Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
296 Cards in this Set
- Front
- Back
|
Testosterone
|
a 19 Carbon steroid
C-III 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 |
|
|
Estradiol
|
an 18 Carbon steroid
Used for anabolic and estrogenic effects |
|
|
Adverse affects of estradiol
|
↓ sperm production, disrupt endocrine system, possible cancer causing agent
|
|
|
Oxytocin
|
a peptide hormone from posterior pituitary
a uterine stimulant; aids in parturition, ↓ post-partum bleeding ↑ milk letdown |
|
|
Misoprostol
|
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)
|
|
|
DMSO
|
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 bleeding acidosis drug interactions-protein binding, microsome induction |
|
|
Aspirin
|
Acetylsalicylic acid
NSAID |
|
|
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
|
NSAID
|
|
|
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 |
|
|
Acetaminophren
|
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 |
|
|
Opiods
|
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
|
|
|
Codiene
|
a full agonist (mu & kappa receptors)
causes analgesia |
|
|
Butorphanol
|
a partial agonist
|
|
|
Morphine
|
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
|
Sedation
Emesis |
|
|
Histamines
|
Produced by mast cells
Cause vasodilation, bronchoconstriction, ↑ 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
|
(Antacids)
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 |
|
|
Epinephrine
|
Direct sympathomimetic, B-2 agonist, used for bronchodilation
|
|
|
Methylxanthines
|
indirect sympathomimetics,
↑cAMP, used for bronchodilation & smooth muscle relaxation |
|
|
Theophylline
|
Princess-bronchodilation
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
|
Gold
Immunosuppressants Mucopolysaccharides Topical analgesics |
|
|
Uses of gold
|
Don't know quite how it works, but effect (expensive treatment of joint diseases
|
|
|
Immunosuppressants as antiiflammatories
|
Glucocorticoids
cytotoxic agents |
|
|
Glucocorticoids for antiinflammatory effect
|
inhibit phospholipase A2
|
|
|
Characteristics of aminoglycosides
|
hydrophilic
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 |
|
|
Gentamicin
|
an aminoglycoside antibiotic
|
|
|
Tetracycline
|
a tetracycline antibiotic
|
|
|
doxycycline
|
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 residues |
|
|
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
parenterally topically IM-flofenicol |
|
|
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 |
|
|
Choramphenicol
|
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
|
fenicols
macrolides lincosamides |
|
|
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
|
Narrow
mainly Gram + usefull for some myobacterium & chlamydia infections |
|
|
Mechanism of action of macrolides
|
-static,
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
|
Diarrhea
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
|
clindamycin
|
|
|
Pharmacokinetics of Lincosamides
|
high protein binding
gets into bone, but not CSF Frequent dosing |
|
|
Administration of Lincosamides
|
BID-TID
Topical PO |
|
|
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 |
|
|
Clindamycin
|
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)
Vomiting anemia 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
|
Imidazoles
|
|
|
Synthetic Antifungal agents to know
|
Ketoconazole
|
|
|
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
ruminants |
large volume=dilutes drugs
pH/pka=traps weak acids pH can change w/ diet motility 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
opiods=morphine xylazine Ipecac |
|
|
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
but hepototoxic if not thrown back up |
|
|
Strategies for locally-acting
antiemetics |
protectants- sucralfate
antacids antibloat |
|
|
sucralfate
|
a mucous membrane protectants
sticks to atomach lining Given PO for: antiemetic 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
antidopaminergic anticholinergic antihistamine antiseratonin |
|
|
metoclopramide
|
an antidopaminergic antiemetic
-best option in animals block d2 receptor also tranquilizers-block α1 |
|
|
atropine
|
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
(Bases) |
|
|
Concerns of Heparin use
|
Only a prevention not treatment
dosage in unit, have to maintain constant concentrations in body to work Toxicity=hemorrhage |
|
|
Vitamin K antagonists
|
anticoagulants
Warfarin rodenticides |
|
|
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
|
Iron
Nutrients 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
Allergies 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 Normosol Dextrose solution |
|
|
Colloids
|
=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 |
|
|
Furosemide
|
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
|
Dehydration
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
|
Thiazides
- 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
|
↓K
= ↑ 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
↑osmolarity - diuresis occurs from body trying to dilute |
|
|
Mannitol
|
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 |
|
|
Enalapril
|
An angiotensin-converting enzyme drug
- prodrug - approved for use only in dogs |
|
|
Adverse effects of angiotensin-converting enzyme inhibitors
|
hypotension
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) |
|
|
Nitroglycerin
|
A vasodilatory drug
-effects veins more than arteries PO, Buccal, Sublingual =very difficult topical admin most popular |
|
|
Adverse effects of Nitrate vasodilators
|
hypotension
-dizziness -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
|
hypotension
activation of baroreceptors = ↑HR 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 ↓ |
|
|
Levothyroxine
|
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
|
|
|
Iodine/Iodide
|
↓ thyroid release/ ↓ size of thyroid gland
|
|
|
Adverse affects of Iodine/Iodide drugs
|
Residues
hypersensitivy immunotoxicity dermal damage from overdose some take long time to work others require use of radiation |
|
|
Thiorylenes
|
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 hepatotoxic 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
|
Infections
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
|
Vasodilation
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
|
Susceptibility
Resistance Mechanism of action Pharmacokinetics 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
|
Sulfasalazine
Trimethoprim Sulfamethoxazole |
|
|
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
|
(Viagra)
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
|
|
|
Digoxin
|
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
|
Susceptibility
Resistance Mechanism of action Pharmacokinetics 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
|
Sulfasalazine
Trimethoprim Sulfamethoxazole |
|
|
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
arrhythmias Visual & behavioral changes |
|
|
Treatment for Cardiac Glycoside overdose
|
Withdraw drug
antiarrhythmia drug Potassium Digoxin antibodies absorbants (activated charcoal) |
|
|
Drug interactions of concern w/ Cardiac Glycosides
|
↑Ca=↑toxicity
↓K=arrhythmias can compete for renal clearance |
|
|
Sympathomimetics for treating heart failure
|
β-1 selective drugs used in acute heart failures
|
|
|
Other treatments for heart failure
|
Diuretics
Vasodilators |
|
|
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
|
Effecacious
safe 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
hypotension GI effects allergies |
|
|
Interactions of concern w/ Class Ia Antiarrhythmia agents
|
can potentiate NMJ blocking of skeletal muscle relaxants & aminoglycosides
|
|
|
Class Ia Antiarrhythmia agents to know
|
Quinidine
Procainamide |
|
|
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 α-blocker=↓BP |
|
|
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 |
|
|
Lidocaine
|
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
Hypotension 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
|
Dilitiazem
|
|
|
Dilitiazem
|
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
|
cardiodepressant
hypotension 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
-Sympathomimetics-isoproterenol -parasympatholytics-atropine |
|
|
Isoproterenol for Bradyarrhythmias
|
sympathomimetic effects
used to treat cardiogenic shock |
|
|
Atropine uses for bradyarrhythmias
|
parasympatholytic
↑ 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 Topical |
|
|
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
|
|
|
Emollients
|
fats obtained from plants
usually used to retain moisture in skin, but can be used as vehicles for other agents Lanolin |
|
|
Lanolin
|
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
|
Emollients
Demulcents, Protectants, Absorbants Irritants 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
|
powders
(Talc, Zinc oxide) |
|
|
Irritants for skin/mucus membranes
|
used for vasodilatory effects
cause hyperesthesia, feel less pain in skin/joints (wintergreen) |
|
|
Keratolytics/cleaners
|
used to cleanse skin/↓keratin
(oticlens) |
|
|
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
|
