketamine ii.  dec motility in dogs ~30 min iii. Bronchodilation, tachycardia iv.  dec lower esophageal stricture fxn h. Indications: to treat/prevent severe bradycardia, young

Answer 25

a. CLASS: Neuromuscular blocking agent b. MOA: Depolarizing NMBA – keeps bound to receptor & maintains depolarization --> acetylcholine won’t bind to already depolarized cell c. PK: not broken down by acetylcholinesterase i. Very rapid metabolism – excreted in urine ii. Very short duration of action d. SE: malignant hyperthermia, muscle soreness i. Hyperkalemia ii.  inc intraocular pressure iii.  inc intracranial pressure iv.  inc intragastric pressure

Answer 26

a. CLASS: local anesthetic b. MOA: Na+ channel blocker c. PK: 4x potent than lidocaine i. Higher lipid solubility and protein binding ii. Slow onset – 45 min d. DOA: 6-8 hrs! e. Toxic effects: chondrotoxicity? i. Cardiotoxicity – DO NOT USE for IV regional ii. >2 mg/kg Cats iii. > 4 mg/kg dogs f. Great for intrapleural tubes

Answer 27

a. CLASS: Local anesthetic / Ib antiarrhythmic drug b. MOA: Primary voltage Na+ channel blocker – inhibits afferent transmission c. PK: very fast onset i. +/- actions on Ca, K channels & NMDA receptors ii. Possible anti-inflammatory effects iii. Improve intestinal motility d. Duration: <1 hour (prolonged 3h with epinephrine) e. Toxic effects: > 6 mg/kg cats; >8 mg/kg dogs i. V+, ileus, nausea, R+, dull mentation --> seizures ii. Really high dose --> cardiotoxicity f. **Bier block – distal to tourniquet i. Smaller fibers need less exposure than large fibers – critical length

Answer 28

a. CLASS: Tranquilizer, atypical antidepressant / serotonin modulator b. MOA: Phenylpiperazine antidepressant --> serotonin antagonist & reuptake inhibitor c. ONSET: Peak plasma conc orally after 7 hrs; ~30-40 min onset? d. SE: IV can cause CV depression e. Indications: anti-anxiety? f. Don’t use with monoamine oxidase inhibitors g. Concern for serotonin reuptake syndrome

Answer 29

a. CLASS: Phenothiazine – sedative b. MOA: blockade of dopamine D2 receptors -->  dec Ca conductance;  dec cAMP / adenyl cyclase activity i. +/- alpha 1 adrenergic, muscarinic, H1 blockage (alpha 1 blockade – hypotension) c. Onset: Within 10 min d. Duration: 4-6 hrs e. PK: Dose-dep  dec in inhalants required; metabolized by liver, excreted in urine f. SE: Hypotension,  dec PCV,  dec platelet aggregation, antiemetic properties i. DOES NOT GIVE ANALGESIA g. CAUTION in severely systemically ill pts with concern for BP h. Indication: sedative, less commonly for  inc BP i. Limit to CV stable pts

Answer 30

a. CLASS: Opioids b. MOA: Full mu agonist c. PK: 100x potent than morphine i. Patch form available. Takes 12-16 hrs (cats) / 18-24 hrs (dogs) for therapeutic levels d. Duration: 20-40 min; do CRI e. SE: less nausea / V+ (has antiemetic effect until ileus forms) i. More likely to cause bradycardia & apnea after rapid bolus ii. Can get “wooden chest;” chest wall rigidity then give naloxone f. Remifentanyl – metab by plasma esterases

Answer 31

a. CLASS: Opioids b. MOA: Full mu agonist c. PK: 8x potent than morphine i. SQ in cats slow absorption d. Duration: 2-4 hrs e. SE: Minimal histamine w IV i. V+ - major ii. +/-  inc bile duct sphincter pressure,  inc pyloric sphincter tone iii. Post-op hyperthermia in cats!!!

