Exam 3 Review: Histamine, Serotonin, NSAIDs, CHF Drugs

A comprehensive set of flashcards to aid in the review for Exam 3 focusing on topics including histamine, serotonin, NSAIDs, and CHF drugs.

What is anaphylaxis?

A severe allergic reaction that can be life-threatening.

What mediates physiological manifestations of anaphylaxis?

Free histamine.

What is the treatment sequence for anaphylaxis?

Epinephrine → Benadryl → Dexamethasone.

Where is mast cell histamine primarily concentrated?

In connective tissue.

What are the two general stashes of histamine?

Mast cell pool and non-mast cell pool.

What receptors do parietal cells have?

H2 receptors.

What do H2 receptors mediate?

Gastric acid secretion.

What physiological effects does histamine cause?

Vasodilation, itching, smooth muscle contraction, and edema.

What type of hypersensitivity is associated with the release of histamine?

Type I hypersensitivity.

What is the primary action of H1 receptor antagonists?

They suppress itching and flare associated with allergic reactions.

What are common H1 receptor antagonists?

Diphenhydramine, chlorpheniramine, and hydroxyzine.

What distinguishes first-generation from second-generation antihistamines?

First-generation antihistamines cross the blood-brain barrier and often cause sedation.

What is the physiological function of H2 receptors?

They mediate gastric acid production.

What is a common effect of morphine and doxorubicin related to histamine?

They can release histamine, causing allergic reactions.

What is an inverse agonist?

A drug that binds to the same receptor as an agonist but exerts the opposite effect.

What physiological role does serotonin play?

Regulates mood, appetite, and sleep.

What is a common side effect of H1 receptor antagonists?

Sedation.

Which drugs can cause unwanted histamine release?

Morphine, vancomycin, and certain antibiotics.

What are H2 antagonists used for?

To prevent gastric ulcers and manage gastric acid conditions.

What does the term "anaphylactoid reaction" refer to?

Reactions similar to anaphylaxis that occur without prior sensitization.

What is the role of prostaglandins (PGs) in inflammation?

They contribute to inflammation, pain, and fever.

What is the general function of NSAIDs?

To inhibit prostaglandin synthesis and provide analgesia.

How do COX-1 and COX-2 differ in action?

COX-1 is involved in normal physiological functions, while COX-2 is associated with inflammation.

What are common uses for non-selective NSAIDs?

Pain relief, anti-inflammatory actions and management of arthritis.

Give an example of a selective COX-2 inhibitor.

Rofecoxib (Vioxx) or Carprofen.

What adverse effects are associated with non-selective NSAIDs?

Gastrointestinal irritation and ulcers.

What is the main action of digitalis (digoxin)?

It increases the force of cardiac contractions (positive inotropic effect).

What effect does digitalis have on heart rate?

It lowers heart rate by increasing vagal tone.

What are the signs of digitalis toxicity?

Nausea, vomiting, diarrhea, and arrhythmias.

What is the preferred positive inotropic agent in heart failure management?

Pimobendan.

What are ACE inhibitors used for?

To manage heart failure and prevent cardiac remodeling.

What are common side effects of ACE inhibitors?

Hypotension and potential renal dysfunction.

What is the function of spironolactone?

It acts as a mineralocorticoid receptor blocker to counteract aldosterone.

What is the standard quadruple therapy for CHF management?

Positive inotrope, ACE inhibitor, spironolactone, and loop diuretic.

What role does renin-angiotensin-aldosterone system (RAAS) play in heart failure?

It contributes to fluid retention and increased workload on the heart.

What is the role of calcium channel blockers in cardiac therapy?

They reduce myocardial contractility and lower heart rate.

What is the mechanism of action of phosphodiesterase inhibitors like Pimobendan?

They enhance the action of calcium in heart muscle, improving contractility.

What is the primary effect of sildenafil in pulmonary hypertension?

It induces vasodilation in the pulmonary vasculature.

What is the therapeutic use of nitroglycerin?

To manage congestive heart failure by reducing preload.

What conditions can lead to the release of prostaglandins?

Trauma, pain, and inflammatory responses.

What is the significance of thromboxane A2?

It plays a role in platelet aggregation and vasoconstriction.

What is the common side effect of diuretics used in CHF?

Hypokalemia.

What is the effect of glucocorticoids on arachidonic acid metabolism?

They inhibit the formation of prostaglandins and leukotrienes.

Why should NSAIDs and glucocorticoids not be used together?

Both can cause gastrointestinal ulceration and other side effects.

What is the benefit of using benzodiazepines in chronic CHF management?

They reduce anxiety and assist with managing chronic edema.

What are common signs of allergic reactions in animals?

Restlessness, anorexia, vomiting, urticaria, and pruritus.

What metabolic mediator do mast cells release upon degranulation?

Histamine.

What is 'red man syndrome' associated with?

Vancomycin use leading to mast cell degranulation.

