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118 Cards in this Set

  • Front
  • Back
Frequent causes of vomiting in dogs
Dietary indiscretion
Intestinal virus
Organ failure
Motion sickness
Chemotherapy
Other: pancreatitis, hepatic disease
What are the advantages and disadvantages of the vomiting reflex?
Advantages: eliminates toxins, reduces pressure during obstructive disease, empties stomach prior to anesthesia (induced vomiting)
Disadvantages: Dehydration, electrolyte and acid/base disturbances, possibility of GI perforation or rupture, aspiration pneumonia
What is the coordinating center responsible for vomiting?
Emetic center (or Vomiting center), located in the medulla.
Where does the vomiting center receive afferent signals from? What conditions might trigger signals from each area?
Higher centers (cerebral structures): Head trauma, increased intracranial pressure
Vestibular apparatus: motion sickness, labyrinthitis
Chemoreceptor trigger zone: toxins, drugs
Pharynx: stimulation=gag reflex
Gastrointestinal organs: inflammation, irritation, or pain
Which emetic pathway does not go directly to the emetic center? Which other site does it pass through?
The vestibular apparatus sends signals through the CRTZ to the Emetic center.
When is emetic therapy (induced vomiting) indicated and contraindicated?
Indicated: expelling non-corrosive poisons (eg. chocolate), prior to general anesthesia to empty the stomach if not fasted.
Contraindicated: seizuring animals, comatose or neurologically impaired animals, ingestion of corrosive material, animals with a history of recent abdominal surgery.
How much of the stomach content will be emptied after vomiting is induced?
40-60%
How do peripherally acting emetics work? What are the three main peripheral emetics used in animals?
Act by irritation or stretching of the stomach (vagal pathway), induce vomiting within 5-15 minutes and a second dose can be given. Not all of them are safe.
Salt/warm salt water, Hydrogen peroxide, Syrup of Ipecac (if repeated use fails, must lavage to remove, potentially toxic).
How do centrally acting emetics work? What are the two main central emetics, and which species are they best used for?
Centrally acting emetics stimulate the CRTZ.
Apomorphine is used in dogs, given IV, SQ, or conjunctival; if the first dose does not work, a second should not be given.
Xylazine is most reliable in cats; if sedation occurs, it can be reversed with yohimbine.
When is the use of anti-emetic agents contraindicated?
GI infections
GI obstructions
Presence of toxin in the GI tract
Systemic hypotension
Epilepsy-varies by drug, some of them lower the seizure threshold.
Anti-dopaminergic anti-emetic: Phenothiazines
Acepromazine, and related drugs
Blocks Dopamine receptors at the CRTZ and emetic center (higher doses)
Broad spectrum (works on a variety of causes)
Anti-emetic doses tend to be low enough to avoid sedation, especially Chlorpromazine
Side effects: Hypotension, CNS depression, tremors, restlessness
Anti-dopaminergic/Serotonin Antagonist anti-emetic: Metoclopramide
Blocks dopamine and seratonin receptors in the CRTZ
Also has peripheral effect, gastric emptying
Broad spectrum
Has gastric promotility effects
IV constant infusion most effective
Contraindications: GI obstruction, DOES LOWER SEIZURE THRESHOLD, restlessness, depression
Serotonin antagonist anti-emetic: Ondansetron an Dolasetron
Antagonizes seratonin receptors in the CRTZ. Ondansetron also acts peripherally on the vagal nerve and gut.
Used in dogs with pancreatitis or parvo, as well as for chemotherapy induced vomiting.
Well tolerated by costly, used as a second line drug.
Serotonin Antagonist anti-emetic: Cisapride
Has prokinetic effects, good for when delayed gastric emptying is the cause of vomiting.
NK1 receptor antagonist anti-emetic: Cerenia (maropitant citrate)
Blocks substance P from binding to NK1 receptors in the emetic center and CRTZ.
Used for acute vomiting and motion sickness. Specifically labeled for dogs, used extralabel for cats. Well tolerated.
Antihistamine anti-emetics: Diphenhydramine, cyclizine, meclizine, etc
Blocks histamine pathways. Primary use is for vestibular disturbances.
More effective in dogs than cats.
May cause sedation.
What are the four primary causes of ulcers?
Physiologic stress
Dietary management-eg. grain fed horses
Ulcer causing drugs-eg. NSAIDs, glucocorticoids
Systemic diseases-eg. uremia
What are the three "excessive factors" that contribute to the formation of ulcers?
