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CLINICAL CORRELATES IM PLAT > CARDIOLOGY > Flashcards

CARDIOLOGY Flashcards

(73 cards)

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1
Q

Triad of Rupture Aneurysm

A

Left flank pain
Hypotension
Pulsation mass

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2
Q

Diagnostic Triad of Wolf-Parkinson-White (WPW) ECG Pattern

A

Wide QRS complex
Relatively short PR interval
Slurring of the initial part of the QRS complex (delta wave

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3
Q

Triad of Chronic Renal Failure in ECG

A

Peaked T waves (hyperkalemia)
Long QT due to ST segment lenthening (hypocalcemia)
LVH (systemic hypertension)

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4
Q

Three principal features of tamponade (BECK’s triad)

A

Hypotension

Soft / absent heart soundJugular venous distension with a prominent x-descent but an absent y-descent

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5
Q

Plaques that have caused fatal thrombosis tend to have

A

Thin fibrous caps
Relatively large lipid cores
High content of macrophages

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6
Q

Triad of Buerger disease

A

Claudication of the affected extremity
Raynaud phenomenon
Migratory superficial vein thrombophlebitis

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7
Q

Virchow triad

A

Stasis
Vascular/endothelial damage
Hypercoagulability

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8
Q

Clinical syndrome of hemochromatosis

A

Cirrhosis
Diabetes
Hypogonadism

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9
Q

Dressler’s triad (post MI pericarditis)

A

Fever
Pleuritic pain
Pericardial effusion

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10
Q

Phases of the cardiac action potential

A

Phase 0: Depolarization (due to rapid Na influx)
Phase 1: Partial Repolarization (Due to K efflux)
Phase 2: Plateau (K efflux balanced by Ca influx)
Phase 3: Complete Repolarization (due to K efflux)
Phase 4: Resting Membrane potential

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11
Q

Has prolongation of PR interval before dropped QRS complex

A

Mobitz type I

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12
Q

Has no prolongation of PR interval before dropped QRS complex

A

Mobitz II

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13
Q

Class of antiarrhythmic drug
Binds to activated Na channels & blocks flow of Na ions in to cardiac myocyte (prolongs action potential)
Used for A-fib, atrial flutter, v-tach

A

Class IA
Quinidine, Procainamide, Disopyramide
(MN: Quiapo Police Department)

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14
Q

Class of anti-arrhythmic drug
Bind to both activated and inactivated Na channels and blocks the flow of Na ions into the cardiac myocyte (shortens action potential)
Use: Post-ischemic arrhythmia, V-fib, V-tach

A

Class IB

Lidocaine, Mexiletine, Tocainide

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15
Q

Class of anti-arrhythmic drug
Binds to activated Na channels and blocks flow of Na ions into cardiac myocyte (no effect on action potential)
Use: treatment of severe refractory ventricular arrhythmia

A

Class IC

Flecainide, Encainid, Propafenone

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16
Q

Class of anti-arrhythmic drug

Blocks beta-adrenergic receptors

A

Class II

-olol group

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17
Q

Class of antiarrhythmic drug

Binds to K channels and blocks flow of K in myocyte (prolongs action potential)

A

Class III

Bretylium, Ibutilide, Amiodarone, Sotalol (BIAS)

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18
Q

Class of anti-arrhythmic drug
Blocks voltage-gated Ca channels thereby blocking the flow of Ca into the cell
Use: supraventricular tachycardia, rate reduction in patients with atrial fibrillation

A

Class IV

Verapamil, Diltiazem

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19
Q

Drugs for HF that increases contractility

A

Digoxin
Dobutamine
Milrinone

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20
Q

Drugs for HF that reduces preload

A

Diuretics
Vasodilator (e.g. nitrates, hydralazine)
Ace inhibitors/ ARBs

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21
Q

Drugs for HF that reduces afterload

A

Diuretics
Vasodilator
ACE inhibitors/ ARBS
Beta blockers

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22
Q

Most common cause of systolic dysfunction that lads to L-sided HF

A

Coronary artery disease (CAD)

