Final Exam 2nd Semster Q Flashcards
- Antiarrhythmic drugs II, III and IV classes: group members, features of antiarrhythmic action, indications, side effects. Example of drug prescription.
-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:
1-Bradyarrhythmia AV block : drugs > Atropin , Adrenaline , isoprenaline
2-tackyarrhythmia : consist of 4 classes
—————— Classes ———
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
———————–
— 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 propranolol > depression
-Uses :
1-Supraventrecular
2-And ventrecular tachyarrhythmia
————————
—3rd class
-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
———————-
-4th class
-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
27 Antiarrhythmic agents used in bradyarrhythmia and AV-block of the heart. Example of drug prescription.
-Classification:
1-M Cholingric blocker : Atropin high dose
2-B agonist : Isoprenaline amp
3-a,B agonist: NorEpinephrine
-Pharmacological effect :
1- Increase contractility , conductivity,Automatcity ,COP
-Side effect :
1-Tachycardia
2-Atropine like action
3-Cardiac aresst
4-Tremors
5-Hypokalemia
28 Principles of pharmacotherapy of coronary artery disease. The main groups of antianginal agents. Nitrates: mechanism of action, indications, side effects. Example of drug prescription.
—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
—————-
–Classification :
1-Nitrates / Nitrates like agent
2-B adrenergic Blockers
3-Calcium channel blocker
4-Other drugs : Ivaberdini tab 0,005
———
—Drugs :
1-Nitroglycerin tab 0.003
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 of nitrate , and cause postural hypotension
- Mechanisms of antianginal action of β-adrenergic blockers and calcium channel blockers, indications, side effects. Example of drug prescription.
–B blockers
—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
————————————————————–
CCB blocker
—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
- Calcium channel blockers: classification, pharmacological effects, indications, side effects. Example of drug prescription.
—Drug groups :
1-Dihydroperiden :1st gen Nifedipine, 3rd gen Amlodipine ,
nicardipine> vascular selective
2-Benzodiazepines: Diltiazem
3-phinylalklamine : Verapamil > Cardio Selective
—mechanism:
1-it decrease peripheral vascular resistance by blocking of potential-dependent L type Ca+ channel which lead to decrease Ca+ in smooth muscles of arteries and result of decreasing vascular tone
2-its also decrease heart rate and Cop negative ion-tropic and chronotropic effect in case of use Verapamil , Diltiazem
—Pharmacological effect :
1-Smoothie muscles relaxtion
2-Cell necrosis: decrease cell necrosis bcs Ca+ is essential for apoptosis
3-decrease insulin release
4-decrease nuronal firing bcs Ca+ is essintial
5-Platelets: decrease platelets aggression because Ca+ is essential
—Side effect :
1- Bradycardia ; verapamil , Diltiazem
2- Reflex tachy : Nifedipine
3-hypotension
4-Constapiation : duo to RAAS reflex
—Uses :
-Verapamil
1-IHD
2-SVT
3-hypertrophic obstractive cardiomyopathy
-Amlodipine
4-ischemic renal failure
5-hypertension im pregnancy : nifedipine
—Contraindications:
1-CHF
2-bradycardia, AV block
3-in combination with digoxin or B.B because all of them nogative iontropic
4-Wolf parkinson syndrome: which the patient have accessory bundle of kent
- Hypolipidaemic drugs: classification, mechanisms of action, side effects. Example of statin prescription.
1- HGM-CoA recutase enzyme inhibitor drugs
—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
——
2- The PCSK9 inhibitor drug
—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
——
3-Fibrates
—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
—–
4-nictonic acid
—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
——–
5- Cholesterol Absorption inhibitor drugs
—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
——
6-Bile acid sequestrants drugs
-Drug : Cholystyramine tab
-mechanism: its bind to bile acid in the intestine and decrease absorption of cholesterol and decrease cholesterol storage in the body
-Side effect :
1-GiT upest
2-Decrease Absorption of the Fat sulobale drugs or Vitamins
—uses :
1-Hypercholestronima
32 Diuretics: classification, comparative characteristics, indications for use, side effects.
Example of drug prescription.
—they are 3 main groups ——
1-loop diuretics
—Drugs :
1-Furosemide amp/tab
2-torasemide amp / tab
3-Ethacrynic acid tab
-mechanism: the location of action is in the ascending loop of henle and they block the transports channel Na/K+/Cl- , also increasing synthesis of PGE1,I2 and improve blood supply of kidney which is lead to excrete :
1-Na/water
2-K+/cl-
3-Ca/mg
4- H+
—pharmacological effect
1-powerful duirsis accompind with loos of K+/Ca/mg
2-Vasodilation
3-increase blood supply of kidney duo to increase synthesis of PgE2,I2
4-VD of pulmonary duo to formation of PG increase
-Side effect:
1-hypovolmia
2-hypotension
3-metabolic alkalosis : duo to loss of H+
4-hyperurecimia : duo to increase uric acid reabsorption in PCT as result of hypovilemia
5-ototoxicty : reversible hearing loss duo to disturbance of ion transportation in inner ear , mostly occurs in high doses
6-allergic reaction : dou to SH group except Ethacryinc acid
-uses :
—Chronic :
1-CHF
2-Liver Cirrhosis
3-RF
—emergency:
1-Pulmonary edema , Cardiac Asthma
2-Acute glucoma attack
3-posinig with water sulable toxins
4-hypertensive crisis : Furosemide IV duo to :
-decrease plasma volume
-decrease vascular smooth muscles
-peripheral VD
———-
2- thiazides drugs
-Drugs :
1-hydrochlorothiazide
2-Clopamide
2-indapamide all tabs
—mechanism: the location of action is the Proximal part of DCT they block
Na/Cl- transport channel and increase Ca reabsorption , and inhibit Carbonic anhydrase enzyme in the PCT , also decrease Na input in smoothie muscles sensitivity to VC
-pharmacological effect :
1-moderate dursis
2-VD
3-decrease production of interocular fluid
4-decrease loos of Ca+
—side effects:
1-hypokalmia
2-hypomagnsimia
3-hyperurecimia ( duo to competition with urates ) ( its ++ uric acid in urine )
4-hyperclacimia
5-hyperglycemia
6-metabolic alkalosis
7-hypotension
—uses :
1-hypertension ( long term treatment )
2-Chronic peripheral edema in :
CHF , liver cirrhosis, miled RF
3-idiopathic hyperclaciuria
——————
3-K+ sparing
—Drugs :
1-Spironolactone tab
2-Amiloride
3-Triamterene
—mechanism: drugs have different mechanism :
1-Spironolactone : its comparative antagonist of aldesteron-dependent-sodium-potassium receptor at the distal site of DCT leading to increase Na/water execration and K+ retention
2-Amiloride/Triamterene : they block the entery of Na/H2o At the distal part of DCT and collecting duct which lead to increase Na/water excration and K+ retention
-side effect :
1-hyperkalamia
2-Acidosis: duo to H+ retention
3-gyncomastia
4-menstrual irregularities
5-erectail dysfunction
-uses of spironolactone:
1-primary hyperaldestornsim ( Cohin syndrome )
2-Secondary hyperaldesttonsim
3-CHF
4-Hypertension
5-hypokalimia
———————–
4- Carbonic anhydrase inhibitor
-drugs :
1-Acetazolamide tab
2-Brinzolamide eye drops
—mechanism: inhibition CAI lead to decrease H+ formation inside the cell , decrease Na/H+ anti-port, increase Na+ and HCO3 in lumen which is lead to increase duress
—mechanism in the eye : its decrease the formation of Aqusomer fluid in the Eye which is lead to decrease IOP
—pharmacological effect:
1-mild duress
2-sever acidosis
3-decrease ICF
4-Decrease IOF
—uses :
1- no druess use anymore duo to acidosis
2-glucoma
3-intercernial hypertension
4-as adjuvant drug for epilepsy
-Contraindications:
1-Liver cirrhosis duo to decrease execration of ammonia which lead to hepatotoxicity
—————————-
NB! tha diffrinses on mechansim , side effect , uses
33 Antihypertensive drugs: the main groups, mechanisms of antihypertensive action, indications for use, side effects. Example of drug prescription.