Gastric acid production
Pepsin production
Bacterial involvement-eg. Helicobacter pylori
What are the four mucosal defenses that prevent ulcers?
Mucus secretion
Rapid epithelial turnover
Bicarbonate secretion
PGE production-promotes above factors and produces other protective factors
What are the three pathways by which gastric acid is produced?
Vagal stimulation: ACh released and reacts with receptors on gastric parietal cells.
G cells: release gastrin which reacts with receptors on gastric parietal cells.
ECL cells: gastrin and ACh both react with receptors on ECL cells which releases histamine that reacts with receptors on gastric parietal cells.
All three of the above mechanisms activate H/K proton pumps in gastric parietal cells to release gastric acid into the stomach.
H2 receptor antagonists
Cimetidine, ranitidine, famotidine, and nizatidine.
Mechanism: Reversibly binds histamine receptors on gastric parietal cells.
Use: gastric and duodenal ulcers from a variety of causes
Side effects: Cimetidine may alter clearance of other drugs by inhibiting chytochrome P450 enyzme pathways.
Other: Famotidine>Ranitidine>Cimetidine. Ranitidine has prokinetic activity as well.
Proton-pump inhibitors
Omeprazole
Mechanism: Irreversibly binds the H/K pump; takes 24-48 hours to produce new H/K pumps.
Use: given once a day for a variety of causes; typically used for ulcers that do not respond to H2 blockers. Drug of choice for ultrasecretory diseases.
Other: only labeled for use in horses, but used very commonly in SA as well. Can be cost prohibitive. Accumulates in parietal cells, prolonged action.
Antacids
Tums, rolaids, etc.
Mechanism: Aluminum, magnesium, or calcium salts neutralize acid in the gastric lumen.
Use: broad spectrum; requires frequent dosing.
Other: Aluminum thought to stimulate mucosal defenses. Can alter pH and interfere with concurrently administered drugs-fluroquinolones, tetracycline, and digoxin.
Sucralfate
AlOH3 and sucrose sulfate salt
Mechanism: When activated by acid, forms a sticky paste that binds to ulcerative sites, stimulates mucosal defenses, and inhibits pepsin.
Use: Any
Other: may cause constipation. Because it requires an acidic environment, administer atleast 30 minutes before an antacid, H2 blocker, or proton-pump inhibitor.
Prostaglandin E1
Misoprostol (synthetic PGE1)
Mechanism: promotes mucosal defense similar to endogenous PGE, inhibits gastric acid secretion.
Use: ulcers from NSAID therapy.
Other: Can cause abortion in pregnant animals.
Protectives and absorbents
Bismuth salts, aluminum hydroxide, pectin, activated charcoal, gums.
Mechanism: either coat the GI epithelium or bind chemical compounds in the gut lumen.
Use: any
Other: may have to be given separate from other medications.
Prokinetics: Metocloprimide
Mechanism: increases ACh release and acts on GI receptors
Use: increases motility in the stomach and small intestines.
Use: Gastroesophageal reflux, post operative ileus, gastritis.
Contraindications: GI obstruction
Side effects: CNS side effects, cats and horses most sensitive.
Prokinetics: Cisapride
Mechanism: same as metocloprimide.
Use: increased motility in the esophagus, stomach, small intestine, and large intestine
Contraindications: GI obstruction or perforation; may cause cardiac arrhythmias if given with azoles or erythromycins
Other: Not available on the human market, must obtain from a vet compounding pharmacy.
Prokinetics: Domperidone
Similar to metocloprimide, but no CNS effects.
Not available in the US.
Prokinetics: Erythromycin
Stimulates motility in the stomach and small intestine when given at sub-antimicrobial doses.
May cause vomiting.
Prokinetics: Lidocaine
Mechanism: Stimulation of smooth muscle.
Use: Used in horses and small animals as a constant rate infusion for post operative ileus.
Prokinetics: Ranitidine
Mechanism: releases ACh; promotes motility of the stomach, small intestine, and large intestine.
What are the three alterations of reabsorption or secretion that lead to diarrhea?
Osmotic changes
Inflammatory processes
Secretory increase
What are the main goals of antidiarrhea therapy?
Reduce discomfort and frequency of bowel movements.
Restoration of flood and electrolyte balance
Bowel rest and modify diet
What are the causes of acute vs. chronic diarrhea?
Acute: diet, toxins, or infections
Chronic: bacterial overgrowth, intestinal fungal disease, and protozoal disease
Anti-diarrheal: opioids
Diphenoxylate, loperamide, paregoric.
