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111 Cards in this Set

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Mannitol
type
MOA
Osmotic diuretic.
Increases tubular osmolarity which produces increased urine flow
Mannitol
Clinical use
Use: shock, drug overdose, decrease intercranial pressure
Mannitol:
SE/Tox
Pulmonary edema
dehydration
Contraindicated to CHF, anuria
Acetazolamide
Type
MOA
Carbonic anhydrase inhibitor
causes self limited diuresis and reduction in total body HCO3
Acts at PCT
Acetazolamide:
Clinical use
Glaucoma
urinary alkanization
metaboilic alkalosis
altitude sickness
Acetazolamide: SE/Tox
Hyperchloremic metabolic ACIDOSIS
Neuropathy
NH3 tox
sulfa allergy
Furosemide:
Type
MOA
Sulfonamide loop diuretic
Inhibits co-transport system ((Na, K, 2Cl) of Ascending
LOP

Abolishes hypertonicity of medulla which prevents concentration of urine

Increases Ca excretion
Furosemide:
Clinical use
Edematous state--CHF, cirrhosis, nephrotic syndrome, PE

hypertension

Hypercalcemia
Furosemide:
SE/ Tox
OH DANG!!
Ototoxicity, Hypokalemia, Dehydration, Allergy (sulfa), Nephritis (interstitial), Gout
Ethcrynic acid
type
MOA
Phenoxyacetic acid derivative--NOT a sulfonamide

Same as furosemide
Ethcrynic acid:
clinical use
Diuresis in pts with allergy to sulfa drugs
Ethcrynic acid: SE/ Tox
Similar to furosemide
can be used in hyperuricemia, acute gout
NEVER used to treat gout
Hydrochlorothiazide:
Type
MOA
Thiazide diuretic
Inhibits NaCl reabsorption in early DT which reduces diluting capacity of nephron.

Decreases Ca excretion
Hydrochlorothiazide:
Clinical use
Hypertension
CHF
idiopathic hypercalciuria
nephrogenic diabetes insipidus
Hydrochlorothiazide:
SE/Tox
hyperGLUC!!!
Hypokalemic metabolic alkalosis
hyponatremia
hyperGlycemia
hyperLipidemia
hyperUricemia
hyperCalcemia
Sulfa allergy
K sparing diuretics
K STAys!!!
Spironolactone
triamterene
Amiloride
eplereone
K sparing diuretics
MOA
Spironolactone--competitive aldosterone receptor antagonist in CCT

Triamterene, amiloride--block Na channels in CCT
K sparing diuretics:
Clinical use
Hyperaldosteronism
K depletion
CHF
K sparing diuretics:
Tox
Hyperkalemia
endocrine effects (spironolactone causes gynecomastia)
Effects of Diuretics:
Who causes what?

1) urine NaCl
2) Urine K
3) blood pH
4) Urine Ca
1) increase-all diuretics (carbonic anhydrase inhibitors, loop diuretics, thiazides, K sparing)

2)increase--all except K sparing

3) decrease/acidosis--carbonic anhydrase inhibitors, K sparing
increase/alkalosis--loop diuretics, thiazides

4) increase-loop diuretics
decrease-thiazides
Hydralazine:
type
MOA
vasodilator

increases cAMP which increases smooth muscle relaxation. So, arterioles vasodilate > veins whihc reduces afterload
Hydralazine
Clinical use
Severe hypertension
CHF
Hydralazine
SE/TOX
Compensatory tachycardia
fluid retention
Lupus-like syndrome
name Ca channel blockers
Nifedipine
Verapamil
Diltiazem
Nifedipine Verapamil Diltiazem:
type
MOA
Ca channel blockers

Block voltage dependent L type ca channels of cardiac and smooth muscle which results in reduced muscle contractility

Vascular SM: N>D>V
Heart: V>D>N
Nifedipine Verapamil Diltiazem:
Clinical Use
Hypertension
angina
arrythmias (not N)
Nifedipine Verapamil Diltiazem:
SE/Tox
Cardiac depresion
peripheral edema
flushing
dizziness
constipation
Name ACE inhibitors
Captropil, Enalpril, Lisinopril
Captropil, Enalpril, Lisinopril:

type
MOA
ACE inhibitors

Inhibit ACE, reduce Ang II, prevent inactivation of bradykinin (potent vasodilator)

increased renin release dt loss of feedback
Captropil, Enalpril, Lisinopril:
Clinical use
Hypertension
CHF
diabetic renal disease
Captropil, Enalpril, Lisinopril:
SE/Tox
CAPTOPRIL
Cough, Angioedema, Proteinuria, Taste changes, hypOtension, Pregnancy problems (fetal renal damage), rash, Increased renin, Lower Ang II levels AND hyperkalemia
Nitroglycerin, isosorbide Dinitrate

MOA
vasodilate: release NO to Smooht muscle which increases cGMP and smooht muscle relaxation

Effect: veins >> arteries
Nitroglycerin, isosorbide Dinitrate:
Clinical use
Angina
PE
aphrodisiac, erection enhancer
Nitroglycerin, isosorbide Dinitrate
tachycardia
hypotension
HA
Monday dz in industrial exposure--develop tolerance for vasodilating effect during week and loss of tolerance during weekend with resulting SE
Antianginal therapy:
1) what is used?
2) Goal
1) nitrates, B-blockers, and a combo of both

2) reduce myocardial O2 (MVO2) use by decreasing one of the determinants of MVO2--end diastolic volume, BP, heart rate, contractility, ejection time
Anginal therapy: nitrates (affect preload)
EDV
BP
Contractility
HR
Ejection time
MVO2
dec
dec

inc (reflex)
inc (reflex response)
dec
dec
Anginal therapy: B-blockers (affect afterload)
EDV
BP
Contractility
HR
Ejection time
MVO2
inc
dec
dec
dec
inc
dec
Anginal therapy: nitrates + B-blockers
EDV
BP
Contractility
HR
Ejection time
MVO2
no effect or dec
dec
little/none
dec
little/no
very dec
Cardiac glycosides
name
Availability,%protein bound, half-life, excretion
digoxin
bioavailability-75%
protein bound-20-40%
half life-40hours
urinary excretion
Digoxin:
type
MOA
glycoside
inhibits Na/K ATPase of cell membrane which causes an increase in cellular Na.

Na-Ca antiport does not fxn as well which causes an increase in intracellular Ca...all of this leads to positive ionotropy

May cause increased PR, decreased QT, scooping of ST, and T wave inversion
Digoxin--
clinical use
CHF-increase contractility
AFib-decrease conduction at AV node
Digoxin--
SE/Tox
N/V/D
Blurry yellow vision
Arrythmias
Digoxin--
How are SE/Toxicity changed?
Tox of digoxin are increased by:
renal failure,
hypokalemia (potentiates drugs effect)
quinidine--decreases drug clearance and displaces dig from tissue binding sites
Digoxin--antidote
Slowly normalize K
lidocaine
cardiac pacer
anti-dig Fab fragments
Antiarrythmics
These are...?
Na channel blockers (Class Ia, Ib, Ic)

B blockers (Class II)-propanolol, esmolol, metoprolol, atenolol, timolol

K channel blockers (Class III)Sotalol, ibutilide, bretylium, amiodarone, dofetilide

Ca channel blockers (Class IV) verapamil, diltiazem
Beta Blockers
B blockers (Class II)-propanolol, esmolol, metoprolol, atenolol, timolol
K channel blockers
K channel blockers (Class III)Sotalol, ibutilide, bretylium, amiodarone, dofetilide
Na channel blockers Class Ia
Queen Amy proclaims Discos Pyramide
Quinidine
Amiodarone
Procainamide
Disopyramide
Na channel blockers Class Ib
Lidocaine
mexiletine
tocainide
Na channel blockers Class Ic
Flecainide
encainide
Propafenone
Na Channel Blocker Ia
Clinical effects of use?
increase AP duration

increase effective refractory period

Increase QT

Affect both atrial and ventricular arrythmias
Na channel blockers Ia:
Tox/SE
quinidine-cinchonism (HA, tinnitus, thrombocytopenia, Torsades de pointes dt increased QT)

procainamide--reversible SLE like syndrome
Na Channel Blockers : Class Ib
clinical effects and when to use
decrease AP

affect ischemic or depolarized Purkinje and ventricular fiber

Useful in acute ventricular arrythmias (especially post MI) and in digitalis induced arrythmias
Na channel blockers : Class Ib
SE/Tox
Local anasthetic
CNS stimulation/depression
CV depresion
Na channel blockers: Class Ic
clinical use or effect
No effect on AP duration

Useful:
in VTachs that progress to VF
intractable SVT

last resort in refractoryt tacharrythmias
Na channel blocker: Class Ic
SE/Tox
proarrythmic esp post MI (contraindicated)
Beta blockers
class?
MOA
Class II antiarrythmics

decrease: cAMP, Ca currents
Suppress abnormal pacemakers by decreasing slope of Phase4

AV node very sensitive--increase PR

Esmolol--short acting
Beta blockers
SE/Tox
Impotence
exacerbation of asthma

CV effects--bradycardia, AV block, CHF

CNS effects-sedation, sleep alterations

May mask signs of hypoglycemia
K channel blockers
class?
MOA/Clinical effects
Antiarrythmics, Class III

Increase duration of AP, refractory period, QT

use when other antiarrythmics fail
K channels blockers
Tox:
Sotalol
torsades
excessive Beta block
K channels blockers
Tox:ibutilide
torsades
K channels blockers
Tox:bretylium
new arrythmias,
hypotension
K channels blockers
Tox:amiodarone
Pulmonary fibrosis
corneal deposits
skin deposits/photodermatitis
neurological effects
constipation
CV effects--bradycardia, heart block, CHF

REMEMBER:YOU MUST CHECK LFT, PFT, TFT
hepatotoxic
hypo/hyperthyroidism
pulmonary fibrosis
Ca channel blockers
class
MOA/effect
class IV

Primarily affect AV nodal cells

Dec conduction velocity,

Inc ERP, PR,

Prevent nodal arrythmias (SVT)
ca channel blockers
Tox
Constipation
flushing
edema
CV effects--CHF, AV block, sinus node depression
Verapamil
Class, MOA, Tox
Ca channel blocker
diltiazem:Class, MOA, Tox
ca channel blocker
Sotalol:Class, MOA, Tox
K channel blocker
ibutilide:Class, MOA, Tox
K channel blocker
bretylium:Class, MOA, Tox
K channel blocker
amiodarone:Class, MOA, Tox
k channel blocker
Na channel blocker, IA
dofetilide:Class, MOA, Tox
k channel blocker
Quinidine Class, MOA, Tox
Na channel, IA
Procainamide Class, MOA, Tox
Na channel, IA
Disopyramide Class, MOA, Tox
Na channel, IA
Lidocaine Class, MOA, Tox
Na channel, IB
Mexiletine Class, MOA, Tox
na channel, IB
Tocainide Class, MOA, Tox
Na channel, IB
Flecainide Class, MOA, Tox
Na channel, IC
Encainide
Na channel, IC
Propafenone
Na channel, IC
Catopril?
ACE I
Enalapril?
ACE I
Lisinopril?
ACE I
Adenosine
family
use
antiarrythmics

drug of choice in diagnosing/abolishing nodal arrythmias
Adenosine:
effect of---
K
(K)--Depresses ectopic pacemakers especially in digoxin tox
Adenosine: effect on (Mg)
(Mg)--Effective in torsades de pointes and dig tox
Lipid Lowering agents

GO MEMORIZE THE TABLE ON P 319!!!!!!!!!!!
HMG-CoA reductase inhibitors (statins)

Niacin

Bile acid resins (cholestyramine, colestipol)

Cholesterol absorption blocker (Ezetimibe)

Fibrates--names end in fibrate
Statins??
HMG-CoA reductase inhibitors
Cholestyramine?
Bile acid resin
Colestipol??
Bile acid resin
Ezetimibe??
cholesterol absorption blocker
Gemfibrozil
Fibrate
hydrochlorothiazide:
family
SE
diuretic

hypokalemia
slight hyperlipidemia
hyperuricemia
lassitude
hypercalcemia
hyperglycemia
Loop diuretics: SE
Potassium wasting
metabolic alkalosis
hypotension
ototoxicity
Clonidine
Family
SE
Sympathoplegics
Dry mouth
sedation
severe rebound HPT
Methyldopa:
family
SE
Sympathoplegics

Sedation
positive Coombs test
Hexamethonium:
family
SE
Sympathoplegics
Severe orthostatic hypotension
blurred vision
constipation
sexual dysfunction
reserpine:
family
SE
Sympathoplegics

Sedation
depression
nasal stuffiness
diahrrea
Guanethidine:
family
SE
Sympathoplegics

Hypotension: orthostatic, exercise
sexual dysfunction
diarrhea
prazosin:
family
SE
Sympathoplegics

1st dose orthostatic hypotension
dizzy
HA
beta blockers
SE
Impotence
Asthma
CV effects--bradycardia, CHF, AV block

CNS effects--sedation, sleep alterations
Vasodilators
Hydralazine
Minoxidil
Nifedipine
Verapamil (ca channel too)
Nitroprusside
Hydralazine
family
SE
notes on usage
vasodilators

nausea
HA
lupus like Syn
reflex tach
angina
salt retention

use with B blocker to prevent reflex tach

use with diuretic to block salt retention
Minoxidil
family
SE
notes on use
vasodilators

Hypertrichosis
pericardial effusion
reflex tach
angina
salt retention

use with B blocker to prevent reflex tach

use with diuretic to block salt retention
nifedipine, verapamil
family
SE
vasodilators

dizzy
flushing
constipation (verapamil)
nausea
Nitroprusside
family
SE
vasodilators

cyanide toxicity--releases CN
ACE I
captopril, enalpril, lisinopril
Captropil
family
SE
H-CAPTOPRIL
Angiotensin II receptor inhibitors
losartan
Losartan
family
SE
Angiotensin II receptor inhibitors

fetal renal tox

hyperkalemia