1. Diuretics
1.1. Types
1.1.1. Thiazide Diuretics
1.1.1.1. Action
1.1.1.1.1. Inhibit Na+ reabsorption (distal convoluted tubules) in nephron
1.1.1.2. Uses
1.1.1.2.1. Hypertension
1.1.1.2.2. Edema ( pulmonary, Ascites , by congestive heart failure, associated by steroids)
1.1.1.3. Side effects
1.1.1.3.1. Hypokalemia
1.1.1.3.2. Hyponatremia
1.1.1.3.3. Hyperglycemia (improper insuline secretion).
1.1.1.3.4. Muscle spasm and cramps
1.1.1.3.5. Nausea, diarrhea, constipation, añorexia, dehydration
1.1.1.3.6. Hypotension
1.1.1.4. Drugs
1.1.1.4.1. Chlorothiazidė (Diuril)
1.1.1.4.2. Hydrochlorothiazide (Hygroton)
1.1.2. Loop Diuretics
1.1.2.1. Action
1.1.2.1.1. Promote diuresis by inhibiting Na+ and CI- reabsorption from loop of Henle
1.1.2.2. Uses
1.1.2.2.1. Hypertension
1.1.2.2.2. Edema (CHF, pulmonary edema, Ascites).
1.1.2.2.3. Nephrotic syndrome
1.1.2.3. Side effects
1.1.2.3.1. Hypotension
1.1.2.3.2. Hyperglycemia
1.1.2.3.3. Nausea, fatigue, Allergy, thirst
1.1.2.3.4. uric acid conc (gout)
1.1.2.3.5. Qtotoxicity (risk of deafness).
1.1.2.4. Drugs
1.1.2.4.1. Furośemide (lasix)
1.1.2.4.2. Bumetanide (Burinex)
1.1.2.4.3. Ethacrynic acid:
1.1.3. Potassium-Sparing Diuretics
1.1.3.1. Action
1.1.3.1.1. Antagonist of aldosterone in the collecting tubules (aldosterone cause NaCl water reabsorption),
1.1.3.1.2. produce mild diuresis and increase Na excretion decrease K* loss by kidney so conserve K+ in the body may cause hyperkalemia
1.1.3.2. Uses
1.1.3.2.1. Usually used in conjugation with a thiazide or a loop diuretics to preventexcessive K+ losss
1.1.3.2.2. In hypokalemia cases (in heart failure)
1.1.3.2.3. On Edema
1.1.3.3. Side effects
1.1.3.3.1. Hyperkalemia
1.1.3.3.2. Nausea – diarrhea
1.1.3.3.3. Antiandrogen effect, gynecomastia
1.1.3.4. Drugs
1.1.3.4.1. Spironolactone (Aldactone)
1.1.3.4.2. Amiloride (Moduretic)
1.1.3.4.3. Triamterene
1.1.4. Osmotic Diuretics
1.1.4.1. Action
1.1.4.1.1. These drugs freely filtered at the glomerulus but poorly reabsorbed from the tubules, drugs remained in tubules and holds water by it's Osmotic effect (creat osmotic gradient and cause migration of water).
1.1.4.1.2. cause mild diuresis.
1.1.4.1.3. No major alteration of Na+ balance (no effect in electrolytes).
1.1.4.2. Uses
1.1.4.2.1. Increase urine excretion in drug poisoning
1.1.4.2.2. Used to maintain high urine flow (oliguria).
1.1.4.2.3. Decreased intraocular or intracranial pressure.
1.1.4.3. Side effects
1.1.4.3.1. Nausea, vomiting, headache, chills
1.1.4.3.2. Precaution: Not given in hypertension or heart failure
1.1.4.4. Drugs
1.1.4.4.1. Mannitol
1.1.4.4.2. Glucose
1.1.4.4.3. Urea
1.1.5. Carbonic Unhydrase Inhibitors
1.1.5.1. Action
1.1.5.1.1. These drugs inhibit action of enzyme carbonic anhydrase ـــــ so very little H+ and HCO3- produce ــــــ no H+ avilable for exchange with Na+ــــــ followed by water excreted in urine ـــــ diurèsis
