CVS Antiangainal - Hyperlipidemia Flashcards
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-HR > 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 , 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 adrenergic 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-HR
4-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 groups of CCB and give the differences
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 hyperlipemia , Basic info. types of lipoprotein,
—Basic info :
-lipids moves in the blood covered by protein called Apolipoprotien inside this cover there is :
1-Triglycerides
2-Cholesterol
> this complex called lipoprotein
—Types of lipoproteins
1-Chylomicrons : 90% triglycerides 10 cholesterol
2-VLDL : 75% triglycerides 25% cholesterol
3-IDL : 50% each
4-LDL : 25% triglycerides 75% cholesterol
5-HDL : 25% triglycerides 75 % Cholesterol
explain the lipoprotein metabolism
—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
Explain HGM-CoA recutase enzyme inhibitor drugs , mechanism, side effect , uses , drug interactions
—Drugs :
1-Atorvastatin tab
2-Rosuvastatin Tab
—mechanism:
they are competitive inhibitor for HGM-CoA enzyme inhibitor which lead to decrease cholesterol synthesis in the liver and increase uptake of LDL
-side effect :
1-hepatic dysfunction : reversible
2-myopathy,myositis
3-GIT upset
4-Cataracts in the eye
-Uses :
1-hypercholystronemia
—Drug interaction :
1-CYP450 inhibitor , which may induce the myopathy and myositis
2- also combined with Fibrates
explain The PCSK9 inhibitor drug , mechanism, side effect , uses
—Drug : Alirocumab Amp S.c
—Alirocumab its monoclonal antibody for PCSK9
-mechanism: PCSK9 its protein synthesis by many tissue in the body including the liver and its promotes lysosomal degeneration of LDL receptor in the liver , So inhibiting of this receptor lead to increase LDL receptors
—Side effect : flu like symptoms
-Uses : hypercholestrolenima
explain Fibrates , Drugs , mechanism, side effect , uses
—Drug : Fenofibrate tab
-mechanism: its act on nuclear receptor called PPAR-a proxisome proliferator activated receptor Alpha leading to increase synthesis of lipoprotein lipase which lead to increase catabolism of VLDL and chylomicrons
—Side effect :
1-GIT upset
2-increase formation of Gall stones
3-reversible hepatic dysfunction
4-myopathy
—Uses :
1-hypertriglyceridnemia
2-Combined hyperlipidnima
3-dysbetalipoprotenima
4-mixed hypertriglycerdenima
explain the Nicotinic Acid , Drugs , mechanism, side effect ,uses
—Nicotinic Acid tab SR NB! its Vitamin B3
-mechanism: Niacin inhibit lipolysis of triglycerides from the adipose tissue
which is lead to decrease the catty acids that reach. the liver results of decrease synthesis of LDL and VLDL
-side effect :
1- skin flushing and burning sensations
2-hyperglycemia
4-GIT upset
-uses :
1-Hypercholstrolenima
2-hypertriglycerdneima
3-Combined hyperlipidenima
Explain the Cholesterol Absorption inhibitor drugs , mechanism, side effect , uses ,
—Drug : Ezetimibe tab
-mechanism: its selective inhibitor of cholesterol absorption and its effect even in absent of diatry fat becs its inhibit Reabsorption of cholesterol that excreted in the bile
-uses : hypercholstrenemia
