Cardiovascular 1/2 Flashcards

(124 cards)

1
Q
A

Answer: Staphylococcus epidermidis

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2
Q
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Answer: colorectal carcinoma.

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3
Q
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Answer: TSH

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4
Q
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Answer: Stroke volume

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5
Q
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Answer: Hyperplastic arteriosclerosis

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6
Q
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Answer: AV node

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7
Q
A

Answer: Blocking calcium channels

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8
Q
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Answer: Inhibits lipolysis in adipose tissue

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9
Q
A

Answer: Wolff-Parkinson-White Syndrome

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10
Q
A

Answer: Third-degree AV block

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11
Q
A

Answer: They block fast sodium channels

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12
Q
A

Answer: Supraventricular tachycardia

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13
Q
A

Answer: Coxsackievirus

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14
Q
A

Answer: Second-degree AV block (Type II)

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15
Q
A

Answer: Option D

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16
Q
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Answer: Hypokalaemia

Note the presence of a U wave, with the associated flattened T wave. The merging of the T wave and the U wave is often misinterpreted as a prolonged or wide QRS; don’t fall for this common student trap! Also note the depressed ST segment, especially marked in Lead II. Causes of hypokalaemia include anorexia, chronic alcohol use, gepphagia, alkalosis, and thiazide/loop diuretics (among others).

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17
Q
A

Answer: Atrial Flutter

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18
Q
A

Answer: II, III, and aVF

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19
Q
A

Answer: Irregularly irregular

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20
Q
A

Answer: Left heart failure

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21
Q
A

Answer: Prolongation of the QT interval

Torsade de pointes is an uncommon and distinctive form of polymorphic ventricular tachycardia (VT) characterized by a gradual change in the amplitude and twisting of the QRS complexes around the isoelectric line (see the image below). Torsade de pointes, often referred to as torsade, is associated with a prolonged QT interval, which may be congenital or acquired. Torsade usually terminates spontaneously but frequently recurs and may degenerate into ventricular fibrillation.