Mechanism: binds to mu and delta receptors to decrease contractions, stimulates water reabsorption, and decreases secretion.
Use: Short term use for nonspecific diarrhea, works best in dogs.
Contraindications: GI infection/toxins, head injuries, respiratory disease, hepatic disease. Collie-breeds, horses, and cats have increased CNS sensitivity.
Side effects: Constipation, respiratory problems, sedation, may cause excitation/dysphoria.
Other: Paregoric mainly used in LA. Diphenoxylate is a controlled substance. Loperamide has no CNS effects (does not cross BBB), and is OTC.
Anti-diarrheal: Bismuth subsalicylate
Mechanism: separates to bismuth and salicylate. Bismuth absorbs toxins, coats surfaces, and has mild anti-bacterial effect. Salicylate has anti-inflammatory effects (anti-PG).
Contraindications: can be toxic to cats (salicylate).
Other: can turn stool black.
Anti-diarrheal: Sulfasalazine
Mechanism: metabolized in colon to sulfapyrindine and Salicylic acid. Salicylic acid has anti-inflammatory effects.
Use: inflammatory diarrhea of the large intestine.
Contraindications: can be toxic to cats (salicylic acid)
Anti-diarrheal: Protectives and absorbents
Same as anti-ulcer. Coats GI and binds to chemicals.
Anti-diarrheal: antimicrobial therapies
Metronidazole-giardia
Tylosin-chronic colitis
Clindamycin and tylosin-E. coli
Enrofloxacin-Campylobacter jejuni
Miscellaneous anti-diarrheals
Clucocorticoids-chronic diarrheal conditions.
Clonidine-increases fluid reabsorption.
NSAIDs-anti-inflammatory (anti-PG).
What is the goal of using a laxative or cathartic? Differentiate between the two.
The goal is to promote evacuation of the intestines by increasing frequency, volume, or consistency of defecation.
Laxitives-elimination of soft-formed stool
Cathartic-rapid fluid evacuation
What are the uses of laxatives and cathartics?
Prior to or during medical proceedures
Rapid passage of toxins or poisons with limited absorption
To relieve impactions (not full obstructions)
Stimulant cathartics
Phenolphthalein and bisacodyl (Dulcolax, Ex-lax); castor oil (converted to ricinoleic acid)
Mechanism: irritates the GI mucosa, increases motility and gut distention, increased fluid secretions, retains H20 in the gut.
Osmotic cathartics
Magnesium sulfate, magnesium hydroxide; Lactulose (synthetic disaccharide)
Mechanism: magnesium compounds are poorly absorbed and act as an osmotic agent. lactulose is poorly absorbed and further ferments in the colon. Both serve to draw water into the lumen, cause distention, and promote peristalsis.
Other: Overdoses can cause fluid loss; lactulose is most effective in cats.
Bulk cathartics
Dietary fiber
Mechanism: binds to water in the colon, causing distention
Other: water should be co-administered to augment action.
Emollient cathartics
Mineral oil
Mechanism: Lubricates and softens feces.
Surfactant cathartics
Docusate
Mechanism: alters surface tension of the intestinal content, mixes and softens stool.
Other: requires 24 hours for effect. Do not mix with mineral oil, may emulsify and allow absorption.
Enemas
Vegetable or mineral oils, warm soapy water, saline.
Primarily distends rectum and increases peristalsis. Soapy water also acts as an irritant to stimulate peristalsis.
Two types of epilepsy
Idiopathic-no identifiable cause.
Symptomatic-variety of causes. Intracranial-brain tumors, encephalitis, etc. Extracranial-metabolic disorders, toxins
Objective of drug therapy for epilepsy
Reduction in the frequency and intensity of seizures while avoiding excessive side effects. (Theraputic range and toxic range can be very close.)
Patient rarely becomes seizure free. If seizures are low in frequency, no medication may be necessary.
Long term control occurs in 60-70% of cases.
Principles of antiepileptic therapy
Theraputic range: should be based on the individual patient. Starting point is based on people, and will change for each patient as tolerance develops or disease states change clearance.
1/2 life effects: Frequency of dosing is dependent on half life. Also, loading dose may need to be given if 1/2 life is long and the situation is urgent.
Owner compliance: Because drugs require regular administration, a drug with a less frequent dosing schedule should be used to increase owner compliance. Drug should not be stopped abruptly, and missed doses should not be doubled up.
Avoid drugs which are known to lower the seizure threshold.
Side effects of anti-epileptic drugs.
