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Phase II > Drugs > Flashcards

Drugs Flashcards

1
Q

Ketamine - class, MOA, PK, SE

A

a. CLASS:
i. Dissociative anesthetic – dissociation of thalamocortical and limbic systems (changes awareness)
b. MOA:
i. Non-competitive antagonist of NMDA receptor – prevents glutamate binding – depress thalamocortical, limbic, & RAS also some action at mu, delta, kappa opioid & antagonist at muscarinic receptors
c. PK:
i. Rapid onset and effective IM (peak 10 min) vs 1 min IV
ii. Crosses BBB
iii. Stimulates sympathetic NS
iv. Metabolized in liver (norketamine) then excreted in kidney (DOG) – avoid if significant renal disease
v. Excreted unchanged in urine after forming norket (CAT)
d. SE:
i. ^ Inc cerebral blood flow / ICP
ii. Dec allodynia / wind up
iii. Muscle rigidity
iv. Dysphoria in cats
v. Increased myocardial work
vi. Negative inotrope effect
vii. Bronchodilation
viii. Increased IOP
ix. Remember – laryngeal reflexes remain intact

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2
Q

Barbiturates

A

a. Increased lipophilicity will increase potency and decrease time to onset/duration
b. MOA:
i. GABAa activation: increase CL conductance – hyperpolarize postsynaptic cells
c. Metabolism: liver, can cause CYPP450 induction
d. Excretion: urine
e. Effects:
i. CNS depression,  Dec CMO2 (cerebral metabolic rate?) : Dec ICP + CBF
ii. Splenic sequestration of RBC
iii. Resp depression, dec responsiveness to hypoxia / hypercapneia
iv. No analgesia
v. Slight dec in renal BF
vi. NOT IN SIGHTHOUNDS

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3
Q

Alfaxalone

A

a. CLASS: injectable anesthetic – schedule IV
b. MOA: steroid enhancing GABA & glycine-mediated CNS depression
c. PK:
i. Cytochrome P450-dep & conjugation dep hepatic metabolism + rapid metabolism
ii. Cannot be stored > 6 hours
iii. Can be given IM
d. SE:
i. Depresses cardiac output
ii. Can cause apnea
iii. Longer recovery than propofol – paddling, rigidity, myoclonus, vocalization
iv.  dec CBF, CMO2 (cerebral metabolic rate?), ICP

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4
Q

Propofol

A

a. CLASS: IV general anesthetic
b. MOA: Agonist at GABA receptor -  inc inhibition of CNS, also inhibition NMDA receptor
c. PK:
i. Emulsion with soybean oil, glycerol, and egg lecithin
ii. 28 emulsion add benzyl alcohol – prevents contamination
1. Avoid formula with liver patients
iii. Rapid + extensive hepatic metabolism – excreted in kidneys
iv. In cats – extrahepatic metabolism in pulmonary tissue
v. Recovery in Greyhouse slower; crosses placenta – neonates rapidly clear
vi. Also extra-hepatic metabolism therefore safe in liver patients
d. SE:
i.  dec intracranial pressure
ii. Respiratory depression
iii.  dec blood pressure
iv. Muscle relaxation
v. Vasodilation – compensatory tachycardia
vi. Oxidative injury to RBC in cats – Heinz body, facial edema

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5
Q
  1. ETOMIDATE
A

a. CLASS: induction agent (imidazole derivative)
b. MOA: Agonist at GABA receptor – CNS depression / hypnosis
c. PK:
i. Onset very quick
ii. Hydrolysis – metabolites excreted (<3%) in urine, bile, feces
iii. Rapid liver + plasma esterase metabolism
d. SE:
i. High dose (> 5 mg/kg) – hemolysis + shock
ii. Emesis
iii. Adrenal suppression (avoid in adrenal disease patients & sepsis!!!)
iv. Alone – muscle rigidity + myoclonus
v.  dec cerebral BF (but MAP same, so CPP same)
vi. Has been associated with seizures
vii. **Minimal effects in CV or respiratory
viii. *** Agent of choice for  ICP, cirrhosis, myocardial disease – from Lumb & Jones