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22
Q
A

Answer: small but sustained inward current of calcium ions

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23
Q
A

Answer: Bundle branch block

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24
Q
A

Answer: First-degree AV block

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25
**Answer: Sinus bradycardia**
26
**Answer: Blocks voltage-gated sodium channels**
27
**Answer: Persistent elevation \>1mm in 2 limb leads and elevation \> 2mm in 2 contiguous chest leads.**
28
**Answer: 1st degree AV block**
29
**Answer: Amiodarone** ## Footnote For a patient with atrial fibrillation who has a normal left ventricular function and no coronary disease, flecainide is preferred. For a patient with atrial fibrillation who has left ventricular dysfunction (left ventricular ejection fraction less than 40%), or coronary disease, amiodarone is preferred as there is no negative inotropic effect.
30
**Answer: Ventricular depolarisation, ventricular repolarisation, and atrial repolarisation**
31
**Answer: Sinus tachycardia**
32
**Answer: Patent ductus arteriosus**
33
34
**Answer: Atrial fibrillation**
35
**Answer: Digoxin**
36
**Answer: Atrial septal defect**
37
**Answer: Mitral valve regurgitation**
38
**Answer: Option A**
39
**Answer: Ventricular tachycardia and ventricular fibrillation**
40
**Answer: K+ efflux**
41
**Answer: Bifascicular block**
42
**Answer: Left bundle branch block (LBBB)**
43
**Answer: Atrial flutter with variable block** ## Footnote The degree of AV block varies from 2:1 to 4:1 The diagnosis of flutter with variable block could be inferred here from the R-R intervals alone (e.g. if flutter waves were indistinct) — note how the R-R intervals during periods of 4:1 block are approximately double the R-R intervals during 2:1 block.
44
**Answer: 2nd degree AV block, Mobitz type I (Wenckebach)**
45
**Answer: S. viridans**
46
**Answer: S. aureus**
47
**Answer: Subendocardial infarct**
48
**Answer: Atrial flutter with 4:1 block only** Atrial flutter with 4:1 block, * There is 4:1 block, resulting in a ventricular rate of 75 bpm.
49
**Answer: Lignocaine** ## Footnote Lidocaine is a class IB anti-arrythmic drug that inhibits sodium channels, shortens repolarisation and decreases the QT interval.
50
**Answer: Normal sinus rhythm**
51
**Answer: Mitral stenosis**
52
**Answer: Atrial fibrillation**
53
**Answer: Supraventricular tachycardia** ## Footnote This arrhythmia has such a fast rate that the P waves may not be seen. Clinical Tip: SVT may be related to caffeine intake, nicotine, stress, or anxiety in healthy adults.
54
**Answer: Class III, Phase 3**
55
**Answer: I, aVL, V5-6**
56
57
**Answer: His-Purkinje system**
58
**Answer: Atrial fibrillation**
59
**Answer: Atrial fibrillation**
60
**Answer: Inhibits HMG-CoA reductase** ## Footnote Statins inhibit the hepatic synthesis of cholesterol. They do this by inhibiting HMG CoA reductase, the enzyme responsible for the rate-limiting step in cholesterol synthesis.
61
62
**Answer: Atrial flutter** There is a 2:1 AV block resulting in a ventricular rate of 150 bpm
63
64
**Answer: atria and ventricles**
65
**Answer: Activates PPARs and thus lipoprotein lipase**
66
**Answer: First-degree AV block** ## Footnote PR Interval: Prolonged (\>0.20 sec)
67
**Answer: Coagulative necrosis**
68
**Answer: Phase 2**
69
70
**Answer: class IV; phase 2**
71
**Answer: Second-degree AV block (Type I)**
72
**Answer: CK-MB**
73
**Answer: Fibrosis**
74
**Answer: Systolic dysfunction**
75
**Answer: Diastolic dysfunction**
76
**Answer: Verapamil** ## Footnote Blocks L-type, voltage-gated, Ca2+ channels which are important in the action potential plateau and in particular affects action potential propagation in the SA and AV nodes. Shows use-dependence so is more active in tachyarrythmias. Decreases automaticity and slows AV conduction.
77
**Answer: Subendocardial ischaemia** ## Footnote Widespread subendocardial ischaemia due to LMCA occlusion
78
**Answer: Left bundle branch block (LBBB)**
79
**Answer: Right coronary artery**
80
81
**Answer: Old inferior MI**
82
**Answer: Second-degree AV block (Type I)**
83
**Answer: Coagulative necrosis with interstitial infiltration of neutrophils**
84
**Answer: Old inferior MI with first-degree heart block**
85
**Answer: Phase 3**
86
**Answer: class III; phase 3**
87
**Answer: First-degree AV block** ## Footnote PR Interval: Prolonged (\>0.20 sec)
88
**Answer: class II; phase 4**
89
**Answer: Spironolactone**
90
**Answer: 3rd heart sound**
91
**Answer: Atrial systole**
92
**Answer: Macrophage influx**
93
94
95
**Answer: None of the above**
96
97
98
**Answer: ECG changes in leads I, aVL, V5, and V6**
99
**Answer: Mitral regurgitation**
100
**Answer: Sinus tachycardia**
101
**Answer: Rapid filling**
102
**Answer: ST segment elevation with Q wave formation in the precordial leads (V1-6) ± the high lateral leads (I and aVL).**
103
**Answer: 1. Funny Na+ channels are open, 2. Transient Ca2+ (T-type) channels open, 3. Long-lasting Ca2+ (L-type) channels open, 4. Opening of K+ channels and closing of Ca2+ (L-type) channels.** ## Footnote Note that the funny channels are called thus as they let sodium into the cell, but also let potassium out of the cell. This mixed permeability allows for a slow, but automatic, depolarisation of the cardiac pacemaker cell.
104
**Answer: Rhythm 1 and 4** ## Footnote Heart rhythms associated with cardiac arrest are divided into two groups: shockable rhythms (ventricular fibrillation/pulseless ventricular tachycardia (VF/pVT)) and non-shockable rhythms (asystole and pulseless electrical activity (PEA)). The main difference in the treatment of these two groups is the need for attempted defibrillation in patients with VF/pVT.
105
106
**Answer: Excess afterload**
107
**Answer: LAD**
108
**Answer: Aortic regurgitation**
109
**Answer: Mitral regurgitation**
110
**Answer: Severe aortic regurgitation is shorter in duration compared with mild aortic regurgitation.**
111
**Answer: Ischaemia**
112
**Answer: Splinter haemorrhages, Osler's nodes, Janeway lesions**
113
**Answer: Tricuspid regurgitation**
114
**Answer: Aortic stenosis**
115
**Answer: Diastasis**
116
**Answer: Third-degree AV block**
117
**Answer: Clopidogrel**
118
**Answer: chronic obstructive airway disease**
119
**Answer: Coagulative necrosis**
120
**Answer: Posterior infarct**
121
122
**Answer: Option B**
123
**Answer: Pericarditis** ## Footnote Patients presenting with acute pericarditis demonstrate diffuse ST segment elevation in all leads except aVR and V1 (see above).
124
**Answer: Tunica adventitia**