Answer 32

a. Low doses i. Beta 1:  inc cardiac output, myocardial O2 consumption, coronary a dilation  dec threshold arrhythmias ii. Beta 2:  dec diastolic BP & peripheral vascular resistance b. High doses i. Alpha 1 – dominates: marked  inc in systemic vascular resistance c. ** Proarrhythmogenic i.  dec threshold for V-fib &  inc VPC/missed beats d. Other effects:  inc temp,  inc glucose,  inc K (then  dec K from B2),  inc renin from kidney

Answer 33

a. Short t ½: 3 min; onset up to 5 min b. Low doses: 1-3 mcg/kg/min i. DA-1 in renal & splanchnic vasculature ii. DA-2 to produce vasodilation &  inc renal BF c. 5-10 mcg/kg/min i. Beta 1&2 effects:  inc myocardial contractility,  inc HR,  inc CO,  inc coronary BF d. >10 mcg/kg/min i. Alpha 1 / 2:  inc systemic & pulmonary vascular resistance, venous return,  inc PCV (splenic contraction) +/-  inc HR e. 25% converted to norepinephrine after metabolism f. Stimulates release of endogenous norepi from presynaptic storge sites – endogenous sympathomimetic effect

Answer 34

a. Very low dose – beta 1 predominates –  inc HR/CO -  dec SVR (beta 2 effects not seen clinically) b. Normal to  inc doses – alpha receptors (1&2) i. Dose-dep  inc systolic, diastolic, & MAP ii. Dose-dep  inc CO,  inc systemic / pulmonary vascular R iii. Cause coronary vasodilation to promote increased coronary BF c. ** Extravasation – tissue necrosis due to localized vasoconstriction

Answer 35

a. Alpha 1 receptor agonist -  inc SVR -  inc BP b. Dose-dep  inc in SVR, MAP, & reflex reduction in HR c. CO usually OK (maybe  dec from increased afterload + bradycardia) d. Other effects:  dec uterine flow,  dec renal hepatic flow,  dec nasal edema e. AVOID IN PREGNANT ANIMALS

Answer 36

a. Primary stimulates beta 1 -  inc CO, HR, SVR b. High doses – beta 2 & alpha 1 receptors – vasodilation i. Can be proarrhythmogenic c. Has both inotropic & chronotropic effects d. In dogs has limited effect on BP

Answer 37

a. Class: Bacteriostatic b. MOA: inhibits protein synthesis R50s (do not use in immunocompromised pts) c. Spectrum: G+, G-, anaerobes (not pseudomonas) d. Resistance: Plasmid mediated – acetylation / destruction of microbial enzymes e. Achieves mod-high conc in all tissues, even CSF f. Eliminated via hepatic metab – glucuronidation major route g. Good for immunocompromised patients?? h. Drug interactions: not with macrolides (some binding it) i. Enhances penicillin inhibition of hepatic metab of other drugs ii. Prolongs barbiturates i. SE: Aplastic anemia (humans), bone marrow suppression in cats

Answer 38

a. Class: Beta lactam b. MOA: Inhibits cell wall synthesis c. Spectrum: Gram +, Gram -, anaerobes d. Resistance: Altered BPs, beta lactamases e. Can not travel barriers – limited to ECF (if inflamed goes into interstitium) f. Conc in urine – eliminate via renal tubules (not hepatic metab) g. Highly protein bound – care with use of other protein bound drugs h. Favors oral absorption but destroyed by GIT acid i. SE: +/- D+, hypersensitivity, decreases seizure threshold

Answer 39

a. MOA: Bacteriocidal; inhibits nucleic acid synthesis (topoisomerase) b. Spectrum: Gram (-) > Gram (+). NO anaerobe c. Resistance: chromosome mediated – decrease cell wall permeability, efflux pump activation, mutation topoisomerase d. Good tissue distribution, goes in WBC & CSF!! (food / antacids decrease abs) e. Elimination varies; but conc in prostate / urine; goes to liver/ kidney well f. Drug interactions: inhibits hepatic drug metabolizing enzymes – prolong elimination i. With NSAID +/- increase risk seizure / CNS activity ii. Cipro increases cyclosporine, prolonged anticoag warfarin effects g. SE: Cartilage damage young pts, seizures / CNS disorders, dose-dep retinal degeneration (cats), V+, D+, GI h. Bacteriophage superguns?

