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Pharmacology - Final - Part 7

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davidwurbel7's version from 2016-08-14 05:46

Diuretics

Question Answer
Major site of Sodium, Chloride and Bicarbonate excretionProximal Convoluted Tubule(PCT)
The major enzyme present in the proximal convoluted tubuleCarbonic Anhydrase
This enzyme is present in the ciliary body and the choroid plexusesCarbonic Anhydrase
Responsible for reabsorption of 20-30% of NaThick Ascending Limb of the Loop of Henle
This segment pumps out sodium, potassium and chloride into the interstitiumThick Ascending Limb of the Loop of Henle
It is also a major site for Mg and Ca reabsorptionThick Ascending Limb of the Loop of Henle
Reabsorption of Na, Cl and K in the Thick Ascending Limb Loop of Henle are accomplished by this carrierNa+/K+/2Cl– Cotransporter
The proximal convoluted tubule actively pumps Na, Cl out of the lumen by this transporterNa+/Cl– Cotransporter
Ca+2 is also reabsorbed in the Distal Convoluted Tubule segment under control of thisPTH
Ca+2 is also reabsorbed in this segment under control of PTHDistal Convoluted Tubule
Inward diffusion of Na+ via this leaves a lumen-negative potential, which drives reabsorption of Cl– and efflux of K+Epithelial Sodium Channel (ENaC)
Na+ reabsorption in the collecting duct is controlled by thisAldosterone
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Diuretic Drugs
Question Answer
This class of drugs act at the PCTCarbonic Anhydrase Inhitors and Osmotic Diuretics
This class of drugs act at the Ascending lopp of HenleLoop Diuretics
This class of drugs act at the DCTThiazides
These classes of drugs act at the Collecting ductAldosterone Antagonist and Calcium Channel Blocker
Acetazolamide, dorzolamideCarbonic Anhydrase Inhibitor
Furosemide, bumetanide, torsemide, ethacrynic acidLoop Diuretics
HydrochlorothiazideThiazides
Spirinolactone & eplerenonePotassium Sparing Diuretics - Aldosterone Antgonists
Amiloride, triamterenePotassium Sparing Diuretics - Na Channel Blockers
MannitolOsmotic Diuretics
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Question Answer
Reduces reabsorption of bicarbonate and Na+ causing urine alkalosis and metabolic acidosisCarbonic Anhydrase Inhibitors
Increases the excretion of potassium resulting in hypokalemiaCarbonic Anhydrase Inhibitors
Can be used to treat Open angle Glaucoma, Urinary Alkalanization for acidic drug toxicity (eg; Aspirin Toxicity), Acute of mountain sickness and Significant metabolic alkalosisCarbonic Anhydrase Inhibitors
Adverse effects of this class of drug are Cross alergenicity with other sulfonamides, Hyperchloremic metabolic acidosis, Renal stones due to alkalinization of urine causing Ca+2 precipitation and hence renal stones and HypokalemiaCarbonic Anhydrase Inhibitors
Acts by inhibiting the carbonic anhydrase (CA) enzymeCarbonic Anhydrase Inhibitors
Reduces reabsorption of Na+, K+, Cl- , Ca+2 and Mg+2Loop Diuretics
Decreases the concentration of urineLoop Diuretics
Can be used to treat edematous states including heart failure (Left Ventricular Failure) , ascites, Mild to moderate congestive heart failure, Severe hypercalcemia (commonly seen in malignancy) Loop Diuretics
These drugs inhibit Na+/K+/2Cl– cotransporterLoop Diuretics
Adverse effects of this class of drug are hypokalemia (avoided usually given with K sparing drugs), Hypomagnesemia, hypocalcaemia, Hypokalemic metabolic alkalosis, Hypovolemia, ***Ototoxicity (additive toxicity when used with aminoglycosides), ***Cross hypersensitivity with sulfa drugsLoop Diuretics
The uses of this class of diuretics is to treat glaucoma, urinary alkalanization for acidic drug toxicity, acute of mountain sickness and significant metabolic alkalosisCarbonic Anhydrase Inhibitors
The uses of this class of diuretics is to treat edematous states including heart failure, ascites, Acute Pulmonary edema, Mild to moderate congestive heart failure and severe hypercalcemiaLoop Diuretics
The adverse effects of this class of diuretics are hyponatremia, hypokalemia, hypocalcemia, hypomagnesemia, and hypochloremiaLoop Diuretics
Acts by inhibiting sodium chloride (NCC) transporter in early segment of distal convoluted tubuleThiazides
The use of this class of diuretics results in increased reabsorption of Ca+2 from urine so urine Ca+2 content is decreasedThiazides
The uses of this class of diuretics is to treat hypertension and chronic renal calcium stoneThiazides
Adverse effects of this class of drug are Severe hyponatremia, Hypokalemia, Cross hypersensitivity with sulfonamides, Hypercalcemia, Hyperuricemia, Hyperlipidemia and HyperglycemiaThiazides
This drug is an aldosterone antagonistSpironolactone
These drugs directly block the Na channelsAmiloride & Triamterene
The use of this class of diuretics is to treat the hypokalemia caused by loop diuretics and thiazidesPotassium Sparing Diuretics
The use of this diuretic is to treat lithium induced diabetes insipidusAmiloride
The use of this diuretic is to treat hyperaldosteronism and congestive heart failureSpironolactone
Adverse effects of this class of drugs can cause hyperkalemia extreme caution needed when given with ACE-IPotassium Sparing Diuretics
The adverse effect of this diuretic is gynaecomastiaSpironolactone
This diuretic is freely filtered in glomerulus but poorly reabsorbed. It holds water by virtue of its osmotic effectMannitol
The use of this diuretic is to treat cerebral edema and acute glaucomaMannitol
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Anti-Diuretics
Question Answer
Facilitates water reabsorption from collecting tubule by activation of V2receptors (Gs) - Increased cAMP causes insertion of additional aquaporin water channels into the luminal membraneVasopressin and Desmopressin
Vesopressin and Desmopressin site of action in the nephron is hereCollecting Duct
Vasopressin and Desmopressin are used in treating this conditionNeurogenic (pituitary) Diabetes Insipidus
Oppose the actions of ADH & other peptides, which act on V2 receptorsDemeclocycline and Conivaptan
This syndrome is treatment with demeclocycline and conivaptanInappropriate ADH Secretion (SIADH)
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Congestive Heart Failure

Question Answer
Characterized by reduction in cardiac outputHeart Failure
Reduction in cardiac contractilitySystolic Dysfunction
Inadequate filling of ventricles during diastoleDiastolic Dysfunction
This class of drugs reduce the preload, afterload and remodelingACE Inhibitors
This class of drugs reduces the remodeling affects on the heartBeta Blockers
This class of drugs is used in systolic heart failureCardiac Glycosides
Hypokalemia due to the use of loop diuretics can increase the toxic effects of this drugDigoxin
Hyperkalemia along with Digoxin can lead to this in a patient with CHFCardiac Arrest
The adverse effects of this class of drug cough (due to bradykinins), Postural hypotention, Hyperkalemia and is contraindicated in pregnant womenACE Inhibitors
Isosorbide dinitrate, Hydralazine and Sodium nitroprusside are usually only used for this type of cardiac failureAcute Decompensated Cardiac Failure
A combination drug of Hydralazine and a nitrateBiDil
Increase force of contraction. All increase intracellular cardiac Ca+2 concentrationInotropes
Digoxin, Dobutamine, Amrinone and milrinone are examples of this class of drugsInotropes
Inotrope that is a cardiac glycosideDigoxin
Inotrope that is a beta-1 agonistDobutamine
Inotropes that are Phosphodiesterase (PDE) InhibitorsAmrinone and Milrinone
The mechanism of action of this drug is increases cardiac contractility by Inhibition of Na/K ATPase pump increase intracellular sodium concentration – eventually increase cytosolic calcium and enhances vagal toneDigoxin
This drug is used in severe LV systolic dysfunction (CCF) (ejection fraction of < 40 %) and management of patients with Atrial Flutter and fibrillationDigoxin
The mechanism of action of digoxin used in atrial flutter and atrial fibrillation is thisReduce AV Node Conduction
The therapeutic range of this drug is 0.5-1.5 ng/mlDigoxin
The signs of this drug toxicity is at first nausea, intestinal cramping, diarrhea. Followed by abnormalities in color vision. Then malaise, confusion, depression, vertigo, vision, anorexia, palpitations, syncope, arrhythmias, bradycardia, AV node block, tachycardia and bigeminyDigoxin
Because this competes with digoxin for binding sites on the Na+/K+-ATPase, hypokalemia results in increased digoxin binding and thereby enhances its therapeutic and toxic effectsPotassium
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Hypercalcemia enhances digitalis toxicity as it increases in intracellular calcium
Hypomagnesemia also sensitizes the heart to digitalis-induced arrhythmias
Question Answer
Quinidine, Amiodarone and verapamil can increase the plasma levels of digoxin because of thisDepressing Renal Digoxin Clearance
Lidocaine, Phenytoin or propranolol can be used to treat thisDigoxin Induced Arrhythmias
Severe digoxin toxicity can be treated with thisDigibind
A preparation of digoxin antibodiesDigibind
This drug stimulates beta-1 receptors and produces a positive inotropic responseDobutamine
Acts by inhibiting the enzyme Phosphodiesterase (PDE) thus lead to increase of intracellular concentrations of cAMP thus causing increased Ca+2 entry into the cell. Increase myocardial contractility by increasing the Ca+2 influx during APPhosphodiesterase (PDE) Inhibitors
Inamrinone (amrinone) and Milrinone (bipyridines) belong to this class of drugsPhosphodiesterase (PDE) Inhibitors
Phosphodiesterase (PDE) Inhibitors are used in this type of heart failureSystolic Heart Failure
Recombinant human Brain Natriuretic Peptide (BNP) approved for treatment of acute decompensated CHFNiseritide
This drug binds to receptors in the vasculature, kidney, and other organs, producing potent vasodilation by increasing levels of cGMPNiseritide
Niseritide is a recombinant form of this naturally occurring chemicalBrain Natriuretic Peptide (BNP)
Part of their beneficial effects may derive from slowing of heart rate and decrease myocardial oxygen consumption. Suggested mechanisms also include reduced remodelingBeta Blockers
The suggested mechanisms include reduced remodelingBeta Blockers
The most commonly used for CCF amongst beta blockersCarvedilol and Metoprolol
A beta blocker that also has some alpha blocker actionCarvedilol
A beta blocker with only beta-1 blocker actionMetoprolol
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Glaucoma Drugs

Question Answer
Dorzolamide and Acetazolamide, Timolol, Betoxolol and apraclonidine, Brimonidine do this to aqueous humorReduce Production
Pilocarpine, physostigmine, Ecothiopate, Mannitol and Latanoprost do this to aqueous humorFacilitate Drainage
Topical eye drops. A non-selective β blockadeTimolol
Eye drops. A selective β1 blockadeBetaxolol
Topical eye drops. Alpha 2 selective agonistsApraclonidine and Brimonidine
Oral carbonic anhydrase inhibitor that reduce the synthesis of aqueous humor by inhibiting the enzyme carbonic anhydraseAcetazolamide
Topical carbonic anhydrase inhibitor that reduce the synthesis of aqueous humor by inhibiting the enzyme carbonic anhydraseDorzolamide
These drugs causes Ciliary muscle contraction which increases the Irido-corneal angle and open the trabecular meshwork. This results in increased drainage of aqueous humorPilocarpine, Ecothiopate and Physostigmine
Prostaglandin that increases the outflow through uveoscleral meshworkLatanoprost
Reduces IOP by reducing vitreous volume through osmotic effectMannitol
Two important group of drugs induces sudden closure of the irido-corneal angle [opposition of iris] and can cause/precipitate glaucoma areMydriatics and SSRIs
Treatment of acute close angle glaucoma until surgical correctionMannitol, Carbonic Anhydrase Inhibitor and Cholinergics
First line drugs for open angle glaucomaTimolol, Latanoprost and Cholinomimtics
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