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1 USMLE - Cardiovascular System > Pharmacology > Flashcards

Pharmacology Flashcards

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USMLE® Step 1 flashcards
1
Q

Class IA Antiarrhythmics. Mechanism. Drugs.

A

Na channel blockers.
-Class IA is moderately strong, decreases slope of phase 0
-Prolongs the refractory period
-Prolong AP duel to K+ blockage in phase 3 (at higher doses)
Procainamide
Quinidine
Disopyramide

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2
Q

Procainamide. Mechanism? Effects? Pharacokinetics? Use? Adverse?

A

Class IA
Decrease vascular resistance causing hypotension
Hepatic metabolism (NAPA is active metabolite that has Class III activity and a longer half life than Procainamide)
Use for Atrial or Ventricular Arrythmias
-2nd or 3rd choice for sustained ventricular arrhythmia with MI
Adverse: Long QT leading to Torsades, Lupus* like disease in chronic use

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3
Q

Quinidine. Mechanism? Effects? Pharacokinetics? Use? Adverse?

A

Class IA
Hepatic metabolism
Rarely used
Adverse: Long QT leading to Torsades, NV&D

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4
Q

Disopyramide. Mechanism? Effects? Pharacokinetics? Use? Adverse?

A

Class IA and also Antimuscarinic
Atropine like effects (urine retention, dry mouth, blurred vision, constapation)
In US only approved for ventricular arrythmias, but also could be used for supra ventricular arrhythmias. DO NOT use in heart failure
Adverse: Long QT leading to Torsades

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5
Q

Class IB Antiarrhythmics. Mechanism? Drugs?

A 
Na channel blockers. 
-Shortens ERP
-WEAK phase 0 changes
-Depression of conduction in depolarized cells, NO effect if patient is in NSR
Lidocaine
Mexiletine
Tocainide
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6
Q

Tocainide. Mechanism? Effects? Pharacokinetics? Use? Adverse?

A

Class IB
Glucuronidation reaction in liver
NOT used in US
Minimal adverse effects

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7
Q

Lidocaine. Mechanism? Effects? Pharacokinetics? Use? Adverse?

A

Class IB
Extensive first pass metabolism (GIVE PARENTERALLY)
Use: Sustained Vtach, Vfib, Post cardioversion in acute ischemia. DO NOT USE prophylactically
Adverse: Very minimal

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8
Q

Mexiletine. Mechanism? Effects? Pharacokinetics? Use? Adverse?

A 
Class IB
(ORAL lidocaine)
Also used for chronic pain or neuropathy
Hepatic metabolism
Use for Ventricular arrhythmias
Adverse: Minimal (tremor, blurred vision, lethargy, N&V)
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9
Q

Class IC Antiarrhythmics. Mechanism? Drugs?

A 
Na channel blockers
-Strongest Class I drugs
-Significant decrease in phase 0 slope
-NO change in ERP
Flecainide
Propafenone
Moricizine
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10
Q

Flecainide. Mechanism? Effects? Pharacokinetics? Use? Adverse?

A

Class IC
-Also Class III effects
Hepatic and renal metabolism
Use for PVC SUPPRESSION and supra ventricular arrhythmias
Adverse: Exacerbation of arrythmias in a patient with a history of arrhythmia or past MI

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11
Q

Propafenone. Mechanism? Effects? Pharacokinetics? Use? Adverse?

A 
Class IC
-Also a weak B-blocker
Hepatic metabolism
Use for Supraventricular Arrhythmias
Adverse: Arrhythmia exacerbation, metallic taste
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12
Q

Moricizine. Mechanism? Effects? Pharacokinetics? Use? Adverse?

A

Class IC
Extensive first pass metabolism (Give PARENTALLY)
NOT used in US, used in ventricular arrhythmia elsewhere

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13
Q

Class II Antiarrhythmics. Mechanism? Drugs?

A 
Beta Blockers
-Inhibit SNS activity in the SA node
-Decrease HR
-Decrease BP
-Decrease Contractilty
-Increase coronary perfusion
Propranolol
Acebutolol
Esmolol
Solatol
Metoprolol
Adverse: May cause HYPOglycemia in Diabetics*
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14
Q

Metoprolol. Mechanism? Effects? Pharacokinetics? Use? Adverse?

A

Cardioselective B1 blocker, MUCH less B2 blocking than propranolol
CYP2D6 Substrate, extensive first pass metabolism
Use: Hypertension in asthma patients, DM, PVD (peripheral vascular disease), CHF, MI
Adverse: Bradycardia

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15
Q

Sotalol. Mechanism? Effects? Pharacokinetics? Use? Adverse?

A

Class II antiarrhythmic
-Some Class III activity
Use in AFIB*, Vfib, Vtach, HTN
Adverse: Long QT leading to Torsades

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16
Q

Acebutolol. Mechanism? Effects? Pharacokinetics? Use? Adverse?

A

Class II Antiarrhythmic
-Cardioselective (B1)
-Partial AGONIST of B2 receptor
Very good to control HTN in asthma patients
Also used for HTN in PVD or patients with bradyarrythmias
Has intrinsic sympathomimetic activity so DO NOT use with ANGINA (may exacerbate it)

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17
Q

Propranolol. Mechanism? Effects? Pharacokinetics? Use? Adverse?

A

Class II Antiarrhythmic
-B1 blocking
-Non specific B blocker
Use for HTN, Prophylaxis of ANGINA, CHF, MI, Reflex tachycardia from vasodilation
DO NOT USE IN ASTHMA PT, PVD, or DM
Adverse: bradycardia, bronchospasm, fatigue

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18
Q

Esmolol. Mechanism? Effects? Pharacokinetics? Use? Adverse?

A

Class II Antiarrhythmic
-B1 selective (cardioselective)
Rapidly metabolized by RBC esterases, must be on a drip (9-10 minute half life)
Used for intra/post operative HTN or in Acute arrhythmia

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19
Q

Class III Antiarrhythmics. Mechanism? Drugs?

A 
Potassium channel blocker
-phase 3 prolongation
-Increase in AP and ERP duration, longer QT
Amiodarone
Dofetilide
Ibutilide
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20
Q

Amidorone. Mechanism? Effects? Pharacokinetics? Use? Adverse?

A

Class III Antiarrhythmic
-Also has Class I, II, and IV effects
Extra: peripheral vasodilation
CYP3A4 substrate (levels of statins, warfarin, and digoxin will GO UP in patients if you give Amiodorone and do not decrease dosing)
First line treatment for sustained VTACH, Vfib, Afib, Aflutter
DO NOT use in a patient with SA or AV nodal disease
Adverse: Pulmonary toxicity*, Hepatitis, corneal deposits, skin deposits, thyroid issues

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21
Q

Dofetilide. Mechanism? Effects? Pharacokinetics? Use? Adverse?

A

Class III anti arrhythmic
CYP3A4 substrate
Use for AFIB* as maintenance
DO NOT use if patient has long QT, bradycardia, or hypokalemia
Adverse: Life threatening ventricular arrhythmias

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22
Q

Ibutilide. Mechanism? Effects? Pharacokinetics? Use? Adverse?

A

Class III anti arrhythmic
-Also slow inward sodium channel ACTIVATOR
-Delays depolarization and inhibits sodium channel INactivation, Increases ERP
Use for Acute conversion of AFLUTTER*, Afib to NSR
Adverse: Long QT leading to Torsades

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23
Q

Class IV Antiarrhythmics. Mechanism? Drugs?

A

Calcium channel blockers
-Smooth muscle relaxation: Vasodilation
-Reduced contractility of myocytes: shortens phase 2
-Decreases HR, conduction, and CONTRACTILITY: Slows phase 0 in Nodal cells
-Increases coronary blood flow
-Decreases Aortic diastolic pressure (reduces preload)
Dihydropyridines
Non-Dihydropyridines (Verapamil, Diltiazem)

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24
Q

Dihydropyridines. Mechanism? Effects? Pharacokinetics? Use? Adverse?

