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Cardio Flashcards

1
Q

Nifedipine

A

Ca++ channel blocker

  • block voltage gated L-type Ca++ channels
    • cardiac + smooth muscle
  • Reduce muscle contractility
  • Vascular smooth muscle *
    • vasodilation
  • Use:
    • HTN
    • Angina
    • Prinzmetal’s angina
    • Raynaud
    • prevent vasospam post subarachnoid hemorrage
  • Toxicity
    • cardiac depression
    • AV bock
    • Peripheral edema
    • Flushing
    • Dizziness
    • Constipation
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2
Q

Verapamil

A

Class IV Antiarr

  • Ca++ channel blocker
  • block voltage gated L-type Ca++ channels
    • cardiac + smooth muscle
  • Reuce muscle contractility
  • **Cardiac smooth muscle * **
    • Decrease heart contractility + rate
  • Use:
    • HTN
    • Angina
    • Prinzmetal’s angina
    • Raynaud
    • Prevent nodal arrhythmias (SVT)
    • rate control in a-fib
  • Toxicity
    • CV:
      • bradycardia
      • 1st, 2nd, 3rd degree AV block
      • Esp if combined with beta blocker!
    • Constipation
    • Gingival hyperplasia
    • Peripheral edema
    • Flushing
    • Dizziness
      *
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3
Q

Diltiazem

A

Class IV Antiarrhythmic

  • MOA
    • Ca++ channel blocker
    • block voltage gated L-type Ca++ channels
      • cardiac + smooth muscle
    • Cardiac smooth muscle
      • Reduce muscle contractility
      • reduce rate
      • increase PR
    • increases effective refractory period
  • Use:
    • HTN
    • Angina
    • Prinzmetal’s angina
    • Raynaud
    • Prevent nodal arrhythmias (SVT)
    • rate control in A-fib
    • prevent vasospasm post subarachnoid hemorrhage
  • Toxicity
    • CV: CHF, AV block, sinus node depression
    • Peripheral edema
    • Flushing
    • Dizziness
    • Constipation
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4
Q

Amlodipine

A

Ca++ channel blocker

  • block voltage gated L-type Ca++ channels
  • Reduce muscle contractility
  • vascular smooth muscle
    • vasodilation
  • Use
    • HTN
    • Angina
    • Arrhythmias
    • Prinzmetal’s angina
    • Raynaud
    • prevent vasospasm post subarachnoid hemorrhage
    • isolated reduction in systolic BP
  • Toxicity
    • cardiac depression
    • AV bock
    • Peripheral edema
    • Flushing
    • Dizziness
    • Constipation
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5
Q

Hydralazine

A

Vasodilator

  • increases cGMP = smooth muscle relaxation
  • Vasodilation
    • arteries > veins
    • decrease afterload
  • Use
    • severe HTN
    • CHF
    • HTN in prego (With methylodopa)
  • Can give with B-blocker to prevent reflex tachycardia
  • Toxcitiy
    • compensatory tachycardia
    • fluid retention
    • nausea
    • headache
    • angina
    • SLE (lupus)
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6
Q

Malignant HTN

A
  • Nitroprusside
    • short acting
    • increase cGMP = release NO
    • Cyanide toxicity
  • Fenoldopam
    • dopamine DI receptor agonist
    • vasodilation: coronary, peripheral, renal, splanchnic
    • decrease BP
    • increase natriuresis
  • Nitroglycerin + Isosorbide Dinitrate
    • vasodilate veins > arteries
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7
Q

Nitroglycerine

A

Vasodilate

  • Release NO = increase cGMP = decrease intracellular Ca+ = myosin dephosphorylation = smooth muscle relaxation
  • Need period without drug in system each day to avoid tolerance
  • Vasodilate
    • Veins > arteries
    • decrease preload
  • ​Use
    • angina
    • pulmonary edema
    • malignant HTN
  • Toxicity
    • reflex tachycardia
    • hypotension
    • flushing, headache
    • monday disease = tolerance of vasodilators during work week but loss of tolerance over weekend
      • dizziness, headache, tachycardia upon reexposure
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8
Q

