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296 Cards in this Set

  • Front
  • Back
a 19 Carbon steroid
used for anabolic-very sick patients & antiestrogenic effect
Cause increase in appetite & muscle mass
Adverse affects of testosterone
Damages liver and germ cells
changes electrolyte balances, causes Na+ retention
an 18 Carbon steroid
Used for anabolic and estrogenic effects
Adverse affects of estradiol
↓ sperm production, disrupt endocrine system, possible cancer causing agent
a peptide hormone from posterior pituitary
a uterine stimulant; aids in parturition, ↓ post-partum bleeding
↑ milk letdown
A prostaglandin used to treat ulcers, particularly ulcers caused by NSAIDs
Mechanism of glucocorticoid action
block phospholipase enzyme from converting phospholipids into arachadonic acid, so can't form prostaglandins or leukotrienes
Mechanism of NSAID action
block cyclooxygenase enzyme from converting arachadonic acid to endoperoxides (precursor of prostaglandins)
Dimethyl sulfoxide,
industrial solvent properties
Scavenges free radicals made from endoperoxides: helps stabilize membranes & block C fibers-neurons of pain perception
Pharmokinetics of NSAIDs
weak acids, 75+% protein bound.
Undergo Phase I & II metabolism.
Some are microsomal enzyme inducers.
Uses of NSAIDs
Antiinflammatory effects.
↓ Prostaglandins & their effects
↓ fever, ↓clotting, ↓endothelial damage.
Adverse affects of NSAIDs
gi irritation/ulcers
liver toxicity
drug interactions-protein binding, microsome induction
Acetylsalicylic acid
Aspirin pharmacokinetics
Oral administration only (expect IcyHot)
Microsomal metabolism
Adverse effects of Aspirin
CNS effects-by acidosis
ear ringing
+all other NSAIDs side effects
Phenylbutazone pharmacokinetics
95+% protein binding
causes microsomal induction
given po or IV
not approved for dairy cows
Adverse effects of Phenylbutazone
all the usual NSAID side effects, especially gi effects
also causes anemia & Na+ retention
Not an NSAID
a weak base
Acetaminophren pharmacokinetics
given po only
undergo Phase I oxidation & Phase II conjugation rxns
Adverse effects of Acetaminophen
feline toxicity-glucuronidation dependent
long term use toxicity in all species-liver & kidney damage
Provide the best pain management
C-II, III, and IV drugs
Codeine, butorphanol, morphine
a CNS depressant
Pharmacodynamics of Opiods
Full or partial agonists or mixed agonist/antagonist depending on drug & species used in
a full agonist (mu & kappa receptors)
causes analgesia
a partial agonist
a full agonist (mu & kappa receptors)
causes analgesia
Pharmacokinetics of Opiods
po or parenteral admin.
metabolism by mixed function oxidases, then by conjugation
Side effects of Opiods
Produced by mast cells
Cause vasodilation,
↑ secretions
Histamine receptors
H1- vasculature & bronchi
H2- gi tract
Function of Antihistamines
Prevent histamine release
Competitive antagonists of H-1 or H-2 receptors
Action of Antihistamines that block release
Stabilize mast cell membranes so histamines can't get out
H-2 receptor antagonists
Used to treat gi disease,
↓ gastric acid
adverse effects= cytochrome 450 inhibition
H-1 receptor antagonists
most often used
best if used prophylacticly
High therapeutic index
Uses of H-1 receptor antagonists
Bronchial smooth muscle relaxation,↓capillary permeability, ↓secretions, ↓itching
CNS depression, antiemetic, anticholinergic
Acepromazine as antihistamine
a H-1 antagonist
also has sedative, antiemetic effects
2nd generation N compounds antihistamines
Polar molecules, so don't cross blood-brain barrier=limited CNS effects
Antihistamine Side effects
Sedation, anticholinergic,
α-1 blocker (given IV), teratogenic
Pharmacokinetics of Antihistamines
weak bases, given po or IM, rarely given IV.
metabolism by cytochrome P450 @ amine site, excreted via kidneys
Other bronchodilators
Direct sympathomimetics, B2 agonists
Indirect sympathomimetics, Methylxanthines
Direct sympathomimetic, B-2 agonist, used for bronchodilation
indirect sympathomimetics,
↑cAMP, used for bronchodilation
& smooth muscle relaxation
a methylxanthine
Side effects of methylxanthines
CNS stimulation, ↑gastric acid, tremors, diuresis
Very low therapeutic index.
Drug interactions with others metabolized by cytochrome P450
Other antiinflammatory treatments
Topical analgesics
Uses of gold
Don't know quite how it works, but effect (expensive treatment of joint diseases
Immunosuppressants as antiiflammatories
cytotoxic agents
Glucocorticoids for antiinflammatory effect
inhibit phospholipase A2
Characteristics of aminoglycosides
large, polar, weak bases
can be -cidal or -static
Absorption/distribution of aminoglycosides
Topical or IV, no PO absorption. PO dosing=topical in GI.
Very limited diffusion
pulse dosing
Clearance of aminoglycosides
Renal clearance
mostly unchanged
long-lasting, low level residuals
Pulse dosing
used for aminoglycosides so that the kidneys don't get overwhelmed & have time to get rid of previous dose
-cidal action of aminoglycosides
require 2-3x the dose of -static effect (boardline toxic levels)
interfer w/ membrane function, cause leaky membranes
-static action of aminoglycosides
inhibt protein synthesis through action of 30S ribosome=cause misreading of mRNA
Spectrum of action of aminoglycosides
G+ & G- aerobes
Bacterial strategies for resistance to aminoglycosides
increased deactivation
altered binding
decreasing O2=no energy-dependent transport
Adverse affects/problems w/ aminoglycosides
low therapeutic index nephrotoxicity neurotoxicity Residues=so no off-label use in food animals
Nephrotoxicity of aminoglycosides
tend to accumulate in kidneys
not good if it occurs
Neurotoxicity of aminoglycosides
predominately affects 8th cranial nerve (vestibulocochlear nerve)= hearing loss/loss of balance
blocks NMJ-decreased ACh release
fast admin IV=drop in BP from blocked ganglia
Characteristics of tetracyclines
lipophilic, weak base, 4 rings, Ca & Fe chelators, Long duration, protein binding, enterohepatic circulation=much longer 1/2 life
Elimination of tetracyclines
excreted mostly unchanged
mainly in feces
-also via kidneys & milk
Administration of tetracyclines
Absorption occurs via all routes, but PO is the safest route
Actions of tetracycline on bacteria
static action= blocks initiation of protein synthesis by effect on 30S ribosome, prevents access to mRNA
Spectrum of action of tetracyclines
Broad spectrum,
G+ & G-, aerobes & anaerobes,
as well as: ricketsia, chlamydophila, mycoplasma & protozoa
an aminoglycoside antibiotic
a tetracycline antibiotic
a tetracycline antibiotic, only excreted via feces
Adverse effects of tetracyclines
predispose to superinfections b/c so broad spectrum.
increasing restance
numerous organ toxicities
drug interaction
Contraindications for tetracycline use
pregnancy & young animals
Ca & Fe chelators=will deposit in bone & teeth
Organ toxicities found with tetracycline use
bone & teeth altered
older drugs can damage liver & kidneys
IV doses can irriate viens (phlebitis)
Drug interaction concerns with tetracycline
inhibit protein synthesis, so keep bacteria from growing & -cidal drugs won't work
Residual concerns with tetracyclines
require withdraw times of 5-12days
Administration of fenicols
PO-as a salt
Distribution of fenicols
little plasma binding, but gets into just about everywhere in the body (including CSF)
Clearance of fenicols
Phase I & II metabolism in microsomes
excreted as glucuronide metabolites in urine
Pharmacodynamics of fenicols
acts on 50S ribosome prevents protein elongation
Spectrum of fenicols
broad spectrum
G+&G-, aerobes & anaerobes
A reserve fenicol antibiotic
Amphiteric molecules
(a characteristic of fenicols)
one side lipid soluble
one side water soluble
allows for a wide (general) distribution
Adverse affects of fenicols
General antibiotic SE (gi irritation, allergies)
Inhibition of protein synthesis, can result in an aplastic anemia
Drug interactions
Drug interactions with fenicols
microsomal enzyme inhibitors-prolong duration of drugs metabolized by microsomal enzymes
Antibiotics that act on 50S ribosome
Administration of macrolides
PO-best if enteric coated (protect from gastric acid breakdown), Parenterally, topically
Pharmacokinetics of macrolides
Lactone ring
general distribution
moderate protein binding
oxidized by hepatic microsomes
Clearance of macrolides
undergo oxidization hepatic microsomes.
