PBL Pharm- Trachte Flashcards
Digoxin
Inhibits Na/K ATPase Positive Inotrope (increases contractility= positive inotrope)
- Inhibits Na/K ATPase
- Increased intracellular Na
- Reduces NCX activity because of high Na levels
- Decreased expulsion of Ca from cell because don’t want MORE Na brought in
- Increased intracellular Ca
- Increased contraction of cardiac sarcomere
NOTE* Ca+ overload can lead to delayed after-depolarizaiton = arrhythmia (why this isn’t first choice!!)
Also a negative chronotrope (decreases SA nodal rate –> HR)
Used in acute CHF management (wehn furosemide and enalapril are not controlling symptoms
Metoprolol
Specific B1 blocker
Decrease heart rate and contractility thus decreasing myocardial oxygen demand
Decreases BP
Used for chronic management in CHF
(Contraindicated in acute CHF, need to perserve heart function and complete diuresis first)
Propranolol
Non-specific B1 and B2 blocker
Decrease heart rate and contractility thus decreasing myocardial oxygen demand
Decreases BP
Used for chronic management in CHF
(Contraindicated in acute CHF, need to perserve heart function and complete diuresis first)
Enalapril
ACE inhibitor
SUprresses RAAS system by inhibiting conversion of angiotensin 1 to angiotensin II
NET EFFECTS:
Decreased aldosterone release - decreased Na+ reabsorption -decreased fluid retention - decreases blood volume and preload
Decreased vasoconstriction - decreased afterload
USE FOR CHRONIC MANAGEMENT OF CHF
Nitroglycerine
Converted to NO by aldehyde dehydrogenase on endothelium - binds smooth muscle g-protein coupled receptor - activates guanylyl cylcase - increased cGMP - decrease in intracellular Ca+ concentration - relaxes smooth muscles
Vasodilator of VEINS!
Acute CHF management
Isosorbide Dinitrate
Same mechanism as nitroglycerine but longer half life (60-90 minutes)
Lisinopril
ACE inhbitor
Metoprolol
Specific B1 blocker
Main activity on heart is to decreased heart rate and contractility thus decreasing myocardial oxygen demand
Decreased BP
Used in MI to reduce ischemia
Chronic management of CHF (NOT ACUTE!)
Eplerenone
Aldosterone receptor antagonists
Blockes aldosterone action
Net effects:
Decreases Na+ reabsorption in the kidney - decreases blood volume and preload
Spirinolactone
Aldosterone receptor antagonists
Blockes aldosterone action
Net effects:
Decreases Na+ reabsorption in the kidney - decreases blood volume and preload
Furosemide
Inhibits NKCC2
Decreases Na and Cl reabsorption
Increased Na and H20 excretion
Decreased blood volume
Decreased Preload
Ceftriaxone
Binds penicillin binding protein (transpeptidase) and prevents peptidoglycan synthesis
Gram + and - bacteria
Less susceptible to penicillianases
Bactericidal
Penicillin G
IV/IM
binds penicillin binding proteins (transpeptidase) and inhibts cross-linking of peptidoglyan
Gram + ONLY
Sensitive to B-lactamases (specifically penicillinases)
Bactericidal
Vancomycin
froms H-bonds with D-ala-D-alanine and prevents the incorporation of NAM/NAG peptide subunits into peptidoglycan matrix (inhibits synthesis)
Broad spectrum for Gram + and -
Bactericidal
Morphine
Analgesic
Works on mu receptor
Nitroglycerin
- forms free radical NO
- Activates guanylyl cyclse
- Increases cGMP
- Dephosphorylation of myosin light chains
- Smooth muscle relaxation
- Vasodilation
- Affects veins more than arteries
- Decreases preload
Aspirin
irreversibly inhibits COX1 & COX2
Inhibits TXA2 synthesis
Inhibits platelet aggregation
Clopidogrel