Isosobide dinitrate

A

Vasodilate

  • Release NO = increase cGMP = decrease intracellular Ca+ = myosin dephosphorylation = smooth muscle relaxation
  • Need period each day where drug is not in system to avoid tolerance
  • Vasodilate
    • Veins > arteries
    • decrease preload
  • Use
    • angina
    • pulmonary edema
  • Toxicity
    • reflex tachycardia
    • hypotension
    • flushing
    • headache
    • monday disease: tolerance of vasodilators during work week but loss of tolerance during weekend
      • tachycardia, dizziness, headache upon reexposure
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9
Q

Angina therapy

A
  • Reduce myocardial O2 consuption by decreasing
    • end diastolic volume
    • blood pressure
    • heart rate
    • contractility
    • ejection time
  • Nitrates
    • preload
    • decrease EDV
    • decrease BP
    • increase contractility (reflex)
    • increase heart rate (reflex)
    • decrease ejection time
    • decrease MVO2
  • B- blockers
    • afterload
    • increase EDV
    • decrease BP
    • decrease contractility
    • decrease heart rate
    • increase ejection time
    • decrease MVO2
  • Together
    • no effect on EDV
    • decrease BP
    • no effect on contractility
    • decrease HR
    • no effect on ejection time
    • decrease MVO2
  • ​Ca++ channel blocker
    • nifedipine = nitrate
    • verapamil = b blocker
  • Partial Beta blockers
    • Pindolol and acebutol = dont use
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10
Q

Niacin

(B3)

A

Niacin

  • Effect
    • Decrease LDL (xx)
    • Increase HDL (^^^)
    • Decrease triglucerides (x)
  • Mechanism
    • inhibit VLDL release from hepatocyte
    • inhibit lipolysis in adipose tissue
  • Toxicity
    • Red, flushed face (due to prostaglandins)
      • decreased by aspirin
    • Hyperglycemia
      • acanthos nigricans
    • Hyperuricemia
      • gout
    • Potentiate effects of hypertensive drugs b/c vasodilatory
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11
Q

Cholestyramine

A

Bile acid resin

  • Effect
    • Decrease LDL (xx)
    • Increase HDL (^)
    • Increase Triglycerides (^)
  • Mechanism
    • prevent bile acid reabsorption from intestine
    • increase hepatic cholesterol synthesis
  • Toxicity
    • Most hated by patients
      • bad taste
      • GI discomfort
    • Decrease fat soluble vit absorption
      • DAKE
    • Cholesterol gallstones
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12
Q

Colestipol

A

Bile acid resin

  • Effect
    • Decrease LDL (xx)
    • Increase HDL (^)
    • Increase Triglycerides (^)
  • Mechanism
    • inhibit bile acid reabsorption from intestine
    • increase hepatic cholesterol synthesis
  • Toxicity
    • patients hate
      • bad taste
      • GI discomfort
    • Decreases absorption of fat soluble vit
      • DAKE
    • Cholesterol gallstones
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13
Q

Colesevelam

A

Bile acid resin

  • Effects
    • Decrease LDL (xx)
    • Increase HDL (^)
    • Increase Triglycerides (^)
  • Mechanism
    • Inhibit bile acid reabsorption from gut
    • Increase hepatic cholesterol synthesis
  • Toxicity
    • Patients hate it
      • bad taste
      • GI discomfort
    • Decreases absorption of fat soluble vit
      • DAKE
    • Cholesterol gallstones
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14
Q

Ezetimibe

A

Cholesterol absorption blocker

  • Effect
    • Decreases LDL (xx)
  • Mechanism
    • prevent cholesterol reabsorption from small intestine
  • Toxicity
    • Increase LFT (rare)
    • Diarrhea
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15
Q

Gemfibrozil

A

Fibrate

  • Effect
    • Decrease LDL (x)
    • Increase HDL (^)
    • Decrease Triglycerides (xxx)
  • Mechanism
    • upregulate lipoprotein lipase (LPL)
      • VLDL –> IDL
    • increase TG clearance
    • increase hepatic cholesterol synthesis*
    • Suppresses 7-alpha hydroxylase
      • decreased cholesterol –> bile acids
      • increased gallstone formation
  • Toxicity
    • Myositis (muscle inflammation)
    • Hepatotoxicity (increase LFT)
    • Cholesterol gallstones
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16
Q

