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Kaplan
Cardiac and Renal Drugs
| Question | Answer |
|---|---|
| Which 2 groups of diuretics are weak acids and how are they secreted in blood? | Loop and Thiazides dietetics are weak acids. They can get filtered into the tubules or secreted via OAT ( organic acid transporter) |
| Which 2 groups of diuretics increases the risk of hyperurecemia/ gout and why? | Loop and Thiazide diuretics bc they compete w other weak acids to get secreted out of the blood via OAT ( example is uric acid). Aspirin can also increase risk of gout dt it being a weak acid going through OAT |
| Which part of the nephron handles potassium? | The collecting duct |
| What are the (2) Carbonic anhydrase inhibitors? | Acetazolamide and Dorzolamide |
| Which renal stone is common in CA inhibitors? | Calcium phosphate stones |
| What are the (3) Loop diuretics? | 1. Furosemide 2. Torsemide 3. Ethacrynic acid (sulfa free) |
| Which channels does Loop diuretics blocks and which is the major ion that it loses? | Na/K 2Cl- cotransporter. The major ion that gets loss it Calcium. Loops lose CALCIUM |
| Which renal stones is common in Loop diuretics? | Calcium stones |
| What are the major (2) side effects of Loop diuretics? | 1. Hyperurecemia (secreted via OAT) 2. Ototoxicity (tinnitus or sense of fullness in ear) |
| What is one important difference between loops and thiazide diuretics? | Loop PROMOTE Ca excretion Thiazides DECREASE Ca excretion |
| What are the (3) Thiazide diuretics? | 1 Chlorthalidone 2 Hydrochlorothiazide 3 Indapamine |
| What channel does thiazide diuretics blocks and which get upregulated? | Blocks: Na/Cl- cotransporter Upregulate: Na/Ca exchanger on the basolateral membrane |
| What is an important/ unique use of thiazide diuretics? | Nephrogenic diabetes insipidus (B/c it causes the nephron to reabsorb more water at the PCT) |
| What are 2 important side effects of Thiazide diuretics? | 1 Hyperglycemia (bc it hyperpolarize pancreatic beta cells which decrease insupine secretion) 2 Hyperlipidemia (except for indapamide) Hyperpolarize is inactivating something. It does it to smooth muscle too which causes dilation |
| V1 and V2 are what type of coupled receptors? | V1 is Gq (bp control) V2 is Gs (water reabsorption) |
| What are the potassium sparing diuretics and where on the nephron do they work? | Aldosterone- receptor antagonist 1. Spironolactone 2. Eplerenone (devoid of anti adrenergic effect) ENac+ channel blockers: 1 Amiloride 2 Triamterine They work on the colllecting duct |
| Which ion can mimic the electrical charge and size of Na and enter the EnaC and produce a neohrogenic diabetes insipidus effect and how does it do so? | Lithium. It enters the EnaC and blocks the V2 receptor ( decrease aquaporins on luminal membrane and decrease h2o uptake) |
| Which diuretics is the STRONGEST and which is the WEAKEST? | STRONGEST : Loop diuretics WEAKEST: Pottasium sparing |
| What are the first line drugs for hypertension (3)? | 1 Thiazide diuretics (inexpensive and effective) 2 ACEIs 3 CCBs AbCDS ( ACEI,ARB, beta blockers, CCB, Diuretics) |
| What are the ACEIs? | “-prils” Captopril Lisinopril |
| What are the ARBs? | “-sartans” Losartan |
| What is the Renin inhibitor? | Aliskiren |
| What is the 2 most common side effect of ACEIs? And what causes it? | Dry cough Angioedema Occurs dt accumulation of bradykinin which is a vasodilator (involved in multiple pathways) |
| Why are ACEIs and ARBs good for diabetics but bad for bilateral renal artery stenosis? | In DIABETICS: Glycosylation of glomerulus increases the pressure in the glomerulus by giving ACEIs it dilates efferent arteriole relive some of pressure In Bilateral RAS: the afferent arteriole hypoperfusion and ACEIs further decrease GFR |
| Which type of ca channels does the Calcium channels blockers drug block? | Block L- type Ca channel in heart and blood vessels |
| Calcium channel blockers are divided into 2 groups, which are they? | 1. Non-dihydropyridines 2. Dihydropyridines |
| What are the names of the Non-dihydropyridines (2)? | 1. Verapamil 2. Diltiazem |
| The CCBs works more on which organ (heart vs blood vessel) | CCBs aka V D Dipines Verapamil - Diltiazem - dipines Heart —————— ——— Blood vessel |
| Orthostatic HYPOtension is dt vasodilation of which vessel? | Venular dilation (NOT arteriole dilation) |
| Which CCBs is most cardiodepressive and mimics HF symptoms? | Verapamil |
| Which CCBs most likely to increase HR? | Dipines (Nifedipine) bc it causes vasodilation leads to reflex tachycardia |
| What are selective venular dilators (1)? | Nitrates |
| What are selective arteriolar dilators? (3 groups) | CCBs, Hydralazine, K channel openers |