have some enterhepatic circulation
Spectrum of macrolides
mainly Gram +
usefull for some myobacterium & chlamydia infections
Mechanism of action of macrolides
act on 50S ribosomes=inhibit protein synthesis, by decreasing enlongation
makes them microsomal enzyme inhibitors
Uses of macrolides
Soft tissue infections
in place of Penicillin (allergies)
feed additives
Adverse effects of macrolides
Microsomal enzyme inhibitor
Exceptions of the macrolide rules
Rifampin-microsomal inducer

tilmicosin-B-agonist activity
Characteristics of Lincosamides
Hexose-w/amides, amphiteric
weak bases
Lincosamides to know
Pharmacokinetics of Lincosamides
high protein binding
gets into bone, but not CSF
Frequent dosing
Administration of Lincosamides
Elimination of Lincosamides
Phase I oxidation (demethylation)
excretion mainly in feces, less so in urine
Pharmacodymanics of Lincosamides
static effect
act on 50S ribosome
Spectrum of Lincosamides
Mainly Gram +
gets some anaerobes, mycobacterium & protozoa
a Lincosamide drug w/ increased lipophilicity (thanks to its -Cl)
can distribute into the bone
Adverse effects of Lincosamides
Diarrhea (really bad)-bad enough to kill pocket pets & horses
NMJ blocker
Classes of Antifungal agents
Antibiotic antifungals
Synthetic antifungals
Antibiotic antifungal agents
Polyenes: large, amphoteric molecules, weak acids
Pharmacokinetics of Polyenes
poorly water soluble
used topically
or IV for very serious fungal infections
highly protein bound
Excretion of Polyenes
Highly metabolized
but metabolites excreted slowly in urine
may last 7 weeks
Pharmacodynamics of Polyenes
-cidal action
bind sterol in fungal cell membrane-making it leaky
Amphotericin B
A Polyene antifungal
for very serious fungal infections, b/c has serious SE's
Adverse effects of Amphotericin B
Nephrotoxic (80%+ of patients)
Drug interaction
Drug interactions of concern w/ Amphotericin B
High protein binding
Microsomal metabolism
Additive nephrotoxicity when given w/ other drugs that target the kidneys
Synthetic Antifungal agents
Synthetic Antifungal agents to know
Drug charactiristics determining
GI therapeutic absorption
oil/water coefficient
ph/pka, preparation, dilution
particle size
Physiological factors determining
GI drug absorption
stomach pH, gastric emptying time, mucosal barrier, absorptive surface
greatest in small intestines
Consideration for GI drug in
large volume=dilutes drugs
pH/pka=traps weak acids
pH can change w/ diet
microflora-can metabolize drugs
very limited absorption
Goals of GI therapeutics
emisis-start/ stop
↓Gastric acid/ treat ulcers
↑GI transport
control diarrhea/constipation
management of pain/inflammation in GI
Drug w/ local action to induce vomiting
3% h2 O2
salt solutions (NaCI)- but can be toxic
Centrally acting drugs for inducing vomiting
Act vomiting center of brain /CRTZ
Morphine for emisis induction
a dopamine agonist
Xylazine in emisis induction
good for cats
acts centrally on vomiting center
Syrup of ipecac
good for vomiting induction
hepototoxic if not thrown back up
Strategies for locally-acting
protectants- sucralfate
a mucous membrane protectants
sticks to atomach lining
Given PO for:
treatmentof ulcers
can bind to other drugs in GI tract
antacids for antiemesis
only work if vomiting is acid-related
↓H+ - by binding
↑H+ - production
antiemetics drug strategies that act on nervous system
act on CRTZ or vestibular apparatus