1.1.5.2. Uses
1.1.5.2.1. Glaucoma (decrease intraocular pressure).
1.1.5.2.2. Urinary alkalinization
1.1.5.2.3. Acute Mountain sickness
1.1.5.2.4. Epilepsy
1.1.5.3. Side effects
1.1.5.3.1. Drowsiness, anorexia,
1.1.5.3.2. GI disturbances
1.1.5.3.3. Renal Stone
1.1.5.3.4. Hypersensitivity
1.1.5.4. Drugs
1.1.5.4.1. Acetazolamide (Diamox)"
1.2. Uses
1.2.1. Hypertension
1.2.2. Heart Failure
1.2.3. Edema-Pulmonary Edema-Ascites
1.2.4. Less Common in glaucoma
1.2.5. Drug Poisoning
2. Anti hypertensive
2.1. Pathephysiology
2.1.1. Hypertension: blood pressure is a measurement of the force exerted by blood circulating in the arteries
2.1.2. Two readings are taken
2.1.2.1. (Systolic pressure)
2.1.2.1.1. force of ventricular contraction
2.1.2.2. (diastolic pressure
2.1.2.2.1. the blood pressure during ventricular relaxation
2.1.3. Notes
2.1.3.1. Blood pressure varies among Individuals if person's blood pressure is higher than normal on at least three separate occasions, a doctör may diagnose hypertension.
2.1.3.2. Blood pressure' may be raised as a result of underlying disorder (Secondary hypertension)
2.1.3.2.1. Ex: kidney failure blood vessel disease 10%
2.1.3.3. Usually, it's not possible to find a cause this condition is known (Essential hypertension) 90%
2.1.3.4. The actual elevation of blood pressure unless serve rarely produce symptoms but over period of times (years of disease)
2.1.3.4.1. complications of disease (damage the heart, blood vessel, kidney heart failure, Stroke, and renal failure)
2.2. Factors contributing to hypertension:
2.2.1. High dietary sodium intake
2.2.2. Weight gain
2.2.3. Smoking
2.2.4. Lack of exercise
2.2.5. Recurrent physical, mental and emotional stress
2.2.6. Diabetes
2.2.7. Heart and kidney disease
2.3. Physiological factors controlling blood pressure
2.3.1. The peripheral vascular Resistance (PR).
2.3.2. The cardiac output
2.3.3. The volume of blood within circulation
2.4. Classification of Hypertension:
2.4.1. Normal <130/85
2.4.2. High normal 130 – 139/85-89
2.4.3. Stage I hypertension (mild) →140 – 159/90- 99
2.4.3.1. Antihypertensive therapy:
2.4.3.1.1. Low salt diet. Smoking cessation. Alcohol moderation. Exercise. Diuretics Change life style
2.4.4. Moderate hypertension 160 - 179/100-109
2.4.5. Severe hypertension 180- 209/110–119
2.4.6. Severe hypertension 180- 209/110–119
2.5. Drugs:
2.5.1. Drugs That Decrease Sympathetic Activity:
2.5.1.1. a-sympathetic blocker
2.5.1.1.1. Block the vasoconstrictor sympathetic nerve supply to the smak arteries and the resulting vasodilation causes a fall in blood pressure
2.5.1.1.2. Drug :
2.5.1.2. B-adrenergic blocker
2.5.1.2.1. Block B1 receptor in cardiac muscle heart rate lead to decrease decrease cardiac output, - so decrease blood pressure
2.5.1.2.2. Drugs
2.5.1.3. Adrenergic Neuronal Blocker
2.5.1.3.1. Supress production and store of Epinephrin
2.5.1.3.2. Drugs
2.5.2. Diuretics
2.5.2.1. Thiazide diuretic
2.5.2.1.1. Used to treat mild - moderate hypertension by inhibit NaCl water.reabsorption
2.5.2.1.2. Drugs
2.5.2.2. Loop diuretics
2.5.2.2.1. Extensive diuresis.
2.5.2.2.2. Drugs
2.5.2.3. K+ sparing diuretic
2.5.2.3.1. Used with other diuretics to conserve K+ spironolactone
2.5.3. Calcium Channel Blocker:
2.5.3.1. This group_of drugs blocks the entry of Calcium ions into the /smooth muscle of the blood vessels resulting in relaxation of arterial walls vasodilation - low BP Also block Ca entry in cardiac muscle - low HR and force of contraction low BP
2.5.3.2. Drugs
2.5.3.2.1. Verapamil
2.5.3.2.2. Diltiazem (Dilzem)
2.5.3.2.3. Nifedipine (Adalat)
2.5.3.2.4. Isradipine
2.5.3.2.5. Amlodipine (Norvasc)
2.5.3.2.6. Felodipine
2.5.3.3. Pharmacokinetics
2.5.3.3.1. All giver orally and broken down by the liver
2.5.3.4. Uses
2.5.3.4.1. Angina
2.5.3.4.2. Tachycardia
2.5.3.4.3. Hypertension
2.5.3.5. Adverse effect:
2.5.3.5.1. Headache, flushing.
2.5.3.5.2. Ankle Oedema due to vasodilation.
2.5.3.5.3. Constipation (verapamil)
2.5.3.5.4. Bradycardia not given to patient with heart failure
2.5.4. Direct Vasodilator
2.5.4.1. Action
2.5.4.1.1. Drugs that dilate blood vessels by acting directly on smooth muscle to cause relaxation
2.5.4.2. Effect
2.5.4.2.1. Decrease BP
2.5.4.2.2. These drugs as a compensatory response (because they cause extensive vasodilation) they cause reflex tachycardia and salt retension, so commonly used with B -blocker and diuretics).
2.5.4.3. Drugs
2.5.4.3.1. Hydralazine
2.5.4.3.2. Minoxidil
2.5.4.3.3. Nitroprusside
2.5.4.3.4. Diazoxide
2.5.5. Drugs Which Act Centrally:
2.5.5.1. This drug lower blood pressure by an action on the (brain which results in decrease activity of the sympathetic system)
2.5.5.2. Drugs
2.5.5.2.1. Methyl dopa (Aldomet)
2.5.5.2.2. Clonidine (catapress)
2.5.6. Angiotension – converting Enzyme inhibitor:
2.5.6.1. Physiology
2.5.6.1.1. Volume of blood within the circulation is ultimately controlled by the kidney, there are receptors which sense changès in the blood volume and if falls the kidney secrets the substance called renin, which via a complex series of changes lead to retention of salt and water by the kidney, and the formațion of-Angiotensin II which čauses vasoconstriction both of which raise the blood pressure.
2.5.6.2. Action of ACEIS:
2.5.6.2.1. ACE inhibitors inhibit the conversion of Angiotensin1 to Angiotensin II in the circulation this reduces the *vasoconstrictioneffect.of Angiotensin II inhibit release of aldosterone and cause less less Na retention → the overall effect is fall in blood pressure.
2.5.6.3. Uses of this group:
2.5.6.3.1. ACE inhibitor may be used as a single drug to lower blood pressure or combined w other drug as diuretic.
2.5.6.4. Side effect
2.5.6.4.1. A few patient develop renal failure.
2.5.6.4.2. Dry cough
2.5.6.4.3. Headaches, diarrhea
2.5.6.4.4. Rash
2.5.6.4.5. Hyperkalemia
2.5.6.5. Drugs
2.5.6.5.1. Captopril (Capoten)":
2.5.6.5.2. Enalapril (Renitec)
2.5.6.5.3. Lisinopril
2.5.7. Angiotensin Il receptor antagonists,
2.5.7.1. also known as angiotensin receptor blockers (ARBS), are a group of pharmaceuticals that modulate the renin- angiotensin-aldosterone system
2.5.7.2. Uses
2.5.7.2.1. Are in the treatment of hypertension, where the patient is intolerant of ACE inhibitor therapy. P.s they are rarely associated with the persistent dry cough
2.5.7.2.2. Congestive heart failure
2.5.7.3. Action
2.5.7.3.1. These substances are receptor antagonists; that is, they block the activation of angiotensin II receptors. Cause directly causes vasodilation, reduces secretion of aldosterone
2.5.7.4. Effect
2.5.7.4.1. The combined effect reduces blood pressure
2.5.7.5. Drugs
2.5.7.5.1. Valsartan ( Diovan)
2.5.7.5.2. Losartan ( cozaar)
3. Anti Arrhythmic Drugs
3.1. Cardiac Conduction System
3.1.1. The heart function is dependent on generation of an impulse in the normal pacemaker (sinoatrial (SA) nodes) = AV node = common bundle of his = Right and left bundle branches = purkinje fibers = contraction of atria = contraction of ventricles.
3.1.2. Electrical impulses has Autorhythmicity initiates its own electrical stimulation.
3.1.3. Electrical activity results in waves we can see on electrocardiogram
3.1.4. So that the heart beat whith regular rhythm
3.1.5. Na+ , Ca++ , K+ are ions that regulate the (electrophysiology) of the the heart.
3.1.6. P wave --> atrial depolarization
3.1.7. PR intervals ---time for electrical impulse to travel from the S.A node to the AV node
3.1.8. QRS - wave mean ventricular depolarization segment
3.1.9. T wave____ ventricular repolarization
3.1.10. So the heart beat with regular rhythm.
3.2. Cardiac Arrhythmias
3.2.1. If this coordination breaks down the heart may beat abnormally the general term arrhythmia
3.2.2. Disorder of cardiac rhythm can be divided into:
3.2.2.1. Abnormal automaticity.
3.2.2.2. Abnormal conduction
3.2.3. Few of important clinical arrhythmias
3.2.3.1. Atrial flutter.
3.2.3.2. Atrial fibrillation
3.2.3.3. Supraventricular tachycardia
3.2.3.4. Premature ventricular beats
3.2.3.5. Ventricular tachycardia
3.2.3.6. Ventricular fibrillation
3.2.3.7. Ectopic beat.
3.2.3.8. Paroxysmal tachycardia
3.2.3.9. Heart block - fail to transmit impulses
3.2.4. Causes of arrhythmias
3.2.4.1. May be due to birth defect to coronary heat disease
3.2.4.2. Heart disorder.
3.2.4.3. Over excitability of thyroid gland
3.2.4.4. Drugs as caffeine
3.2.5. Drugs
3.3. Antiarrhythmics
3.3.1. drugs used in cardiac arrhythmia
3.3.1.1. Ca++ Channel blocker Beta blocker Na+ Channel blocker others
3.3.2. B-adrenergic blocker
3.3.2.1. Action
3.3.2.1.1. B – blocker inhibit adrenergic nerve at ßi receptor in heart (block sympathetic effect on heart).
3.3.2.2. Effect
3.3.2.2.1. Slow heart rate, decrease (AV conduction, decrease cardiac output, decrease blood pressure
3.3.2.3. Drugs
3.3.2.3.1. Propranolol
3.3.2.3.2. Atenolol
3.3.2.3.3. Sotalol
3.3.2.4. Uses
3.3.2.4.1. Ectopic beat
3.3.2.4.2. Supraventricular tachycardia
3.3.3. Calcium channel blocker:
3.3.3.1. Action
3.3.3.1.1. These of drug block the flow of calcium ions group into the muscle cell of heart.
3.3.3.2. Effect
3.3.3.2.1. Reduce force of contraction of the heart muscle and slow conduction of the AV node.
3.3.3.3. Drugs
3.3.3.3.1. Verapamil (isoptin)
3.3.4. Lidocaine
3.3.4.1. Action
3.3.4.1.1. Block conduction (block Na+ channel).
3.3.4.2. Effect uses
3.3.4.2.1. Used as local anesthetics.
3.3.4.2.2. Used antiarrhythmic in acute ventricular arrhythmias specially in MI (myocardial infarction).
3.3.5. Phenytion
3.3.5.1. Action
3.3.5.1.1. Na-Channel blocker
3.3.5.2. Uses
3.3.5.2.1. Anticonvulsant in Epilepsy.
3.3.5.2.2. Antiarrhythmics in digitalis – induced arrhythmias.
3.3.6. Quinidine
3.3.6.1. Alkaloid from cinchona park.
3.3.6.2. Action
3.3.6.2.1. Used in all type of arrhythmia
3.3.6.2.2. Antimalarial
3.3.6.2.3. Anticholinergic effect
3.3.6.2.4. Enhance uterine contraction in labor.
3.3.6.3. Side effect
3.3.6.3.1. Cinchonism (headache, vertigo, tinnitus).
3.3.6.3.2. GI disturbance
3.3.6.3.3. Cardiac depression
3.3.6.4. Dosage form
3.3.6.4.1. oral, IV.
3.3.7. Procainamide
3.3.7.1. Action
3.3.7.1.1. Block Na- channels and slow conduction velocity
3.3.7.2. Uses
3.3.7.2.1. Antiarrhythmic, given orally or IV
3.3.7.3. Side effect
3.3.7.3.1. Microcrystalline deposit in conea
3.3.7.3.2. Thyroid dysfunction (hypothyroidism).
3.3.7.3.3. Pulmonary fibrosis
3.3.7.3.4. Deposits in skin
3.3.7.3.5. Photosensitivity
3.3.7.3.6. Hypotension if IV (given gradually).
4. Drugs used In Coagulation disorder
4.1. Blood Clotting Mechanism
4.1.1. Fibrin formation depends on presence in the blood of several clotting factor proteins (13 factor) figure 5:9 shows clotting process
4.1.2. Blood clots normally form only response to injury. In some people, however, there is a tendency for clots to form in blood vessels without appearance causes. Distributed blood flow as a result of the presence of fatty deposits – atheroma inside the blood vessels increasę the risk of the formation of this type abnormal clot (thrombus) in addition, a portion of blood clot (embolus) formed in response to injury or surgery may some time break off and carried away in blood stream.
4.1.3. The likelihood of this occurring is increased by long period of little or no activity. When an abnormal clot forms there is risk that it way become lodged in a blood vessel
4.1.4. When a thrombus plaque (atheromatous plaque) is formed it may block the artery and cutt off the blood supply to the organ (for example Myocardium and cause infarction).
4.1.5. Thromboembolism = blocked vessel by thrombus impending blood flow.
4.2. We can see that important process on clotting:
4.2.1. Prothrombin ــــــــ Factor x ـــــــــThrombin FibrinogenـــــــــــThrombinـــــــــــFibrinogen
4.2.2. When a blood vessel wall damaged platelet accumulate at site to form a plug.
4.2.3. Platelets activate blood clotting factor
4.2.4. These factor together with vitamin k = fibrin
4.2.5. Fibrin enmeshed in the platelet plug blood clot
4.3. Drugs
4.3.1. Anticoagulant drugs
4.3.1.1. Anti coagulant drugs help to maintain Torrnal blood flow in people who are at risk from clot formation .
4.3.1.2. Although the precise mode of action of each drug differs . They don't however dissolve clot that have already formed .
4.3.1.3. Uses
4.3.1.3.1. Used to prevent ( venous thrombosis ) and pulmonary embolism , coronary occlusion , by interfering with coagulation process
4.3.1.4. Side effect
4.3.1.4.1. Patient must constantly monitored for bleeding complications
4.3.1.5. Drugs
4.3.1.5.1. Heparin
4.3.1.5.2. Coumarin groups:
4.3.2. Antiplatelet drugs
4.3.2.1. Effect
4.3.2.1.1. Inhibit platelet aggregation and inhibit clot formin.
4.3.2.2. Uses
4.3.2.2.1. MI (myocardial infarction), (heart ischemia...).
4.3.2.3. Drugs
4.3.2.3.1. Aspirin 100 mg
4.3.2.3.2. Dipytidamole (persantin)
4.3.3. Thrombolytics
4.3.3.1. Uses
4.3.3.1.1. Also called fibrinolytic, these drugs used to dissolve clots that have already formed usually administered hospital (IV) to clear blood vessel in coronary thrombosis
4.3.3.2. Drugs
4.3.3.2.1. Streptokinase
5. Hemostatic Agents, Drugs Used In Bleeding Disorders
5.1. Systemic effect
5.1.1. Fibrinolytic inhibitors;
5.1.1.1. Aminocaproic acid
5.1.1.1.1. Action
5.1.1.1.2. Effect
5.1.1.1.3. PK
5.1.1.1.4. Uses
5.1.1.2. Tranexamic acid
5.1.1.2.1. Same of aminocaproic acid.
5.1.1.3. Aprotinin (Trasylol)
5.1.1.3.1. Inhibit fibrinolysis
5.1.1.4. Adrenaline
5.1.1.4.1. vasoconstrictor
5.1.1.5. Vitamin K'
5.1.1.5.1. synthesis of clotting factor.
5.1.1.6. Thrombin + fibrin + prothrombin
5.1.1.6.1. natural coagulation factor
5.2. Local Hemostatic
5.2.1. Used locally to prevent bleeding wounds.
5.2.2. Åbsorbable dressing
5.2.2.1. Applied locally has absorption capacity used in bleeding wounds
5.2.2.2. Oxidized Cellulose.
5.2.2.3. Gelatin Sponge.
5.2.2.4. Ca-alginate
5.2.3. Alum
5.2.3.1. Astringent substance stop bleeding.
6. Vasodilator and the treatment of angina pectoris
6.1. Angina pectoris
6.1.1. Introduction
6.1.1.1. Angina (pain), Angina pectoris when coronary blood flow is inadequate to supply the oxygen required by the heart
6.1.1.2. By far the most frequent cause of angina is theromatour obstruction of large coronary vessels, thickened calcified arteries and decrease blood flow to heart (ischemia).
6.1.1.3. The primary cause of angina pectoris is an imbalance between the oxygen requirement of the heart and oxygen supplied to it via the coronary vessels
6.1.1.4. In classic angina, the imbalace occurs when the myocardial oxygen requirement increases as during exercises (angina of effort).
6.1.1.5. However transient spasm of localized portion of these vessels can also cause significant myocardial ischemia and pain (variant or angiospastic angina), often occurs at rest (unstable angina).
6.1.1.6. The primary objective of treatment in both form of angina is to improve coronary blood flow
6.1.1.7. A secondary objective is reduction of the myocardial oxygen requirement
6.1.2. Drugs
6.1.2.1. Therapeutic Strategies:
6.1.2.1.1. The defect that cause anginal pain is inadequate coronary oxygen delivery relative to the myocardial oxygen requirment. This defect can be corrected in two ways:
6.1.2.2. Nitrates
6.1.2.2.1. Most widely used vasodilators for relief of acute angina pectoris.
6.1.2.2.2. Action
6.1.2.2.3. Uses
6.1.2.2.4. Side effect
6.1.2.2.5. Drugs
6.1.2.3. B-adrenergic blocker
6.1.2.3.1. Action
6.1.2.3.2. Uses
6.1.2.3.3. Drugs
6.1.2.4. Calcium channel blocker
6.1.2.4.1. Action
6.1.2.4.2. Uses
6.1.2.4.3. Drugs
6.2. Vasodilators
6.2.1. Introduction
6.2.1.1. Vasodilators are drugs that widen blood vessels - so increase oxygen supply.
6.2.1.2. Also dilation of blood vessels throughout the body reduce the force with which the heart need to pump and decrease it's workload pain.
6.2.1.3. Because blood pressure depends partly on the diameter of blood vessels, vasodilator are often helpful in treatments of hypertension.
