Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmocology > Cardiopulmonary Disease Pharm > Flashcards

Cardiopulmonary Disease Pharm Flashcards

1
Q

What drug is used commonly to treat CHF?

A

Furosemide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Furosemide

A

Lasix
Loop Diuretic
Impairs Na+/Cl-/K+ cotransport in ascending loop of Henle • Increases excretion of Na+, Cl-, K+, H+, Ca++, Mg++ (Can produce hyponatremic hypochloremic alkalosis)
Oral administration -> diuresis in ~1 hr, peaks in 1-2 hrs, duration ~6 hrs
Oral, injectable preparations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

AE of Furosimide?

A

Adverse Effects: Dehydration, electrolyte disturbance (see above) esp. hyponatremia and hypokalemia. Ototoxicity (esp. at high doses and concurrent use of aminoglycoside antibiotics)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Spironolactone

A

Aldosterone antagonist (as a diuretic it produces only a mild degree of diuresis)

  • Inhibits Na+/K+ exchange, when used together with furosemide (K+ wasting), some of the potassium loss is offset (hence its category name ‘potassium-sparing diuretic’)
  • Aldosterone blocking may directly benefit CHF via aldosterone receptor-mediated effects in heart, including cardiac remodeling.
  • Slow onset diuresis, peaks in 2-3 days.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

AE of Spironolactone?

A

Adverse Effects: Hyperkalemia, facial dermatitis (cats)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Hydrochlorothiazide

A

Decreases Na+, Cl- and increases Ca++ absorption in distal convoluted tubule • Increases excretion of Na+, Cl-, K+, Mg++

  • Mild to moderate diuresis
  • Oral administration -> onset ~1 hr, peaks ~4 hrs, duration 6-12 hrs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

AE of Hydrochlorothiazide?

A

Adverse Effects: Dehydration, electrolyte disturbance (see above) esp. hypokalemia. Can cause hypochloremic alkalosis, hyperuricemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

ACE Inhibitors

A

“PRIL” Captopril, Enalapril, Afosiopril

Antihypertensive. Blocks ACE in lungs from converting angiotensin I to angiotensin II (powerful vasoconstrictor). Decreases BP, Decreased Aldosterone secretions, Sodium and fluid loss.

Check BP before giving (hypotension)

*Orthostatic Hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Enalapril

A

Prodrug, activated in liver.

  • Prodrug and active metabolite undergo primarily renal clearance, consider dose modifications in renal failure.
  • Oral preparation.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Benazepril

A

Prodrug, activated in liver.

  • Less renal clearance than other ACEI’s, 50% in dog, 15% in cats (preferred ACEI for patients with renal disease).
  • Oral preparation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Angiotensin Receptor Blocker (ARBs)

A

Antagonists at the Angiotensin-II receptor
Telmisartan (ARB names generally end in -sartan). Oral preparation • Approved to treat feline systemic hypertension (more effective than ACEI’s), limited data in dogs
Adverse Effects: GI effects (nausea/vomiting/diarrhea), lethargy, weight loss in cats. Hypotension may require dose reduction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Positive Inotropes

A

These drugs increase myocardial contractility and in doing so they increase cardiac output in heart failure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Pimobendan

A

Called an ‘inodilator’ because it also causes systemic and pulmonary vasodilation.

  • Targets multiple processes in the pathology of heart failure • Positive inotrope by increasing the affinity of contractile regulatory proteins to Ca++. Inotropic effect occurs without increased myocardial oxygen demand.
  • May also inhibit elements of the neurohumoral response
  • Primarily hepatic clearance, biliary excretion (feces)
  • oral
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

AE of Pimobendan?

A

Adverse Effects: Rarely arrhythmogenic-use cautiously in animals with history of arrhythmia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Sympathomimetics

A

These drugs are not typically used to manage chronic heart disease, and are included here because they may be used in other contexts to manage cardiovascular function (e.g. shock, anaphylaxis, severe hypotension…)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Epinephrine

A
  • Agonist at a-1, a-2, b-1 and b-2 receptors, used in CPR, anaphylaxis
  • Vasoconstriction, positive inotropy/chronotropy, bronchodilation
  • inj preparations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

AE of Epinephrine?

A

Adverse Effects: Hypertension, arrhythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Norepinephrine

A

Agonist at a-1, a-2. Moderate agonist at b-1. Little/no agonism at b-2

  • Used as pressor in hypotension, particularly in patients with no other systemic pathology (e.g. renal failure, CHF)
  • Administered as CRI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Dopamine

A

Dose-dependent receptor agonist
-Administered as CRI
- When given at low doses, primary activity at dopaminergic receptors
Dopaminergic receptors, when stimulated, increase renal and mesenteric perfusion.
- Increasing the dose results in beta-1 stimulation (positive inotropy, chronotropy).
- High doses cause activation of the alpha-1 receptors leading to peripheral vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Dobutamine

A

Primarily beta-1 agonist, lower level alpha-1 and beta-2 agonism

  • Less dramatic changes in blood pressure than dopamine
  • Administered as CRI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Vasodilators

A

Arteriolar dilators relax arteriolar smooth muscle and thereby decrease systemic vascular resistance and left ventricular afterload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Amlodipine (Dihydropyridine CCB category)

A

CCBs of the dihydropyridine category have their primary effect on vascular smooth muscle (compared to non-dihydropyridine CCBs that have a greater effect in myocardial cells)

  • Amlodipine primarily acts on systemic arterioles, reducing LV afterload
  • Oral preparation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

AE of Amlodipine?

A

Adverse Effects: Hypotension, bradycardia, gingival hyperplasia (infrequent, in dogs with chronic use, reversible)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Hydralazine

A

Arterial vasodilator

  • Most commonly used in initial management of severe systemic hypertension/hypertensive crisis
  • Not preferred for long-term management of heart failure
  • Oral, injectable preparation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

AE of Hydralazine?

A

Adverse effects: Hypotension, reflex tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Nitroprusside

A

Nitrates

  • Not widely used, very $$$. Primarily venous dilation, restricted to IV administration with very close monitoring of blood pressure.
  • Injectable preparation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Sildenafil

A

Phosphodiesterase-V (PDE-V) inhibitor

  • -Inhibits PDE-V, which is localized to specific tissues and degrades the vasodilator, cGMP
  • Used to treat pulmonary arterial hypertension (also megaesophagus), owing to the tissuerestricted distribution of PDE-V
  • Oral preparation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Antiarrhythmics

A

It is worth noting that most drugs used to manage cardiac arrhythmias can also cause arrhythmias as adverse effects of those drugs. This is not surprising when one considers that these drugs work by modulating electrical impulse formation and conduction in a highly-electrically active organ

  • Generally antiarrhythmic drugs work through a relatively small set of electrophysiological changes:
  • Slowing tachycardia
  • Terminating the re-entry of an aberrant impulse
  • Preventing abnormal impulse formation or conduction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Antiarrhythmics Class I

A

Class I drugs, including lidocaine and mexiletine, block Na+ channels that are key to the rapid action potential upstroke (Phase 0). This slows the speed of the conduction of an electrical impulse. Most drugs in this class lose effectiveness in hypokalemic patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Lidocaine

A

Generally the first-choice IV drug for ventricular arrhythmias (bolus, followed by CRI)

  • With some exceptions it is generally ineffective in supra-ventricular arrhythmias.
  • Ineffective orally, complete clearance by first-pass metabolism
31
Q

AE of Lidocaine?

A

Adverse Effects: Arrhythmias, CNS (tremors, seizures) at high doses. Cats more prone to adverse effects.

32
Q

Mexiletine

A

Similar MOA to lidocaine

  • Orally effective, primarily hepatic clearance
  • oral prep
33
Q

AE of mexiletine?

A

Adverse Effects: GI, arrhythmias, excitement

34
Q

Antiarrhythmics Class II

A

Class II is composed of beta-adrenergic antagonists. Both non-selective (b-1 and b-2 antagonism) and cardioselective (b-1 antagonism) drugs comprise this class. Beta-1 blockade slows heart rate, slows atrioventricular conduction velocity, and increases refractoriness to impulses. Beta blockers are used in both supraventricular and ventricular arrhythmias, particularly those induced by enhanced SNS output. Beta blockers are considered first line drugs for both supraventricular and ventricular arrhythmias in cats.

35
Q

Atenolol

A

Selective b-1 blocker

  • Commonly used to slow sinus rate and AV conduction, and to suppress sympathetically mediated ventricular premature beats
  • Oral preparation
36
Q

AE of Atenolol?

A

Adverse Effects (more common in elderly, severe heart disease): Bradycardia, lethargy, inappetence, hypotension. Negative inotropic effects can exacerbate heart failure.

37
Q

Sotalol

A

Sotalol has both non-selective beta blocking activity (Class II) as well as potassium-channel inhibiting activity (Class III)
Non-selective beta-blocker, with Class III effects at higher doses.
-Renal clearance
-oral preparation

38
Q

AE of Sotalol?

A

Adverse Effects: Negative inotropic effects can exacerbate heart failure, arrhythmias, dyspnea, bronchospasm

39
Q

Antiarrhythmics Class III

A

Class III antiarrhythmics block a subset of potassium channels that open in Phase 3 repolarization, prolonging the action potential duration and the effective refractory period (the period in which the cell will not generate a new action potential if stimulated). Conduction velocity is not prolonged by Class III drugs. These drugs are effective treatments for ventricular arrhythmias, particularly those cause by reentry.

40
Q

Antiarrhythmics Class IV

A

Class IV antiarrhythmics are calcium-channel blockers (CCB’s). Class IV drugs target calcium channels in vascular tissue, where they regulate vasoconstriction, and in the heart, where they regulate pacemaking and myocardial contractility

41
Q

Diltiazem

A

Non-dihydropyridine CCB, targeting both vascular and cardiac tissue.

  • Slows AV conduction, potent coronary and mild peripheral vasodilation
  • Positive lusiotrope (increases rate of myocardial relaxation), particularly beneficial in restrictive heart disease, e.g. feline HCM
  • Comparatively lower negative inotropy than other non-dihydropyridine CCB’s
  • Hepatic clearance, chronic dosing prolongs t 1/2
  • Oral preparations available as immediate release and extended-release (e.g. Diltiazem ER), also available as injectable
42
Q

AE of Diltiazem?

A
  • Adverse effects: GI, lethargy, hypotension
43
Q

Digoxin

A

Positive inotrope, this indication largely now filled by pimobendan

  • Negative chronotrope
  • Anti-arrhythmic effect via increasing PNS output to SA, AV nodes, atria
  • Narrow therapeutic range -> therapeutic monitoring of plasma levels
  • Clearance primarily renal in dogs, combined renal/hepatic in cats
  • Digoxin toxicity not uncommon (narrow therapeutic range), long list of factors that predispose to toxicity (e.g., azotemia, hypokalemia drug-drug interactions)
  • Oral preparations
44
Q

AE of Digoxin?

A

Adverse Effects: GI (vomiting/diarrhea), cardiac (arrhythmias), CNS (depression, disorientation) Treatment symptomatic, correct predisposing factors (e.g., K+), Fab anti-digoxin

45
Q

Anti-thrombotics

A

Thrombosis is a well-characterized sequela to cardiovascular pathological processes. Feline hypertrophic cardiomyopathy (HCM) is a prototypical disease process that benefits from anti-thrombotic therapy. Given the role of platelet attachment/aggregation in initiating thrombus formation, it is not surprising that drugs targeting platelet aggregation can be effective anti-thrombotics

46
Q

Aspirin

A
  • Irreversibly inhibits COX-1 production of thromboxane in platelets (necessary for platelet activation/adhesion/aggregation)
  • Inconsistent therapeutic effect at low doses
  • oral preparation
47
Q

AE of Apirin?

A

-Adverse Effects: Narrow therapeutic range, GI: vomiting, Gastric ulcer disease, Bleeding

48
Q

Clopidogrel

A

Antagonist at ADP receptor responsible for signaling platelet activation

  • Superior platelet inhibition vs. aspirin
  • Prodrug, hepatic metabolic activation, substantial individual variability
49
Q

AE of Clopidogrel?

