Veterinary Pharmacology

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Local Anesthetics
Eg. Lidocaine, Bupivicane
MOA: To decrease the rate of depolarization at the NMJ by decreasing the membranes permeability to sodium and elevating the threshold

Opiods
Ei. Tramadol, Fentanyl, Tramazol
MOA: Bind to Gi protiens activating the receptor leads to INHIBITION of Adenylase Cyclase and decreased production of cAMP, which leads to inhibition of voltage-gated K+ channels and
activation of Ca2+ dependent K+ channels

NSAIDS
Aspirin, Paracetamol, Flunixin
MOA: To inhibit the Cyclooxygenase enzymes

Phenothiazine Tranquilizers
Acepromazine, Chloropromazine, Promazine
Block Dopamine receptors non-selectively and reduce the action of serotonin
ei are dopamine antagonists

Butyrophenones Tranquilizers
Doperol, Azaperone
Block Dopamine Receptors
(ei are dopamine antagonists)

Alpha 2 Agonists
Xylazine, Detomidine, Medetomidine
MOA: Stimulate central alpha 2 adrenergic receptors locally at both pre and post synaptic level
Reduce the NT release from the Nerve Terminal

Benzodiazepine hypnotics
Diazepam, Midazolam, Zolazepam
Potentiates the inhibitory action of GABA. Activation of the receptor causes an influx of Cl- ion movement into the neuron and hyperpolarization and inhibition of membrane depolarization

Antirhythmic Drugs – Class 1a
Quinidine, Procainamide
To block Na+ channels in the heart and reduce the rate of depolarization at phase 0
(medium dissociation from the channel)

Antirhythmic Drugs – Class 1b
Lidocaine, Mexilitine, Phenytoin
To block Na+ channels in the heart and reduce the rate of depolarization at phase 0
(fast dissociation from channel)

Antirhythmic Drugs – Class 1c
Flecainide, Encainide
To block Na+ channels in the heart and reduce the rate of depolarization at phase O
(slow dissociation from the channel)

Antirhythmic Drugs – Class II
Propanolol, Sotalol, Atenolol, Carvedilol
B-adrenergic receptor blockers (B adrenergic antagonists). Act by inhibiting the effect of catecholamines on the heart. Are negative inotropes.

Antirhythmic Drugs – Class III
Amiodarone, Bretylium, Sotalol
K+ channel blockers
Selectively prolong the AP duration and refractory period in the heart muscle w/o decreasing the conduction velocity

Antirhythmic Drugs – Class IV
Verapamil, Diltiazem
Block L-type Ca2+ channels (Ca2+ channel antagonist
Decreases the slow inward current of Ca2+ which has its greatest effects on the SA and AV nodes

Benzimadazoles Anthelmintics
Albendazole, Flubendazole, Mebendazole
Binds to nematode, cestode, and trematode beta tubulin. Prevents microtubule formation, which is important for parasite feeding. Microtubules are not present for 6-24 hours the parasite starves.

Also binds to and inhibits Fumarate Reductase, an enzyme found only in parasite mitochondria, leads to the uncoupling of oxidative phosphorylation and energy generation for the parasite.

Probenzimadoles anthelmintics
Netobimin, Febantel, Thiophanate (All pro-drugs)
Binds to nematode, cestode, and trematode beta tubulin. Prevents microtubule formation, which is important for parasite feeding. Microtubules are not present for 6-24 hours the parasite starves.

Also binds to and inhibits Fumarate Reductase, an enzyme found only in parasite mitochondria, leads to the uncoupling of oxidative phosphorylation and energy generation for the parasite.

Imidazoles anthelmintics
Levamisole
Acts on the parasitic nicotinic Ach receptors, producing depolarization and spastic paralysis of the worm. Is reversible but while the worm has convulsing it can’t hang on and gets passed out in the feces

Tetrahydropyrimidines anthelmintics
Pyrantel, Morantel, oxantel
Acts on the parasitic nicotinic Ach receptors, producing depolarization and spastic paralysis of the worm. Is reversible but while the worm has convulsing it can’t hang on and gets passed out in the feces

Organophosphate anthelmintics
Dichlorvos, Trichlorfon, Naphthalophos
Irreversibly inhibits AchE, and inhibits Ach breakdown at the synaptic cleft.

Macrocyclic Lactone anthelmintics
Ivermectin, Doramectin, Abamectin
Targets glutamate gated chloride channels in the invertebrate nerve and muscle cells lead to hyperpolarization of the post synaptic cells, which interferes with neurotransmission and leads to flaccid paralysis

May also increase the rate of GABA release from the Nerve terminals

Heterocyclic compounds
Piperazine, Diethylcarbamazine
P-hyperpolarization of NMJ of the muscles resulting in flaccid paralysis
DEC – Opsonizes larval heartworms causing them to be covered in complement and then destroyed by the hosts immune system

Cyclooctadepsipeptides
Emodipside
Binding to a Lacrophillen-like receptor leading to Inhibition of Ach elicited muscle contractions at the presynaptic terminal resulting in flaccid paralysis of the worm

Praziquantel – Anticestodal drugs
Causes Tetanic contraction of the parasite musculature due to increased Ca2+ intracellularly which paralysis the tapeworm. Digestion and irreversible focal vacuolization leads to digestion of the parasite integument.