Hepatotoxicity
Sedation
What are the ideal characteristics of anti-epileptic drugs?
Non-sedating
Safe and effective
High bioavailability and long 1/2 life
What are the most commonly used anti-epileptic drugs?
Phenobarbital and Potassium Bromide
Which anti-epileptic drugs work on GABA receptors? Which work thourhg other methods?
Barbiturates (phenobarb) and benzodiazepines (valium) act at GABA receptors.
Barbiturates also inhibit neurotransmitter release from presynaptic channels.
Potassium bromide hyperpolarizes post synaptic membranes to prevent signal transmission.
Phenobarbital
Classic choice for chronic treatment of epilepsy.
Pharmacokinetics: Weak acid (pKa = 7.3). Oral absorption slow but complete (80-100%). Widely distributed, but slow distribution to CNS. Primarily metabolized by liver. Half-life 40-80 hrs in dogs, 35-55 hrs in cats.
Can induce liver metabolism both of itself and other drugs, which may decrease effectiveness over time. Theraputic range is between 20-40 ug/mL
Side effects: Sedation and polyphagia, patient will develop tolerance in 10-14 days. Potentially hepatotoxic, blood dyscrasias, and hypothyroidism; important to monitor CBC/chem @45 days and every 6 months.
Dose: 20 mg/kg loading, 3-5 mg/kg for dogs and 2-3 mg/kg for cats every 12 hours maintenance.
Monitoring: @14-21 days, 45 and 90 days, then every 6 to 12 months based on clinical signs. Both peak(4-6 hours post pill) and trough (just prior to next dose) concentrations should be monitored.
Potassium Bromide
Oldest antiepileptic. Add on drug of choice but can be used alone.
Pharmacokinetics: Stabilizes neuronal cell membranes by hyperpolarization. Eliminated by the kidneys. 1/2 life-24 days in dogs, 1-2 weeks in cats
Side effects: Sedation and hind limb weakness. Contraindicated in renal disease. Diets high in chloride will increase elimination of KBr.
Dose: 20-30 mg/kg as add-on; 30-50 mg/kg as monotherapy. Does require loading dose.
Monitoring: Target-1.5 to 2.0 mg/mL of KBr. Should allow target of 25 ug/mL of phenobarb. Monitoring occurs at 3 months then yearly.
Diazepam
First choice in status epilepticus or emergency situations. Not used for long term control in dogs; can be used in cats, but phenobarb still better.
Pharmacokinetics: Acts on GABA receptors, rapidly distributed to CNS, low oral bioavailability, 1/2 life-3.2 hours in dogs, 15-20 hours in cats.
Side effects: Dogs develop tolerance. Hepatotoxicosis, emesis, lethargy, ataxia.
Dose: CRI @ 0.5-2mg/kg/hr; IV dose of 0.2-2mg/kg; Rectal 1.0 mg/kg up to three times per day.
Monitoring: No theraputic monitoring, but if long term use, monitor serum chem for hepatotoxicity.
Primidone (Mylepsin)
Metabolized to phenobarbital.
Expensive but not classified as a controlled drug.
Felbamate
Good for use in dogs that are refractory to phenobarbital and KBr.
Pharmacokinetics: Acts on GABA receptors, blocks glutamate receptors, and acts on sodium and calcium channels. Good oral absorption in adult dogs. 1/2 life-5-6 hours. 70% eliminated in urine.
Side effects: Does NOT cause sedation. Liver dysfunction.
Dose: 15 mg/kg TID
Monitoring: Serum chemistry for liver function every 4-6 months. Theraputic range 20-100 mg/L.
Gabapentin
Used in adjunct to phenobarbitol and KBr.
Pharmacokinetics: works on GABA receptors and inhibits sodium and calcium channels. Well absorbed, 60-70% elimination in urine, 1/2 life- 3-4 hours
Side effects: None currently reported
Dose: 10 mg/kg every 6-8 hours (4 x/day dosing).
Monitoring: none
Zonisamide(Zonegran)
Good add-on choice for refractory epilepsy.
Pharmacokinetics: Multiple mechanisms of action. 1/2 life-15 hours; 8 hours in dogs taking phenobarb. Tolerance may develop.
Side effects: transient sedation, ataxia, vomiting.
Dose: 5 mg/kg every 12 hours, 10 mg/kg if given with phenobarb.
Monitoring: Theraputic window 10-40 ug/mL. Start 1 week after treatment.
Levetiracetam (Keppra)
Add on or monotherapy. First choice of add on in cats.