A

bleeding

50
Q

Melarsomine

A

Arsenic-based drug that impairs metabolism in adult worms

  • Not recommended in feline HWD (often self-limiting, low adult worm load, complications from adulticide). Not recommended for dogs with Class 4 HWD until after surgical removal of adult worms.
  • AHS recommends 3-dose treatment for dogs, 1st after 8 weeks of macrocyclic lactone/doxycycline, 2nd and 3rd one month later separated by 24 hrs.
  • Deep IM injection into epaxial muscles. Injection site reactions common.
51
Q

AE of Melarsomine?

A

Adverse Effects: Narrow therapeutic range: anorexia, injection site reactions, lethargy/ depression, inc. hepatic enzymes

52
Q

Doxycycline

A

Tetracycline-class antimicrobial

  • In HWD, doxycycline targets Wolbachia, an obligate endosymbiont bacteria essential for D. immitis development, reproduction, and adult survival. Wolbachia likely releases biomolecules that contribute to systemic inflammatory response that is prominent in HWD pathology
  • AHS recommends doxycycline treatment for weeks 1-4 following diagnosis (4 weeks prior to adulticide)
  • Oral solid and suspension, injectable preparations
53
Q

AE of Doxycyclin?

A

Adverse Effects: Renal tox at high doses, esophageal irritation/damage with solid dose formulations, esp. in cats -Recommend “chasing” oral dose with water

54
Q

Prednisone/Prednisolone

A

Glucocorticoid anti-inflammatory

  • Used to reduce immune response to Wolbachia, adult worms, and microfilariae as well as the immune response to their biomolecule release during treatment.
  • In patients with substantial microfilarial loads, treatment with glucocorticoids and antihistamines prior to macrocyclic lactones may reduce immune response/anaphylaxis
  • Prednisone is a prodrug requiring hepatic activation. Use prednisolone in patients with hepatic impairment, and in cats and horses (poor absorption and/or bioactivation of prednisone)
  • Oral, injectable preparations
55
Q

AE of Predisone?

A

Adverse Effects: Polyphagia, PU/PD, GI ulceration, hepatopathy, hyperglycemia, delayed wound healing, immunosuppression. In patients with heart disease, glucocorticoid-induced increased systolic blood pressure can worsen status.

56
Q

Ivermectin

A

Avermectin class of macrocyclic lactones

  • Lipophilic drug, primarily hepatic-biliary-GI clearance of un-metabolized drug (this explains why dogs eating feces from recently treated horses can ingest toxic levels of ivermectin)
  • Excluded from CNS by mdr1 efflux pump. Some dogs carry variant mdr1 genes/proteins and are susceptible to CNS toxicity at high doses (e.g. mitocidal therapy). At microfilaricidal/HWD prophylactic doses these patients are not at elevated risk of toxicity. Review Multidrug Sensitivity in Herding Breeds from the Veterinary Clinical Pharmacology Laboratory at Washington State University
  • Oral, injectable, spot-on preparations
57
Q

AE of Ivermectin?

A

Adverse Effects: Primarily focused on CNS: salivation, depression, ataxia, visual, coma, death.
-Treatment of toxicity supportive, intravenous lipid emulsion may be beneficial

58
Q

Milbemycin

A

Milbemycin class of macrocyclic lactones

  • Similar MOA, toxicity as ivermectin, used as microfilaricidal/HWD prophylactic
  • Better tolerated at high (e.g. mitocidal) doses than other macrocyclic lactones
  • Milbemycin is the most potent microfilaricide of the macrocyclic lactones, may precipitate immune reaction in patients with substantial microfilarial loads.
  • Oral preparation
59
Q

AE of Milbemycin?

A

Adverse Effects: CNS toxicity risk elevated in dogs with variant mdr1 treated with high doses

60
Q

Moxidectin

A

Milbemycin class of macrocyclic lactones

  • Similar MOA, toxicity as ivermectin, used as microfilaricidal/HWD prophylactic
  • Oral preparations
61
Q

Antitussives

A

Coughing can be a beneficial response to some respiratory disorders by moving exudative secretions and foreign material out of the airways. In other contexts, excessive coughing can be non-beneficial, potentially harmful, and become self-perpetuating in that the irritation produced from coughing can further stimulate the cough reflex. In animals susceptible to, or suffering from, tracheal collapse excessive coughing can contribute to the pathology.