A 
Class IV antiarrhythmics
-Smooth muscle SELECTIVE
-drugs end in '-pine'
Use to treat HTN
DO NOT USE WITH A BETA BLOCKER
Adverse: HA, flushing, hyptension, reflex tachycardia, edema
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25
Q

Verapamil. Mechanism? Effects? Pharacokinetics? Use? Adverse?

A

Class IV antiarrythmic
-NONdihydropyridine
-Myocardium selective, decreases HR and contractility
Use for SVT, Afib, Aflutter, Angina, coronary vasospasm
DO NOT USE with a B-BLOCKER or in WPW
Adverse: bradycardia, AV block

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26
Q

Diltiazem. Mechanism? Effects? Pharacokinetics? Use? Adverse?

A

Class IV antiarrhythmic
-NONdihydropyridine
-Smooth muscle and cardiac, slows HR, Contractility, and increases vasodilation
Use for hypertension or prophylaxis of angina (will NOT get reflex tachycardia like the dihydropurines may produce)
DO NOT USE with a B-Blocker

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27
Q

Adenosine. Mechanism? Effects? Pharacokinetics? Use? Adverse?

A

Activation of inward K channels
Inhibition of Ca channels (hyperpolarization), slowing of APs in nodal cells
Slowed conduction velocity
Increased ERP
First line treatment for SVT conversion to NSR
DO NOT USE if pt has preexisting 2’ or 3’ block
Adverse: hypotension

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28
Q

Digitalis. Mechanism? Effects? Pharacokinetics? Use? Adverse?

A 
Inhibits Na/K ATPase pump
-increase intracellular Na
-decreases action of Na/Ca pump so more Ca IN CELL
-increases CONTRACTILITY
-Depolarizes RMP
-Activates vagal efferents to heart
-Decreases SA/AV conduction
-Increases ERP
-Decreases Ventricular rate
Use in HEART FAILURE*, Afib, Aflutter
DO NOT use if AV block, WPW, Hypokalemia
Adverse: AV block, digitalis effect on EKG (increase PR, flat T waves, decreased QT)
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29
Q

Nitrates & Nitrites. Mechanism? Drugs?

A 
Arteriole and Venodilation
-VENODILATION > arteriol dilation
-Decreases Preload (V filling pressure)
-Decreased pulmonary resistance
-Decreases LV end-diastolic pressure
-Slight decrease in TPR
-Minimal INCREASE in HR at high doses (reflex response)
-MINIMAL change in coronary blood flow, but less pressure  redistributes it to endocardium
Nitroglycerine
Isosorbide Dinitrate
Isosorbide Mononitrate
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30
Q

Nitroglycerine. Mechanism? Effects? Pharacokinetics? Use? Adverse?

A

Releases NO in smooth muscle, activates guanylyl cyclase and increases cGMP
-Smooth muscle relaxation (VEINS>arterioles)
-Decreased venous return and heart size
-May increase coronary blood flow
USE: Angina
sublingual for acute episodes, oral and transdermal for prophylaxis, IV for acute coronary syndrome
HIGH first pass metabolism (sublingual dose much smaller than oral)
Adverse: Orthostatic HPTN, REFLEX tachycardia, HA
Synergistic hypotension if patient is on other phosphodiesterase type V inhibitor (viagra, cialis, levitra)

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31
Q

Isosorbide Dinitrate

A

Mechanims similar to nitroglycerin but has a slightly longer duration of action

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32
Q

Isosorbide Mononitrate

A

Active metabolite of isosorbide denigrate used ORALLY for prophylaxis of Angina

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33
Q

Nifedipine. Mechanism? Effects? Pharacokinetics? Use? Adverse?