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6
Q
  1. MEDETOMIDINE / DEXMEDETOMIDINE
A

a. CLASS: alpha 2 agonist – tranquilizer
b. MOA: binds to alpha 2 receptor -  dec NorEpi from CNS
c. Onset: within 20 min, peak analgesia at 20 min
d. Duration: Med – 60-90 min; Dex - ~45 min
e. PK: alpha 2:alpha 1 – Med 1600:1; Dex ~1600:1
i. Dexmed is dex + rotary isomer; less sedation than med
f. SE:
i.  dec HR ( dec CO); vasoconstriction
ii.  inc plasma BG
iii.  dec uterine motor activity (low dose or inc) (dose dep) (high dose)
iv.  inc urine production
v. Respiratory depression mainly with opioid combo
g. Indications: Sedative, pre-med, analgesia (low-level)

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7
Q
  1. What receptor effects of each hydrocone, codeine, oxycodone?
A

a. Hydrocodone -
i. Mu effects metabolized to hydromorphone
b. Codeine
i. Mu effects
c. Oxycodone
i. Mu effects – not recommended in dogs

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8
Q
  1. Inhalants x2 ?? Not sure what this means – perhaps how does solubility affect onset, induction, absorption, and what are the MACs of iso/sevo/des
A

a. Highly soluble – slower onset
b. Poorly soluble – faster onset
c. Higher CO – slower absorption (higher blood pool)
d. High minute ventilation – faster updake
e. MAC
i. ISO – dog 1.3%, cat 1.7%
ii. SEVO – dog 2.1%, cat 3.1%
iii. DES – dog 7.2%, cat 10.3%

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9
Q
  1. Midazolam
A

a. CLASS: Benzodiazepine – tranquilizers
b. MOA:
i. Enhance GABA effects -  inc Cl- conductance & hyperpolarize
ii. Cell – prevent action potentials
c. Duration: 1 hour
d. PK:
i. Very water soluble; IM or IV, sensitive to light
ii. Metabolized by liver, but better with liver disease than diazepam bc mam ?? (1-hydroxymethyl midazolam) metabolite has minimal biological activity
iii. Lipid soluble at physiologic pH – crosses BBB
e. SE: Muscle relaxation, sedation, mild excitement or agitation in both dogs & cats; HR/CO  dec, +/- mild  dec BP
f. Indications:  dec excitation from ketamine, sedative, to help with induction

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10
Q
  1. What are reversal agents for NMBAs? What are side effects?
A

a. Neostigmine & edrophonium
b. Inhibit acetylcholinesterase at nerve terminal thus  inc Ach concentration to bind to more receptors
c. SE: cholinergic crises: salivation, emesis, bradycardia, potentially death

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11
Q
  1. Meperidine
A

a. CLASS: Opioids
b. MOA: Full mu agonist
c. PK:
i. Duration 0.5-2 hours (1 hour in TJ)
ii. 10x less potent than morphine
iii. Has negative inotropic effects & anti-muscarinic effects
iv. Serotonergic effects
d. SE:
i. Significant histamine release!!!
ii. Local analgesia?? effects
iii. Does not really cause panting
iv. Hypotension
v. Vomiting, nausea
e. DO NOT GIVE with other monoamine oxidase inhibitors –> serotonin syndrome

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12
Q
  1. METHADONE
A

a. CLASS: Opioid
b. MOA: Full mu opioid agonist; also NMDA antagonist
c. PK:
i. Duration 2-4 hours
ii. Metabolized by enzymes inhibited by chloramphenicol and other similar drugs
iii. Synergistic with other opioids
iv. 2x potent than morphine
d. SE:
i. Less panting
ii. Less nausea/ vomiting
iii. Because NMDA Antagonist – less excitement in cats

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13
Q
  1. Examples of antisecretory drugs?
A

a. Diphenoxylate HCl – meperidine to control D
i. Potential for abuse??
b. Loperamide HCl – butyramide derivative – helps with D
i. Doesn’t cross BBB
ii.  transit time and luminal capacity
c. Glucocorticoids – stimulate Na absorption in jejunum –
d. Ca-calmodulin antagonists
e. NSAIDs
f. Sulfasalazine: 5-ASA (e.g. aspirin) - 5-aminosalicylate

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14
Q
  1. What are 2 peripherally active (reflex emetics)?
A

a. H2O2
b. Ipecac syrup -  inc lacrimation, salivation, bronchial secretions

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15
Q
  1. How do anti-cholinergics serve as anti-emetics?
A

a. Peripherally acting
b. Blocks muscarinic receptors in emetic center
c. Inhibits cholinergic transmission
d. Those that don’t cross BBB well: glycopyrrolate, propantheline, etc
e. Efficacy related to inhibition of afferent vagal impulses release of GI spasms + inhibits GI secretions
f. Can cause delayed gastric emptying – so DON’T USE with drugs like metoclopramide, cisapride, opioids – all rely on cholinergic receptors