—ACEi , drug groups —–
—Drug groups :
1-Sulfhydrnal group : Captopril tab
2-non SH group : Enalapirl,Enalaprilate tab
—mechanism of Renal hypertension:
-when renal ischemia occurs and RBF , GFR decreased this lead to Acute oliguria that may develop acute tubular necrosis
- As comoplasatory mechanism , renin is released from jaxtaglumular cells as rescue message to stimulate RAAS as its follows :
-Renin > Angitensigen > Angiotensin’s 1 > ACE / kinins > ACE convert Angiotensin to Angiotensin 2 , And kinins metabolis bradykinies .
-Explanation : renin which released from the kidney goes to Angiotisgen which is inactive form and activating it which lead to Angiotensin 1 and with enzyme ACE converted to be Angiotensin 2 , also with ACE there is Another Enzyme called kinins which metabolise bradykinase which is responsible for VD
-Ang 2 : Acts on 2 receptors
1-AT1 : -its cause V.C and thus mentaine Adequate GFR , in another vascular tissue Ang2 act on AT1 casuing systemic V.C , cell hypertrophy, Increase Apoptosis
2-AT2 : V.D
—Mechanism of ACEI : by inhibition of ACE and kinase the affect will be :
1-decrease conversion of Ang1 to Ang2 = decrease vascular tone
2-decrease Aldesteron > decrease Na/water retention = increase K+
3-increase Bradykinin > increase synthesis of PG > decrease vascular tone
—Receptors of Ang2 :
1–AT1 : activating of AT1 : located mostly in efferent and its G-Protein linked receptor when its activated cause V.C duo to :
1-increase intraglumular hydrostatic pressure = Increase GFR
2-Systemic V.C
3-increase Aldesteron release = salt and water retention
4-Increase Vasopressin > V.C
5-increase proapoptotic protein which is lead to Increase apoptosis , so inhibtaion of this enzyme lead to decrease apoptosis and thats useful in IHD
2— AT2 : V.D
—Pharmacological effect :
-CVS :
1-hypotension without reflex tachycardia : duo to resting of baroreceptor
2-direct V.D action in artery and veins which lead to decrease pre/after load
3-increase Cop ( in patient with CHF)
4-decrease cardiac remodeling: duo to decrease apoptosis, and decrease hypertrophy
-side effect :
1-Cough : duo to accumulation of bradykinin
2-Angioedema :
3-protenuria
4-test changes
5-postural hypotension
6-pregnancy tetrognsis
7-skin rush: duo to sh group
8-hyperkalemia
—uses :
1-hypertension duo to RAAS
2-systemic hypertension
3-CHF : bcs its decrease pre/after load , and increase Cop and decrease Cardiac remodelling
4-late stage of MI
—Contraindications:
1-hypotension
2-Severe RF or renal artery stanosis
3-pregnancy : duo to fetal tetroginisis
4-hyperkemia
5-neutrophilina , thrombocytopenia: duo to bonemarrow depression
6-immunological problems
–ARA , Drugs ——-
—Drugs :
1-Losartan
2-Valsartan
-mechanism: they are selectively antagonist of Ang2 receptor AT1 which lead to :
1-decrease vascular tone
2-decrease aldesteron release = salt and water retention
3-increase renin > angiotensin 2 > AT2 lead to VD
4-have no effect of metabolism of Bradykinin
-Side effect :
1-hypotension
2-hyperkalima
3-hypatotoxcity
-uses :
1-hypertension in patient who used ACEI and casue cough or Angioedema
-Contraindications:
1-renal artery stenosis
2-pregnancy
- Classification of antihypertensive agents for localization of action. Central sympatholytics: mechanisms of action, indications, side effects. Example of drug prescription.
-First line drugs :
1-B.B
2-CCB
3-ACEI
4-ARA
5-diuretics
-2nd line :
1-Alpha 1 blocker
2-a+B blockers
3-Adrenergic neruon blocker > methyldopa
4- Vasodilators
——————————–
-Drug: Sodium nitroprusside Amp
-mechanism: it consist of nitric oxide which increases cGMP which result of dilation of both veins and arteries and decrease pre/after load
-side effect :
1- it consist of cyanid so it can convert to toxic form and accumulation could casue toxicity more often happens with RF,LF and its antidot its Sodium thiosulfate
-uses :
-hypertension crisis
—————————————
-Drug : methyldopa Tab
-mechanism: alpha methyldopa convert to methyl norepinephrine centrally to decrease the adrenergic out flow of alpha 2 agonist action from CNS leading to decrease total peripheral resistance and systemic Bp
-uses : hypertension in pregnancy
——————————————-
-drug : Clonidine Amp ( central acting )
-mechanism: its stimulating the presynaptic a2 adrenoreceptor which lead to decrease noradrenaline reales from both central and peripheral sympathetic nerve terminal
-side effect
1-sedation
2-postural hypotension
3-Constipation
-uses : hypertension crisis
- Cardiac glycosides: mechanisms of action, pharmacological effects, comparative
characteristics of drugs, indications. Symptoms of cardiac glycoside intoxication and
treatment principals. Example of drug prescription.
