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Pharmacology II Midterms - Unit 3 Angina Pectoris (PDF)

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Summary

This document is a lecture outline on Angina Pectoris, focusing on stable, atypical, silent, unstable, and rest angina, detailing associated symptoms, causes, and treatment strategies. It covers topics like therapeutic strategies and anti-anginal drugs and may be part of a pharmacology course for undergraduates.

Full Transcript

MIDTERMS PHARMACOLOGY II LECTURE UNIT 3: ANGINA PECTORIS OUTLINE STABLE ANGINA I...

MIDTERMS PHARMACOLOGY II LECTURE UNIT 3: ANGINA PECTORIS OUTLINE STABLE ANGINA I. DEFINITION II. CONDITIONS THAT MAY PRECIPITATE FROM AKA: Effort Induced Angina, Classic or Typical ANGIINA Angina III. CAUSES OF ANGINA Short-lasting, burning, heavy or squeezing feeling of IV. TYPES OF ANGINA PECTORIS the chest V. THERAPEUTIC STRATEGIES VI. ANTI-ANGINAL DRUGS Associated with plaques that occlude coronaries. This obstruction results in accumulation of acidic ANGINA PECTORIS metabolites and ischemic changes that stimulate Other name: myocardial pain endings A spasmodic, cramp-like choking feeling Decreased coronary perfusion (Perfuse of the blood characterized by severe sudden constricting from cell to cell) due to atherosclerosis substernal pain often radiating from the pericardium ATYPICAL ANGINA to the left shoulder down to the arm. o Patients can experience extreme fatigue, o Feel in the heart portion (Lower area) and nausea or diaphoresis radiate to the arm going down. SILENT ANGINA o Note if feel a distinct pain consult a doctor o Not associated with any symptoms but there is chest pain CONDITIONS THAT MAY PRECIPITATE FROM Pain can be relieved in 15 minutes of rest: relieved by ANGINA Nitroglycerin ISCHEMIA: o Happens in hypoxia state USTABLE ANGINA o Cells are still alive AKA: Crescendo Angina o Treatment is IHF Chest pain occurs in increased frequency, duration INFARCTION: and intensity o Happens in anorexia state Can be precipitated by progressively less effort o Cells are already dead Angina can last longer than 20 minutes Form of acute coronary syndrome CAUSES OF ANGINA REST ANGINA SETTING CONDITION AKA: Prinzmetal Angina, Variant Angina, Vasoprastic Coronary Artery Disease/ Ischemic Heart Disease Angina o Hardening of the plaque in the blood Pain can be felt at rest vessels or artery Due to coronary spasm causing decreased blood o There is imbalance of myocardial flow to the heart oxygen supply and demand Angina attacks are unrelated to physical activities, heart rate or blood pressure During normal situations: Responds to vasodilator or CCB ↑ oxygen demand & ↑ oxygen supply THERAPEUTIC STRATEGIES During CAD/ IHD: Increase oxygen delivery (if patient is conscious ↑ oxygen demand but ↓ oxygen supply give water- if unconscious give air) Decrease oxygen requirement (rest) Increase efficiency of oxygen utilization PRECIPITATING EVENTS Conditions that require high oxygen demand: ANGINA-ANGINAL DRUGS o Vigorous exercise (same like cramps) o Too much work NITRITES/ NITRATES o Strong emotions (Lack of oxygen) MOA: o Have direct relaxant effect on vascular TYPES OF ANGINA PECTORIS smooth muscles and dilation of ORIA, N. & AYENZA, S 1 UNIT 3: ANGINA PECTORIS coronary vessels improving oxygen o Causes (-) Inotropy: ↓ Cardiac Force supply to the myocardium. ▪ Therefore: o Effect is vasodilation ↓ myocardial fiber tension USES: ↓ oxygen requirement o To relieve acute anginal attacks USES: o Prophylactic treatment (prevention) o Prophylaxis of atherosclerotic angina o For long term management of angina o Prophylaxis of chronic angina together ADR: with nitrates o Headache ADR: o Hypotension o Worsen CHF o Tachycardia o Bradycardia o Methemoglobinemia o Hypotension ▪ Presence of methemoglobin in the o Reduce blood flow blood o Edema Dysfunction form of hgB iron component has been CALCIUM CHANNEL BLOCKERS oxidized from the ferrous to MOA: ferric state o Blocks calcium entry into the smooth ▪ Cyanosis, impaired aerobic muscles respiration, metabolic acidosis o Causes smooth muscle relaxation (vasodilation) o Monday Disease o Faster blood flow to the myocardium ▪ Develop tolerance to nitrates (better delivery of oxygen/ oxygen during the weekdays then loss demand on the body supplied) of tolerance in the weekend. AGENTS: ↑ oxygen delivery ↔ ↑ vasodilation o Amyl nitrite ▪ Administered through USES: inhalation o Treatment of stable angina pectoris ▪ Very volatile and flammable AGENTS: o Nitroglycerin o Nifedipine ▪ Very high first pass effect o Amlodipine (FPE) o Diltiazem ▪ Relaxes the vascular smooth o Verapamil muscles causing an increase ADR: in blood flow and oxygen DRUG-DRUG INTERACTION: delivery o CCB + Beta blockers ▪ SL: short acting ▪ Additive Cardiac Depression ▪ Patch: long acting o CCB + Vasodilators o Isosorbide Mononitrate (ISMN) ▪ Additive Vasodilation ▪ Does not undergo first pass effect SODIUM CHANNEL BLOCKERS ▪ Half-life: 4-6 hours ▪ Sublingual MOA: o Isosorbide Dinitrate (ISDN) o Inhibits the late phase of the sodium ▪ Undergoes first pass effect current improving the oxygen supply ▪ Half-life: 40 minutes and demand equation ▪ Available in tablet ▪ Reduced intracellular sodium and calcium overload DRUG-DRUG INTERACTIONS improving diastolic function o Phosphodiesterase 5 Inhibitors o Can prolong the QT interval therefore it (Sildenafil) + Nitrates should be avoided with other drugs that Ex. Viagra cause QT prolongation Phosphodiesterase 5 Inhibitors: Erectile dysfunction USES: Nitrates: Angina Pectoris o Chronic angina Results to SYNERGISTIC HYPOTENSION o Used in patients who have failed in Note: relax the veins of ED need to have other anti-anginal drugs vasodilation AGENT: o Ranolazine BETA BLOCKERS Reference(s): APA Format MOA: Handout & Discussion: GBAYENGRPhCIP©2024 MJASTUDILLO©2024 o Inhibits NE in occupying the receptors o Causes (-) chronotropy: ↓ HR ORIA, N. & AYENZA, S 2

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