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140 Cards in this Set

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4 Species that have a poorly developed emetic center
Horses
Ruminants
Rodents
Rabbits
These hormones can act on the CRTZ to trigger the Emetic Pathway
Dopamine D2
Serotonin 5-HT
Histamine H1
A-2 Adredergic
What percentage of the Stomach contents are emptied with emesis?
40-60%
Name 3 peripherally-acting emetics
Salt water (unreliable)
Hydrogen peroxide orally
Syrup of ipecac (emetine)
What's the problem with syrup of ipecac?
If they don't vomit, you have to get that out, too. Emetine is nephro and cardiotoxic.
Name 2 Centrally-acting emetics
and how they work.
Apomorphine (dopamine agonist - works on the CRTZ)

Xylazine (a-2 agonist - works on the CRTZ)
What's something you need to know about Apomorphine vs. Xylazine?
Apomorphine won't work in cats, but xylazine will. Also, Apomorphine at high doses will act as a CNS depressant and shouldn't be given repeatedly if emesis fails. Xylazine can cause hypotension, respiratory depression and cardiac arrythmias, but can be reversed.
Contraindications of Anti-emetics
Epilepsy
GI Infections
GI Obstructions
Systemic Hypotension
Name classes of Anti-emetic agents
Anti-dopaminergic
Seratonin Antagonists
NK-1 receptor Antagonists
Anti-histamine Agents (H1 antagonists)
Name the Anti-dopaminergic Agents
Phenothiazines
Metaclopramide
Phenothiazine specifics
-D2 at CRTZ AND acts at emetic center
-Side effects include: hypotension, sedation, and extrapyramidal signs.
Metaclopramide specifics
-D2 at CRTZ and seratonin (5HT3) antagonist
-Peripheral Cholinergic effect
Side effects: Increased GI motility, depression, aggression, hyperactivity, seizures
USE SPECIFICALLY FOR:
Metabolic disease
Acid-base imbalances
Vomiting due to delayed gastric emptying
Gastroesophageal reflux
Post-op ileus
Name the Seratonin antagonists
Ondansetron
Dolasetron
Metoclopramide
Cisapride

Work on:
Vagal nerve and Gut
Ondasetron/Dolasetron specifics
-S3 receptor in CRTZ (ond)
-5HT receptor (Dol)
-$$$
-No extrapyramidal effects
-Great for pancreatitis or parvo
Cerenia specifics
-Acts on NK-1 receptors found in emetic center, CRTZ, Intestinal epithelium
-Blocks Substance P
-Rapid onset
-No side effects
-dose OID
Antihistamine Specifics
-Benadryl, meclizine, Promethazine
-Sedation
Name the H2 Receptor blockers and what they do
Famotidine
Ranitidine
Cimetidine
Nizatidine
They reversibly inhibit Histamine action in the GI, decreasing Proton pump activity, thereby reducing the release of H+ ions.
Potency of H2 Receptor Blockers

And Primary uses
Famotidine>Ranitidine>Cimetidine

Cimetidine inhibits P450, and may slow metabolism of some drugs.
GI and duodenal ulcers
Gastritis
Gastric erosions
Omeprazole specifics
-Dose OID
-more potent than H2 Blockers
-inactive at neutral pH
-$$$
- Irreversibly binds to proton pumps
-use with MCT
Gastrinoma
Gastroduodenal ulcers
gastric erosions
gastric acid unresponsive to H2s
FDA approved in horses
Antacid specifics
Antacids including:
Sodium Bicarbonate
Calcium carbonate
Magnesium Hydroxide
Aluminum Hydroxide
- Increases pH of GI lumen
- Al stimulates mucosal defenses with pepsin and PG
Sucralfate specifics
Stimulates mucosal defenses
Protects against ulcers by making a gel over potential ulcer areas
Misoprostol specifics
Use with:
Ulcers from NSAIDs