- Irreversible ADP receptor antagonist that prevents activation of ADP receptor (lasts the lifetime of the platelet)
- Inactiavtion of ADP receptor prevents more GpIIbIIIa receptors from being exposed
- Decreases plateles adhesion
Heparin
Enhances activity of antithrombin III in the degradation of thrombin and factor 10
Since thromin is inhibited fibrinogen is not converted to fibiring to form the clot
Eptifibatide
- Fibrinogen analgogue that binds GpIIbIIIa receptor and prevents binding of adhesive glycoproteins such as fibrinogena nd vWF to activated platelets
Alteplase (tPA)
- ACtivates plasminogen (preferentially that is bound to fibrin so you don’t get systemic activation)
- Dissolbes existing thrombi
Hydrochlorothiazide
Diuretic
Blocks sodium ion transport across the renal epithelium
Blocks Chloride transport as well (via unknown mechanism)
Results in more NaCl and H20 excretetion
Used to treat = Hypertension and CHF
Losartan
Angiotensin II Receptor Blocker
Reversibly and non-competitvely binds AT1, thus blocking directly the vasoconstriction of Angiotensin II and secondarily the actions of Aldosterone
***Decrease in systemic vascular resistance without and increase in HR
Used for HYPERTENSION
Hyzaar
Combo durg of Losartan and Hydroclororthiazide
Small dose of diuretic greatly increases an ARBs efficacy
Losartan also reduced Potassium loss from HCTZ
Used for HYPERTENSION
Amlodipine
Ca+ Channel Blocker
Dihydropyridine
Main action is on the arteriolar vasculature - vasodilates
Blocks Ca+ influx thus decreasing basal contractility of coronary and systemic arteries
Decreased coronary resistance and increased O2 delivery to myocardium
NOTE** decreased pressure and vasodilation may lead to an increase in caridac stimulation = reflex tachycardia…..can greatly increased myocaridal O2 demand. THUS NOT used for angina
Fluticasone/ Salmerterol
Fluticasone - acts on intracellular receptors to alter transcription resulting in:
- Decreased inflammatory allergen response by decreasing histamine, eosinophil chemotactic factor, PGs, bradykinins, & others
- Also up-regulates B-receptors
Salmeterol - B-2 agonist
- B2 activation -> Gs -> adenylyl cyclase -> increased cAMP -> PKA -> dephosphorylates MLCs -> BRONCHODILATION
USED FOR ASTHMA/ COPD
STATINS
Inhibit cholesterol synthesis
- HMG-CoA Reductase inhibitors = decreases mevalonic acid a precursor of cholesterol
- Decreased de novo synthesis also increases LDL reuptake/clearance
Cilstazol
Platelet aggregate inhibitor with vasodilator abilities
- Blocks Phosphodiesterase
- Increases intracellular cAMP
- Decreased platelet activation by ADP, AA, collagen, etc.
Used for intermitent claudication
Niacin
Lipid-lowering Agent
Inhibits lipolysis in adispose tissue, reduces hepatic VLDL synthesis
Decreases LDL, and Triglycerides
Increases HDL
Bile Acid Resins
(Cholestyramine Colestipol, Colesevelam)
Lipid-lowering agents
Prevents intestinal reabsorption of bile acids
Liver must used cholesterol to make more
Decreases LDL
Slightly increases HDL and Triglycerides
Ezetimibe
(Cholesterol Absorbtion Blockers)
Prevent cholesterol absorption at small intesting brush border
Decrease LDL, no effect on HDL, Triglycerides
Gemifbrozil (Fibrates)
Upregualtes lipoprotein lipase
Increase TG clearance
Activates PRAR-alpha to induce HDL synthesis
Decrease LDL, Increase HDL, REALLY Decrease Tri
Aliskiren
Direct Renin Inhibitor
Binds to S3 binding site, decreases activity of enzyme.
Less conversion of angiotensinogen to angiotensin I