A 
Class IV antiarrythmic
-Dihydropyridine
-Blocks vascular Ca L-type channels MORE than cardiac Ca channels
Use in prophylaxis of ANGINA, HTN
Adverse: HPTN, reflex tachycardia
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34
Q

Atenolol. Mechanism? Effects? Pharacokinetics? Use? Adverse?

A 
Class II anti arrhythmic
-B1 Selective
Decrease HR, BP, Contractility
Increase coronary blood flow
Use: HTN or ANGINA
Adverse: HPTN, bronchospasm (but less risk than propranolol)
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35
Q

Aspirin

A 
Mech: Inhibitor of plately COX1&2
-inhibits thromboxane A2
-Irriversible
-Platelets cannot aggregate
-Decreases risk of thrombosis
Use in MI
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36
Q

Hydralazine

A

Arteriole vasodilator

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37
Q

Enalapril

A

l

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38
Q

Diabinase

A

L

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39
Q

Zaroxolyn

A

Loop dieuretic

-Use in CHF if allergy to furosemide

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40
Q

Warfarin

A

io

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41
Q

Furosemide

A

s

42
Q

Acetazolamide

A

l

43
Q

Dobutamine

A

Used in acute CHF in hospital

44
Q

Apresoline

A

Arterial vasodilator

45
Q

ACE inhibitors

A

CHF!!!
Catopril
Enalapril

46
Q

ARBs (Angiotensin II Receptor Blockers)

A

Losartan

47
Q

Spironolactone

A

Aldosterone antagonist

CHF

48
Q

Carvedilol

A

Cardio selective B-Blocker

  • Decreases catecholamines
  • Improves survival in CHF
49
Q

What drug do you never use in a patient with diastolic dysfunction CHF?

A

Diuretics and Vasodilators

50
Q

Indirect-Acting Sympathomimetics

A

Induce release of NE but not dopamine B hydroxylase
-Reverse direction of axoplasmic catecholamine transporter
-Inactive in presence of axoplasmic pump inhibitors (imipramine, cocaine)
Tyramine
Amphetamine
Ephedrine

51
Q

Alpha 1 Receptor

A

Epinepherine > Norepi&raquo_space;> Isoproterenol
-Smooth muscle contraction
-Vasoconstriction
Activates phophsolipase C, Gqalpha dependent, increases intracellular Ca

52
Q

Alpha 2 Receptor

A

Epinepherine > NE&raquo_space;> Isoproterenol

  • Inhibition of neural NE release
  • Decreases cAMP
  • Activates Na/H antiporter
  • Gialpha dependent
53
Q

Beta 1 Receptor

A

Isoproterneol > Epi = NE

  • Adrenergic cardiac effects (SA node inc.)
  • Renin Release (inc BP, volume)
  • Increases cAMP via Gsalpha
54
Q

Beta 2 Receptor

A

Isoproterenol > Epi&raquo_space; NE

  • Relaxation of smooth muscle Bronchiodilation in LUNG (use Epi in anaphylaxis)
  • Vasodilation
  • Increase cAMP via Gsalpha
55
Q

Dopaminergic Receptor

A

Dopamine

-Dilation of renal and mesenteric vasculature

56
Q

Muscarinic Receptor

A

NE

57
Q

Nicotinic Receptor

A

Ach, Nicotine release from preganglionic neuron

  • Nicotinic receptor on post ganglionic neuron
  • Stimulates release of ACh from vagus nerve on muscarinic receptor (heart and vessels)
  • Stimulates release of NE if adrenergic neuron (heart, vessels)
  • Stimulates ACh if cholinergic neuron, muscarinic rec. (sweat glands, vessels)
  • Stimulates release of dopamine if dopaminergic neuron (renal vessels)
  • Stimulates release of NE, EPI into blood if acting in ADRENAL gland (heart and vessels)
58
Q

COMT

A

Inactivates catecholamines in liver

59
Q

MAO

A

Oxidizes catecholamines

-Pargyline

60
Q

Dobutamine

A

Selective B1 AGONIST
-Positive inotrope (inc. HR, BP)
Use in CHF or acute MI
DO NOT USE in AFib