| What is the action of CCBs on the heart and blood vessel ? | Heart: DECREASE CO Blood vessel: DECREASE TPR |
| What are the signs of hypoglycemia? And why are beta blockers contraindicated? | Signs: Tachycardia Tremor Sweating Beta blockers contraindicated bc Tremor (skeletal muscle b2) and Tachycardia (b1 on cardiac muscle) are masked |
| What other drug classes can be used for hypertension but are not first liners? | Beta blockers Alpha 1 blockers Alpha 2 agonist |
| What are the direct- acting vasodilators which act through NO? (2 ) | Hydralazine Nitroprusside |
| What are the direct-acting vasodilators which act through opening K channels? | Minoxidil Diazoxide |
| Which drugs for hypertension affect the lipids levels? | Beta blockers (B blockade decrease lipolysis in adipose tissue, less FAs deliver to the liver) Thiazides |
| What are the drugs for pulmonary hypertension? (3) | 1. Bosentan 2. Epoprostenol (a prostacyclin) 3. Sildenafil |
| How does Bosentan work? | It is an ET-A receptor antagonist. ET is Endothelin which is a potent vasoconstrictor through ET-A / ET-B receptors |
| What is the effect of heart failure on CO? | CO DECREASES |
| Which ANS system is activated in heart failure? | The Sympathetic nervous system |
| What is remodeling of the heart? | Loss of cardiac myocytes and fibrosis formation (causes increase SANS and Aldosterone) |
| Which substrate in the RAAS pathway is responsible for heart remodeling? | Aldosterone |
| What is the connection between a beta blocker and spironolactone? | Both decrease Aldosterone (B1 is found in juxtaglomerular cells, once stimulated release of renin) |
| When treating HF what are the (4) aim in pharmacotherapy? | 1 Decrease preload ( by venular dilation) 2 Decrease afterload ( by decreasing the TPR) 3 Increase contractility 4 Decrease remodeling ( anything that decrease Aldosterone) |
| Which drugs stops remodeling and improve survival? | Spironolactone and Eplerenone (because they are the ones that INHIBITS ALDOSTERONE) |
| What are the (3) positive inotrpes used in HF? | 1. Digoxin 2. Phosphodiesterase inhibitors ( Inamrinone, Milrinone) 3. Synpathomimetic ( Dobutamine, Dopamine) |
| How does Dobutamine increase contractility? | B1 agonist. Gs protein which increase cAMP, activates PKA which increase the Ca influx through the Ca channel on the heart |
| Is Dobutamine used for acute or chronic HF? and why | ACUTE ONLY. Bc chronic use leads to tachyphylaxis (fast tolerance) Only Digoxin is used chronically |
| What is the MOA of Digoxin | Inhibition of Na/K channel (on cardiac) —> accumulation of Na inside cell —> Na/Ca channel stop working —> accumulation of Ca inside cell —> storage in SERS —> more calcium available for contraction |
| What is an important/ late sign of Digoxin toxicity? | Disorientation, visual defects ( YELLOW- GREEN color disturbances, blurry vision) |
| Why does DECREASED POTASSIUM cause increased risk of Digoxin toxicity? | Digoxin binds at the same spot of K on the Na/K channel on cardiac so if there is a decreased K there is no competition and Digoxin can bind freely and cause effects |
| Sacubitril and MOA | Drug for CHF MOA: INCREASE ANP and BNP ( it is a neprilysin inhibitor, nephrylysin is an enzyme that degrades atrial and brain natriuretic peptide) ANP and BNP reduce blood pressure ( via inhibition of RAAS) |
| Sacubitril is used in combination with which other drug and their side effect? | Used with VALSARTAN (ARB) S/e : cough, angioedema (similar to ACEIs) |
| Ivabradine and MOA | Blocks funny sodium channels of the pacemaker cells. This drug decrease the HR wo effect on the contractility. Funny sodium channels current are dysfunctional in a CHF patient |
| What are the 2 types of arrhythmias? | 1. Ventricular tachycardia (below AV node) 2. Supra ventricular (AV node and above) |
| Fast response fibers cause which type of arrhythmia? | Ventricular tachycardia |
| What are the (2) drug class used for fast response fibers arrhythmias? | 1. Na channel blockers (prolong QRS) 2. K channel blockers (prolong QT) Group 1 and 3! |
| Slow response fibers causes which type of arrhythmia? | Supra ventricular tachycardia (AV node and above) |
| Drugs for slow response fibers arrhythmias | CCBs (direct or indirect) B blockers Digoxin Vagal techniques (Valsalva and carotid massage) |
| Slow response fibers vs Fast response fibers | Slow fibers: set the rhythm (SA/AV node) Fast fibers: contractile cells (ventricular muscle) |
| Anti arrhythmic drugs target which state of Na channel? ( resting, open, inactive) | Open and inactive but mostly INACTIVE (that goes for every Na channel blockers) Coincides with late 0 phase- mid phase 3 |
