Pharm - winter

• Carbonic Anhydrase enzyme Inhibitor 
• Proximal tubule
• Inhibit CA to prevent HCO3- reabsorption

Use: Glaucoma, oral 

Osmotic Diuretic 

Works on filtrate limiting the reabsorption

Use: 1. Maintain function in acute renal failure 2. acute angle closure

• Given orally and topically
• Less effective but safe

Carbonic anhydrase inhibitors 

Use: Glaucoma, topical 

Thiazide diuretics

• Distal tubule on the luminal side 
• Increased Na+ and Cl- EXCRETION by blocking the co-transport protein found in the DT  

Oral hypertension

Thiazide diuretics

• Distal tubule on the luminal side Increased
• Na+ and Cl- EXCRETION by blocking the co-transport protein found in the DT  

Oral hypertension

Thiazide diuretics

Distal tubule on the luminal side Increased Na+ and Cl- EXCRETION by blocking the co-transport protein found in the DT  

Oral hypertension

high ceiling/loop diuretics - best diuretics

• TAL of the LOH
• Block the Na/Cl/K co-transport protein leading on the luminal surface to increase in the loss of NaCl and K 

high ceiling/loop diuretics - best diuretics

• TAL of the LOH
• Block the Na/Cl/K co-transport protein leading on the luminal surface to increase in the loss of NaCl and K 

Hepatic, renal, cardiac edema/ oral, IV/ combination therapy in hypertension 

Antagonizes aldosterone receptor as a steroid 

• Collecting Tubule 
• Block aldosterone's action of increasing Na/K exchange so to conserve K+ 

Collecting tubule 

Works without aldosterone (directly blocking the Na/K exchange mech), and block Na+ channels in the lumen side of tubular cells   

collecting tubule 

block Na+ channels in the lumen side of tubular cells   

hydrochlorithiazide + triamterene

theophylline /  caffein / theobromine

• Block phosphodiesterase and adenosine receptors
• Increase NaCl excretion, increase GFR, decreased reabsoprtion 

• Blocks ADH release 
• Osmotic activity 

• Class 1a anti-AR
• Block Na+ channel: decrease membrane responsiveness, increase threshold, and decrease conduction velocity (increase conduction time) 

Blockade of K+ efflux current also increases refractory period, increase action potential duration

Class 1a anti-AR

• Block both Na+ and K+ channel
• (same as Quinidine)

class 1b anti-AR

• Block both active and inactive Na channels
• NO increase in action potential duration or increase in refractory period 
• Increases threshold for excitability

class II anti-AR 

Beta blocker: decrease rate contractibility and conductive velocity (AV node)

class 2 and class 3 anti-AR

Both beta blocker and K+ channel blocking activities

class III anti-AR 

Block K channel involved in repolarization prolonging the the cardiac action potential  

Class IV anti-AR

blocks Ca influx at SA and AV node to decrease impulse formation and conduction especially in AV node 

Class IV anti-AR

blocks Ca influx but less selective for cardiac muscle and more problems with hypotension

Acts on adenosine receptor: no class Anti-AR

• Increases K+ outward current to decrease rise in Phase 4: Hyperpolarize nodal cells
• Decrease spontaneous depolarization, decreases automaticity

Use: supraventricular tachycardia

• Anti-AR
• Decreases SNS, increase PNS, slows HR

Anti-AR, anti-muscarinic 

Treatment of sinus bradycardia by blocking AV node activity 

Anti-AR

Treatment of cardiac arrest 

Treatment of digoxin induced fibrillation 

• Digoxin
• Verapamil
• Adenosine 

(effective choice in flutter or fibrillation)

Cardioversion then Lidocaine

in vitro only 

• Ca++ chelator
• Prevent coagulation

in vitro only 

• Ca++ chelator 
• Prevent coagulation

in vitro and in vivo 

• Accelerates anti-thrombin III activity to inactivate several clotting factors:
• IIa, Xa, IXa, XIIa, XIa

only in vivo 

vitamin K antagonists

• Inc vitamin K in diet Dec anticoagulant effect
• Dec vitamin K in diet Inc anticoagulant effect
• Hepatic disease Inc anticoagulant effect
• Hyperthyroid Inc anticoagulant effect
• Very young/ old age Inc anticoagulant effect
• Pregnancy Dec anticoagulant effect

blocks synthesis of vitamin K and increases anticoagulant effect 

potentiates anticoagulant effect 

disrupt protein binding to transiently increase warfarin blood level 

increases anticoagulant metabolism and decreases effect 

inhibits metabolism of anticoagulant and decreases effect

blocks fat absorption and vitamin K (lipid soluble) to block anticoagulant absorption ?? decrease or increase anticoagulation 

Direct thrombin inhibitor

• Competitive reversible antagonist 
• Orally active 
• Less risk of bleeding than warfarin

active factor Xa inhibitor, oral

direct inhibitor of active factor Xa 

Plasminogen activator

from the streptococcus bacteria 

must bind to plasminogen to plasmin to dissolve the clot

DNA recombinant tPA 

a tissue plasminogen activator

DNA recombinant tPA 

a tissue plasminogen activator

Given IV to control bleeding from excessive plasmin activation (Antidote)

Given orally and IV to control bleeding from excessive plasmin activation (Antidote)

anti-platelet 

• 1. Irreversibly inhibits prostaglandin synthesase (COX-1 and COX-2)
• 2. Block thromboxane A2 synthesis (TXA2)