—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
–Groups :
1-Positive Iontropic
- Cardiac glycosides > digoxin
- Debutamine ( for short term only )
- phosphodiestrase inhibitor > Milrinone
2-ACE inhibitors
3-V.D
4-B.Blockers
——-
—– glycosides
—Drugs :
1-Digoxin Tab 0.003
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
– sympotoms of glycosides intoxication:
1-CVs ; sevser bradycardia , AV block
2-CNS : fatugi
3-GIT : anuroxia , vomating , nausea
4-Kindeny : decrease durisis
5-hypokalemia and hypercalcima
–Treamtnet of toxicity :
1-Stop digitalis
2-curratrion of hyopkalimia by giving K+
3-Atropine high dose if there is bradycardia or AV block
4-antiarrhythmic drug
- Non-glycoside inotropic agents: mechanisms of action, indications for use, side effects. Example of drug prescription.
1-Positive Iontropic
- Cardiac glycosides > digoxin
- non glycosides - Debutamine ( for short term only )
- non glycosides - phosphodiestrase inhibitor > Milrinone
2-ACE inhibitors
3-V.D
4-B.Blockers
———————
1–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)
—————
2–Calcium Sensitizer
-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
——————-
3— Dobutamine and Dopamine Amp 0.1 5ml
-mechansim : the CAMP actevates protein kinase which turn on the phosphoralation of Ca2+ channels leades to increase calcium influx and result of increase the cardiac work
-side effect :
1-tachycardia , hypertantion , cardiac arrethmia
-uses acute HF short term only
- Principles of drug therapy for chronic heart failure. The main groups and drugs, mechanisms of action, side effects.
—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
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-Classification of drugs :
1-Positive Iontropic
- Cardiac glycosides > digoxin
- non glycosides - Debutamine ( for short term only )
- non glycosides - phosphodiestrase inhibitor > Milrinone
2-ACE inhibitors : Captopril
3-V.D : Verapamil
4-B.Blockers : propranolol , metoprolol
- the mechansims already known and all of them lead to :
1- Decrease BP
2- decreas aldesteron which is lead to decrease salt and water retntation and lead to decrease PRe/AFter load and Bp
3-perevent mycordial wall thinkness
4-Decrease cardiac remodling by inhbation of RAAS
-Side effect :
1-Hypotnation
2-Bradycardia
3-renal inufficncy
4-hyperkalemia
5-Dry cough and angioedema with ACEI
- Anticoagulants: classification, mechanisms of action, a comparative characteristic of
anticoagulants of direct and indirect action, indications for use, side effects. Example of
drug prescription.