Pharmacokinetics: Mechanism of action not well known. Almost 100% bioavailability in dogs. 70-90% eliminated in urine. 1/2 life- 3-4 hours in dogs, 4-8 hours in cats. Tolerance may develop.
Side effects: Hepatotoxicity reported rarely.
Dose: 20 mg/kg every 8 hours in both dogs and cats. May work BID for some dogs.
Monitoring: Target is 5-45 ug/mL. Due to high safety margin, theraputic monitoring is probably not required.
What drugs are commonly used for emergency control of status epilepticus?
Diazepam IV (or CRI) is 1st choice.
Phenobarbital-requires 15-20 minutes to work
Propofol
Etomidate
Levetiracetam IV
What is the most extensive use for sedatives and tranquilizers?
Short-term chemical restraint.
What is the only class of sedatives that also has an analgesic effect?
Alpha-2 agonists
What are the only two classes of sedatives that have a paired antagonistic class of drugs?
Benzodiazepines, and alpha-2 agonists.
What factors should be considered when picking a sedative/tranquilizer?
Procedure: length of sedation needed, is the procedure painful?
Status of the patient: will side effects of the drug worsen a condition that the patient has?
Contraindications of the drug.
Benzodiazepines
Drugs: Diazepam, midazolam, lorazepam, zolazepam.
Mechanism: GABA agonist-promotes the binding of GABA to the GABA-A receptors.
Pharmacologic effects: Dose dependant. Sedation, decreased anxiety, anticonvulsant activity.
Side effects: Minimal cardiovascular depression, respiratory depression, muscle relaxation, profound CNS depression at high concentrations.
Species specific: Horses may have muscle fasciculations, weakness and ataxia; Cats may have hepatic failure, changes in behavior, and appetite stimulation; Dogs may have cardiotoxicity (multiple doses), be hyper responsive to stimulus, and develop tolerance with prolonged use (1-2 weeks).
Contraindications: Painful procedures; patients with hepatic failure, cardiac problems, uncontrolled hypertension, shock, or respiratory depression. Do not use with already aggressive animals.
What is the reversal drug for benzodiazepines? What is its mechanism of action?
Flumazenil
Mechanism: competitively antagonizes the binding and allosteric effects of benzodiazepines.
Phenothiazines
Drugs: Acepromazine, promazone, chlorpromazine.
Mechanism: Inhibits dopaminergic receptors, alpha-1 adrenergic receptors, and serotonin receptors.
Pharmacologic effects: Sedative, muscle relaxant.
Side effects: Vasodilation, hypotension, reflex tachycardia. Inhibition of intestinal motility, antiemetic. Decreases hematocrit. Causes hyperglycemia. Affects thermoregulation (can lead to hypo or hyperthermia).
Contraindications: Painful procedures, hypotention, liver dysfunction, coagulopathies, thrombocytopenia, decreased platelet aggregation, uncontrolled hyperglycemia.
Species specific: can cause persistent paraphimosis in stallions (rare but use cautiously, warn owners).
Butyrophenones
Drugs: Azeperone, droperidol (typically +fentanyl)
Mechanism of Action: inhibits dopaminergic, alpha-1 adrenergic, and serotonin receptors; also antihistaminic effects.
Pharmacologic effects: sedation, muscle relaxation.
Side effects: Hypotension, reflex tachycardia, extrapyramidal signs (muscle rigidity, tremors), dysphoria, antithrombotic effect.
Species specific: Pigs and horses-reduced mean arterial pressure following IM admin. Dogs-aggressive behavior, esp in dobermans.
Contraindications: Painful procedures, coma, cardiac arrhythmias, pre-existing hypotention.
Alpha-2 agonists
Drugs: Xylazine, detomidine, medetomidine, dexmedetomidine, romifidine.
Mechanism of action: agonizes alpha-2 adrenergic receptors (also has some effect on alpha-1 receptors). Inhibits release of norepinephrine and acetylcholine from nerve endings. Drugs with higher a2:a1 activity have more specific sedative and analgesic effect with fewer side effects.
Pharmacologic effects: Sedation and analgesia.
Side effects: Biphasic cardiovascular response (1. vasoconstriction with hypertension and bradycardia, 2. hypotension and bradycardia.), ileus, vomiting, diuresis, hyperglycemia, may induce hyperexitation.
Species specific: Cattle are most sensitive to alpha-2's, can cause abortion in late gestation cattle. Can cause pulmonary edema in sheep.