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16
Q

a. Peripherally acting
b. Blocks muscarinic receptors in emetic center
c. Inhibits cholinergic transmission
d. Those that don’t cross BBB well: glycopyrrolate, propantheline, etc
e. Efficacy related to inhibition of afferent vagal impulses release of GI spasms + inhibits GI secretions
f. Can cause delayed gastric emptying – so DON’T USE with drugs like metoclopramide, cisapride, opioids – all rely on cholinergic receptors

A

a. Choline – make phospholipids to prevent fatty liver
i. Lipotropic agent – convert liver fat to PL?
b. Selenium – catalyzes oxidation of  dec glutathione
i. GP – removes H2O2 & FA hydroperoxides
c. Vit E – enhances selenium
i. Maintains glutathione in  dec form to prevent H2O2
ii. Acts as anti-oxidant
d. Vit B12 – utilizes fat, lipolysis
e. Vit K – helps absorb factors for 2,7,9,10 coag pathway
f. Glucose -  inc glycogen protects liver from cell damage

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17
Q
  1. Domperidone
A

a. Dopamine antagonist – prokinetic similar to met
b. No cholinergic activity
c. Not inhibited by atropine
d. Does not cross BBB
e. Can modulate temp control, prolactin secretion, and activity at CTZ
f. Coordinates antiduodenal contractions

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18
Q
  1. Dirlotapide (Stentrol)
A

a. MOA: microsomal +G transfer protein inhibitor
i. Blocks release of lipoprotein into bloodstream
b. Adverse effects: V+, D+,  dec cholesterol, retinopathies, cataracts
i. DO NOT GIVE TO CATS
c. Tx: to target energy intake / anti-obesity

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19
Q
  1. Mirtazapine – MOA?
A

a. Serotonin 5-HT1 agonist – also inhibits serotonin reuptake

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20
Q
  1. Valium / Oxazepam – MOA?
A

a. Gabaminergic + central inhibition of satiety center in hypothalamus

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21
Q
  1. Cyproheptadine – MOA?
A

a. Antihistamine + anti-serotonin properties
b. Oral bioavailability 100%
c. Appetite stimulant

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22
Q
  1. Milk thistle
A

a. Silymarin – hepatoprotective
b. MOA??: ~ hepatic regeneration, scavenging oxygen free radicals
i. Stabilize cell membranes, competitive inhibition of toxin
c. PK: poorly water soluble
i. Concentration products needed for absorption
d. Drug interactions: inhibition of P-glycoprotein
i. Also inhibits CYP450 socare??

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23
Q
  1. S-adenosyl-L-methionine
A

a. SAMe
b. Functions: transmethylation – helps with detoxification, energy utilization, transcription, cell growth
i. Helps form phospholipid layer of cell membranes
ii. Shown to improve bile secretion and  dec drug toxicity
c. PK: oral bioavailability low
i. Ensure correct formulation!!!
d. Drug interactions: inhibits uptake of serotonin!!!
i. So care with behaviour modifying drugs

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24
Q
  1. Pentosan polysulfate
A

a. Beechwood hemicellulose
b. Treat cystitis in people
c. Stimulates HA synthesis
d. Maintains PGAG content in joints
e. SE: prolong clotting times,  inc PTT, TT, thrombocytopenia

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25
Q
  1. Pentoxifylline
A

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

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26
Q
  1. Phenylbutazine
A

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

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27
Q
  1. Deracoxib
A

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

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28
Q
  1. What is the difference between a cholagogue & a choleretic ( & hydrocholeretic)? Give examples.
A

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

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29
Q
  1. Hyaluronic acid
A

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

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30
Q
  1. Meloxicam
A

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

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31
Q
  1. Aspirin
A

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

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32
Q
  1. Carprofen
A

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.

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33
Q
  1. Piroxicam
A

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

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34
Q
  1. Firocoxib / Previcox
A

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?

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35
Q
  1. Etodolac
A

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

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36
Q
  1. Acetaminophen
A

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

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37
Q
  1. Lipoxygenase inhibitors
A

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

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38
Q
  1. Dual-acting NSAIDs
A

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

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39
Q
  1. Morphine
A

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)

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40
Q
  1. Butorphanol
A

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

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41
Q
  1. Tramadol
A

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

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42
Q
  1. Buprenorphine
A

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

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43
Q
  1. Atracurium / vecuronium
A

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

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44
Q
  1. Xylazine
A

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

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45
Q
  1. Diazepam
A

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

46
Q
  1. Oxymorphone
A

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

47
Q
  1. Atropine
A

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

48
Q
  1. Glycopyrrolate
A

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

49
Q
  1. Succinylcholine
A

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

50
Q
  1. Bupivacaine
A

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

51
Q
  1. Lidocaine
A

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

52
Q
  1. Trazodone
A

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

53
Q
  1. Acepromazine
A

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

54
Q
  1. Fentanyl
A

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

55
Q
  1. Hydromorphone
A

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!!!

56
Q
  1. Epinephrine
A

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

57
Q
  1. Dopamine
A

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

58
Q
  1. Norepinephrine
A

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

59
Q
  1. Phenylephrine
A

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

60
Q
  1. Dobutamine
A

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

61
Q
  1. PHENICOLS (eg. Chloramphenicol) – note more detail than needed
A

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

62
Q
  1. PENICILLIN – note more detail than needed
A

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

63
Q
  1. FLUOROQUINOLONE – note more detail than needed
A

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?

64
Q
  1. LINCOSAMINES (eg. Clindamycin) – note more detail than needed
A

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

65
Q
  1. CEPHALOSPORINS
A

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

66
Q
  1. MACROLIDES (eg. Erythromycin)
A

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

67
Q
  1. List the static vs cidal abx (classes)
A

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)

68
Q
  1. RIFAMYCIN
A

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

69
Q
  1. AMINOGLYCOSIDES (Eg. Gentamicin, amikacin)
A

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)

70
Q
  1. Which abx are GOOD penetration of CSF?
A

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

71
Q
  1. Which have POOR penetration?
A

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

72
Q
  1. What have moderate penetration with meningitis?
A

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

73
Q
  1. TETRACYCLINES (eg. Mino, doxycycline)
A

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

74
Q
  1. Metronidazole
A

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!!!

75
Q
  1. TRIMETHOPRIM-SULFA
A

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

76
Q
  1. Glycopeptides (eg. Vancomycin)
A

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

77
Q
  1. Phenothiazine
A

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

78
Q
  1. Omeprazole
A

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

79
Q
  1. Sucralfate
A

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?

80
Q
  1. Metoclopramide
A

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.

81
Q
  1. Famotidine
A

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

82
Q
  1. Ondansetron
A

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+

83
Q
  1. What drugs work at vestibular apparatus specifically to control emesis?
A

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

84
Q
  1. Bethanechol
A

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

85
Q
  1. Maropitant (Cerenia)
A

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

86
Q
  1. Antacids – examples, MOA, PK, SE
A

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

87
Q
  1. Misoprostol
A

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

88
Q
  1. Cisapride
A

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

89
Q
  1. PGAGs
A

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

90
Q
  1. Glucosamine
A

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

91
Q
  1. Chondroitin sulfate
A

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

92
Q
  1. Antihistamines
A

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

93
Q
  1. What are adverse effects of inhalant anesthetics?
A

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

94
Q
  1. Inhalants
A

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

95
Q
  1. Tiletamine
A

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)

96
Q
  1. Which antibiotics are conc dep? Time dep?
A

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

97
Q
  1. Which abx that we learned of are primary excreted in urine?
A

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)

98
Q
  1. Which antimicrobials are NOT effective for gram (-)?
A

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

99
Q
  1. Ranitidine
A

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 (&laquo_space;cimetidine)
e. SE: thrombocytopenia, otherwise minor
f. Tx: gastritis, etc. may help with EPI to  dec enzymatic / acid hydrolysis of replacement enzymes

100
Q
  1. Butyrophenone derivatives: haloperidol/ droperidol
A

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

101
Q
  1. What are examples of digestive enzymes & anti-flatulence drugs?
A

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

102
Q
  1. How do opioids affect GI motility? Secretion?
A

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

103
Q
  1. Cimetidine
A

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

104
Q
  1. What are examples of non GI drugs impacting motility?
A

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

105
Q
  1. How do erythromycin, ranitidine, & misoprostal affect motility?
A

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

106
Q
  1. What are the 2 types of cathartics? List examples & how they work.
A

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

107
Q
  1. Apomorphine HCl
A

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

108
Q
  1. List 2 types of laxatives & how they work
A

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

109
Q
  1. GI protectants / absorbents + comparisons
A

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

110
Q
  1. What are the most helpful flora in probiotics? How does body know not to attack own flora?
A

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

111
Q
  1. Drug: megesterol acetate – MOA, SE, Therapeutic?
A

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

Phase II (4 decks)

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