—Df: Anticoagulant medication thats help to prevent blood clots formation
—Classification:
1-Directly acting
1.1 Heparin
1.2 low molecular heparin ( dalteparin,Enoxaparin)
1.3 syntactic pentasaccraid : Fondaparinux
2-directly acting factor inhibitor:
2.1 Rivaroxaban ( inhibit factor 10)
2.2 Dabigatran ( inhibit factor 2 )
3-Indirectly acting :
3.1 Warfarin tab
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—-Direct acting :
—Drug:Heparin S.c / IV
-Pharmacokinetics:
1.1 Absorption: no because breakdown by HCL
1.2 distributable: dosnt pass BBB/Placenta
—mechanism: its action depends on the presence of Natural cloting inhibitor called ( heparin cofactor : Antithrombine 3) in the plasma small amount of heparin cofactor can activate Antithrombine 3 which lead to inhibition of several clothing factor especially factor 10 and 2
-pharmacological effect :
1- Anticougulant in vivo and vitro
2- Stimulate lipoproteins which decrease TGs in serum
—Adverse effect :
1-bleeding the most common side effect : Anti dot its Protamine sulfate
2-hematoma
3-osteoprosis : prolonged use of heparin inhibit proteins that stimulate osteoblast
—uses :
1-treatment of established thrombosis : to decrease its expand
2-prevention of thrombosis
—Contraindication:
1-MI
—-
-Low mulecular wight heparin
—Drugs :
1-Enoxaparin Amp s.c
2-Dalteparin Amp s.c
—mechanism: same mechanism of heparin but more specific on Anti factor 10
—–
-low molecular wight heparin Direct Acting on factors
1-Factor 10 inhibitor
1.1 Drug : Fondaparinux amp
- synthetic polysaccharides that has the same mechanism of lwmh selective inhibitor of Factor 10 and long acting
1.2 Drug : Rivaroxaban Tab
-Selective factor 10 inhibitor has. the same mechanism of LwMH
2- Direct Inhibitor of Factor 2 ( thrombin)
-drug: Dabigatran Tab
-synthetic compound thats acts as thrombin inhibitor, its can be used as alternative to heparin to treat patient with heparin-indenednt thrombocytopenia
————————
–indirct acting :
—Drug : Warfarin tab
-pharmacokinetics:
1-Absorption: good bioavailability
2-distribution : Can cross BBB
—mechanism: Warfarin inhibit Vit K epoxied reeducates enzyme in the liver leading to inhibition of formation of the active form of Vit K which is lead to decrease synthesis of Vit k-dependent cloting factor ( 2,7,9,10) which is lead to inhibation of carboxlase resulting in decrease modification of factors
—pharmacological effect :
1-Anticougulant in vivo
2- long acting 3-7 days
—Adverse effect :
1-bleeding of major organs : can be antagonis by Vit K
—uses :
1- treatment and prevention of : DVT,post operative thrombosis , Cerebral veouns thrombosis
-Warfarin Polymorphism : Variation in dose requirements is different for everyone, and genetic factors have an effect on dose variation. Polymorphism of vitamin K epoxide reductase complex 1 (VKORC1) gene is identified as the main genetic factor involved in warfarin dosage requirement variations.
–CYP2C9 and VKORC1 polymorphisms influence warfarin dose variability in patients on long-term anticoagulation.
- Antiaggregants (antiplatelet drugs): classification, indications for use, side effects. Example of drug prescription.
—Classification:
1-NSAIDS
2-grel
3-phosphodiestreas inhibitor
4-Monoclonal Antibody
——
1-NSAIDs
—Drug : Acetylsalisalic Acid Tab 0.1
-mechanism: its inhibt Cox irrivarsbaly witch lead to decrease THA2 which is responsible for platelet agg
-Pharmacological effect :
1-in low dose : anti agg
2-in high dose : analgasic and antypyratic , anti inflammatory
—side effect :
1-Git ulceration
2-risk of bleeding
3-bronchospasm
—uses :
1-prophylaxis of thrombosis’s
2-to reduce MI recurrent
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2-Grel
-Drugs :
1-Clopidogrel Tab
2-Prasugrel
3-Ticagrelor
—mechanism: they bind to receptor in the platelets called P2Y12 in site of the chemical mediator ADP should bind to start the aggression , so they bind to this receptor and inhibit ADP from binding and activate of GP2b/3a which is required for platelets to bind to fibrinogen and each other
—Pharmacokinetics:
1-Ticagerlor : 1-3 h and bind irreversibly
2-prasugrel : 2-4 h bind reversible
3-Clopidogrel : 3-5 days bind reversible
—metabolism: they metabolic by CYP450
-Clopidogrel : this drug is pro drug witch mean is that need to metablose to be active , So clopidogrel is metabolize By CYP2C19 , People with polymorphism of this gene lead to reduce clinical responseof Clopidogrel ,
-Drug such as Omeprazole is inhibit the CYP2C19 which is lead to drug drug interaction
—Side effect : bleeding
-uses : prophylaxis of thrombosis
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3-Phophodiestrase
-drug : Dipyridamole tab
-mechanism: they are phosphodiesterase inhibitor which is responsible for converting the cAMP to AMP which is important for increasing Ca2 and increase platelets agg
-Pharmacokinetics:
1-good bioavailability
2-high protein bounded
3-VD
-Side effect :
1-headech
2-hypotension especially in IV
-uses :
1-Protection of stroke with. companion of Aspirin
—Contraindications:
1-Unstabil angania duo to VD effect which can increase the ischemia
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4/Monoclonal Antibody
-Drug : Abciximab Amp ivi
-mechanism: they are monoclonal antibody , binde to Gp3/2a and blocks the binding site which is responsible for fibronogen linking and agg will not occur
-pharmacokinetics:
inhibiton of platelets in 30min
-uses :
in combination with heparin and aspirin for percoutnes Cornary intervantion , and cardiac ischemic complications
- Drugs affecting fibrinolysis: classification, mechanisms of action, indications for use, side effects. Example of drug prescription.