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23
Q

Most common cause of diastolic dysfunction that leads to L-sided HF

A

Concentric LVH due to HPN

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24
Q

Most common cause of R-sided HF

A

L-sided HF

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25
Earlier she cardinal symptom of L-side HF
Dyspnea
26
Earliest Cardinal sign of L-sided HF
L-sided S3
27
Most sensitive index of cardiac function
Ejection fraction
28
Single most important bedside measurement to estimate volume status
JVP (internal jugular vein is preferred)
29
Cardinal symptoms of HF
Fatigue | Shortness of breath
30
Most important mechanism f dyspnea in HF
Pulmonary congestion with accumulation of interstial or intra-alveolar fluid, which activates juxtacapillary J receptors
31
Cornerstone of modern therapy for HF with depressed EF
ACE-I / ARBs and Beta blockers
32
most common reason for rehospitalization in HF
Failure to meet criteria for discharge
33
Gold standard for imaging valve morphology/motion, detection of pericardial effusion and tamponade, and assessment of LVcavity size, systolic function & wall thickness
2D echo
34
Gold standard for assessing LV mass/volumes
Cardiac MRI
35
Gold standar in assessing anatomy and physiology of the heart & associated vasculature
Cardiac catheterisation and coronary angiography
36
Cornerstone in he diagnosis of acute and chronic ischemic heart disease
ECG
37
Most common underlying cause of myocardial ischemia and injury
Obstruction of coronary arteries by atherosclerosisa
38
Infection associated with accelerated atherosclerosis
Chlamydophila pneumoniae (pneumonia)
39
Most common cause of anterior chest musculoskeletal pain
Costrochondral and chondrosternal syndromes
40
Myocardial perfusion occurs during this time
Diastole
41
represents the initial lesion of atherosclerosis
Fatty streak
42
Major features of metabolic syndrome
``` Central obesity Hyperglycemia Hypertriglyceridemia Hypertension Low HDL cholesterol ```
43
Age when lipid screening should start (based on current ATP III guidelines)
All adults >20years (lipid profile : TC, TG LDL, HDL) | Q5y
44
Key feature of metabolic syndrome
Central adiposity
45
Most accepted and unifying hypothesis to describe Pathophysiology of metabolic syndrome
Insulin resistance
46
Driving force behind the metabolic syndrome
Obesity
47
Most common cause of myocardial ischemia
Atherosclerotic disease of pericardial coronary artery
48
Most common major vessel involved in MI
Left anterior descending artery
49
Sites of predilection for atherosclerotic plaques to develop due to increased turbulence
Branch points in epicardial arteries
50
Time frame for reversible damage in myocardium
<20mins for total occlusion in the absence of collaterals
51
Most widely used test for both the diagnosis of IHD and estimating the prognosis
Electrocardiographic stress testing
52
Most common Pathophysiology cause of unstable angina
Plaque rupture or erosion with superimposed non-occlusive thrombus
53
Only absolute contraindications to nitrate use
Hypotension | Sildenafil (or similar drug) in previous 24-48 hours
54
Most common artery involved in Prinzmetal angina
Right coronary artery
55
main agents for acute episodes of and to abolish recurrent episodes of prinzmetal’s angina
Nitrates and Ca channel blockers (nifedipine)
56
Type of necrosis seen in MI
Coagulation necrosis (preserve architecture, faded details)
57
Earliest detectable feature of myocyte necrosis
Sarcolemmal membrane disruption (which leads to leakage cardiac enzymes into circulation)
58
Time frame where gross changes in MI occur
12 hours after the onset of symptoms
59
Color changes in MI
Mottling: 4 hours Bright yellow: 1 wk Surrounding red granulation tissue : 2 weeks Gray-white scar: 2 mos
60
Fibrinous pericarditis (bread and butter pericarditis) post MI
Dressler syndrome
61
Preferred biochemical markers for re-infarction
CK-MB
62
Preferred biochemical markers ruptur in MI
Cardiac-Specific Troponin T and Cardiac-Specific Troponin I
63
Level of coronary artery stenosis sufficient to produce ischemia (%)
70%
64
Primary cause of out-of-hospital deaths.from STEMI
V-fib
65
Primary cause of in-hospital deaths form STEMI
Pump failure
66
Principal goal for fibrinolytic
Prompt restoration of full coronary arterial potency
67
Extent of LV involvement that usually results in cardiogenic shock
Infarction > 40%
68
Most common complication of angioplasty
Restenosis
69
Most common thrombi found in NSTEMI (composed mainly of platelets)
White thrombi
70
Most common thrombi found in STEMI (composed of cells and fibrin
Red thrombi
71
Most common cause of sudden cardia death
Coronary artery disease
72
Most common arrhythmia post-MI
Premature ventricular contraction
73
Most common lethal arrhythmia post MI
V-fib

CLINICAL CORRELATES IM PLAT (3 decks)

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