Download Free Medical Antianginal Drugs PowerPoint Presentation

Antianginal Drugs PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical presentation on Pharmacology, which is titled "Antianginal Drugs", to know about the antianginal drugs.

Tags : Pharmacology, Antianginal Drugs

Published on : Jul 18, 2021 | Views : 4019 | Downloads : 18

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Assoc. Prof. Ivan Lambev (www.medpharm-sofia.eu) ANTIANGINAL DRUGS
Slide 2-

Angina pectoris is a symptom of reversible myocardial ischaemia and is most frequently experienced as chest pain on exertion, which is relieved by rest. Pain is the consequence of an imbalance between oxygen supply and oxygen demand in the ischaemic area of myocardium.
Slide 3-

ppt slide no 3 content not found
Slide 4-

This imbalance results from an inability of the coronary blood flow to meet the metabolic demands of the heart, due to a fixed atheromatous narrowing of coronary artery. Usually reversible coronary artery spasm participates too.
Slide 5-

ECG Stress Test (10–20 min) Non- Invasive method
Slide 6-

ECG Stress Test: Recordings
Slide 7-

Iopramide (Ultravist®) in a. femoralis Invasive method
Slide 8-

X-ray a. femoralis
Slide 9-

They can be given to relieve rapidly the ischaemia during an acute attack, or as prophylaxis to reduce the risk of subsequent episodes. Antianginal drugs increase oxygen supply by improving coronary blood flow or reduce oxygen demand by decreasing cardiac work.
Slide 10-

Major sites of actions of antianginal drugs
Slide 11-

Glyceryl- 3-nitrate Isosorbide dinitrate Organic nitrates – indirect donors of NO
Slide 12-

Organic nitrates are vasodilators which relax vascular smooth muscle. They connect with thiol groups (-SH) and release nitric oxide (NO). NO combines with thiol groups in vascular endothelium to form nitrosothiol (R-SNO). Nitrosothiol activates guanylate cyclase which raises the concentration of cyclic GMP. This reduces the availability of intracellular calcium and produces vasodilation in three main vascular beds.
Slide 13-

Ca2+ Organic nitrate (R-ONO2) Endothelium Smooth muscle Celullar action of nitrates SR – sarcoplasmatic reticulum GTP – guanosine triphosphate GMP – guanosine monophosphate
Slide 14-

Organic nitrates dilate: Venous capacitance vessels and lower left ventricular filling pressure (“preload”) Arterial resistance vessels and reduce ventricular emptying (“afterload”). This is less important than venodilation during long treatment but it lowers blood pressure, decreases cardiac work and contributes to reduced oxygen demand.
Slide 15-

Coronary arteries. Nitrates have little effect on the total coronary flow but they improve the blood flow through collateral vessels. Nitrates also relieve coronary artery spasm. The net effect is increased blood flow supply to ischaemic areas of the myocardium.
Slide 16-

ppt slide no 16 content not found
Slide 17-

Glyceryl trinitrate is the most widely used organic nitrate. It is well absorbed orally but undergoes extensive first-pass metabo- lism in the liver to inactive metabolites. Usually glyceryl trinitrate is given by one of three routes to avoid first-pass effect and hence increases its bioavailability: Sublingually (as a tablets). Its effect begins after 1-2 min and lasts 18–20 min. Tablets lose their potency with prolonged storage.
Slide 18-

ppt slide no 18 content not found
Slide 19-

Glyceryl trinitrate Nitrolingual® spray: 0.4 mg/dose Nitroglycerin®: ling. 0.5 mg Nitroderm® TTS Perlinganit® - i.v. inf. (+ Heparin)
Slide 20-

Isosorbide dinitrate (prodrug) Isoket®: spray and tabl. (sub linguam) Isodinit®: tablets 20 mg Kardiket®: tabl. 20 mg Isosorbide-5-mononitrate t1/2 4–5 h (Olicard® 40 retard: 12 h)
Slide 21-

Adverse reactions of nitrates: Venodilation may lead to postural hypo- tension, dizziness, syncope, tachycardia. Arterial dilation causes throbbing headache and flushing, but tolerance is common during treatment with long-acting nitrates (retard tablets). Tolerance to the therapeutic effects. This may be due to depletion of vascular thiol groups. It can be avoided by a “nitrate-low” period of 10-12 h each day.
Slide 22-

II. Beta-adrenoceptor antagonists (b-blockers) (1) (b1 & b2 ) Propranolol Oxprenolol Pindolol Carvedilol (antioxidant) (b & a ) Atenolol Acebutolol Bisoprolol Celiprolol Metoprolol
Slide 23-

VDCC ROCC Receptor AP Ca2+ Ca2+ Sarcoplasmatic reticulum Cell wall (–) Beta-blockers AP – action potential, NA – noradrenaline VDCC – voltage dependent calcium channels ROCC – receptor operating calcium channels (–)
Slide 24-

All b-blockers act as competitive antagonists of catecholamines at beta-adrenoceptors: decrease heart rate; reduce the force of cardiac contraction; lower blood pressure; reduce oxygen demand. Lipophilic -blockers (e.g. propranolol) are well absorbed from the gut, but undergo extensive first-pass metabolism in the liver, with considerable variability among individuals.
Slide 25-