Clofibrate

Bezafibrate

Fenofibrate

A

Fibrates

  • Effect
    • Decrease LDL (x)
    • Increase HDL (^)
    • Decrease Triglycerides (xxx)
  • Mechanism
    • Upregulate lipoprotein lipase (LPL)
    • Increase TG clearance
    • Increase hepatic cholesterol synthesis
    • Suppress 7-alpha hydroxylase
      • decrease cholesterole –> bile conversion
      • increase cholesterol gallstones
  • Toxicity
    • Myositis (muscle inflammation)
    • Hepatotoxicity (increase LFT)
    • Cholesterol gallstones
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17
Q

Digoxin

A

Cardiac Glycoside

  • 75% bioavailable
  • Urinary excretion
  • Antagonised by actions of K+
  • Mechanism
    • Directly inhibits Na+/K+ ATPase
      • indirections inhibits Na+/Ca+ exchanger
      • inceases incracellulat Ca++
      • Positive ionotropy
    • Stimulates CN X
      • decrease heart rate
    • ​​Increases refractoriness in AV node
  • Toxicity
    • Cholinergic (DUMBBELSS)
      • Diarrhea, Urination, Miosis, Bradycardia, Bronchospasm, Excitation of skeletal m and nervous system, Lacrimation, Salivation, Sweating
    • Changes in color perception
    • occurs with decreased renal function b/c renally cleared
  • ECG:
    • increase PR
    • decrease QT
    • ST scooping
    • T wave inversion
    • Arrythmia
    • AV block
  • Hyperkalemia (poor prognostic factor)
  • Digitalis induced tachycardia = increased Ca+ = Delayed Afterdepolarization
    • most serious and potentially fatal effects
  • Factors predisposing to toxicity
    • renal failure, hypokalemia, quinidine use
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18
Q

Na+ / K+ ATPase

Na+ / Ca+ Exchanger

A
  • Na+ / Ka+ ATPase
    • Na+ out
    • K+ in
  • –> decreases intracellular Na+ turning on exchanger
  • Na+ / Ca+ Exchanger
    • Na+ in
    • Ca+ out
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19
Q

Quinidine

A

Class 1A antiarrhythmic

  • double, quarter, pounder
  • Medium Na+ binding strength
  • Mechanism
    • Na+ block
      • preferentially active and inactive channels in pacemaker cells
    • K+ block
  • Effect
    • Prolong action potential
    • increase effective refractory period
    • increase QT interval
  • Use
    • atrial + ventricular arrhythmias
    • esp: reentract + ectopic supraventricular and ventricular tachycardias
  • Toxicity
    • Thrombcytopenia
    • Torsades de pointe
    • Q: headache, tinnitus
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20
Q

Procainamide

A

Class **1A **Antiarrhythmic

  • double quarter pounder
  • medium Na+ binding strength
  • Mechanism
    • Na+ block
      • preferentially block active and inactive channels in pacemaker cells
    • K+ block
  • Effect
    • Prolong action potential
    • Increase effective refractory period
    • Increase QT interval
  • Use
    • atrial + ventricular arrhythmias
    • esp: ectopic supraventricular and ventricular tachycardia
  • Toxicity
    • thrombocytopenia
    • torsades de pointe
    • P: SLE
21
Q

Disopyramide

A

Class 1A Antiarrhythmic

  • double, quarter, pounder
  • Medium Na+ channel binding affinity
  • Mechanism
    • Na+ block
      • preferentially block active and ianctive Na+ channels in pacemaker cells
    • K+ block
  • Effect
    • Prolong action potential
    • increase effective refractory period
    • Increase QT interval
  • Use
    • atrial and ventricular arrhythmias
    • esp: reentrant supraventricular and ventricular tachycardia
  • Toxicity
    • thrombocytopenia
    • torsades de pointe
    • D: heart failure
22
Q

Lidocaine

A

Class 1B antiarrhythmic

  • Lettuce, mayo, tomato
  • Weakest Na+ channel blocker
    • rapid dissociation
    • minimal cumulative effect over many selectives
  • Mechanism
    • Na+ channel blocker
    • Shortens AP
    • Selective for ischemic or depolarized Purkinje ventricular tissue
  • Use
    • Post MI - acute ventricular arrhythmias
    • Digitalis induced arrhythmias
  • Toxicity
    • local anesthetic
    • CNS stimulation/ depression
    • CV depression
23
Q