61
Q

Dopamine

A

B1 Agonist, Dopaminergic agonist
-At high doses A1 Agonist
-Inc. HR, BP (positive inotrope)
Use in Shock (maintains renal blood flow), HPTN, Chronic refractory HF

62
Q

Phenylephrine

A

A1 AGONIST
-Vasoconstriction (inc. BP)
Use in HPTN or for paroxysmal atrial tachycardia

63
Q

Metaproterenol

A 
B2 AGONIST
-Bronchodilation in lungs
Use for Asthma, difficulty breathing
Adverse: Tachycardia (B1), tremor, HA (B2 vasodilation)
-Decreases BP
64
Q

Albuterol

A 
B2 AGONIST
-Bronchodilation in lungs
Use for Asthma, difficulty breathing
Adverse: Tachycardia (B1), tremor, HA (B2 vasodilation)
-Decreases BP
65
Q

Isoproterenol

A 
B1 and B2 Agonist
-Vasodilation* 
-Bronchodilation
-Increase HR
What about BP? 
-MAP = HR*SV*TPR
-HR and SV increase
-TPR decreases (but much more than HR and SV (radius^4))
-So BP WILL DROP*
Use: Cardiac stimulant
66
Q

Norepinepherine

A 
A1 Agonist, B1 Agonist
-Vasoconstriction
-Positive Inotrope
-HR, Contractility, SV, BP all increase
-Then reflex reduction in HR
Used to treat HPTN
67
Q

Terazosin

A

A1 ANTAGONIST

  • Vasodilation
  • Decreased BP
68
Q

Epinepherine

A 
A1 Agonist, B2 Agonist, B1 Agonist
-Vasoconstriction
-Bronchodilation
-Vasodilation
-Positive Inotrope (Inc. HR)
-Reflexive decrease in HR
-If large dose it will RAISE BP
Used in hypersensitivity Reactions or with local anesthetics
69
Q

Loop Diuretics

A

Furosemide, Torsemide
-inhibit Na K Cl pump in acending loop lf Henle
Used in CHF or to reduce pulmonary hypertension
ALWAYS check electrolyte levels*

70
Q

Furosemide

A

Loop Diuretic

71
Q

Torsemide

A

Loop Diuretic

72
Q

Thiazide Diuretics

A 
Block NaCl transporter in distal convoluted tubule
-Used to treat HTN
Chlorthalidone
Hydrochlorothiazide
Metalzone
Adverse: HYPERGLYCEMIA (thiazides are sufonylureas, bind to SUR (sufonyl urea receptor) on potassium channel and OPENS it, hyper polarizing the cell - thus suppressing insulin release)
Hyperuricemia (GOUT)
Hypokalemia
Hyperlipidemia
Hyponatremia
73
Q

Chlorthalidone

A

Thiazide Diuretic

74
Q

Hydrochlorothiazide

A

Thiazide Diuretic

75
Q

Metalzone

A

Thiazide Diuretic

76
Q

Why are using thiazide diuretics with ACE inhibitors Synergistic?

A

when you use a thiazide it shifts body to use renin-angiotensin system.. So blocking both is SYNTERGISTIC*

77
Q

Potassium Sparing Diuretics

A

Inhibit aldosterone receptos in collecting duct (SPIRONOLACTONE)
-Inhibit Na exchange for K and H (E NAC channels) in the cortical collecting duct (AMILORIDE, TRIAMTERENE)
Used in hyperaldosteroneism or to PREVENT K WASTING caused by other diuretics
Use in HEART FAILURE or POST MI
Adverse: Hyperkalemia, hyperchloremic metabolic acidosis, kidney stones

78
Q

Spironolactone

A

K Sparing Diuretic
-Inhibits aldosterone receptor in collecting duct
Adverse: hyperkalemia, acidosis, Gynecomastia