62
Q

Dextromethorphan

A

Little/no activity at opioid receptors. May have analgesic/behavioral effects by blocking NMDA receptors. Antitussive activity likely due to receptor agonism in cough center (omega-1 receptors) that inhibits neurotransmission

  • Effectiveness in dogs is variable, low bioavailability
  • Adverse Effects: GI, ataxia
63
Q

Opioid antitussives

A

Opioid antitussives acting at the mu receptors reduce responsiveness of the cough center (medulla) to afferent stimuli and may also modulate activity at peripheral afferent sensory neurons.

64
Q

Hydrocodone

A

mu-active opioid prodrug with hepatic bioactivation

  • oral preparations, standard and extended release
  • may be combined with atropine (theoretically could provide decreased respiratory secretions, but typically included at doses that prevent drug abuse/diversion and not at parasympathetic inhibitory doses)
  • Adverse Effects: Sedation, constipation, bradycardia, paradoxical excitement in some animals.
  • Adverse effects more prominent in cats.
65
Q

Butorphanol

A

Primarily agonist at kappa receptor, weak mu antagonist -Antitussive effects more potent than morphine or codeine

  • Adverse Effects: mu adverse effects are minimal. Sedation, dysphoria (esp cats), reduced GI motility can occur.
  • Oral, injectable preparations
66
Q

Bronchodilators

A

Patients with respiratory disease processes that involve reversible constriction of small airways can benefit from drugs that cause smooth muscle relaxation leading to bronchodilation

67
Q

Adrenergic Agonists

A

In the context of respiratory disease adrenergic agonists are primarily used for beta-2 agonist activity that provides dilation of the small airways in diseases such as feline asthma, as well as in bronchospasm in inflammatory airway disease.

68
Q

Terbutaline

A

b-2 selective agonist

  • Adverse Effects: Tachycardia, arrhythmia, muscle tremors (“spillover” to b-1 agonism). Inhibit uterine contraction in pregnancy. Hypokalemia at high doses.
  • injectable and oral preparations
69
Q

Albuterol

A

b-2 selective agonist

  • similar adverse effect profile as terbutaline
  • oral, solutions for inhalation, and aerosolized preparations (inhalers)
70
Q

Methylxanthines

A

Bronchodilators that function through non-specific phosphodiesterase inhibition, increasing cAMP levels. These drugs possibly also act as adenosine receptor antagonists. They may also have antiinflammatory properties. Primarily used in inflammatory airway disease.

71
Q

Aminophylline

A

salt of theophylline, formulated to enhance oral absorption without gastric side-effects. Rapidly converted to theophylline (also available as a therapeutic drug).

  • nonselective phosphodiesterase inhibitor, increases cAMP concentration in airway smooth muscle cells leading to bronchodilation
  • CNS stimulant (use with caution in patients w epilepsy). Stimulates gastric secretion.
  • Adverse effects: GI: nausea, vomiting/diarrhea. Cardio: tachycardia, arrhythmias. CNS effects: excitement, tremors, seizures. -Narrow therapeutic range, therapeutic drug monitoring recommended
72
Q

Anti-inflammatory Drugs

A

The anti-inflammatory effects of glucocorticoids provide benefit in the treatment of non-infectious inflammatory airway disease (e.g., canine chronic bronchitis, feline asthma). Systemic therapy (e.g., prednisone/ prednisolone) or local installation (fluticasone proprionate) in metered dose inhalers are treatment options. Local therapy has the advantage of allowing locally high concentrations of drug to the affected respiratory tissue, while offering lower ‘total body’ dose that would reduce the risk of some adverse effects seen at systemic doses.

73
Q

Atropine

A

Adverse effects predictable for PNS inhibition: include xerostoma, ileus, constipation, tachycardia, urine retention
- Injectable preparations

74
Q

Glycopyrrolate

A

primarily used in anesthesia/surgical procedures • longer duration of effect vs. atropine

  • Injectable preparations
  • Similar adverse effects as atropine

Pharmocology (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions