CVS - Zatchot Flashcards
explain Heart failure , DF,Classification , Clinical manifestation
—Df: its progressive clinical syndrome in which either structural or functional abnormalities impair the ability of the heart to meet the metabolic demands of the body
—Classification: they are 2
1-Anatomical:
1.1 Anatomical left-sided : usually duo to systemic hypertension
1.2 Anatomical right-sided : caused by to many things such as pre load , left-sided HF cause Pulmonary Conjation which lead to fail of the right side
1.3 in both sided
2-Pathophysiological :
2.1 systolic : ventricle cant pump the blood through systolic phase which is bcs the muscle are week Ex> ischemic heart disease
2.2 diastolic : duo to hypertrophy the heart cant pump the required amount if the blood in the filing phase
—Clinical manifestation:
decrease Cop leads to following mechanism:
1-sympathetic over activity duo to decreased oxygen to brain leading tachycardia
2-renal ischemia : increase of RAAS ( renin angiotensin aldosterone system) lead to V.C and aldosterone lead to salt and water retention which lead to increase after load and preload and more heart failure
explain the drug therapy of HF
1-Positive Iontropic
- Cardiac glycosides > digoxin
- Debutamine ( for short term only )
- phosphodiestrase inhibitor > Milrinone
2-ACE inhibitors
3-V.D
4-B.Blockers
explain the Glycosides Drugs , chemical structure , molecular mechanism,Autonomic effect , pharmacological effect , uses , Contraindications,
—Drugs :
1-Digoxin Tab
2-Strophanthin K Amp
-Chemical structure: it consists of :
1-Steroid nucleus : lipophilic and essential for activity
2-Lacton ring : hydrophilic and essential for activity
3-Series of sugar : linked to C 3 of steroid and isn’t essential for activity , changing in the glucose would lead to changes in the pharmacokinetics
—molecular mechanism:
its inhibit Na+K+ atapse enzyme , Entering of the sodium to the cell is Passive action so we dont need The
Na+/K+atapes pump so accumulation of the Sodium inside the cell and K+ extracellular, Accumulation of intercellular Sodium leads to :
1-increase the Calcium release from the Sarcoplasmic reticulum
2-Displacement of intercellular Calcium from binding site
3-increases intercellular Sodium prevent Calcium explosions from the cell by inhibition of Na+/Ca+ exchanger
—Autonomic effect :
1-increase Vegal activity > bradycardia
2-decrease sympathetic activity duo to better Oxygenation
—Pharmacological effect :
1-increase Contractility duo to accumulation of Calcium
2-decrease RAAS secretion
3-relief of lung conjation
4-decrease HR duo to vegal increase of vegal tone
5-Normalization of of the Bp
—Uses :
1- chronic HF> digoxin
2- Acute HF > Strophanthin K
3-Arterial fibrillation
—Contraindications
1-sever bradycardia
2-AV block
3-CNS: fatigue ,insomnia , change in the color of vision
4-GIT : Anorexia , Vomating, nausea
5- decrease Duress
explain the Phosphodieastrase inhibitor drugs in HF ( Bipyradins )
-Drug : Milrinone Amp
-mechanism: they inhibit PDE enzyme type 3 which lead to increase cAMP and cAMp leads to Increase Calcium influx in myocardial cells which results of increase the strength of Contraction
—Adverse effect :
1-Thrombocytopenia
2-increase liver toxicity
-uses :
1-they are used IV only for short term treatment of CHF for patient who digoxin doesn’t affect on them
2-For acute AHF ( Acute Atrium Failure)
Explain the Calcium Sensitizer Drug For HF
-Drug : Levosimendan Falcon 0,25%-5ml
-mechanism:
1-increase the sensitivity of Cardiomyocytes to Calcium by increasing myofilment Calcium by binding to Cardiac troponin in the calcium dependent manner
2- also its selective of Phosphodiestrase enzyme type 3 inhibitor which lead to Accumulation of cAMP which lead to
1-improve contractility
2-and vascular smooth muscle relaxation
—pharmacological effect :
1-V.D
2- decrease pre load and after load
3-Arrhythmoginc effect
-uses :
1-Acute HF
2-Acute decomposition CHF
Explain the Df , AP of Cardiac and its Phases , differences between Phase 4 in Atrium and ventricular, pathophysiology of Arrhythmia
-DF of AP : in the resting state K+ ions is found mainly intracellular while Na+ and Ca+ extracellular making the intracellular is negative
-phases :
Phase 0 : rapid depolarization of the cells duo to rapid influx of Na+
Phase 1 : short period of Redepolazation duo to slow influx of K+
Phase 2 : Plateu delay in repolarization duo to slow influx of Ca
Phase 3 : second period of Rapid repolarization duo to rapid out influx of K+
Phase 4 : the resting state is restored , Na is extracellular , K+ back to intracellular by Na/K+ pump
- Difference between Phase 4 in Atrium and ventricular : is the slop the atrium consist of Slop duo to pre entering of Ca+ to the cells in this phase
—Pathophysiology of Arrhythmia:
-Df : its disturbance in the normal heart rhythm and its results from :
1-Abnormal impulse generation
2-abnormal impulse conduction
Classification of Arrhythmia, and its drugs
- Classification of arrhythmia:
1-Bradyarrhythmia AV block : drugs > Atropin , Adrenaline , isoprenaline
2-tackyarrhythmia : consist of 4 classes
Explain Class 1A/1B/1C in arrhythmia
1A class
—its increase the APD by inhibition of Na channel
-Drugs :
1-Quinidine tab
2-Disopyramide tab
3-Procainamide tab
—mechanism:
1-they block Na+ channel leading to decrease the Rate of Phase 0 depolarization which lead to increase The APD
2-decrease the exitibality on the atrial side slop which lead to decrease the firing of SA nodes
—pharmacological effect :
1- Arropine like action duo to blocked of muscranic receptor
2-hypotension duo to block of à receptor
Automatism↓
Excitability ↓
Conductivity ↓
Contractility ↓
-side effect :
1-Atropin like action
2-hypotension
3-small doses cause increase AV conduction
4-negative Iontropic effect
- uses :
1-Supraventrecular Arrhythmia
2-ventricular tachyarrhytmia
—NB : the difference between Procainamide and Quinidine is that Procainamide cause SLE like
——————————————————————
-1B class
—they are decrease the APD
-drugs :
1-Lidocaine Amp ,
2-Mexiletine Caps
3-Phenytoin tabs
—mechanism: it decrease the APD by increasing K+ in the 3rd phase ( repolarization) which llead to decreas APD
–pharmalogical effect :
Automatism↓
Excitability ↓
Conductivity ↓
Contractility ↓
—uses :
1-ventricular tachyarrhythmia
2-Acute MI > lidocaine
3-Arrhythmia with over dose of cardiac glycosides > phenytoin
—————————————————————-
Class 1C
—they have no effect of the APD
-Drugs : Propafenone amp ,Ethacyzin tab
-mechanism: by slowing the influx of sodium ions into the cardiac muscles cells causing decrease in :
Automatism↓
Excitability ↓
Conductivity ↓
Contractility ↓
-uses :
1-Supraventrecular
2-ventricular Arrhythmia
explain class 2 in arrhythmia
— class 2 are B.Blockers
-Drugs :
1-selective : B1> metoprolol ,Atenolol
2-nonselective : Propranolol tabl
-mechanism: they block Sodium, Potassium, Calcium , channel’s which lead to inhibition of phase 4 and depress Autmoticity and prolong Av conduction , alsodecrease HR , :
Automatism↓
Excitability ↓
Conductivity ↓
Contractility ↓
—Side effect :
1-CVS : decrease conductivity, bradycardia , AV block , hypotension
2-Respiratory: bronchispasm
3-GiT : dyspipsia
4- CNS : inly lipophlic drug such as Atenolol > depression
-Uses :
1-Supraventrecular
2-And ventrecular tachyarrhythmia
Explain Class 3 in arrhythmia
—They are K+ channel blocker
-Drugs :
1- Amiodarone Tab / Amp
2-Sotalol
-mechanism: inhibition of K+ channel in phase 3 which prolongate The Apd also inhibit Na+ and Ca+ , also casue Cornary V.D
-side effect :
1-Bradycardia
2-Arterial hypotension
4-Pulmonary fibrosis
5- photo sensitivity
6-hyperthyroidism
-uses : most type of arrhythmia