May cause abortions
Primary Ulcer treatment plan
Famotidine
Famotidine + Sucralfate
Omeprazole if unresponsive (or ranitidine in larger animals)
Anti-ulcer drugs
Antacids
Misoprostol
H2 Antagonists
Name the Prokinetic drugs including Benzamides and others
Metaclopramide
Cisapride

Domperidone
Erythromycin
Lidocaine
Ranitidine
Cisapride specifics
Increases motility
Good for dogs, cats, horses
CNS effects
Can cause fatal arrhythmias when combined with -conazoles.
More potent than metoclopramide
Erythromycin specifics
motilin antagonist
Stomach and SI motility
Ranitidine Specifics
Preferred in Large animal
Increases ACH release
Good for increasing GI motility
Cisapride Uses and contraindications
Uses:
Chronic constipation, Post-op ileus, esophageal reflux, delayed gastric emptying
Contraindications:

GI obstruction
Cardiac
drug interactions
Drugs affecting the GI
Opioids
-paregoric
-diphenoxalate
-Loperamide
Bismuth Subsalicylate
Sulfasalzine
Antimicrobials
Glucocorticoids
Clonicine
NSAIDs
Opioids GI specific effects
Uses:
-bind to mu and delta receptors
-prolong transit
-Inhibit secretion
-stimulate reabsorption

Contraindications:
Contraindications:
-GI infections
-Head injuries
-Respiratory disease
-Hepatic disease
-Small dogs
-Collies
Bismuth Subsalicylate GI Specific effects
Antibacterial (helicobacter)
Turns stool black
Toxicosis in cats
Binds toxins
What drugs can cause an imbalance between absorption and secretion?
Opioids (diphenoxalate, loperamide)
Bismuth
Sulfasalazine
antimicrobials
Sulfasalazine mechanism/use
5-Amino salicylic adic inhibits leukotrienes

LI inflammation
Name two GI drugs to avoid in cats
Bismuth
Sulfasalazine
Bismuth Subslicylate mechanism/use
metabolized to bismuth/salicylate

bismuth binds toxins, salicylate blocks PG
GI Stimulants
Phenolphthalein and bisacodyl
Castor Oil
Osmotic Agents for GI stimulation
Mg
Na Salts
PEG
Sugar alcohols
Lactulose
Synthetic disaccharides
Bulk forming Agents for GI stimulation
bran, whole grains, psyllium
linseed, wheat bran, pumpkin
Lubricating/surface acting agents for GI stimulation
Mineral oil

Docusates
What drugs can typically cause interactions with Anti-epileptics?
Chloramphenicol
Metoclopramide
Enrofloxacin
Pen G
Phenobarbital mechanism/metabolism
Stabilizes the post-synaptic neurons by increasing Cl- conductance and decreaseing Ca+2 influx into cell

Potentiates GABA
Liver - induces some drugs including itself
Phenobarbital specifics
Well absorbed
Widely distributed
Slow into CNS
Test trough at
14-21 d
45
90
180
360
Potassium Bromide mechanism/metabolism
Stabilizes the neuronal cell membranes via hyperpolarization
Kidney
KBr Specifics
Only contraindicated in renal failure
Monitor at 3 mos, then yearly
Diazepam/ Primidone (mylepsin) mechanism/metabolism
Increases the action of GABA on Nerve
Liver
Diazepam specifics
THE drug for status epilepticus
Rapid CNS penetration
Tolerance develops in dogs
Drugs to avoid in animals
vigabatrin
lamotrigine
tiagabine
oxcarbaxepine
topiramate
phenytoin
carbamazepine
valproate
ethosuximide
Name the second generation Anti-epileptic drugs and their mechanism of action
Felbamate (Felbatol)
Gabapentin (Neurontin)
Zonisamide (Zonegran)
Levetiracetam (Keppra)
Felbamate -
Gabapentin - increases [GABA]; inhibits Na and Ca channels
Zonisamide - multi-faceted
Levetiracetam - binds to synaptic vesicle
Felbamate specifics
70% eliminated in urine
Does not cause sedation
May cause liver dysfunction
Gabapentin specifics
70% urine elimination
No induction of hepatic enzymes
Zonisamide specifics
Eliminated by liver
Very safe
Levetiracetam specifics
100% bioavailability
Mostly urine elimination
Extremely safe in dogs
May develop tolerance
Good for cats
In case of Status Epilepticus...
Give Diazepam IV
or...
pentobarb, phenobarb
Propofol
Etomidate
Levetiracetam
Name the benzodiazepines
diazepam
lorazepam
midazolam
Alprazolam
oxazepam

