pharmacy all semester notes and study material previous year qus

KEPPRA

KEPPRA

CVS PART 1: ANATOMY OF CARDIOVASCULAR SYSTEM 1️⃣ HEART – Structural Anatomy Location Middle mediastinum Between lungs Apex at left 5th intercostal space Coverings Pericardium (fibrous + serous) 2️⃣ Layers of Heart Wall Endocardium (inner) Myocardium (muscular layer) Epicardium (outer) Myocardium thickness: Left ventricle > Right ventricle (because systemic circulation requires more force) 3️⃣ Chambers and Flow Sequence Venous blood → Right Atrium → Tricuspid Valve → Right Ventricle → Pulmonary Valve → Lungs → Left Atrium → Mitral Valve → Left Ventricle → Aortic Valve → Aorta → Body 4️⃣ Conducting System of Heart Sequence SA node → AV node → Bundle of His → Right & Left bundle branches → Purkinje fibers SA node = natural pacemaker (60–100/min) AV node delay allows ventricular filling PART 2: PHYSIOLOGY (FUNCTIONAL CONCEPTS) 1️⃣ Cardiac Cycle Duration ≈ 0.8 sec Phases: Atrial systole Ventricular systole Diastole 2️⃣ Stroke Volume (SV) Amount pumped per beat ≈ 70 mL 3️⃣ Cardiac Output (CO) CO = SV × HR = 70 × 70 ≈ 5 L/min Regulation: ↑ Sympathetic → ↑ HR + ↑ contractility → ↑ CO ↑ Vagal tone → ↓ HR → ↓ CO 4️⃣ Blood Pressure BP = CO × Peripheral Resistance Normal: 120/80 mmHg Determinants: Cardiac output Total peripheral resistance Blood volume Elasticity of vessels PART 3: REGULATION OF BLOOD PRESSURE 1️⃣ Neural Regulation (Short term) Baroreceptors: Carotid sinus Aortic arch If BP ↑ → Baroreceptor firing ↑ → ↓ sympathetic → BP falls 2️⃣ Renal Regulation (Long term) Kidney controls: Sodium balance Water balance RAAS system 3️⃣ RAAS SYSTEM ↓ BP → Kidney releases renin → Renin converts Angiotensinogen → Angiotensin I → ACE converts → Angiotensin II → Angiotensin II: Potent vasoconstrictor ↑ Aldosterone ↑ Sodium retention ↑ BP PART 4: PATHOPHYSIOLOGY OF MAJOR DISORDERS 1️⃣ HYPERTENSION Definition: Persistent BP > 140/90 mmHg (exam value) Types: Primary (90–95%) ↑ RAAS activity Sympathetic overactivity 2️⃣ CONGESTIVE HEART FAILURE (CHF) Definition: Heart unable to pump adequate blood. Pathophysiology: ↓ CO → Kidney senses low perfusion → RAAS activated → Fluid retention → Edema Compensatory: Ventricular hypertrophy Sympathetic stimulation 3️⃣ ANGINA PECTORIS Cause: Imbalance between oxygen supply and demand. Types: Stable Unstable Variant (Prinzmetal) 4️⃣ ARRHYTHMIA Abnormal impulse: Formation problem Conduction problem Causes: Ischemia Electrolyte imbalance Drug toxicity (e.g., digoxin) PART 5: PHARMACOLOGY 1️⃣ ANTIHYPERTENSIVE DRUGS Classification: A. Diuretics Thiazides (Hydrochlorothiazide) Loop (Furosemide) K⁺ sparing (Spironolactone) Mechanism: ↓ Blood volume → ↓ CO → ↓ BP B. Sympatholytics 1. Beta blockers Propranolol Atenolol Metoprolol Mechanism: ↓ HR + ↓ Renin release 2. Alpha blockers Prazosin Mechanism: Vasodilation 3. Central acting Clonidine Methyldopa Mechanism: ↓ Sympathetic outflow C. RAAS Inhibitors ACE inhibitors: Enalapril Ramipril ARBs: Losartan Telmisartan Direct renin inhibitor: Aliskiren D. Calcium Channel Blockers Amlodipine Verapamil Diltiazem Mechanism: ↓ Ca²⁺ entry → Vasodilation → ↓ BP 2️⃣ DRUGS FOR CHF Diuretics ACE inhibitors Beta blockers Aldosterone antagonists Digoxin Vasodilators SGLT2 inhibitors 3️⃣ ANTIANGINAL DRUGS Nitrates → Venodilation → ↓ Preload Beta blockers → ↓ Oxygen demand CCB → Vasodilation Ranolazine Ivabradine 4️⃣ ANTIARRHYTHMICS Class I – Na⁺ channel blockers Class II – Beta blockers Class III – K⁺ channel blockers Class IV – Ca²⁺ channel blockers Others: Adenosine Digoxin Magnesium sulfate 5️⃣ DIURETICS (Nephron Based) PCT – Acetazolamide Loop of Henle – Furosemide DCT – Thiazides Collecting duct – Spironolactone

Mahashivratri ki shubhkamnaye sbhi ko Mahadev ap sbhi ka mansik santulan banaye rakhe ap ak Khushal jeewan pradan kre

GERD vs GASTRITIS vs PUD

Diuretics sites of Action