-contraindication: Arrhythmia duo to thyrotoxicosis
Explain Class 4 in arrhythmia
-They are clacium channel blocker
-Drugs :
1-Verapamil
2-diltiazem
-mechanism:its prolongate the APD through inhibation of Ca+ in phase 2 pleatue ,:
Conductivity ↓
Contractility ↓
Excitability ↓
Automatism:
atria ↓
—Side effect :
1- Decrease conductivity
2-bradycardia
—uses : superventercular tachyarrhythmia
Explain Cardiac Angaina , DF, Pathophysiology , Pathogenesis
—DF: impaired blood flow through the coronary Artery duo to :
1-Organic Athresclerosis
2-Thrombosis
—Pathophysiology:
-Types of IHD
1-Chronic Stable angaina
1.1 its duo to atherosclerosis and narrowing of the major branch of the heart
1.2 pain induce by effort
2-Acute Coronary Syndrome:
2.1 unstable Angina: its duo to rupture of the plaque
2.2 MI : its next stage of which above and charectrazed by complete occludes of the Epicardial Coronary Artery
3-Prenzmetal Angina ( vasospasmtic ) : its duo to a receptor overactivity , and its happen even in rest
—Pathogenesis:
- its imbalance between oxygen demand and supply of the heart
Explain Antianginal drugs Classification
1-Nitrates / Nitrates like agent
2-B adrenergic Blockers
3-Calcium channel blocker
4-Other drugs
Explain Organic nitrates , Classification, Pharmacokinetics ,Mechanism , Additional effect ,Side effect , Uses , Contraindications
—Drugs :
1-Nitroglycerin
2-Isosorbide Dinitrate
3-Isosorbide Mononitrate
4-Molsidomine
— Classification:
1-Short acting
1.1 Nitroglycerin ( Suplingual )
1.2 Isosorbide Dinitrate (Suplingual)
2- Nitrate like Agent: Molsidomine
3-Intermediate Act
3.1 Isosorbide dinitrate ( tab)
4-long acting
4.1 Isosorbide Mononitrate
—Pharmacokinetics:
-Absorption: good
-FPM: 90% While Mononitrate have no FPM
—Mechanism of Action :
-Nitrate release nitrate Oxide (NO) by the effect of Enzyme called Mitacondrial Aldahyed dehydrogenase 2 , NO stimulate Soluble Guanyly Cyclase and cause increase of the second massenger cGMP which is results of Smooth muscles relaxation by stimulating dephosphorlation of myosin light-chain phosphate which lead to :
1-Arterial dilation > decrease Pulmonary vascular resistance which is decreasing post load = decrease myocardial demand of O2
2-venous dilation > decrease venous return > decrease endosystolic volume > decrease pre load = decrease myocardial O2 demand
3-when Endosystolic decrease leads to decrease ventricular wall tension which lead to increase Sub endocardial blood flow = increase myocardial oxygen supply
4-Coronary vessels dilation > increase myocardial oxygen supply
—Additional effect :
1-relaxation of most smooth muscle ~ git , bronchi
2-decrease aggregations
—Side effect :
1-reflex tachycardia
2-Postural hypotension
3-Fascial flushing > duo to venous dilation
4-headache and dizziness
5-Tolerance
—Uses :
1-Acute HF > Nitroglycerin, Isosorbide dinitrate suplingul
2-IHD > isosorbide mononitrate
3-Acute Coronary syndrome , MI > IV nitroglycerin
—Contraindications:
1- mixed it with drug of PhospateDieastrase type 5 such as Sildenefi its potent the action id nitrate , and cause postural hypotension
Explain B adrenergic blocker in Angaina , Drugs , mechanism,side effect , uses , Contraindications
—Drugs :
1-Propranolol > lipophilic , 1st gen , no selective
2-Bisoprolol > 2gen , selective B1
3-Metoprolol > lipophilic ,2gen , selective B1
—mechanism of action : They block B adrenergic receptor and decrease
cAMP which lead to decrease Ca result in effect on the heart and kidney which lead to :
1-decrease HR
2-decrease contractility
3-Decrease Renin
—side effect :
1-headache drawnness
2-bradycardia , AV block
3-hypotension
—Uses :
1-chronic classic angina
—Contraindications:
1-Vasospastic angina ( Premzemtal )
2-AV block
3-AHF
3-Bronchial asthma
explain Calcium channel blocker , Drugs , mechanism, pharmacological effect , side effect , uses