79
Q

Amiloride

A

K Sparing Diuretic

-Inhibits E NAC channels, inhibits Na exchange for K and H in collecting duct

80
Q

Triamterene

A

K Sparing Diuretic
-Inhibits E NAC channels, inhibits Na exchange for K and H in collecting duct
Adverse: RENAL Failure

81
Q

Vasopressin (ADH)

A

Natural hormone that uses G-protein coupled receptors in the collecting duct of the nephron to recruit aquaporins and increase water reabsorption to CONCENTRATE urine
-Desmopressin is a synthetic congener of ADH
Used to treat diabetes insipid us and bed wetting in young children

82
Q

Desmopressin

A

Vasopressin (ADH) congener

83
Q

Reason to use a potassium sparing diuretic?

A

HTN in Heart Failure or Post MI patient

84
Q

Demecocycline

A

Antibiotic that has some ADH antagonistic activity

85
Q

Osmotic Diuretics

A

Mannitol is the primary osmotic diuretic
-It is NOT reabsorbed in the nephron, therefore it exerts and osmotic effect to RETAIN water IN the nephron, thus increasing urine output
-Reduces body water or intracranial/ocular pressure
Adverse: Extracellular volume expansion, dehydration, hyperakalemia

86
Q

Mannitol

A

Osmotic Diuretic

87
Q

Carbonic Anhydrase Inhibitors

A

Acetazolamide is major CA inhibitor
-Not useful as diuretic since it has so many large effects in body
Used to treat Glaucoma, to ALKALINIZE urine (anecdote for barbiturates), treating metabolic ALKALOSIS, Acute Mountain Sickness
Adverse: Hyperchloremic metabolic acidosis, Renal stones, Renal K wasting (hypokalemia)

88
Q

Acetazolamide

A

Carbonic Anhydrase Inhibitor

89
Q

Organic Anion Transporters

A

Transport small hydrophilic molecules into or out of nephron
-Dicarboxylate drives this process (an alpha keto glutamate)
Used in the treatment of GOUT (along with NSAIDS, DO NOT use ASA)
Probenicid
Sulfinpyrazone
-Inhibits renal organic acid transporters of irate to facilitate excretion

90
Q

Allopurinol

A

Inhibits xanthine oxidase

-Used to treat GOUT

91
Q

Probenicid

A

Inhibits Organic Anion Transporters (OATs)

-Used for Gout

92
Q

Sulfinpyrazone

A

Inhibits Organic Anion Transporters (OATs)

-Used for Gout

93
Q

How to thiazides cause Gout?

A

Thiazides are substrates

94
Q

Eplerenone

A

Potassium sparing diuretic

-Aldosterone Receptor blocker similar to spironolactone

95
Q

What do you use to acidify urine?

A

Ammonium Chloride

-Probably will never use

96
Q

What is important to monitor when using Loop Diuretics?

A

Electrolyte levels, hypokalemia can be and adverse effect

97
Q

What reasons (comorbidities) should thiazide diuretics be used?

A

HTN and high risk of STROKE
HTN in diabetics (even though hyperglycemia may be an AE)
HTN and Coronary Artery Disease

98
Q

Pindolol. Mechanism? Use? Adverse?

A

Class II Antiarrhythmic
-Cardioselective (B1)
-Partial AGONIST of B2 receptor
Very good to control HTN in asthma patients
Also used for HTN in PVD or patients with bradyarrythmias
Has intrinsic sympathomimetic activity so DO NOT use with ANGINA (may exacerbate it)

99
Q

Treatment for polycystic kidney disease along with HTN?

A

ACE Inhibitors

  • Reduce HTN
  • Increase renal blood flow
  • Renal protective
100
Q

Methamphetamine

A

Facilitates release of NE from post ganglionic neuron in the synaptic junction.

  • NE stimulates alpha 1 adrenergic receptors causing smooth muscle contraction leading to hypertension
  • NE stimulates beta 1 adrenergic receptors in the SA node causing an increased HR - it is a positive inotrope

1 USMLE - Cardiovascular System (3 decks)

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