Name the reversal
flumazenil
Name the phenothiazines
Acepromazine
Chlorpromazine
Name the Butyrophenones
azaperone
Droperidol
Name the A-2 Agonists
xylazine
Detomidine
Dexmedetomidine
Romifidine

Name the reversals
yohimbine
Atipamazole
Tolazoline
Benzodiazepines mechanism
promote binding of GABA to the GABA receptors leading to hyperpolarization of the post-synaptic membrane
Mechanism of Phenothiazines
Inhibits dopaminergic receptors
Antagonist of seratonin receptors
Blocks A-1 receptors peripherally
Phenothiazine Specifics
May cause ileus.
May cause hypotension
Reflex tachycardia
Sinus bradycardia and 2nd degree heart block
Extrapyramidal signs
Sedation
Hyperglycemia
Antiemetic
Decreased hematocrit (sequestration of blood in spleen)
Hyper/hypothermia
No analgesia
Butyrophenones
Azaperone
Droperidol

Mechanism:
Antagonist of:
dopamine receptors
seratonin receptors
A-1 receptors
Also, antihistaminic effect.
Butyrophenones effects
Mild respiratory depression
CV depression
Hypotension
Reflex tachycardia
Extrapyramidal signs
Neuroleptic
Dysphoria
Antithrobotic effect
No Analesia

Contraindications
painful
Hypotensive
Cardiac arrythmias
Coma
Dobermans
A-2a Receptors in the ___ ____ are the primary site of action of A-2 agonists
Locus Coeruleus


What's the mechanism for that?
Gets into the post-synapse and prevents Influx of Ca+2
Peak sedation with an A-2 is at ____ minutes
~5 IV
~12 IM
Phases of CV effects by A-2s are
1. Hypertension/Bradycardia
2. Hypotension/bradycardia

Those further breakdown into:
1. Peripheral vasoconstriction>increased BP>Reflex bradycardia

2. Vasodilation>Hypotension>decreased Cardiac output
A-2 specifics
Cows
require 10% of horse dose
Brahman-influenced Highly sensitive

Sheep
May activate PIMs
Name the 4 mechanisms of Heart failure
Systolic - Pump
Diastolic - Filling
Volume Overload - Preload
Pressure Overload - Afterload
Name 5 types of Systolic Failure
DCM
Muscular dystrophy
Taurine Deficiency
Myocarditis
Arrhythmias
Name 4 types of Diastolic Failure
HCM
Pericardial effusion
Pericarditis
Lymphosarcoma
Name the 2 types of Volume overload
Chronic valvular disease
-L: Mitral, aortic
-R: Pulmonary, tricuspid

AV Shunting
Name the 2 types of Pressure Overload
Left ventrical
-systemic arterial hypertension
-Aortic stenosis

Right ventrical
-Pulmonary hypertension
-Pulmonic stenosis
Explain the pathophysiology of Cardiohypertrophy
myocytes degnerate>low contractility>low stroke volume>triggers RAAS>high afterload>overworked muscles>huge muscles
Explain the pathophysiology of Cardiodilation
myocytes degnerate>low contractility>low stroke volume>triggers RAAS>high preload>Stretched muscles>weak muscles
These drugs are used to relieve edema/effusion/preload
Diuretics and aldosterone antagonists
ACE Inhibitors and ARBs
Venodilators
These drugs are used to decrease cardiac workload/afterload
ARBs
Ca channel blockers
Arteriolar dilators
Pulmonary hypertension reducers
These drugs improve short-term contractility
catecholamines IV