Answer 40

a. Bacteriostatic b. MOA: Inhibits protein synthesis (50s) ribosome c. Resistance: Plasmid mediated – change in ribosome prevents binding d. PK: Highly protein bound, distributes to most tissues i. Excellent bone / skin. NOT brain or CSF well ii. Can penetrate biofirm iii. Excreted in BILE & hepatic metabolism e. Drug interations: do not combine with chloramphenicol or erythromycin f. CAN combine with aminoglycosides g. SE: rate dogs/cats – severe D+ herbivores / horses

Answer 41

a. Beta lactam b. Bacteriocidal c. Inhibits cell wall synthesis d. Gram + (more first gen), Gram – (more 3rd gen), anaerobes e. Resistance: Beta lactamases, loss of porins, altered BPs, pumps f. Drug interactions: other high protein bound drugs g. Primarily urine conc, excreted in urine (+/- hepatic) h. Cannot travel through barriers / 1st/2nd gen =/ CNS i. 1st gen: cephalexin, cefazolin (t ½ 45 min) j. 2nd gen: cefoxitin – great for anaerobes, lower GIT k. 3rd gen: ceftazidime, cefpodoxime (long t ½, conc inc with food, <50% drug readily interstitium) l. Cefovecin (Convenia) – avid protein binding, may have enterohepatic circulation; t ½ 136 hrs!!! IV or SQ

Answer 42

a. MOA: Inhibit protein synthesis (50s ribosome) b. Baceriostatic; cidal – high dose c. Spectrum: Gram +, Anaerobes (except bacteroides), NOT Gram – d. Resistance: Plasmid mediated – pump efflux from cell, altered ribosome binding protein e. PK: food may delay abs, diffuse through membrane slowly i. Tissue conc exceed in many tissues > plasma ii. Erythro / azithro – eliminated in BILE; clarithro – bile + feces f. Drug interactions: antacids decreased rate abs i. May inhibit CYP 450 enzymes – impairs drug metab ii. Don’t pair with those drugs that need bacterial growth to work g. SE: pair with IM, GI upset (V+), inc gastric emptying i. Mimics mutilin = stimulates gastric, pyloric, and duodenal contractions

Answer 43

a. STATIC i. Macrolides (low dose) ii. Lincosamides iii. Chloramphenicols iv. Trimethoprim (alone) v. Tetracyclines vi. Sulfonamides (alone) b. CIDAL i. Beta lactams ii. Glycopeptides iii. Aminoglycosides iv. Fluoroquinolones v. Rifamycin vi. Metronidazole vii. TMS (together)

Answer 44

a. MOA: Bacteriocidal – inhibits beta subunit suppressing RNA synthesis b. Spectrum: Gram + primarily, +/- clostridium, chlamydia, E-coli (Gram – limited) c. Feeding may delay absorption, mostly protein bound, good for intracellular orgs d. Excreted in bile – enterohepatic circulation e. Drug interactions: inc toxicity associated with drug metab (if met by liver) i. Cyclosporine, imidazoles ii. Inc catabolism of steroids iii. Decreased biliary secretion of compounds like contrast f. SE: GI dz, icterus, immunosuppression of lymphocytes i. Orange color urine / feces / sweat ii. CNS depression after IV

Answer 45

a. MOA: inhibits protein synthesis – target 30s & 50s ribosomal subunit b. Spectrum: gram (-); Not anaerobes or G+. c. Bacteriocidal d. Resistance: plasmid mediated enzymatic destruction primarily seen in anaerobes e. Poor oral absorption (d/t weak base) – give IV/local – doesn’t distribute to CNS, ocular, bile, milk, prostate f. Eliminate via kidneys – alkaline urine facilitates absorption g. Tissue penetration poor (bronchial > penicillins) h. SE: Renal (tubule toxicity reversible), ototoxicity, NM blockade, cardiac (if IV rapid) i. Drug interactions: NSAIDS, Ace inhibitors, amphotericin B, other nephrotoxic drugs j. May inactivate weak acids (like penicillin)

Answer 46

a. 3rd gen ceph b. Fluoroquinolones c. Metronidazole d. TMS e. Chloramphenicol

Answer 47

a. 1st/2nd gen ceph b. Aminoglycosides c. Clindamycin d. Vancomycin (GPs)

Answer 48

a. Tetracyclines (doxo/mino) b. Erythromycin c. Penicillins d. Rifampin

Answer 49

a. MOA: Inhibits protein synthesis ribosome 30s b. Bacteriostatic c. Spectrum: Broad gram +, gram -, anaerobic & rickettsial d. Resistance: plasmid mediated – interfere with influx / efflux e. Doxy/mino – lipid soluble f. Biliary excretion (*other tetracyclines renal & biliary) g. Abs decreases with milk products / antacids; goes into brain but NOT CSF h. Doxy 99% protein bound; do NOT give IM i. Drug interactions: cation-containing drugs (antacids, sucralfate, Ca supplement?) j. All except doxy should NOT be given with food k. SE: GI signs, esophageal structure (cat), collapse if rapid IV, renal, discolored teeth, enamel hypoplasia, NOT IN PREGNANT ANIMALS

Answer 50

a. Class: nitroimidazoles b. MOA: inhibits microbial RNA/DNA synthesis c. Bacteriocidal; a prodrug – both concentration & time dep d. Spectrum: All Gram (-) anaerobic & most gram (+) anaerobic bacilli e. Resistance: Rare; aerobes – lack e- systems / decrease intracellular drug activation f. Penetrates BBB, minimally protein bound g. Eliminated – hepatic metabolism 59-100% bioavail h. IV should be neutralized, reacts with AI needles i. SE: discolor urine, GI upset, dose dep neurotox, teratogenic – DO NOT GIVE with preggo!!!

Answer 51

a. Class: sulfonamide / pyrimethamine = bacteriostatic (w/o other abx = cidal) b. MOA: inhibit nucleic acid synthesis / impair folic acid synthesis c. Spectrum: Gram (+), gram (-), and anaerobes (NOT pseudomonas or mycoplasma d. Resistance: if microbe can make folic acid elsewhere – plasmid-mediated & chromosomal e. PK: highly insoluble (in GIT long time) but rapid oral absorption i. Sulfasalazine – enterohepatic circ, elim in urine, excreted in renal tubules ii. Sulfadiazine can get to CNS f. SE: KCS, hypersensitivity, decrease TH synthesis, Doberman arthropathy, thrombocytopenia, hepatopathy g. Drug interactions: oral hypoglycemic agents, warfarin, procainamide, increased elimination of cyclosporine

Answer 52

a. Bacteriocidal b. MOA: inhibit cell wall synthesis & affects RNA synthesis c. Spectrum: G+, anaerobes. Not G- d. Resistance? e. SE: hypersensitivity, nephrotoxicity, ototoxicity

Answer 53

a. MOA: Antidopaminergic (D2) & 2nd antihistaminergic i. Weak antiserotonergic (low dose) ii. Acts at CTZ > vest apparatus (low dose) iii. High dose: anticholinergic at central sites – V+ center b. SE: sedation, hypotension (peripheral alpha blockade), caution seizure patients c. Tx: Antiemetic

Answer 54

a. Proton Pump Inhibitors – antisecretory drugs b. MOA: Antagonist of H1K1ATPase c. PK: unstable in acid – needs capsule form i. Selective partition into canaliculi of parietal cells ii. Binds to sulf-hydryl group of H1K-ATPase pump iii. Take up to 3-5d for full effect iv. Clearance through liver d. Partial inhibitor of CYP450 e. SE: D+, fluctuations hepatic enzymes, increase acid secretory capacity

Answer 55

a. MOA: Disaccharide AlOH binds to damaged?? epithelial cells i. Binds to exposed anions of GI ?? membrane b. PK: 30 before antacids, empty stomach (1hr before) i. Inactivates bile acids; increase mucosal BF ii. stimulate local mediators: PGs, GF, etc iii. Decreases absorption of several drugs (eg abx) c. SE: constipation?

Answer 56

a. Anti-emetic; prokinetic b. MOA: Dopamine antagonist; 5HT3 antagonist; 5HT4 agonist i. Enhanced release of Ach intrinsic neurons c. PK: well absorbed oral – 1st pass met; bioavail 50-70% i. Tissue distribution rapid – excrete renal + hepatic; ½ life 90 min d. SE: nervousness, restless, listless, depression, disorientation, tremors (cats), constipation e. Drug interactions: anticholinergics and opioids decrease prokinetic efficacy f. Tx: increase tone esophageal sphincter, increase gastric contractile force, relax pylorus, stimulate peristalsis --> GI motility, emesis, etc.

Answer 57

a. Antisecretory: H2 antagonist b. PK: 9x potent > R; 32x > cimetidine i. Longest duration of action ii. 37% bioavailable, but more potent iii. Least drug interactions c. SE: minor, thrombocytopenia d. Tx: gastritis, esophagitis, etc

Answer 58

a. Anti-emetic b. MOA: Serotonin antagonist (5HT3) --> CTZ c. PK: low oral bioavailability d. SE: maybe GI upset? e. Tx: great for V+, even more so with chem drug induced V+

Answer 59

a. Antihistamines – cyclizine HCl, meclizine HCl, diphenhydramine HCl

Answer 60

a. Cholinergic – prokinectic b. MOA: Works at M2 receptors i. Enhances amplitudes of contractions throughout GIT c. SE: enhanced parasympathomimetic – cramps, D+, salivation, decreased HR, lacrimation

Answer 61

a. MOA: NK antagonist – blocks actions of Substance P at CTZ & vomit center b. PK: protein bound i. Dogs: ½ life 9 h after SQ, 5 oral ii. Cats: ½ 13-17 h in cats c. SE: pain on injection, BM hypoplasia (<11 weeks of age) d. Tx: anti-emetic

Answer 62

a. AlOH, Mg-products, CaCO3 b. MOA: neutralize HCl so pH Increases, inactivate pepsin, binds bile salts i. Induce local PG synthesis, affect electrolyte absorption c. PK: cleared within 30 min from stomach i. Neutralization – removes negative feedback on gastric – increases HCl secretion ii. Food prolongs effect d. DI: alkalinizes urine – increase elimination of weak acids (NSAID, phenobarb) i. Affects drug absorption e. SE: inc risk food allergies, incomplete food digestion i. AlOH: Constipation, slow acting, decrease P abs in intestines ii. Mg: cathartic, laxative, prompt & prolonged, avoid in renal dysfunction iii. CaCO3: rapid acting, prolonged, mAlk (?), increase Ca, calcifying urolithiasis, constipation

Answer 63

a. Prostaglandin E1 analog b. MOA: interact with basolateral receptor – intracell dec cAMP -->  dec PK & H+ c. PK: food delays onset; metabolized by liver i. Doesn’t alter gastrin levels; no rebound hypersecretion d. SE: intestinal secretion, smooth m contracts  D+ i. Induce uterine contractions – NOT FOR PREGGO e. Treats NSAID ulceration

Answer 64

a. Prokinetic (C < D) b. MOA: indirect stimulation of cholinergic n. i. Serotonin – stimulates 5-HT4 & stimulates colonic contractions via 5-HT2a c. PK: bioavailability 30% in cats i. Elimination long with liver disease ii. Better at lower GIT d. SE: block K influx – prolong QT i. Myocardial? – greater when combine with drugs that inhibit CYP450

Answer 65

a. Eg. Adequan b. Closely mimics proteoglycan complexes in normal articular cartilages c. MOA: largely not understood i. Collage, proteoglycan, & HA synthesis increases ii. Inhibit collagenase, leukocyte elastase, proteases iii. Inhibit complement iv. No effect on IL-1 d. SE: +/- anticoagulant, so care with patients that have bleeding disorders