—Drugs :
1-Verapamil 1gen
2-Diltiazem 1gen
3-Amlodipine 3 gen
—mechanism:
-They Block potential-dependent L-Type of calcium channel which decrease transmembrane Ca2+ current to heart and arteries which lead to :
1-Decrease myocardial oxygen demand duo to :
1.1 decrease HR ( verapamil )
1.2 decrease Post load
2-increase myocardial oxygen supply duo to :
2.1 Coronary dilation
2.2 increase subendoccardial blood flow
—Phramalogical effect :
1-Antihypertinsive
2-Antiarrhytmic
3-decrease Platelets aggregations
—Side effect :
1-CVS : bradycardia, AV block , reflex tachycardia
2-GIT : dyspepsia
3-CNS: headache
4-Allergic reaction
—uses :
1-Stable angina
2-Vasospastic Angina
3-hypertension
4-tachyarrhythmia
Explain the newer drugs , Pfox inhibitor, Ivabradine
1-Pfox inhibitor
-Drug:
1-Trimetazidine tab
2-Ranolazine tab
-mechanism: inhibit fatty acid oxidation in the myocardial which lead to metabolic switch from fat to carbohydrates which is making the heart require less oxygen demand , also by inhibition of fatty acid oxidation they decrease intercellular lactic acidosis leading to decrease intercellular calcium , Sodium accumulation and ion disturbance , and prevent cell necrosis
——
-newer drug
-Ivaberdini tab 0,005
-mechanism: its heart rate lowering drug agent that act by selectively inhibit the cardiac peacemaker (If ) mixed sodium potassium channel which lead to bradycardia
-side effects: sever bradycardia
-uses : Chronic Classic Angina
explain the lipoprotein metabolism ( just for reading )
—it consist of 4 phases
1—1st Phase in the intestine: the diatry fats which is cholesterol and triglycerides comes to intestine and in order to get absorbed:
1- need to become fatty acid again by help of pancreatic lipase
2-and then get coverd by bile acid which is synthesized from cholesterol then its enter the enterocytes which its covered again and thorough out to blood stream in shape of chylomicrons
2—Phase 2 in blood : the chylomicrons in the blood get metabolism by enzyme found in the walls of the arteries called lipoprotein lipase its only metabolis the triglycerides in the chylomicrons till its reach the liver As chylomicrons Remanent
3—Phase 3 in the liver : in the liver the source of lipids are 3 :
1-Chylomicrons remanent = cholesterol
2-Synthesis of cholesterol by endogenous by Cholesterol precursors and with help of HMG-CoA reducase enzyme to form Cholesterol
3-Adipose tissue : release triglycerides by lipolysis and its reach the liver
— the liver combined all these lipids together and through them in the blood stream in shape of VLDL
4–Phase 4 in blood stream: in the blood stream we have VLDL and also there is lipoprotein lipase so the VLDL get metabolic > IDL> LDL the LDL then get to liver and bind to receptor called LDL receptor then the liver make these lipids into hormons , bile acid , ETC
-NB! in case of genetical problems and the body doesn’t have LDL the LDL remain in the blood and gets into the endothelial layer of the Arteries and with calcium form sold substance which is lead to Athreoscelerosis
- some time the body break this sold substance and resend it to the liver in the shape of HDL in this case is good because the body is correcting the huge amount of lipid. and the LDL doesn’t need receptor.
Explain DF of Hyperlipidima , Classification
—Df : its abnormal elevated levels of any or all lipids in the blood
-Normal levels
1-Tottal Cholesterol: < 240/dl
2-Tottal triglycerides:< 150/dl
—Classification:
-genetic :
-type 1 : increase chylomicrons : chylomicronimia
-types 2:
-A : increase LDL : hypercholystronemia
-B : increase LDL + VLDL : combined hyperlipidnima
-type 3 : increase IDL : Dysbetalipoprotinima
-type 4 : increase VLDL : hypertruglycerdnimia
-type 5 : increase VLDL + cholesterol: mixed triglycerdnima
—Aqauierd : DM , RF alcohol , Drugs