an antidopaminergic antiemetic
-best option in animals
block d2 receptor
also tranquilizers-block α1
an anticholinergic antiemetic
-block M1 receptors in CRTZ
Characteristics of Heparin
a systemic anticoagulant
large MW
Weak acid
dosed in units
a glucosamine-containing mucopolysaccharide
Kinetics of Heparin
IV admin (SC sometimes)
Doesn't cross placenta
Zero-order clearance
Metabolism by plasma enzymes & liver
Zero-order kinetics
An absolute amount is cleared/time,
No fractional excretion
Pharmacodynamics of Heparin
effects clotting factors 2,9,10,11,12
Concerns of Heparin use
Only a prevention not treatment
dosage in unit, have to maintain constant concentrations in body to work
Vitamin K antagonists
Characteristics of warfarin
Vitamin K antagonist=anticoagulant
a weak acid
Pharmacodynamics of warfarin
effect Vitamin K dependent clotting factors
=II, VII, IX & X
Kinetic of warfarin
Only given PO
-takes 12-24 hours to start working
highly protein bound
broken down in microsomes
2-5 days to be cleared
Uses of Vitamin K antagonists
Limited uses in Vet med
can be used as long term clotting preventative
usually seen as a toxicity from ingestion of rat poison
Other anticoagulants
NSAIDs-decrease thromboxaneA2
Methylxanthine-decrease fibrinogen
Systemic coagulants
Vitamin K
Pharmacokinetics of Vitamin K
oil soluble
6-12 hours to onset
given PO or SC
Side effects of Vitamin K
High therapeutic index
allergies can cause hemolysis= lysed RBC build up in kidneys
Uses of Hematinics
Treat anemia
Types of Hematinics
Blood products
Uses of Iron to treat anemias
used for anemias due to decreased hemoglobin
PO admin=low Bioavailibility
Ferrous sulfate
Most common Iron preparations for treating anemia
Side effects of ferrous sulfate
Gi irritation that causes hemorrhage, constipation/diarrhea
deposits in the skin/liver
Things to consider w/ Ferrous sulfate
Bioavailability decreases as dose increases
F better when give Vit C, + helps keep as Fe++
Chelators given w/=antagonism
Fluids given to treat cariovascular system
to replace or maintain body fluids/electrolytes
isotonic saline
Ringers/Lactated Ringers
Dextrose solution
=Plasma extenders
help keep H2O in vessels (prevents leakage into tissues), by affecting osmotic pressure
usefull in treating trauma
Action of Diuretics
↑ urine volume w/o changing GFR
- interfere w/ Na reabsorption
Uses of Diuretics
↓ Edema
treatment of congestive heart failure
Similarities of site1,2&3 diuretics
weak acids
contain sulfur
protein bound
urinary excretion
can cause K loss
Pharmacodynamics site 1 diuretics
in proximal convoluted tubules
Carbonic anhydrase inhibitors
-prevents bicarbonate formation
can it be broken down=less H to go out
=less Na can go in
via H-Na transporter
↑Na in lumen=↑h2O loss
Uses of site 1 diuretics
Po or topical
-↓ Na in CNS, or glaucoma
-↑eye pressure in cataract surgery
Adverse effects of site 1 diuretics
tolerance common = no use in congestine heart failure
↓K =↑sensitivity to digoxin
↑acidosis from H retention
Pharmacodynamics of site 2 diuretics
Act in loop of Henle
- on Na, K, 2 Cl cotransporter
=causes ↓ Na, k, Cl, = ↓h2O,
Ca, + Mg
↑PGE 2x = vasodilation, ↑ renal blood flow
↓ water reabsorption
Kinetics of site 2 diuretics
most efficacious of diuretics
sterp dose-response curve after threshold
- amount to reach threshold varies due to tolerance
short-acting + 1/2 = 1-2 hrs.