Phosphodiesterase inhibitors IV
These drugs improve long-term contractility
Digitalis glycosides

Oral phosphodiesterase inhibitors
These drugs improve diastolic filling by reducing HR
Beta blockers

Calcium channel blockers
These drugs improve diastolic filling by improving early relaxation
Calcium channel blockers
Name the loop diuretics
Furosemide
Ethacrynic acid
Name the Thiazide diuretics
hydrochlorothiazide
chlorothiazide
Name the potassium sparing diuretics
Spironolactone
Name the ACE Inhibitors
enalapril
captopril
benazepril
lisinopril
ramipril

And what was it that those do?
block production of AT-2
3 facts about Enalapril
decreases filling pressure;increases output
<24hr duration in dogs
Renal elimination
3 facts about Captopril
have to administer TID
Bioavailability 4>3 with food
2 facts about lisinopril
Not affected by feeding
lasts longer than captopril
Possible side effects of ACEIs
vomiting
diarrhea
hyperkalemia
azotemia
How do Digitalis Glycosides work?
increase myocardial contraction
increase vagal tone
Increase diuresis (blocks renin)
decreases SNS tone

NARROW therapeutic range
Where would you NEVER use Digitalis Glycosides?
Sinus AV node
HCM
Diastolic dysfunction
4 facts about Digoxin
BID in dogs; SID in cats
Base dose on lean mass
HIGHLY VARIABLE Renal elimination
Toxicity is common (cats) - GI, arrhythmias
4 facts about Digitoxin
TID dosing
Hepatic elimination
95% Oral availability
95% bound to albumin
4 facts about hydralazine
arteriolar dilator
significant 1st pass hepatic metabolism
Alternative to ACEI for mitral regurg.
5 facts about nitroglycerin
venodilator
variable dose
takes effect in 15 minutes
Pre-load reducer
improves circulation, reduces O2 demand
4 facts about Nitroprusside
potent, balanced vasodilator
Afterload AND preload reducer
Fast acting/shortlived - CRI that shit
start @ low dose work up
DOC for emergency arterial BP reduction
4 facts about Prazosin
A-1 receptor blocker
artery/venodilator
Tolerance
Use when hydralazine prohibited
What do positive inotropes do?
Increase contractility
4 facts about Inamrinone
+inotrope
balaced vasodilation (low preload, afterload)
SHORT TERM TREATMENT OF SEVERE HF OR MYOCARDIAL DEPRESSION WHEN CONVENTIONAL THERAPY FAILS
Hypotension, arrhythmia, GI upset common (Overdose)
3 facts about milrinone
+inotrope
~35x more potent than inamrinone with fewer side effects
3 facts about pimobendan
+inotrope
Artery/venodilator
Reduces plasma NE, cytokines
3 facts about catecholamines
act on A and B adrenergic receptors
increase contractility, HR, BP, CO
Increase workload and O2 demand
DOC for cardiac arrest
What are the dose ranges for Dopamine?
low - ARF
High - Cardiogenic shock
Dobutamine is reserved for what
cases of sever intractable HF by myocardial failure
Non-selective Antiarrhythmics
propanolol - avoid if asthma
carvedilol - also vasodilates
sotalol - K blocker
Selective (B-1) Antiarrhythmics
Altenolol
Metoprolol
Esmolol (IV)
Antiarrhythmics in general
improve diastolic performance
negative inotropes
negative chronotropes
Calcium channel Antiarrhythmics
Diltiazem - HCM
Verapamil - HCM
Amlodipine - peripheral vasodilator
Tx for acute DCM (dog)
furosemide
dobutamine
nitroglycerin
lidocaine
O2
Tx for chronic DCM (dog)
furosemide
digoxin
ACEI