6.2.2. Patient recommendation
6.2.2.1. Stop smoking
6.2.2.2. Change diet
6.2.2.3. Loose weight
6.2.2.4. Change life style
6.2.2.5. Proper medication.
7. Drug Therapy Of Hyperlipoproteinemia
7.1. The blood contains several types of fats or lipids. They are necessary for normal body function but can be damaging if present in excess, particularly saturated fat and cholestrol, the main risk is atherosclerosis, in which fatty deposits called atheroma build up in the arterioles, restricting and disturbing the flow of blood, this lead to great likelihood of the formation of abnormal blood clots. Leading to potentially fatal disorders such as stroke and heart attack.
7.2. Hyperlipidemia
7.2.1. LDL low density lipoprotein, associated with increase 4 cholestrol level, atherosclerosis, coronary disease and increased risk of MI (contain cholestrol and triglycerides).
7.2.2. (HDL) high density, lipoprotein, good fats, involve of removal of cholesterol from the atheroma.
7.2.3. (VLDL) very low đensity lipoprotein
7.2.4. Chylomicron
7.3. Lipoprotein
7.3.1. Substance composed of fats and proteins and are produced by the liver.
7.4. → determined by dietary Concentration of lipoprotein intakes of fat and by metabolic process in body.
7.5. it therefore seems reasonable to lower the blood coholestrol concentration and thereby reduce the risk of coronary artery disease
7.6. Therapy
7.6.1. Diet and Weight Reduction:
7.6.1.1. Decrease Total fat in take specially saturated fat and cholesterol
7.6.2. Drugs
7.6.2.1. Cholestyramine
7.6.2.1.1. Action
7.6.2.1.2. Side effect:
7.6.2.2. Fibrates derivative:
7.6.2.2.1. Action
7.6.2.2.2. Side effect
7.6.2.2.3. Drugs
7.6.2.3. Statins derivatives
7.6.2.3.1. Action
7.6.2.3.2. Drugs
7.6.2.3.3. Uses
7.6.2.3.4. Adverse effect
7.6.2.4. Antioxidant
7.6.2.4.1. vitamin E
7.6.2.5. Niacin (Vit B3)
7.6.2.5.1. need high doses (1-3 gm) this dose cause vasodilation.
8. Cardiac Glycosides and other Drugs used in congestive heart failure
8.1. Pathophysiology of the heart failure:
8.1.1. Cardiac output in congestive heart failure is usually below the normal range, the contractility of the heart muscle is reduced so the ventricles fail to empty properly, the blood accumulate in the chambers cause an increase in size of the heart, the pump becomes insufficient for needs of the body and various organs receive an inadequate blood and oxygen supply.
8.1.1.1. This causing the kidney to retain salt and water high BP
8.1.1.2. Oedema of dependent parts amd lung develops. Cause "dyspnea (short of breath).
8.1.1.3. Low oxygen supply to the heart and brain, this account for the fatigue.
8.1.1.4. This cause an increase in sympathetic activity causing additional vasoconstriction tachycardia
8.1.1.5. When left side of heart fail pulmonary edema - shortness of breath.
8.1.1.6. When right side of heart fails accumulation of fluid in the abdominal cavity Ascites
8.2. Causes of cardiac failure
8.2.1. Increase in work load over along period (anemia, beriberi, hyperthyroidism).
8.2.2. High blood pressure, valve disease.
8.2.3. Heart muscle may be damaged (MI, coronary thrombosis, cardiomyopathy).
8.3. Drugs
8.3.1. Cardiac Glycosides:
8.3.1.1. Source
8.3.1.1.1. group of compounds obtained mainly from plant leaves of
8.3.1.2. pharmacokinetics
8.3.1.2.1. individual glycosides differ mainly in absorption rate and duration of action.
8.3.1.3. Digitalization
8.3.1.3.1. Process of establishing therapeutic dose of digitalis for optimum functioning without toxic effect, treatment is started with a full dose, of the drugs until a satisfactory response is obtained, this followed by maintenance dose to establish drug within therapeutic window monitor HR, ECG, cardiac function and blood digoxin level to determine maintenance dose.
8.3.1.4. Dose