Contraindications: Pre-existing cardiac conditions, dehydration, hypovolemia, urinary obstruction, hepatic impairment, epilepsy (may trigger seizures), diabetes mellitus, hypothermia.
Alpha-2 agonist reversal drugs
Atipamezole, yohimbine, tolazoline.
What are the 4 mechanisms of heart failure?
1. Systolic failure-not enough power to pump blood out of the chambers.
2. Diastolic failure-Not enough room to fill the heart completely.
3. Volume overload(excess preload)-excess blood enters during diastole
4. Pressure overload (excess afterload)-heart has to pump against too much pressure.
What are the 4 mechanisms of heart failure?
1. Systolic failure-not enough power to pump blood out of the chambers.
2. Diastolic failure-Not enough room to fill the heart completely.
3. Volume overload(excess preload)-excess blood enters during diastole
4. Pressure overload (excess afterload)-heart has to pump against too much pressure.
Principles of managing heart failure.
Early intervention may be beneficial.
Must understand pathophysiology of disease and pharmacology of the drugs being used to effectively treat.
Goal is management, not cure.
Principles of managing heart failure.
Early intervention may be beneficial.
Must understand pathophysiology of disease and pharmacology of the drugs being used to effectively treat.
Goal is management, not cure.
What are the 4 possible goals of therapy?
1. Improved contractility (systolic failure): Short term, catecholamines; Long term, digoxin, pimobendan.
2. Improve filling (diastolic failure): Beta-blockers, propanalol, atenolol; calcium channel blockers, diltiazem.
3. Treat edema and pleural effusion (reduce preload)-Diuretics, ACE inhibitors, venodilaors
4. Reduce cardiac work load (reduce afterload): ACE inhibitors, calcium channel blockers, arterioloar dilators.
What are the 4 possible goals of therapy?
1. Improved contractility (systolic failure): Short term, catecholamines; Long term, digoxin, pimobendan.
2. Improve filling (diastolic failure): Beta-blockers, propanalol, atenolol; calcium channel blockers, diltiazem.
3. Treat edema and pleural effusion (reduce preload)-Diuretics, ACE inhibitors, venodilaors
4. Reduce cardiac work load (reduce afterload): ACE inhibitors, calcium channel blockers, arterioloar dilators.
Diuretics for reducing preload, and treating edema and pleural effusions associated with cardiac failure.
Furosemide is the most commonly used. Will be discussed later.
Diuretics for reducing preload, and treating edema and pleural effusions associated with cardiac failure.
Furosemide is the most commonly used. Will be discussed later.
ACE inhibitors
Enalapril, captopril, benazepril, lisinopril, ramipril.
Effect: Decreases filling pressures, decreases vascular resistance, increases cardiac output.
Pharmacokinetics/dynamics:
1. Enalapril: Good oral absorption; 0.5mg/kg/sid, may have to give BID in dogs; lasts less than 24 hrs in dogs, 2-3 days in cats. Converted to enalaprilat in the liver. Renal elimination.
2. Captopril: must be administered while fasted. BID to TID dosing, shorter half-life.
3. Lisinopril: Lysine derivative of enalaprilat; also dosed at 0.5 mg/kg/day.
All are fairly safe.
Side effects: GI signs, hyperkalemia (rare), hypotension (important to monitor blood pressure), renal dysfunction and pre-renal azotemia (may need to decrease concurrent diuretic use).
ACE inhibitors
Enalapril, captopril, benazepril, lisinopril, ramipril.
Effect: Decreases filling pressures, decreases vascular resistance, increases cardiac output.
Pharmacokinetics/dynamics:
1. Enalapril: Good oral absorption; 0.5mg/kg/sid, may have to give BID in dogs; lasts less than 24 hrs in dogs, 2-3 days in cats. Converted to enalaprilat in the liver. Renal elimination.
2. Captopril: must be administered while fasted. BID to TID dosing, shorter half-life.
3. Lisinopril: Lysine derivative of enalaprilat; also dosed at 0.5 mg/kg/day.
All are fairly safe.
Side effects: GI signs, hyperkalemia (rare), hypotension (important to monitor blood pressure), renal dysfunction and pre-renal azotemia (may need to decrease concurrent diuretic use).
Digital Glyosides
Digoxin and digitoxin
Effects: Increased mycardial contractility, vagal tone, diuresis; decreases sympathetic tone; normalizes baroreceptor reflexes.