Mexiletine

A

Class IB antiarrhythmic

  • lettuce, tomato, mayo
  • Weakest Na+ block
    • rapidly dissociate from Na+ channels
    • minimal cumulative effect over time
  • Mechanism
    • Na+ channel block
    • **Shorten AP **
    • Selective for ischemic or depolarized Purkinje and ventricular tissue
  • Use
    • Post MI
      • acute ventricular arrhythmias
    • Digitalis induced arrhythmias
  • Toxicity
    • local anesthetic
    • CNS stimulation/ depression
    • CV depression
24
Q

Tocainide

A

Class IB antiarrhythmic

  • lettuce, tomato, mayo
  • Weaknest Na+ channel blocker
    • rapid dissociation from channel
    • minimal cumulative effect over time
  • Mechanism
    • Na+ channel blocker
    • Shorten AP
    • Selective for ishcmeic or depolarized Purkinje and ventricular tissue
  • ​Use
    • Post MI​
      • acute ventricular arrhythmias
    • Digitalis induced arrhythmias
  • Toxicity
    • Local anesthetic
    • CNS stimulation/ depression
    • CV depression
25
Q

Fenoldopam

A

Malignant HTN Fenoldopam

  • Dopamine D1 receptor agonist
  • Arteriol Vasodilator:
    • coronary
    • peripheral
    • renal
    • splanchnic
  • Decrease BP
  • increase natriuresis

dopamine DI receptor agonist

vasodilation: coronary, peripheral, renal, splanchnic

decrease BP

increase natriuresis

26
Q

CHF

A
  • Decrease mortality
    • ACE inhibitors
      • captopril
      • enalapril
      • lisinopril
    • B- blockers
    • **ARBs **
      • (sartans)
    • Spironolactone
  • Decrease symptoms
    • thiazide diuretic
      • hydrochlorathiazide
    • **loop diuretic **
      • furosamide
27
Q

Flecainide

MOA? AP effect? Uses?

A

Class IC antiarrythmic

  • MOA: Na+ blocker
    • binds strongly
    • slow dissociation
      • Use dependence= na+ block increases as heart rate increases (prolong QRS with faster rate)
      • blocking accumulates b.c less time between action potentials for drug to dissociate
  • No effect on AP
  • Use:
    • ventricular tachycardia that progresses to VF
    • intractable SVT
    • Last resport in refractory tachyarrythmias
    • *** NO structural abnormalitites
  • Toxicity
    • proarrythmias if post MI
    • prolonges refractory period in SA node
      *
28
Q

Propafenon

MAO?

AP effect?

Use?

A

Class IC antiarrhythmic

  • MOA: Na+ inhibitor
    • binds tightly
    • slow dissociation
      • Use dependence = sodium blocking effect increases with heart rate (prolong QRS with faster rate)
      • blocking effect accumulates b/c less time between action potentials for medicine to dissociate from receptor
  • AP effect
    • no effect on duration
  • Use
    • ventricular tachycardias that progress to VF
    • intractable SVT
    • last resport in refractory tachyarrhythmias
    • ** no structural abnormalities
  • Toxicity
    • proarrhythmic post MI
    • prolongs refractory period in AV node
29
Q

Metoprolol

Selective nonselective?

MOA?

Use

Toxicity

A

Class II antiarrhythmic

  • B-blcoker
  • B1 selective = heart (ABEAM)
  • MOA:
    • decrease SA + AV node activity
      • decrease cAMP
      • decrease Ca++ currents
    • suppress abnormal pacemakers
      • decrease phase 4 slope
    • Decrease heart rate
    • decrease ionotropy
    • decrease conduction velocity
  • Use
    • ventricular tachycardia
    • SVT
    • a-fib
      • slow ventricualr rate
    • a-flutter
    • CHF
  • Toxicity
    • impotence
    • CV = bardycardia, av block, chf
    • CNS = sedation, sleep alterations
    • Mask signs of hypoglycemia ***
    • Do not use in cocaine users = unopposed alpha-adrenergic receptor agonists
    • dislipidemaia
      • treat with glucagon
30
Q

Propranolol

Selective?

MAO?

Use?

Toxicity

A

Class II Antiarrhythmic

  • B-blocker
  • Non- selective
  • MAO
    • decrease SA and AV node activity
      • decrease cAMP
      • decrease Ca++
    • suppress abnormal pacemakers
      • decrease slope of phase 4
    • decrease HR
    • decrease ionotropy
    • decrease conduction velocity
  • Use
    • v-tach
    • SVT
    • a-fib + a-flutter
      • slow ventricular rate
    • CHF
  • Toxicity
    • impotence
    • exacerbation of asthma
      • prevent brochodilation
    • CV = bradycardia, AV block, CHF
    • CNS = sedation, sleep alteration
    • Mask signs of hypoglycemia ***
    • Do not give to cocaine users = unooposed alpha adrenergic receptor agonist
    • Exacerbate vasospasm in Prinzmetal’s angina
31
Q

Esmolol

Selective?