Answer 66

a. Amino sugar needed for synthesis of chondroitin, heparin, & HA so needed for PGAG synthesis b. Derived from bovine cartilage orchitin c. Good absorption d. No side effects

Answer 67

a. Glycosaminoglycans b. Bind to & support collagen c. Derived from bovine trachea d. Inhibit MMP effects in cartilage matrix e. Increase synthesis of PGAGs f. Other uses: CV disease associated with thrombogenesis & PSS, IVDD, tracheal collapse

Answer 68

a. MOA: competitive antagonists at H receptors (keeping inactive state) i. Smooth m inhibition in GIT / resp tract, inhibition of vasodilation, ii. 2nd gen do not penetrate BBB, but 1st gen do iii. Anticholinergic activity for motion sickness b. Drug interactions: when using other P-glycoprotein substrates c. Adverse effects: i. 1st gen – CNS effects! “hangover” ii. GI side effects iii. Dry respiratory tract, urinary retention, dysuria

Answer 69

a. Hypotension b. Decreased cardiac output c. Respiratory depressants d. Increased intracranial pressure e. Disrupted thermoregulation * f. Malignant hyperthermia * g. +/- arrhythmias * h. * = NOT dose dependent

Answer 70

a. Analgesia from loss of consciousness b. MOA unknown / side effects dose dependent c. MAC = conc (volume/volume %) required to prevent purposeful movement in 50% normal patients d. MAC – BAR: conc needed to bloc CV response to painful stimulus (typically higher than MAC) e. Dose for sx ~1.2-1.5x MAC f. Affected by temp, age, dz, other drugs g. Adverse effects: i. CV – hypotension (SVR/CO) 1. Halothane sensitizes myocardium to catecholamines  arrhythmias ii. Resp  dec,  inc ICP, disrupt thermoregulation dose dep except malignant hyperthermia, arrhythmias, thermoregulation

Answer 71

a. CLASS: dissociative anesthetic – dissociation of thalamocortical & limbic systems b. MOA: non-competitive antagonist of NMDA receptor – prevents glutamate binding – depress thalamocortical, limbic, & RAS also some action at mu, delta, kappa opioid, & antagonist at muscarinic c. PK: rapid onset, crosses BBB, stimulate sympathetic NS i. Hepatic metabolism & excreted in urine ii. Combined with zolazepam – zolazepam longer duration in cats; tiletamine duration longer in dogs d. SE:  inc salivation,  inc ICP i. Muscle rigidity ii. Bronchodilation iii. Emergence delirium iv. Sympathomimetic actions e. DURATION 45-60 min > Ketamine (15-20min)

Answer 72

a. CONCENTRATION: i. Aminoglycosides ii. Fluoroquinolones iii. Metronidazole iv. Azithromycin (a type of macrolide FYI) v. Ketolides b. TIME: i. Beta lactams ii. Glycopeptides iii. Macrolides iv. Linezoline v. Tetracyclines vi. Clindamycin vii. TMS

Answer 73

a. Beta lactams – penicillin & cephalosporins b. Aminoglycosides – c. +/- fluoroquinolones (depends on specific ones) d. TMS (trimethoprim/sulfa) e. Some (few) tetracyclines (basically not doxy/mino)

Answer 74

a. Glycopeptides b. Macrolides c. Lincosamides d. Nitroimidazoles (metronidazole)

Answer 75

a. Reversible competitive H2 receptor antagonist b. MOA:  dec H+, pepsin, & intrinsic factor c. PK: 5=12x potent > cimetidine i. Hepatic elim 30% IV, 73% oral ii. 50% BA, ½ 2.5 h, not impaired by food d. Drug interaction: can inhibit CYP (<< cimetidine) e. SE: thrombocytopenia, otherwise minor f. Tx: gastritis, etc. may help with EPI to  dec enzymatic / acid hydrolysis of replacement enzymes

