Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

1 USMLE - Cardiovascular System > Pharmacology > Flashcards

Pharmacology Flashcards

(100 cards)

Start Studying
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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*
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Verapamil. Mechanism? Effects? Pharacokinetics? Use? Adverse?
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
26
Diltiazem. Mechanism? Effects? Pharacokinetics? Use? Adverse?
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
27
Adenosine. Mechanism? Effects? Pharacokinetics? Use? Adverse?
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
28
Digitalis. Mechanism? Effects? Pharacokinetics? Use? Adverse?
``` 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) ```
29
Nitrates & Nitrites. Mechanism? Drugs?
``` 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 ```
30
Nitroglycerine. Mechanism? Effects? Pharacokinetics? Use? Adverse?
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)
31
Isosorbide Dinitrate
Mechanims similar to nitroglycerin but has a slightly longer duration of action
32
Isosorbide Mononitrate
Active metabolite of isosorbide denigrate used ORALLY for prophylaxis of Angina
33
Nifedipine. Mechanism? Effects? Pharacokinetics? Use? Adverse?
``` 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 ```
34
Atenolol. Mechanism? Effects? Pharacokinetics? Use? Adverse?
``` 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) ```
35
Aspirin
``` Mech: Inhibitor of plately COX1&2 -inhibits thromboxane A2 -Irriversible -Platelets cannot aggregate -Decreases risk of thrombosis Use in MI ```
36
Hydralazine
Arteriole vasodilator
37
Enalapril
l
38
Diabinase
L
39
Zaroxolyn
Loop dieuretic | -Use in CHF if allergy to furosemide
40
Warfarin
io
41
Furosemide
s
42
Acetazolamide
l
43
Dobutamine
Used in acute CHF in hospital
44
Apresoline
Arterial vasodilator
45
ACE inhibitors
CHF!!! Catopril Enalapril
46
ARBs (Angiotensin II Receptor Blockers)
Losartan
47
Spironolactone
Aldosterone antagonist | CHF
48
Carvedilol
Cardio selective B-Blocker - Decreases catecholamines - Improves survival in CHF
49
What drug do you never use in a patient with diastolic dysfunction CHF?
Diuretics and Vasodilators
50
Indirect-Acting Sympathomimetics
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
Alpha 1 Receptor
Epinepherine > Norepi >>> Isoproterenol -Smooth muscle contraction -Vasoconstriction Activates phophsolipase C, Gqalpha dependent, increases intracellular Ca
52
Alpha 2 Receptor
Epinepherine > NE >>> Isoproterenol - Inhibition of neural NE release - Decreases cAMP - Activates Na/H antiporter - Gialpha dependent
53
Beta 1 Receptor
Isoproterneol > Epi = NE - Adrenergic cardiac effects (SA node inc.) - Renin Release (inc BP, volume) - Increases cAMP via Gsalpha
54
Beta 2 Receptor
Isoproterenol > Epi >> NE - Relaxation of smooth muscle Bronchiodilation in LUNG (use Epi in anaphylaxis) - Vasodilation - Increase cAMP via Gsalpha
55
Dopaminergic Receptor
Dopamine | -Dilation of renal and mesenteric vasculature
56
Muscarinic Receptor
NE
57
Nicotinic Receptor
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
COMT
Inactivates catecholamines in liver
59
MAO
Oxidizes catecholamines | -Pargyline
60
Dobutamine
Selective B1 AGONIST -Positive inotrope (inc. HR, BP) Use in CHF or acute MI DO NOT USE in AFib
61
Dopamine
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
Phenylephrine
A1 AGONIST -Vasoconstriction (inc. BP) Use in HPTN or for paroxysmal atrial tachycardia
63
Metaproterenol
``` B2 AGONIST -Bronchodilation in lungs Use for Asthma, difficulty breathing Adverse: Tachycardia (B1), tremor, HA (B2 vasodilation) -Decreases BP ```
64
Albuterol
``` B2 AGONIST -Bronchodilation in lungs Use for Asthma, difficulty breathing Adverse: Tachycardia (B1), tremor, HA (B2 vasodilation) -Decreases BP ```
65
Isoproterenol
``` 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
Norepinepherine
``` A1 Agonist, B1 Agonist -Vasoconstriction -Positive Inotrope -HR, Contractility, SV, BP all increase -Then reflex reduction in HR Used to treat HPTN ```
67
Terazosin
A1 ANTAGONIST - Vasodilation - Decreased BP
68
Epinepherine
``` 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
Loop Diuretics
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
Furosemide
Loop Diuretic
71
Torsemide
Loop Diuretic
72
Thiazide Diuretics
``` 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
Chlorthalidone
Thiazide Diuretic
74
Hydrochlorothiazide
Thiazide Diuretic
75
Metalzone
Thiazide Diuretic
76
Why are using thiazide diuretics with ACE inhibitors Synergistic?
when you use a thiazide it shifts body to use renin-angiotensin system.. So blocking both is SYNTERGISTIC*
77
Potassium Sparing Diuretics
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
Spironolactone
K Sparing Diuretic -Inhibits aldosterone receptor in collecting duct Adverse: hyperkalemia, acidosis, Gynecomastia
79
Amiloride
K Sparing Diuretic | -Inhibits E NAC channels, inhibits Na exchange for K and H in collecting duct
80
Triamterene
K Sparing Diuretic -Inhibits E NAC channels, inhibits Na exchange for K and H in collecting duct Adverse: RENAL Failure
81
Vasopressin (ADH)
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
Desmopressin
Vasopressin (ADH) congener
83
Reason to use a potassium sparing diuretic?
HTN in Heart Failure or Post MI patient
84
Demecocycline
Antibiotic that has some ADH antagonistic activity
85
Osmotic Diuretics
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
Mannitol
Osmotic Diuretic
87
Carbonic Anhydrase Inhibitors
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
Acetazolamide
Carbonic Anhydrase Inhibitor
89
Organic Anion Transporters
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
Allopurinol
Inhibits xanthine oxidase | -Used to treat GOUT
91
Probenicid
Inhibits Organic Anion Transporters (OATs) | -Used for Gout
92
Sulfinpyrazone
Inhibits Organic Anion Transporters (OATs) | -Used for Gout
93
How to thiazides cause Gout?
Thiazides are substrates
94
Eplerenone
Potassium sparing diuretic | -Aldosterone Receptor blocker similar to spironolactone
95
What do you use to acidify urine?
Ammonium Chloride | -Probably will never use
96
What is important to monitor when using Loop Diuretics?
Electrolyte levels, hypokalemia can be and adverse effect
97
What reasons (comorbidities) should thiazide diuretics be used?
HTN and high risk of STROKE HTN in diabetics (even though hyperglycemia may be an AE) HTN and Coronary Artery Disease
98
Pindolol. Mechanism? Use? Adverse?
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
Treatment for polycystic kidney disease along with HTN?
ACE Inhibitors - Reduce HTN - Increase renal blood flow - Renal protective
100
Methamphetamine
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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions