-
Acetazolamide (Diamox)
- Carbonic Anhydrase enzyme Inhibitor
- Proximal tubule
- Inhibit CA to prevent HCO3- reabsorption
Use: Glaucoma, oral
-
Mannitol
Osmotic Diuretic
Works on filtrate limiting the reabsorption
Use: 1. Maintain function in acute renal failure 2. acute angle closure
-
glycerol
- Given orally and topically
- Less effective but safe
-
Dorzolamide (Trusopt)
Carbonic anhydrase inhibitors
Use: Glaucoma, topical
-
hydrochlorothiazide (HydroDiuril)
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
-
indapamide (lozol)
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
-
chlorthalidone (Hygroton)
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
-
furosemide (Lasix)
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
-
bumetanide (Bumex)
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
-
spironolactone (Aldactone)
Antagonizes aldosterone receptor as a steroid
- Collecting Tubule
- Block aldosterone's action of increasing Na/K exchange so to conserve K+
-
triamterene (Dyrenium)
Collecting tubule
Works without aldosterone (directly blocking the Na/K exchange mech), and block Na+ channels in the lumen side of tubular cells
-
amiloride (Midamor)
collecting tubule
block Na+ channels in the lumen side of tubular cells
-
Dyazide
hydrochlorithiazide + triamterene
-
Methylxanthine derivatives
theophylline / caffein / theobromine
- Block phosphodiesterase and adenosine receptors
- Increase NaCl excretion, increase GFR, decreased reabsoprtion
-
Alcohol
- Blocks ADH release
- Osmotic activity
-
Quinidine
- 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
-
disopyramide (Norpace)
Class 1a anti-AR
- Block both Na+ and K+ channel
- (same as Quinidine)
-
lidocaine (Xylocaine)
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
-
propranolol (Inderal)
class II anti-AR
Beta blocker: decrease rate contractibility and conductive velocity (AV node)
-
sotalol
(d-sotalol)
class 2 and class 3 anti-AR
Both beta blocker and K+ channel blocking activities
-
amiodarone (Cordarone)
class III anti-AR
Block K channel involved in repolarization prolonging the the cardiac action potential
-
verapamil (Isoptin)
Class IV anti-AR
blocks Ca influx at SA and AV node to decrease impulse formation and conduction especially in AV node
-
diltiazem
Class IV anti-AR
blocks Ca influx but less selective for cardiac muscle and more problems with hypotension
-
adenosine
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
-
Digoxin
- Anti-AR
- Decreases SNS, increase PNS, slows HR
-
Atopine
Anti-AR, anti-muscarinic
Treatment of sinus bradycardia by blocking AV node activity
-
epinephrine
Anti-AR
Treatment of cardiac arrest
-
magnesium chloride
Treatment of digoxin induced fibrillation
-
Atrial Tachycardia (acute)
- Digoxin
- Verapamil
- Adenosine
(effective choice in flutter or fibrillation)
-
Ventricular Tachycardia (acute)
Cardioversion then Lidocaine
-
EDTA
in vitro only
- Ca++ chelator
- Prevent coagulation
-
Oxalate
in vitro only
- Ca++ chelator
- Prevent coagulation
-
Heparin
in vitro and in vivo
- Accelerates anti-thrombin III activity to inactivate several clotting factors:
- IIa, Xa, IXa, XIIa, XIa
-
warfarin (Coumadin)
only in vivo
vitamin K antagonists
-
Wafarin in the system
- 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
-
Tetracycline with warfarin
blocks synthesis of vitamin K and increases anticoagulant effect
-
Aspirin with warfarin
potentiates anticoagulant effect
-
phenylbutazone with warfarin
disrupt protein binding to transiently increase warfarin blood level
-
Phenobarbital with warfarin
increases anticoagulant metabolism and decreases effect
-
Allopurinol with warfarin
inhibits metabolism of anticoagulant and decreases effect
-
Cholestyramine with warfarin
blocks fat absorption and vitamin K (lipid soluble) to block anticoagulant absorption ?? decrease or increase anticoagulation
-
dibigatran (Pradaxa)
Direct thrombin inhibitor
- Competitive reversible antagonist
- Orally active
- Less risk of bleeding than warfarin
-
rivaroxaban (Xarelto)
active factor Xa inhibitor, oral
-
apixaban (Eliquis)
direct inhibitor of active factor Xa
-
streptokinase
Plasminogen activator
from the streptococcus bacteria
must bind to plasminogen to plasmin to dissolve the clot
-
alteplase (Activase)
DNA recombinant tPA
a tissue plasminogen activator
-
tenecteplase (TNKase)
DNA recombinant tPA
a tissue plasminogen activator
-
aminocaproic acid (Amicar)
Given IV to control bleeding from excessive plasmin activation (Antidote)
-
tranexamic acid (Lysteda)
Given orally and IV to control bleeding from excessive plasmin activation (Antidote)
-
Aspirin
anti-platelet
- 1. Irreversibly inhibits prostaglandin synthesase (COX-1 and COX-2)
- 2. Block thromboxane A2 synthesis (TXA2)
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