Answer 76

a. Antiemetic / tranquilizers b. MOA: dopaminergic c. SE: sedation,  dec BP

Answer 77

a. DE: pancreatin – add with each meal i. Diastases – used to replace alpha amylase ii. Bile acids – eg dehydrocholic acid b. AF: simethicone – antifoaming agent covering bubbles with thin layer – creates collapse

Answer 78

a. Motility i. Exogenous depress normal peristaltic reflex 1. MOA: presynaptic inhibition of Ach release / post-syn modulation  --> depletes neuron contract 2. Reduce Ca++ entry during AP  --> depletes neuron contraction ii. Endogenous in GI modulate normal GI motility / gastrin release b. Secretion i. Enhance gastric acid secretion via histamine ii. Stimulates net absorption H20 / electrolytes S/L intestines 1. Via delta receptors 2. Pre-syn inhibition of Ach release & inhibition of PG mediated adenylate cyclase iii.  inc HCO3- secretion from gastroduodenal mucosa

Answer 79

a. Anti-secretory drug: H2 receptor antagonist b. PK: least potent i. Rapidly absorbed (70% BA) ii. Excreted in urine unchanged & conjugated forms iii. ½ life 1 hour c. Drug interactions: impairs oral absorption of # drugs by altering pH & binds other drugs i. Microsomal enzyme inhibitor  Decreases metabolism of drugs (especially cyclosporine) d. SE: minor, TCP

Answer 80

a. Benzos – disrupt migration. MEC, also contractility jejunum i. Ace / diazepam -  dec G-E sphincter tone b. Morphine – dose  dec duodenal SM activity  dec bile flow c. Xylazine + ace + torb -  inc total gastric emptying time

Answer 81

a. Erythromycin i. Mimics effects of motilin (low doses) ii.  inc lower esophageal sphincter pressure b. Ranitidine i. H2 antagonist (remember H2 inhibits contraction) c. Misoprostol i. PgE: prokinetic in colon

Answer 82

a. Osmotic cathartics --> Mg salt, NaPO4, mannitol / sorbitol / lactulose i. Salts / compounds partially or slowly absorbed & H2O osmotically retained or attracted into lumen ii. Mg salts --> release CCK  inc peristalsis iii. Eg. Lactulose --> 1)  dec pH of colon --> favours NH4 so  dec NH3 1. 2) also causes osmotic effect b. Irritant cathartics --> stimulates mucosal lining of GIT --> initiate local myenteric reflex to enhance GI transit & activate secretion i. Eg. Irritating soaps or oils, castor oil, etc

Answer 83

a. MOA: derivative of morphine --> stimulates dopamine receptors & emesis at CTZ b. Depresses emetic center (?) c. SE: depressant d. Tx: induce emesis – esp in patients ingesting toxins

Answer 84

a. Emollient eg. Dioctyl Na Sulfosuccinate / mineral oil i. Not absorbed --> soften & lubricate fecal mass b. Simple bulk laxatives eg. Psyllium seed, methylcellulose, wheat brain, prunes i. Hydrophilic & not digested – absorbs H2O & swell --> distension / reflex contract for peristalsis

Answer 85

a. Bismuth salts – antisecretory & antimicrobial i. Antiprostaglandin effects b. Activated charcoal – ignite, wood, or peat forms pores i. Use with cathartic (sorbitol) ii. Food  dec efficacy iii. Absorptive & rapid action c. Cholestyramine – anion exchange resin binds acidic side chains i. Binds bile salts &  dec abs of cholesterol / lipoproteins ii. GIVE WITH FOOD or H2O

Answer 86

a. Lactobacillus b. Bifidobacterium c. Pattern recognition receptors & pathogen associated molecular patterns

Answer 87

a. MOA: binds progesterone receptors A/B & heat shock proteins i.  inc insulin conc,  inc lipase (lipoprotein) ii. Stimulate appetite & antagonize catabolic effect of cytokines b. SE: thromboembolic (humans) c. Therapy: treats nausea / inappetence for dogs with chemotherapy