—Drugs :
1-Urokinase iV , : its products from kidney
2-Streptokinase IV : its from streptococcal
3-Alteplase IV : tissue plasminogen activator or TPA made by genatic engeneering
—– all pwoder
—explainion of the mechanism: normally when fiber clot is formed plasminogen get in contact with the clot and becomes activated into plasmin By the help do naturally occurring tissue called
( tissue Plasminogen activator T-PAs)
and plasmin causes fibrolysis
—mechanism:these drugs cause Rapid activation of T-PAs to form plasmin , and cause fibrolysis
-side effect :
1-systemic bleeding
2-allergic reaction , fever , hypotension ( streptokinase)
—uses : Acute MI
- Glucocorticoids. Mechanisms of anti-inflammatory, immunosuppressive and anti-allergic action. Indications and contraindications to the prescription of drugs. Example of natural glucocorticoid prescription.
—Classification:
1-Drug: Hydrocortisone ( natural ) tab,oint,Amp AntiF= 1 SW=1
2-Drug: Prednisolone tab,oint,Amp AntiF=4 SW=0,3
3-Drug: Triamcinolone tab,oint,Amp AntiF= 5 SW=0
4-Drug: Dexamethasone , tab,Eye,Amp AntiF= 30 SW=0
5-Drug: Betamethasone oint,Amp
AntiF= 30 SW=0
6-Drug: Beclomethasone Aerosoli
AntiF= 30 SW=0
—pharmacokinetics:
1-Absorption : All glucocorticoids are absorbed completely
2-Distribution: 85% bind to globin and 10% bind to albumin
3-Metabolism: by the liver CYP450 and execration by kidney
—mechanism: glucocorticoids bind to cell surface receptor then cytoplasm receptor ( carrier ) transferred to nucleus where it interacts with DNA the. transcription Activated and results of RNA
———–
-michaism of antiinflammatory action , -michism of antiallrrgic , immunusuprrasive mechansim
-Anti inflammtory , anti immunological
-1 they inhibt B cells function : which lead to decrease Antigen-Antibody reaction ( immeune supprqasive )
-2 they inhibit T cell function : which lead to decrease inflammatory mediators and cytokines (antiinflammatory )
-3 inhibit macrophages activity and stabilize lysosomes membrane ( immune supprasive )
-4 inhibit mast cells : which lead to decrease Histamine release and capillary permeability ( antiallargic )
-5 they inhibit PLsA2 enzyme: which lead to decrease synthesis PGs and LTs ( anti inflammatory )
—
—therapeutic uses :
1-inflammatory disease: bcs it decrease PLA2
2-Autoimmune disease: bcs decrease B cells
3- Allergic disease: ex asthma , bcs its decrease histamine release
4-organ transplantation: bcs its immune suppression ( Dexamethason)
5- adrenal inefficiency : (hydrocortisone)
6-anaphylactic shock : bcs its decrease histamine release and do SW to correct the pressure
7-Cerebral edema : Dexamethason bcs it has no SW effect
8-Stamulation of lung maturation in the fetus : betamethasone / lung maturation in fetus is regulated by fetus secretion of cortisol , when the fetus should be delivered per-term we use the glucocorticoids to reduce the incidence of respiratory destress syndrome ( lack of surfactant in fetus alveoli)
we choose betamethasone bcs most of it is free part which allows the drug to cross the placenta and reach the fetus
— Contraindication :
1- Presence of viral infection : especially TB
2-DIabetus mellitus
3-hypertension and heart failure: bcs they cause SW retention
4-peptic ulcer : they decrease the synthesis of PGE2 and I2 which protect the stomach
5-in early pregnancy : may cause cleft palate