| What are the 2 gates that the Na channel has? | M gate (activating) H gate (inactivating) |
| What receptors are the class 1A anti-arrhythmic drugs work on? | Na channel blockers + K channel |
| What are the ECG changes seen after giving a class 1A? | Prolonged QRS and QT QRS bc slower Na entering, lows phase 0 QT bc blockade of K, slower depolarization |
| What are the drugs that cause drug induced Lupus? (2of the 3 are a drug used for the heart) | 1 Hydralazine (vasodilator via NO) 2 Procainamide (class 1A antiarrhythmic) 3 Isonazid (TB drug) |
| What are the Class 1A anti-arrhythmic drugs (2)? | 1. Quinidine 2. Procainamide (Quater Pouder) |
| What are the Class 1B anti-arrhythmic drugs (2)? | 1. Lidocaine 2. Mexiletine (Lettuce and Mayo) |
| What are the Class 1C anti-arrhythmic drugs (1) ? | Flecainide (chemical cardioversion) |
| What is Cardioversion? | A medical procedure used to restore a normal heart rhythm when the heart is beating irregularly |
| What are the drugs in Class 3 antiarrhythmic drugs? (3) | Amiodarone, Dronedarone Sotalol Potasium channel blockers |
| How to treat Torsades? | MAGNESIUM (exact mechanism not known) |
| What is the most common arrhythmia in the US and what is the 2 method of treatment? | A fib 1. Ventricular rate control (CCB,Digoxin or b blockers) 2. Anticoagulant |
| Wolf Parkinson White syndrome is treated w which drugs? | Class 1 and 3 antiarrhythmics. Do not slow down AV conduction just control the accessory pathway |
| What Channel’s does the 4 antiarrhythmc drugs block? | Saved By Pharm Class 1 sodium (+potassium) 2 B blocker 3 Pottasium blocker 4 CCBs |
| What drugs are used for Supra ventricular arrhythmias? (4) | 1. Class 3 AA 2. Class 4 AA 3. Digoxin 4. Adenosine ( v short half life) |
| What drugs are used for ventricular arrhythmias? (2) | 1. Class. 1 AA 2. Class 3 AA |
| What drugs are used to treat STABLE angina? (3) | 1. Nitrates 2. B blockers 3. CCBs |
| What drugs are used to treat VASOPASTIC angina? (2) | 1. Nitrates 2. CCBs |
| Adenosine MOA | Decreases SA and AV nodal activity VERY SHORT HALF LIFE (8sec) By binding to adenosine receptor —> Gi receptor —> decrease cAMP Ps: antagonized by methylxanthines |
| What property of a drug makes it more susceptible to getting Tosades de Pointes? | Any drug that blocks POTASSIUM channels |
| What are the extra effects of Quinidine? | is it PROARRHYTHMIC dt muscarinic blocking effects and a1 blocking effects (leads to reflex tachycardia) |
| Procainamide gets metabolized to which active metabolite and its action? | into N-ACETYL PROCAINAMIDE (NAPA) by acetyltransferase. NAPA blocks K+ channel. |
| Which antiarrythmic drug can cover all types of arrhythmias and its S/E? | AMIODARONE because it mimics all the antiarhythhmic classes. S/E Interstitial pneumonitis, pulmonary fibrosis, corneal deposits and iodine-related side effects |
| What is the goal of antihyperlipidemic drugs? | to LOWER LDL cholesterol and atheroma plaque formation. |
| What are the "statins" and how do they work? | Atorvastatin, Rosuvastatin HMG-CoA Reductase inhibitors (cannot make cholesterol) |
| Side Effects of "STATINS" and drug interactions with? | 1. Mild myalgia can progress to rhabdomyolysis drug interaction with: GRAPEFRUIT juice bc it is an CYP450 inhibitor |
| What are the bile acid sequestrants? (2) | 1. Cholestyramine 2. Colestipol |
| MOA of Bile sequestrants? | Sequesters/complexation of bile salts in the gut --> Increase LDL receptor --> decrease LDL in blood |
| What are the S/E of Bile acid sequesterants and contraindicated in? | S/E: Increase VLDL and triglycerides Contraindications: HYPERTRIGLYCERIDEMIA |
| MOA of Nicotinic Acid (vitamin B3) ? | DecreasecAMP + Inhibits lipolysis in adipose tissue --> DecreaseTG and VLDL synthesis |
| S/E of Niacin/vitamin B3? | 1. Flushing, pruritis, burning pain (use Aspirin as pretreament to prevent these) 2. Hyperglycemia |
| What are the Fibrates (2) and their MOA? | 1. Fenofibrate 2. Gemfibrozil MOA: bind to PPAR alpha and INCREASE expression of lipoprotein lipases Used in: HYPERTRIGLYCERIDEMIA |
| S/E of Fibrates? | 1. Gallstones 2. Myositis (mostly w Gemfibrozil) |
| MOA of Ezetimibe (antihyperlipidemics) | Prevents intestinal absorption of cholesterol --> DECREASED LDL |
| What are the PCSK9 inhibitors (2) and their MOA? | 1. Alirocumab 2. Evolocumab MOA: PCSK9 targets LDL receptor for lysosomal degradation. Block of PCSK9 --> DECREASE LDL |
| MOA of Orlistat | INHIBITS pancreatic lipase --> Decrease TG breakdown in intestine (cant absorb fat) USE FOR WEIGHT LOSS |
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DVD27