Maybes:
Taurine
antiarrhythmics
Tx for chronic HCM (cat)
furosemide
ACEI
diltiazem
low dose aspirin (thrombi)
Name the 4 classes of Anti-arrhythmic drugs
I - Sodium channel blockers
II - B-blockers
III - K blockers
IV - Ca blockers
Class I Anti-arrhythmics do what?
slow phase 0
increase threshold
inhibit misfire
Class Ia Anti-Arrhythmics do what?
Depress phase 0
depress conduction
slow repolarization

Those drugs are:
quinidine
procainamide
Disopyramide
3 facts about Quinidine
Oral use only
cardiac, GI, and dermal side effects
negative inotrope
What's the deal with Diopryamide?
potent negative inotrope reserved for when the other drugs stop working.

DO NOT USE WITH CHF!
Class Ib Anti-arrhythmics do what?
shorten AP
Shorten repolarization
increase fibrillation threshold

(goes from Batman to Batman running)

Those drugs are:
lidocaine - IV only
tocainide - ARF in dobies
Mexiletine - 80% urine elim.
Class II Anti-Arrhythmics do what?
Negative inotropic, chronotropic, dromotropic

Decrease heart O2 needs

Which makes them good for?
Supraventricular tachycardias
Atrial fibrillation
Refractory ventricular tachyarrhythmias
HCM
Class III Anti-Arrhythmic drugs do what?
inhibit K channel
prolong AP
Prolong refractory period
increase threshold

And those drugs are?
Amiodarone
Sotalol - Neg Inotrope
Class IV Anti-Arrhythmic drugs do what?
Ca channel blockers
depress contractility
reduce CO

That drug is?
diltiazem - atrial fib, HCM, supraventricular arrhythmias
These drugs are for acute supraventricular arrhythmias
Diltiazem
esmolol
Procainamide (IM)

These are for chronic
Digoxin and beta blockers/calcium blockers/procainamide
These drugs are for acute ventricular tachycardias
lidocaine
Procainamide

These are for chronic
Mexiletine and altenolol/procainamine/sotalol

Procainamide and altenolol
This is absorbed in the PCT
bicarb
sodium
water
This is absorbed in the DLOH
Water
This is absorbed in the ALOH
Na
Later, K, Cl, Na

NOT WATER.
This is absorbed in the DCT
Na

This gets tweeked
H
K
Na
This is altered in the CD
water out
Na out
K in
Name the 5 types of diuretics
Osmotic
Thiazide
Loop
K sparing
Carbonic Anhydrase Inhibitors
These drug classes work at the PCT
CAI
Osmotic
These drug classes work at ALOH
Loop
These drug classes work at the Early DCT
thiazide
These drug classes work at Late DCT
Potassium Sparing
These drug classes work at the CD
Potassium sparing
Osmotic diuretics are used for
Oliguric RF
Cerebral edema
Acute glaucoma
well-hydrated

But contraindicated for
Pulmonary edema
HF
dehydration
DM
hemorrhage
Thiazide diuretics work by
blocking Cl, the cotransport for Na. This prevents Na resorption

This causes loss of
Na
Cl
K (due to aldosterone)
Mg

But Ca is retained.
2 Facts about Thiazide diuretics
can cause arrhythmias when given with cardiac glycosides
diminish effects of insulin

And particular uses
edema
NDI
prevention of Ca stones

(largely replaced by Loop diuretics)
Loop diuretics work by
blocking Cl resorption in the LOH

so you lose
Na (~30%)
Cl
K (due to aldosterone)
Loop diuretics are great for
edema (all)
Congestive HF
Ascites
Hepatic fibrosis
EIPH in horses
K sparing diuretics work by
blocking the production of Na/K pumps

The two types are:
Na channel - miloride, triamterene
Ald antagonists - sprionolactone
K sparing diuretics specific uses
edema (liver disease, adrenal tumors)
Hyperald
cirrhosis

Don't use with
hyperkalemic
ACEI
CAI drugs
Acetazolamide
Methazolamide

Mainly used to reduce IOP

They work by
preventing the formation of bicarb in PCT, reducing H ions, thus less NA reabsorbed