Hydrophilic beta-blockers (e.g. atenolol) are less completely absorbed from the gut and are eliminated unchanged by the kidney. The dose range to maintain effective plasma concentrations is narrower than that for drugs which undergo metabolism and the clinical response in angina pectoris is more predictable. Adverse reactions of beta-blockers Blockade of beta1-receptors may cause bradycardia, AV block, heart failure.
Slide 26-

Blockade of beta2-receptors may cause bronchospasm, intermittent claudication (reducing peripheral blood flow) and hypoglycemia. CNS effects: sleep disturbance, dreams and hallucinations (more common with lipophilic drugs which cross the BBB). Most β-blockers raise the plasma concentration of triglycerides and lower the concentration of HDL. Induratio penis pastica (fibrosis …) Sudden withdrawal syndrome: Beta-blockers should be stopped gradually.
Slide 27-

III. Calcium antagonists Calcium is essential for excitation and contraction in muscle cells. Free calcium must either enter the cell or be released from intracellular stores (e.g. SR). Calcium antagonists have widely different chemical structures.
Slide 28-

Calcium antagonists block predominantly L-type calcium channels, localized in myocardium and myocytes of blood vessels. L-type channels are connected to the plateau of the AP. Plateau phase of AP
Slide 29-

VDCC ROCC Receptor AP Ca2+ Ca2+ Sarcoplasmatic reticulum Cell wall NA (–) Calcium antagonists AP – action potential, NA – noradrenaline VDCC – voltage-dependent calcium channels ROCC – receptor operating calcium channels
Slide 30-

Calcium antagonists cause a reduction in coronary and peripheral resistance, lower the blood pressure and oxygen demand. Dihydropyridine derivatives (e.g. amlodipine, felodipine, nifedipine, nisoldipine) have no negative chronotropic effect and do not impair myocardial contractility.
Slide 31-

(Tipathy, 2003)
Slide 32-

Calcium antagonists Amlodipine normal frequently dihydropyridine t1/2 31–47 h, 55–91% p.o. bioavailability 5–10 mg/24 h p.o. (once daily) Nifedipine (tachycardic dihydropyridine) – effective in vasospastic angina Diltiazem (in SR dosage forms) Verapamil (Isoptin SR® – tabl. 120 mg) (22% p.o. bioаvailability, first pass effect – extensive liver metabolism)
Slide 33-

ADRs of calcium antagonists Arterial dilation: headache, flush, dizziness, ankle swelling (resistant to treatment with diuretics but not with ACE inhibitors). Bradycardia and AV block (verapamil). Verapamil + beta-blockers: potentiate cardiodepression. Tachycardia (nifedipine, nisoldipine). Constipation (verapamil 8%, nifedipine 3%) Haemorrhagic gingivitis (inhibition of collagen synthesis)
Slide 34-

4. Metabolic cardioprotective agents Trimetazidine (Preductal MR®) has prolonged concentration plateau lasting up to 11 h. It increases ATP synthesis and decreases acidosis in ischemic tissues. Trimetazidine supplies energy for the Na+/K+ transmembrane pump, but can cause parkinsonism.
Slide 35-

Angiotensinogen Angiotensin I Angiotensin II AT1- receptor AT2- receptor ACE Enalapril (-) Kinins PGs: vasodilation (kininase II) (-) ACE 5. ACE inhibitors: Enalapril, Lisinopril Ramipril, Trandolapril …
Slide 36-

6. If-blockers delays pulse rate with
Slide 37-

IV. OTHER DRUGS USED IN CORONARY HEART DISEASE (CHD) Platelet antiaggregants Antifibrinolytics (Alteplase - t-PA) Antidyslipidemic drugs Anxiolytics, etc.
Slide 38-

V. ALTERNATIVE METHODS FOR TREATMENT OF ISCHAEMIC HEART DISEASE
Slide 39-

ppt slide no 39 content not found
Slide 40-

ppt slide no 40 content not found
Slide 41-

Rotational atherectomy (Rotablation) – Chronic narrowing's or blockages may become calcified or have a lot of atheroma in them making them very difficult to treat with just a balloon. Rotablation is a procedure where, once again, a very fine wire is guided through the narrowing and then a catheter with a small device called a burr, similar to drill, mounted at its tip is guided to the beginning of the narrowing. The burr is connected to an external device which when activated by the cardiologist causes the burr to spin at very high speeds inside the narrowing, thereby creating a channel wide enough for a balloon or stent to then be used.
Slide 42-

ppt slide no 42 content not found
Slide 43-

ppt slide no 43 content not found
Slide 44-

ppt slide no 44 content not found
Slide 45-

ANGIOGENESIS PDGF TGF- TNF- (+) (+) (-) VEGF (+)
Slide 46-

Regenerative medicine
Slide 47-

ppt slide no 47 content not found
Slide 48-

ppt slide no 48 content not found
Slide 49-

ppt slide no 49 content not found
Slide 50-

BMI > 30: >>> saturated fatty acids >>> salt and >>> sugar >>> alcohol <<< fruits and vegetables Smoking Lipid status Stress 2/3 of the risk Risk factors for CVD Chomocysteine > 15 mmol/l  Diabetes mellitus Metabolic syndrome Sedentary life style Tachycardia
Slide 51-

Никотинът е и ензимен индуктор.
Slide 52-

ppt slide no 52 content not found
Slide 53-

ppt slide no 53 content not found
Slide 54-

“The heart never stops. When it stops, it stops forever”. Leonardo da Vinci Modern medicine often disproves this saying.