-only dose SID, or BID to prevent too much dehydration
A site 2 diuretics
-used to treat edema from cardiac, hepatic or renal origin
+ to↓capillary pressure in racing horses
(↓risk of epistaxis)
Adverse effects of site 2 diuretics
ion inbalance - ↓ K, Ca
-↑sensitivity to digoxin
Ototoxic, rephotoxic when used w/ other drug w/ same effects
protein binding
NSAIDs = antagonists - ↓PG = renal vasoconstrition
Pharmacodynamics site 3 diuretics
- act in distal tubules
↓Na + Cl reabsorption
↑ Ca reabsorption
Kenitics of site 3 diuretics
good Po absorption
+1/2 = longer than site 2 diuretics (5-20 hr)
less harsh acting than sire 2
Uses of site 3 diuretics
primary use in vet. med = treat mammry edema
may also be used to treat edema of cardiac origin
Adverse effects of site 3 diuretics
= ↑ effects of digoxin
Site 4 diuretics
no veterinary uses (yet)
↓Na/K exchange in distal tubule
= Na loss w/o lossing K
Pharmacodynamics of osmotic Diuretics
Put " particles " in urine to
- diuresis occurs from body trying to dilute
an osmotic diuretic
- a osmotic saturated solution
used to traet acute renal failure + cerebral edema = emergency management
Pharmacodynamics of Angiotensin-converting enzyme inhibitors
blocks conversion of angiotensin I →angiotensin II
=prevents aldosterone production
-aldosterone -↑Na +h2O retention
-angiotensin II - vasoconstriction + hypertension + aldosterone production
Uses of angiotensin - converting enzyme inhibitors
to treat cardiac disease
- not raelly used in cats
kenitics of angiotensin-converting enzyme inhibitor
PO admin
many given as prodrugs
renal excretion
An angiotensin-converting enzyme drug
- prodrug
- approved for use only in dogs
Adverse effects of angiotensin-converting enzyme inhibitors
bradykinin-induced cough
not tested for safety duirng pregnancy
gi problems-oral drugs
Pharmacodynamics of vasodilators
vasodilation = ↑cGMP
↓ preload + afterload
Uses of vasodilators
to treat hypertensive emergencies
-acute congestive heart failure
-ischemic heart disease
also chronic conditions(like laminitis)
A vasodilatory drug
-effects veins more than arteries
PO, Buccal, Sublingual =very difficult
topical admin most popular
Adverse effects of Nitrate vasodilators
-tachy cardia
Kinetics of vasodilatory drugs ( nitrates)
high lipid solubility
= absorbed by any route
- short duration of action
Sodium nitroprosside
nitrate vasodilator
emergency drug-given IV
- 1 min onset→ 10 min. duration
potential toxicity in chronic use from - CN groups
Pharmacodynamics of Hydralazine vasodilators
↑cGMP, in smooth muscle
- directly arts @ arterioles
Uses of hydralazine vasodilators
to treat congestive heart failure w/ mitral regurgitation
- especially if left atrium enlarged.
mainly in dogs
Adverse effects of hydralazine vasodilators
activation of baroreceptors =
gi disorders
Kinetics of hydralazine vasodilators
usually P.O. admin
-I.V. available
protein binding
highly conjuction -t1/2=4hr
Uses of hormones & antagonist drugs
Specific THERAPEUTIC goals, don't cure
Diagnose, Metabolism/ antimetabolism, manipulation of growth/reproduction
Supplement, replace or antagonize natural hormones
diagnostic goals of Hormones
to see if target organ works
Actions of Metabolic/antimetabolic hormones
work on Calcium equilibrium
work on Iodine metabolism
either to increase or decrease
Drugs to increase Calcium in body
No PTH replacement
Give soluble Calcium salts, i.e. calcium gluconate
Hormones controlling body calcium concentrations
PTH-Parathyroid ↑
Calcitonin-thyroid ↓
T4-thyroid hormone
Characteristics of T4 durgs
dosage in mg
given as prodrugs
long t1/2, but dosed every 4 days
Characteristics of T3 drugs
dosage in mcg
short t1/2
dosed bid-tid
much more potent than T4
Pharmacokinetics of thyroid drugs
highly protein bound
liver metabolism
higher dosages needed in dogs b/c ↑ clearance
Uses of Antithyroid drugs
used to treat hyperthyroid=↑ activity, ↓ weight
↓ thyroid release/ ↓ size of thyroid gland
Adverse affects of Iodine/Iodide drugs
dermal damage from overdose
some take long time to work
others require use of radiation
prevent Iodine from be converted to T4=↓ thyroid hormones
given PO
Type I diabetes
Insulin dependent diabetes
B-cells don't make insulin
Type II diabetes
Insulin indepent diabetes
most common form in vet med.