MOA?

Use?

Toxicity

A

Class II Antiarrhythmic

  • B-blocker
  • B1 selective = heart (A BEAM)
  • Shortest acting
  • MOA
    • decrease SA and AV node activity
      • decrease caMP
      • decrease Ca++
    • supress abnormal pacemakers
      • decrease slope of phase 4
    • decrease ionotropy
    • decrease HR
    • Decrease conduction velocity
  • Use
    • v-tach
    • SVT
    • a-fib and a-flutter
      • slow ventricular rate
    • CHF
  • Toxicity
    • CV = bradycardia, AV block, chf
    • CNS = sedation, sleep alteration
    • mask signs of hypoglycemia ***
    • done give to cocaine users = unopposed alpha adrenergic receptor agonists
32
Q

Atenolol

Selective?

MOA?

Use?

Toxicity

A

Class II antiarrhythmic

  • B-blocker
  • B1 selective = heart (A BEAM)
  • MOA
    • decrese SA + aV node activity
      • decrease cAMP
      • decrease Ca++
    • suppress abnormal pacemakers
      • decrease slope phase 4
    • decrease ionotropy
    • decrease HR
    • decrease conduction velocity
  • Use
    • v-tach
    • SVT
    • a- fib + a-flutter
      • slow ventricular rate
  • Toxicity
    • CV = bradycardia, AV block, CHF
    • CNS = sedation, sleep alteration
    • Mask signs of hypoglycemia***
    • dont give to cocain users = unopposed alpha adrenergic receptor agonists
33
Q

Timolol

Selective

MOA

Use

Toxicity

A

Class II antiarrhythmic

  • B-blocker
  • Non selective
  • MOA
    • decrease SA + AV node activity
      • decrease caMP
      • decrease Ca++
    • suppress abnormal pacemakers
      • decrease slope phase 4
    • decrease ionotropy
    • decrease HR
    • decrease conductionv velocity
  • Use
    • v-tach
    • SVT
    • a-fib + a-flutter
      • slow ventricular rate
    • CHF
  • Toxicity
    • impotence
    • exacerbation of asthma (no bronchodilation)
    • CV = bradycardia, AV block, CHF
    • CNS = sedation, altered sleep
    • Mask signs of hypoglycemia**
    • dont give to cocaine users = unopposed alpha adrenergic receptor agonist
34
Q

Amiodarone

MAO

Use

Toxicity

A

Class III antiarrhythmic (AIDS)

  • K+ channel blocker
    • also has class I, II, IV effects
      • Na+, B-blocker, K+, Ca+ block
  • MOA
    • increase AP duration
    • increase effective refractory period
    • increase QT interval
      • but low risk torsades de pointes
    • fail when used with other antiarrhythmics
  • Use
    • A-fib + left ventricle dysfunction
    • A-flutter
    • V-tach
  • Toxicity
    • Pulm: pulmonary fibrosis (most common)
      • ​amiodarone interstitial pneumonitis
      • dyspnea, cough, fever, pulm infiltrate
      • reversible
    • Endo: hypothyroid( no T4–> T3 conversion) + hyperthyroid
      • 40% iodine by weight
    • GI/ Hepatic:
      • constipation
      • elevated transaminases
    • Cardiac: bradycardia, heart block, QT prolongation, torsades de pointes
    • Neuro: peripheral neuropathy
    • Ocular: optic neuropathy, corneal microdeposits
    • Derm: blue gray skin discoloration
35
Q

Sotalol

MAO

Use

Toxicity

A

Class III antiarrhythmic (AIDS)

  • K+ channel blocker
    • B blocker
  • MOA
    • increase AP duration
    • increase effective refractory period
    • increase QT interval
    • decrease HR (b block)
  • Use
    • A-fib
    • A-flutter
    • V-tach
  • Toxicity
    • torsades de pointes
    • excess beta block
36
Q

Dofetilide

MAO

Use

Toxicity

A

Class III antiarrhythmic (AIDS)

  • K+ channel blocker
  • MOA
    • increase AP duration
    • increase effective refractory period
    • increase QT interval
  • Use
    • A-fib
    • A-flutter
    • V-tach
  • Toxicity
    • torsades de pointes
37
Q

Ibutilide

MAO

Use

Toxicity

A

Class III antiarrhythmic (AIDS)

  • K+ channel blocker
  • MOA
    • increase AP duration
    • increase effective refractory period
    • increase QT interval
  • Use
    • A-fib
    • A-flutter
    • V-tach
  • Toxicity
    • torsades de pointes (prolonged QT)
38
Q

Lovastatin

Pravastatin

Simvastatin

Atorvastatin

Rosuvasatin

A

HMG-Co-A Reductase inhibitors

  • LDL: xxx
  • HDL: ^
  • TG: x
  • MOA:
    • inhibit HMG-CoA –> mevalonate
      • cholesterol precursor
    • **Increase surface LDL receptors on hepatocytes **
      • Increase LDL uptake
  • Use
    • commonly prescribed post MI (lower cholesterol adn satbilize plaques)
  • Toxicity
    • hepatotoxicty
      • increased LFT
    • Rhabdomyolysis (muscle tissue breakdown)
      • Myalgia = low dose, no rise in CK
      • Myositis = high dose, rise in CK
  • Risk of myopathy is increased when used with fibrates
39
Q

Nitroprusside

Use

MOA

Toxicity

A

Malignant HTN

  • Use: emergency setting when you need to control blood pressure quickly
  • MOA: mixed arterial + venous dilation
    • inceases cGMP via release of NO
  • Toxicity: Cyanide poisoning
    • metabolized to CN + NO
    • Signs: altered mental status + lactic acidosis
    • Treatment: **sodium thiosulfate **
40
Q

Adenosine

MOA

Use

Toxicity

Block effect

A
  • MOA: Decreases If
    • increases K+ out of cell –> hyperpolarize cell and decrease Ca++
  • Use:
    • diagnose and abolish supraventricular tachycardia
    • very short acting (15 sec)
  • Toxicity
    • flushing
    • hypotension
    • chest pain
  • Block effects with
    • theophylline
    • caffeine
41
Q

Mg2+

Use

A
  • Use:
    • torsades de pointe
    • digoxin toxicity
42
Q

Isoproterenol

A
  • Isolated beta agonist
    • increase contractility of heart
    • decrease systemic vascular restistance
  • use
    • torsades de pointes (tachycardia decrease QT interval)
    • braduarrhythmias (worsen ischemia)
    • rarely used due to AV block
43
Q

Atropine

A
  • Muscarine receptor bocker
    • blocks vagal influence on SA + AV node
    • increases heart rate
  • Use: bradycardia
    • most inferior MI
  • Toxicity
    • normal antimuscarinic effects
    • acute closed angle glaucoma
      • unilateral severe ye pain and visual disturbance (halos)
44
Q

Phosphodiesterase 3 Inhibitors

A
  • MOA: Increase contractility in heart
    • inhibit phosphodiesterase = no metabolism of cAMP
    • increased cAMP –> inceased conductance of Ca+ channels in SR –> strengthen contraction
  • Use: CHF
  • Toxicity
    • vasodilation
      • do not use in hypotension
45
Q

Dobutamine

A
  • MOA: B1 receptor agonist
    • increased production of cAMP causing
      • positive ionotropic efffect
      • increased heart rate = weak chronotropic effect
        • increased myocardial O2 consumption
      • increased cardiac conduction velocity
  • Use: heart failure
  • cardiac stress test
46
Q
A
47
Q

Essential HTN

A
  • Diuretics
  • ACE inhibitors
    • prevent unfavorable heart remodeling
  • Angiotensin II receptor blocler (ARB)
  • Ca+ channel blocker
48
Q

CHF

A
  • Diuretics
  • ACE inhibitors
  • Angiotensin II receptor blockers (ARBs)
  • B-blockers (compensated)
    • use cautiously
    • do not use in cardiogenic shock
  • K+ sparing diuretics
49
Q

Diabetes Mellitus

A
  • ACE inhibitors
    • protect against diabetic nephropathy
  • Angiotensin II receptor blocker (ARB)
  • calcium channel blocker
  • diuretics
  • B-blocker
  • A-blocker

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