PK/PD: Narrow theraputic index. Good oral absorpion. BID dosing in dogs(24 hr 1/2 life), SID or every other day dosing in cats (48 hr 1/2 life). Dosage should be based on lean body mass, as it is not absorbed into adipose or fluid. Renal elimination.
Adverse effects: cardiac arrhythmias, GI upset, many drug interactions.
Contraindicated: Hypertrophic cardiomyopathy, conditions with diastolic dysfunction.
Digital Glyosides
Digoxin and digitoxin
Effects: Increased mycardial contractility, vagal tone, diuresis; decreases sympathetic tone; normalizes baroreceptor reflexes.
PK/PD: Narrow theraputic index. Good oral absorpion. BID dosing in dogs(24 hr 1/2 life), SID or every other day dosing in cats (48 hr 1/2 life). Dosage should be based on lean body mass, as it is not absorbed into adipose or fluid. Renal elimination.
Adverse effects: cardiac arrhythmias, GI upset, many drug interactions.
Contraindicated: Hypertrophic cardiomyopathy, conditions with diastolic dysfunction.
Arterial Vasodilators
Hydralazine
Effect: Reduces impedance to left ventricle ejection. Alternative to ACE inhibitors with chronic mitral regurg.
PK/PD: BID dosing; large individual variability, should be titrated to effect.
Adverse effects: Hypotension and tachycardia; Gi disturbances.
Arterial Vasodilators
Hydralazine
Effect: Reduces impedance to left ventricle ejection. Alternative to ACE inhibitors with chronic mitral regurg.
PK/PD: BID dosing; large individual variability, should be titrated to effect.
Adverse effects: Hypotension and tachycardia; Gi disturbances.
Venous Vasodilators
Nitroglycerin
Effect: Reduces preload, useful in cases with pulmonary edema. Indicated in acute treatment.
PK/PD: Effect in 15-30 min. Dose is variable and should be titrated to effect. Tolerance develops with long term use.
Venous Vasodilators
Nitroglycerin
Effect: Reduces preload, useful in cases with pulmonary edema. Indicated in acute treatment.
PK/PD: Effect in 15-30 min. Dose is variable and should be titrated to effect. Tolerance develops with long term use.
Balance Vasodilators
Nitroprusside
Effects: Reduces afterload and preload. First choice for emergency reduction of arterial blood pressure.
PK/PD: Fast acting and short lived. Must be give by CRI.
Adverse affects: Easy to cause hypotension, blood pressure should be monitored while administrating.
Balance Vasodilators
Nitroprusside
Effects: Reduces afterload and preload. First choice for emergency reduction of arterial blood pressure.
PK/PD: Fast acting and short lived. Must be give by CRI.
Adverse affects: Easy to cause hypotension, blood pressure should be monitored while administrating.
Phosphodiesterase III inhibitor
Pimobendan
Effect: Positive inotropic effect (increased contractility), arterial and venous dilator.
Also sensitizes myofibrils to intracellular calcium (pos inotrophic effect).
Phosphodiesterase III inhibitor
Pimobendan
Effect: Positive inotropic effect (increased contractility), arterial and venous dilator.
Also sensitizes myofibrils to intracellular calcium (pos inotrophic effect).
Catecholamines
Purpose: improved pumping function.
Epinephrine: Drug of choice for cardiac arrest, short term use. Increases cardiac contractility, heart rate, blood pressure, and cardiac output.
Dopamine: High doses used for support during cardiogenic shock.
Dobutamine: Used in cases of severe intractable heart failure caused by myocardial failure.
Beta-blockers
Purpose: reduce sympathetic stimulation in diastolic disturbances; provides early relaxation to give longer filling time.
Nonselective: Propranolol
Selective: Atenolol.
Note: non-selectives will also cause bronchoconstriction and should be used with caution in animals with respiratory compromise.
Calcium channel blockers
Diltiazem, verapamil, amlodipine.
First two depress contraction of the myocardial muscles, allows for longer filling time.
Amlodipine acts as a peripheral vasodilator.
Class IA Antiarrhythmics
Depress phase 0 of depolarization.
Used for supraventricular arrhytmias.
Contraindicated in systolic disfunction because of negative inotropic effects.
Quinidine: BID dose, oral only.
Procainamide: TID dose, Oral and IV.
Disopramide: Used for refractory arrhythmias.
Class IB Antiarrhythmics
Shorten duration of action potential.
Safe to use with systolic failure, less effect on contractility.
Lidocaine: Acute life-threatening ventricular arrhythmias. IV only, must be given by CRI, can cause seizures at high doses.