Salicylanides – Antitrematodal drugs
Oxyclosanide, Rafoxanide, Closantel
Is a proton ionospore ei it creates a pore through the fluke membrane and allows H+ ions to flow in
Changes homeostasis and uncouples phosphorylation

Nitroxynil – Antitrematodal drugs
Uncouples oxidative phosphorylation in the trematode fluke

Clorsulon – Antitrematodal drugs
Inhibits 3-phosphoglucerate kinase and phosphoglycero-mutase and blocks the Embden-Myerhof glycolytic pathway

Diamphenethide – Antitremodal drugs
Deacylation to the active compound in the liver parenchyma changes the parasite integument effectively killing the parasite

Duddintonia flagrans
reduces the infective larvae of Haemonchus contortus in the feces of the sheep
It does not reduce GI nematode infections in the ewes

Positive Inotropes – Drugs that treat HF
Cardiac Glycosides, B agonists,
Phosphodiesterease III Inhibitors, Ca2+ sensitizers

Cardiac Gycosides – Positive Inotrope
Digoxin
Competatively binds to ATPase pump in the heart myocardial cells, increased intracellular accumulation of Na2+ promotes Ca2+ entry via the Na+/K+ enchanger. Result: Increased force of cardiac M contraction.

B agonist – A positive inotrope that treats HF
Dobutamine
Stimulates Cardiac B1 adrenergic receptors, activates Adenylate Cyclase, which converts ATP into cAMP, which stimulates Protein Kinase A to release intracellular Ca2+ from the Sarcoplasmic Reticulum. Result: Increased force and contractility of the Heart

Phosphodiesterase III Inhibitors – Positive Inotropes that treat HF
Amrinone, Milrinone
Inhibits phosphodiesterase III, an intracellular enzyme that degrades cAMP. Inhibition of cAMP degredation leads to increased cAMP, increased Ca2+ influx and increased contractility of the myocardial cells

Ca2+ Sensitizers – Positive Inotropes that treat HF
Pimobenden
Sensitized the myocardium to Ca2+ so that the same intracellular Ca2+ concentration will give you BIGGER contractile effect. Inhances the interaction w/in cell b/w Ca2+ and Troponin C complex
Used as a Front-line treatment for HF

Vasodilators – Drugs to treat HF
Reduce the load on the heart by decreasing preload, decreasing afterload, and decreasing central venous pressure.
2 types: Pure Vasodilators
Vasodilators with additional properties

Pure Vasodilators
Ca2+ channel blockers, Hydralazine, Prazosin, Nitrates

Ca2+ channel blockers – Pure vasodilators
Verapamil
Blocks L-type Ca2+ channels, decreases depolarization of heart and reduces contraction of heart muscles
Main vasodilator used

Hydralazine – Pure vasodilators
Directly relaxes smooth arteriole smooth muscle. Has little effect on venous system

Prazosin – Pure vasodilators
Selectively blocks alpha 1 adrenoceptors

Nitrates – Pure vasodilators
Isosorbide dinitrate, Trinitroglycerin,
Mimics endogenous Nitrous Oxide and directely dilates both arterial and venous smooth muscle

Phosphodiesterase V inhibitors – Vasodilators w/ additional properties
Sidafil, Viagra
Block phosphodiesterase V.
Result lowers hypertension

Drugs that treat HF
Diuretics, Positive Inotropes, Vasodilators, Neuroendocrine modulators, Negative inotropes

Neuroendocrine modulators
Ace inhibitors, B blockers, Aldersterone antagonists, Cardiac Glycosides

Ace inhibitors – Neuroendocrine modulators
Enalpril, Benazepril, Ramipril ALL are PRODRUGS
Binds to and blocks binding site of Angiotension Converting Enzyme inhibiting it. Angiotension Converting enzyme normally converts Angiotension I into Angiotension II. Brings Renin-Angiotension-Aldersterone system under control.
A mainstay of tx for HF

Angiotension II Receptor Antagonists
Specifically targets AT1 receptor. Inhibits its action and blocks its effects on vascular growth, Vasoconstriction, Salt retention

Aldersterone Antagonists
Block aldersterone action and cause body to RELEASE water

B Blockers – Negative Inotropes
Atenolol, Carvediol
Used to slow down the HR so it can fill better and each beat will then push more out
Ei Positive Lusiotrophic effect

Calcium Channel Blockers – Negative Inotropes
Diltiazen

Negative Inotropes – Drugs that treat HF
B blockers, Negative inotropes

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