still treat animals with insulin
Action of glucocorticoids as antiinflammatories
Inhibit phospholipase A2
Side effects of Glucocorticoids
Change fat distribution
altered integument
Decreased wound healing
Action of cytotoxic agents as antiinflammatories
general immunosuppressants
kills cells (usually used for anticancer therapies)
Topically for keratoconjunctivitis
Systemic use for rheumatoid arthritis, atopic dermatitis, autoimmune diseases, & cancers
Adverse effects of cytotoxic agents
tissue damage
Action of mucopolysaccharides
used to replace normal joint components by stimulating collagen & glucosaminoglycan synthesis
Think Glucosamine, Cosequine
Kinetics of mucopolysaccharides
Given IM or Intraarticular
but take 4-6 weeks to take effect
2 Types of Topical analgesics
Counterirritants/natural substances
Local anesthetics
Action of Counterirritants
Think Icy Hot (oil of wintergreen)
Increase blood flow to an area
Action of local anesthetics in topical analgesia
Use to relieve local joint pain
Inhibit Na transport across neural membrance=↓ nerve conduction
Adverse affects of local anesthetics
CNS Stimulation if absorbed
4 Factors to consider when using antiinfectives
Diagnosis- main concern
Drug Choice
Host Factors
Client Factors
Factors to consider with Drug choice
Mechanism of action
Adverse effects
Drug interactions
3 Mechanisms of Drug Resistance
↓ Penetration
↓ Binding to target
↑ Degradation of drug
Mechanisms of antiinfective action
act on cell wall/membrane
act on protein synthesis
act on nucleic acids
act on metabolites, & metabolism
Targets of -Cidal drugs
Cell wall/membrane
nucleic acids
Targets of -static drugs
Protein synthesis
cell metabolism
Host factors to consider w/ antiinfectives
Preexisting disease
Host immune system=needed to help fight infection-if compromised need -cidal drug
Sulfonamide drugs to know
Chemistry of Sulfonamides
Weak acids w/ Sulfur group
water insoluble
Pharmacokinetics of Sulfonamides
Usually PO admin, well absorbed
high protein binding
may require loading dose
Mechanism of action of Isoxsuprine
A vasodilator
acts directly on skeletal muscle blood vessels=decreases peripheral resistance
indirectly stimulates heart
Pharmacokinetics of Isoxsuprine
PO administration
Short t1/2
Hepatic metabolism
main use is to ↑ blood flow in horses legs
Methylxanthines use in the vasculature
smooth muscle relaxant & vasodilator
inhibit phosphodiesterase & ↑cAMP
Sympathomimetics affecting the vascular system
α-1 agonists=vasopressors (norepinephrine)
α-2 agonists=↓ BP (xylazine)
β-2 agonists=no use
Direct Sympatholytics affecting the vascular system
α-1 blockers (Acepromazine, quinidine)
β blockers=↓ BP (propranolol)
Indirect Sympatholytics affecting the vascular system
Decrease activity of the SNS
-antidopaminergic (ACE)
-decrease catecholamines storage/release (Diltiazem)
-α-2 agonists-↓SNS outflow (Xylazine)
Uses for Cardiotonic Drugs
For treating Congestive Heart Failure (no Cure)
Goal of Cardiotonic Drugs
↓HR & ↑ventricular filling= ↑Cardiac Output
A Cardiac Gylcoside
Derived from plant sources
Pharmacodynamics of Cardiac Glycosides
Inhibit Na/K/ATPase Pump
-less Na pumped out here= more out by Na/Ca pump
-More Ca in=actin-myosin activated
=↓SA rate, ↓AV conduction
↑ Myocardial contractility
4 Factors to consider when using antiinfectives
Diagnosis- main concern
Drug Choice
Host Factors
Client Factors
Factors to consider with Drug choice
Mechanism of action
Adverse effects
Drug interactions
3 Mechanisms of Drug Resistance
↓ Penetration
↓ Binding to target
↑ Degradation of drug
Mechanisms of antiinfective action
act on cell wall/membrane
act on protein synthesis
act on nucleic acids
act on metabolites, & metabolism
Targets of -Cidal drugs
Cell wall/membrane
nucleic acids
Targets of -static drugs
Protein synthesis
cell metabolism
Host factors to consider w/ antiinfectives
Preexisting disease
Host immune system=needed to help fight infection-if compromised need -cidal drug
Sulfonamide drugs to know
Chemistry of Sulfonamides
Weak acids w/ Sulfur group
water insoluble
Pharmacokinetics of Sulfonamides
Usually PO admin, well absorbed
high protein binding
may require loading dose
Pharmacokinetics of Cardiac Glycosides
Usually given PO
Bioavailability differs greatly by prep & patient (that's why monitor levels)
Low TI
Highly protein bound, ↑ t1/2
Toxic effects of Cardiac Glycosides
GI effects (vomiting)-actually used to monitor dosage
Visual & behavioral changes
Treatment for Cardiac Glycoside overdose
Withdraw drug
antiarrhythmia drug
Digoxin antibodies
absorbants (activated charcoal)
Drug interactions of concern w/ Cardiac Glycosides
can compete for renal clearance
Sympathomimetics for treating heart failure
β-1 selective drugs used in acute heart failures
Other treatments for heart failure
Phases of Cardiac action potential
Phase 0-Na in
Phase 1,2-Cl/Ca in, K out
Phase 3-K out
Phase 4-resting phase
Ideal drug to treat dysrhythmias
no significant side effects or interactions
PO or IV uses
reliable kinetics
Class I Antiarrhythmia agents
Target Na channels-↓Na transport
Used for atrial & ventricular arrhythmias
Class II Antiarrhythmia agents
Target β receptors of SA node
=β blockers (β1,β1β2 drugs)
Class III Antiarrhythmia agents
Not used much in Vet med
↓membrane responsiveness- prolongs repolarization
Class IV Antiarrhythmia agents
Block Ca channels
indirect sympatholytics
Class V Antiarrhythmia agents
the miscellaneous class
Target Na/K/ATPase pumps
(digitalis glycosides)
also includes new drugs that don't fit into other classes
Class Ia Antiarrhythmia agents
Low TI
↓Na going in, by targeting open Na channels (during Phase 0)
Action of Class Ia Antiarrhythmia agents
Slow Phase 0=↓ conduction velocity=↓rate & force of contractions
↑refractory period
goal is to allow SA node to reestablish control
Adverse effects of Class Ia Antiarrhythmia agents
can cause arrhythmias
GI effects
Interactions of concern w/ Class Ia Antiarrhythmia agents
can potentiate NMJ blocking of skeletal muscle relaxants & aminoglycosides
Class Ia Antiarrhythmia agents to know
Characteristics of Quinidine
Class Ia Antiarrhythmia agent
Low TI
↓ HR=treatment for chronic premature atrial beats
Pharmacokinetics of Quinidine
Blood concentrations directly related to therapeutic/toxic effects (for monitoring b/c absorption can vary)
highly protein bound
Side effects of Quinidine
↑digoxin effects-compete for renal excretion=results in overdose in one or the other
Microsomal enzyme induction
immune-mediated thrombocytopenia
Pharmacokinetics of Procainamide
good PO absorption
no protein binding
much shorter t1/2 than Quinidine
Characteristics of Procainamide
can cause immune-mediated reactions if given long term
Less α-blocking than Quinidine
Characteristics of Class Ib Antiarrhythmia agents
work on closed Na channels
little effect @ phase 0
work to ↑ depolarization threshold
used for ventricular arrhythmias
have no effect on HR
Low TI
Class Ib antiarrhythmia agent
a local anesthetic
↓ atrial excitability & Purkinje depolarization
no effect on SA or AV nodes=no effect on HR
Pharmacokinetics of Lidocaine
only used IV
very short t1/2
hepatic metabolism
Adverse effects of Lidocaine
Very low TI
Vasodilation-↓BP if given too fast
CNS stimulant
Interactions of concern w/ Lidocaine
Microsomal enzyme induction
affects blood flow to liver
Characteristics of Class II antiarrhythmia agents
β-blockers @ SA & AV nodes & ventricular muscles
↓HR by ↓rate of AV conduction
Pharmacokinetics of Class II antiarrhythmia agents
Low absorption when given PO
Protein bound
t1/2 ~4 hrs
Side effects of Class II antiarrhythmia agents
antagonism of β-2 & β-1= bronchoconstriction & hypoglycemia
sudden withdraw can cause arrhythmias
Class II antiarrhythmia agents to know
Propranolol-IV or PO admin
(β1β2 blocker)
Class III antiarrhythmia agents
Not really used in Vet med yet
↓ norepinephrine release
↑ duration of action potential
emergency uses
Class IV antiarrhythmia agents
Ca channel blockers
Cardiodepressants @ SA/AV nodes-slow Ca coming in
↓ conduction velocity
No Vet labeled drugs
Uses of Class IV antiarrhythmia agents
used for arrhythmias, hypertension
not specific for cardiac tissue-affect smooth muscle=vasodilation & ↓ BP
Classification of Class IV antiarrhythmia agents
Classified by structure
Dihydropyridines-more effect on vascular system than heart
Others-effect the heart more than the vascular system
Class IV antiarrhythmia agents to know
Class IV antiarrhythmia agent
used for hypertrophic cardiomyopathy in cats b/c better antiarrhythmia effects than vascular effect
Pharmacokinetics of Class IV antiarrhythmia agents
Usually given PO
high protein binding
short t1/2
Side effects of Class IV antiarrhythmia agents
inhibit mixed function oxidases
Class V antiarrhythmia agents to know
Digoxin-digitalis glycosides
target Na-K-ATPase pump to ↓ HR
Digoxin uses for antiarrhythmias
used for atrial tachyarrhythmias
Action to
Drugs used for Bradyarrhythmias
ANS Drugs
Isoproterenol for Bradyarrhythmias
sympathomimetic effects
used to treat cardiogenic shock
Atropine uses for bradyarrhythmias
↑ HR
Chemistry of local anesthetics
All are esters or amides
weak bases
easily metabolized=short acting
Uses of local anesthetics
infiltration anesthesia (SC)
nerve blocks (regional)
Spinal anesthesia
Lidocaine as a local anesthetic
an amide
can be used by any route for local anesthetics (topical, SC, local infil., epidural)
Pharmacokinetics of local anesthetics
Senistive pH-pKa relationship
unionized outside the cell (to get inside), ionized once inside the cell (to take effect)
quickly broken down in plasma or in liver
Pharmacodynamics of local anesthetics
Target Na channels to ↓Na transport @ nerve membranes
Membrane stabilizers
Effects automonic nerves> sensory>motor
vasodilators (except coke)
Adverse effects of local anesthetics
Occur after systemic absorption
Vasodilators (except coke)
CNS stimulation
How to prevent systemic adverse effects of local anesthetics
use low dose @ proper site
use vasoconstrictors to prevent absorption & spread
How to treat systemic adverse effects of local anesthetics
control convulsions
treat hypotension & arrhythmias
Local adverse effects to local anesthetics
may see immune-mediate response to topical applications
fats obtained from plants
usually used to retain moisture in skin, but can be used as vehicles for other agents
An Emollient
used to retain moisture in skin
can be used as vehicle for other agents
Types of agents for specifically for effects on skin or mucus membranes
Demulcents, Protectants, Absorbants
Keratolytics, cleaners
Wound treatments
Demulcents for skin/mucus membranes
High MW, water soluble
usually in lotions, ointments & artificial tears
Protectants and Absorbants for skin/mucus membranes
(Talc, Zinc oxide)
Irritants for skin/mucus membranes
used for vasodilatory effects
cause hyperesthesia, feel less pain in skin/joints
used to cleanse skin/↓keratin
Wound treatment agents
Used for wound debridement, to close wounds, aid in healing
Also antiseptics & ulcer healing agents
Povidone Iodide
An antiseptic used for wound treatments