Tocainide: Given orally, as follow up to lidocaine.
Mexiletine: Given orally, follow up to lidocaine, fewer side effects.
Class IC Antiarrhythmics
Depress phase 0, depress conduction velocity.
Not used often in animals; only as conjunction therapy.
Flecainide: contraindicated in systolic dysfunction.
Encainide: no info given.
Class II Antiarrhythmics
Beta-blockers-Propranolol, Atenolol, Sotalol, Metoprolol, Esmolol.
Mechanism: Inhibits sympathoadrenal excitation, and decreases RAAS activation. Effect depends on baseline sympathetic tone.
Uses: Supraventricular tachycardias, refractory ventricular thacyarrhythmias (add on), Hypertrophic cardiomyopathy.
Class III Antiarrhythmics
Inhibit K+ Channels.
Amiodarone: longer half life when given repeatedly (often start BID then reduce), better when combined with IA or IC drugs. used for supraventricular arrhythmias.
Sotalol: Has class II and III effects. Used for supraventricular and ventricular arrhythmias.
Class IV Antiarrhythmics.
Calcium channel blockers, works in phase 1 and 2, depresses contractility.
Diltiazem: negative inotrope. Contraindicated in systolic failure.
Osmotic diuretics
Mannitol, urea, glucose.
Function at the proximal tubule
Thiazide diuretics
Hydrochlorothiazide, chlorthalidone, chlorothiazide.
Function at the early distal tubule.
Loop diuretics
Furosemide, ethacrynic acid, bumetanide.
Function at the ascending loop of Henle.
Potassium sparing diuretics.
Spironolactone (aldosterone antagonist), amiloride and triamterene (sodium channel blockers).
Function in the late distal tubule and collecting duct
Carbonic anhydrase inhibitors
Acetazolamide, ethazolamide, ethoxzolamide.
Function in the proximal tubule.
Mannitol (osmotic diuretic)
Filtered at the glomerulus, but little to no reabsorption. Osmotically pulls water into the tubular lumen.
Uses: Oliguric renal failure, cerebral edema, acute glaucoma.
Contraindications: Congestive heart failure, pulmonary edema, pre-existing osmotic diuresis (eg. diabetes). Use cautiously in dehydrated patients, rehydrate first.
Thiazide diuretics
Inhibit sodium chloride channels in the early distal tubule. Inhibits a maximum of 5-10% of sodium reabsorption.
Side effects: electrolyte disturbances (dec serum Na, Cl, magnesium, and potassium; inc Ca). Diminishes effect of insulin. Increase risk of cardiac arrhythmias if coadministered with cardiac glycosides.
Uses: Nephrogenic diabetes insipidus. Can be used as a back up to loop diuretics for edema.
Furosemide (loop diuretic)
Actively secreted in the proximal tubule, blocks sodium transport (Na/Cl/K transporter) in the ascending loop of henle. Inhibits up to 30% of Na reabsorption.
Side effects: hypokalemia, ototoxicity in cats at high doses. Drug interactions: cisplatin and aminoglycosides (inc ototoxicity), digoxin (arrhythmias), alters insulin requirements, NSAIDs may alter diuretic effect.
Use: Edema. Esp. acute pulmonary edema and nephrotic syndrome.
Spironolactone (aldosterone antagonist potassium sparing diuretic)
Competitively inhibits aldosterone in the late distal tubule; blocks aldosterone induced synthesis of Na/K pumps. More effective if aldosterone activity is high.
Uses: Hyperaldosteronism states. Blunts potassium loss due to other diuretics.
Contraindications: Hyperkalemia. Monitor potassium levels if given with ACE inhibitors.
Acetazolamide, methazolamide (Carbonic anhydrase inhibitors)
Inhibits carbonic anhydrase in the proximal tubule, less H is secreted and less Na is reabsorbed.
Use: Glaucoma.
What is "Aldosterone effect"?
Increased sodium in the early portions of the nephron reach the distal tubule, activating the RAAS system. Aldosterone is released, causing Na to be reabsorbed in the distal tubule and K to be secreted.
ACE inhibitors and Angiotensin II receptor blockers effect on the kidney.
Work to decrease ADH, aldosterone and thirst. Overall increase in water loss.
Urinary acidifiers
DL-mehtionine sulfate, Ammonium chloride.
Used to enhance efficacy or solubility of a drug, excrete toxins, or dissolve struvite stones.
Urinary antiseptics
Methenamine mandelate.
Used to treat fungal UTI's, urine must be acidic for drug to work.