What are the cardinal signs of inflammation?

Redness, heat, swelling, and pain.

What effect does histamine have on blood pressure?

It causes hypotension.

What are the primary pharmacological effects associated with H2 receptor antagonists?

Reduction of gastric acid secretion and treatment of ulcers.

What role does serotonin play in gastric function?

It modulates gastrointestinal motility and secretion.

What does the term 'iatrogenic' refer to?

Reactions or complications caused by medical treatment or advice.

How does the body metabolize digoxin?

Primarily through hepatic metabolism and renal excretion.

What should clinicians monitor when using digoxin?

Serum drug concentration and signs of toxicity.

Pimobendan mechanism

Calcium sensitizer and PDE III inhibitor that increases contractility without raising myocardial oxygen demand.

Pimobendan contraindication

Contraindicated in hypertrophic cardiomyopathy or outflow obstruction.

Digoxin mechanism

Inhibits Na⁺/K⁺-ATPase → increased intracellular Ca²⁺ and stronger contractions.

Digoxin toxicity

Early signs include vomiting and cardiac arrhythmias.

Dobutamine receptor target

Selective β₁-adrenergic agonist producing potent inotropy.

Dobutamine duration

Used for short-term CRI (48–72 hr) due to β₁ receptor downregulation.

Dopamine low-dose effect

Stimulates D₁ receptors → renal vasodilation and increased urine output.

Dopamine high-dose effect

Stimulates α₁ receptors → systemic vasoconstriction.

Enalapril class

ACE inhibitor (prodrug converted to enalaprilat).

Benazepril renal advantage

Dual biliary and renal excretion; safer in renal dysfunction.

Telmisartan drug class

Angiotensin II receptor blocker (ARB).

Telmisartan pregnancy warning

Teratogenic—pregnant women must avoid handling.

Spironolactone mechanism

Mineralocorticoid receptor blocker; prevents aldosterone-induced fibrosis/remodeling.

Amlodipine therapeutic use

Drug of choice for systemic hypertension in cats.

Sildenafil mechanism

PDE V inhibitor enhancing nitric oxide-mediated pulmonary vasodilation.

Sildenafil primary use

Treatment of pulmonary hypertension (PHT) in dogs.

Furosemide mechanism

Inhibits Na⁺/Cl⁻ reabsorption in the loop of Henle → potent diuresis.

Nitroglycerin mechanism

Releases nitric oxide → venodilation and decreased preload.

Hydralazine mechanism

Direct arteriolar vasodilator reducing afterload.

Firocoxib selectivity

Highly selective COX-2 inhibitor (COXIB) used for OA or TCC.

Robenacoxib unique feature

COXIB approved for cats; accumulates in inflamed tissue for short duration.

Piroxicam special use

Nonselective NSAID used as adjunct therapy for transitional cell carcinoma.

Phenylbutazone primary species

Used primarily in horses for musculoskeletal inflammation.

Flunixin meglumine main indication

Treatment of equine colic and endotoxemia.

Meloxicam feline caution

Chronic use in cats can lead to renal failure and death.

Aspirin MOA

Irreversibly acetylates COX-1 → inhibits platelet aggregation.

Aspirin use in cats

Low-dose antithrombotic due to irreversible COX-1 inhibition.

Grapiprant mechanism

Selective EP₄ receptor antagonist; bypasses COX and spares GI/kidney.

Solensia mechanism

Feline monoclonal antibody targeting Nerve Growth Factor (NGF).

Librela mechanism

Canine monoclonal antibody targeting NGF for osteoarthritis pain.

Famotidine receptor target

H₂ receptor antagonist reducing gastric acid secretion.

Diphenhydramine generation

First-generation H₁ antagonist; sedating and crosses BBB.

Cetirizine generation

Second-generation H₁ antagonist; non-sedating due to poor CNS penetration.

Cisapride mechanism

5-HT₄ agonist used as prokinetic; must be compounded.

Metoclopramide receptor action

5-HT₄ agonist and weak 5-HT₃ antagonist; enhances GI motility.

Ondansetron class

5-HT₃ antagonist; antiemetic for severe or chemo-induced vomiting.

Mirtazapine dual role

5-HT₃ antagonist functioning as antiemetic and appetite stimulant in cats.

Cyproheptadine therapeutic use

Treatment for serotonin syndrome; also appetite stimulant.

Spironolactone formulation combo

Often combined with benazepril in “Cardalis.”

Benazepril class

ACE inhibitor; slows cardiac remodeling in CHF.

Pimobendan administration

Administer on empty stomach; unstable if compounded.

NSAID + glucocorticoid interaction

Contraindicated—can cause life-threatening GI ulceration.

Drugs causing histamine release

Morphine, codeine, vancomycin, polymyxins, doxorubicin.

Digoxin therapeutic monitoring

Requires serum level checks due to narrow therapeutic window.

Hydroxyzine metabolite

Converted to cetirizine (active antihistamine).