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Phase 2a > Cardio > Flashcards

Cardio Flashcards

1
Q

Which three conditions is atherosclerosis the principal cause of?

A

Stroke, heart attack and gangrene

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2
Q

What are the 7 risk factors for atherogenesis?

A
  1. Age
  2. Tobacco smoking
  3. High serum cholesterol
  4. Obesity
  5. Diabetes
  6. Hypertension
  7. Family history
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3
Q

What is the term for a new plaque?

A

Neointima

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4
Q

What are the 4 components of an atherosclerotic plaque?

A
  1. Lipid
  2. Necrotic core
  3. Connective tissue
  4. Fibrous cap
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5
Q

What are the two ways that atheroma can cause problems?

A
  1. Rupture which precipitates a thrombus that occludes the vessel
  2. The plaque can grow so big that it occludes the vessel. This leads to the tissue being supplied to become ischaemic
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6
Q

How is an atheroma caused by injury?

A
  1. Endothelium is injured- “endothelial dysfunction”
  2. Signals sent to circulating leukocytes which then accumulate and migrate into the vessel wall.
  3. Inflammation ensues
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7
Q

What happens when LDL is present in the blood in excess?

A

It accumulates in the arterial wall and then undergoes oxidation and glycation

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8
Q

What happens after inflammation is initiated after injury?

A

Chemoattractants are released from the endothelium and they send signals to the leukocytes

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9
Q

What are the 7 inflammatory cytokines found in plaques?

A
  1. IL-1
  2. IL-6
  3. IL-8
  4. IFN-gamma
  5. TGF- beta
  6. MCP-1
  7. C reactive protein
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10
Q

What are the 5 stages of leukocyte recruitment to vessel walls?

A
  1. Capture
  2. Rolling
  3. Slow rolling
  4. Firm adhesion
  5. Transmigration
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11
Q

When do fatty streaks begin to appear?

A

Under 10 years

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12
Q

What do fatty streaks consist of?

A

Lipid-laden macrophages and T lymphocytes within the intimal layer of the vessel wall.

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13
Q

What do intermediate lesions consist of? (5)

A
  1. Lipid laden macrophages called foam cells
  2. Vascular smooth muscle cells
  3. T lymphocytes
  4. Adhesions and aggregations of platelets on the cell wall
  5. Isolated pools of extracellular lipid
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14
Q

What is the fibrous cap made up of in an atheroma?

A

Collagen and elastin

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15
Q

What causes a plaques to rupture?

A

A fibrous cap needs to constantly be resorbed and redeposited. If the balance shifts in favour of inflammatory conditions then the cap becomes weak and the plaque ruptures.

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16
Q

How do you treat coronary heart disease?

A

PCI- percutaneous coronary intervention

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17
Q

How do some stents reduce the chances of restenosis?

A

They are drug eluting

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18
Q

How does aspirin work?

A

It is an irreversible inhibitor of platelet cyclo-oxygenase

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19
Q

How does Clopidogrel/ Ticagrelor work?

A

Inhibits the P2Y12 ADP receptor on platelets

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20
Q

How do statins work?

A

Inhibit HMG CoA reductase, reducing cholesterol synthesis

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21
Q

Which node is the dominant pacemaker node?

A

SA

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22
Q

What is the intrinsic rate of the SA node?

A

60-100 bpm

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23
Q

What is the intrinsic rate of the AV node?

A

40-60 bpm

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24
Q

What is the intrinsic rate of ventricular cells?

A

20-45 bpm

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25
Q

What is the standard calibration of an ECG?

A

25 mm/s

0.1mV/mm

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26
Q

What does an upright deflection in an ECG signify?

A

An electrical impulse that is travelling towards the electrode

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27
Q

What is the sequence of impulse conduction in the heart?

A

SA node- AV node- Bundle of His- Bundle branches- Purkinje fibres

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28
Q

What does the P wave signify on an ECG?

A

Atrial depolarisation

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29
Q

What does the QRS complex signify on an ECG?

A

Ventricular depolarisation

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30
Q

What does the T wave signify on an ECG?

A

Ventricular repolarisation

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31
Q

What does the PR interval signify on an ECG?

A

Atrial depolarisation and the delay in the AV junction

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32
Q

What makes up a 12 lead ECG?

A

3 standard limb leads, 3 augmented limb leads, 6 precordial leads

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33
Q

Which anatomical group of the heart does lead I monitor?

A

Lateral

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34
Q

Which anatomical group of the heart does lead aVR monitor?

A

None

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35
Q

Which anatomical group of the heart does lead V1 monitor?

A

Septal

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36
Q

Which anatomical group of the heart does lead V4 monitor?

A

Anterior

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37
Q

Which anatomical group of the heart does lead II monitor?

A

Inferior

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38
Q

Which anatomical group of the heart does lead aVL monitor?

A

Lateral

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39
Q

Which anatomical group of the heart does lead v2 monitor?

A

Septal

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40
Q

Which anatomical group of the heart does lead V3 monitor?

A

Lateral

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41
Q

Which anatomical group of the heart does lead III monitor?

A

Inferior

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42
Q

Which anatomical group of the heart does lead aVF monitor?

A

Inferior

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43
Q

Which anatomical group of the heart does lead V3 monitor?

A

Anterior

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44
Q

Which anatomical group of the heart does lead V6 monitor?

A

Lateral

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45
Q

How long should a PR interval be?

A

120 to 200 miliseconds. 3 to 5 little squares

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46
Q

How long should the QRS complex be?

A

No bigger than 110ms, 3 little squares

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47
Q

In which leads should the QRS complex be upright?

A

I and II

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48
Q

What is special about lead aVR?

A

all waves are negative

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49
Q

What is the difference in R waves between leads V1 and V4?

A

They grow in magnitude

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50
Q

What is the trend in S waves V1- V6?

A

The S wave must grow from V1 to at least V3 and then disappear in V6

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51
Q

What is the rule regarding the ST segment in a normal ECG?

A

The ST segment should start isoelectric except in v1 and v2 where it may be elevated

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52
Q

In which leads should the P wave be upright?

A

I, II, v2 and v6

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53
Q

What is the rule regarding Q waves?

A

There should be no Q wave or a very small one in I, II, V2-6

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54
Q

What is the rule regarding T waves?

A

Must be upright in I, II, V2-6

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55
Q

how does right atrial enlargement present on an ECG?

A

Tall, pointed P waves (P pulmonale)

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56
Q

How does left atrial enlargement present on an ECG?

A

Notched P wave (P mitrale) in the limb leads

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57
Q

What does a short PR interval indicate?

A

Wolff-parkinson-white syndrome.

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58
Q

What does a long PR interval indicate?

A

First degree heart block

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59
Q

What does an tall QRS complex in V1-6 mean?

A

Left or right ventricular hypertrophy

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60
Q

How do you calculate heart rate?

A
  1. Divide 300 by the number of big boxes between QRS complexes
  2. Count the number of beats in the 10 second strip and x6
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61
Q

What is the normal weight of a heart in a male?

A

280-340g

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62
Q

What is the normal weight of a heart in a female?

A

230- 280g

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63
Q

What is heart failure?

A

failure to transport blood out of the heart

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64
Q

What is cardiogenic shock?

A

Severe heart failure

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65
Q

Which parts of the heart does the right coronary artery supply?

A

Right ventricle, posterior part of the intraventricular septum and part of the posterior wall of the left ventricle

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66
Q

What does the left coronary artery supply?

A

The left ventricle and the anterior part of the intraventricular septum

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67
Q

Where is ANP produced in the heart?

A

In the right atrial wall

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68
Q

What does increased sympathetic tone cause?

A

tachycardia

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69
Q

What are the signs of left heart failure?

A

pulmonary congestion and oedema

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70
Q

What are the signs of right heart failure?

A

prominent systemic venous congestion, raised jugular venous pressure, enlargement of the liver

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71
Q

What does cor pulmonae mean?

A

Describes right heart failure second to lung disease

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72
Q

What is the most common cause of cor pulmonae?

A

chronic obstructive airway disease

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73
Q

What is dysponea?

A

subjective symptom of shortness of breath

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74
Q

What is orthponea and what does it suggest?

A

Dysponea when lying down. It suggests left heart failure because it is a result of oedema in the legs returning to the lungs.

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75
Q

What are the 4 principle causes of heart of heart failure?

A
  1. Ischaemic heart disease
  2. systemic hypertension
  3. Valvular heart disease
  4. lung disease leading to right then congestive heart failure
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76
Q

Why is there increased fluid retention by the kidney in heart failure?

A

It is a compensatory mechanism

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77
Q

What does increased fluid retention by the kidney lead to?

A

Increased venous return, increased in ventricular preload and volume overloading of the ventricles

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78
Q

Why is the liver enlarged in congestive heart failure?

A

because the centrilobular veins and hepatic sinusoids are engorged.

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79
Q

What triggers the hypertrophic response in heart failure?

A

Angiotensin 2, ET-1 and insulin-like growth factor.1, TGF-Beta.

80
Q

When does the heart (in utero) become formed of two chambers?

A

After the fifth week of gestation

81
Q

What is tachypnoea?

A

Abnormally fast breathing

82
Q

What is polycynthaemia?

A

Raised haematocrit, raised percentage of rbc.

83
Q

Why does probe patent foramen ovale occur? ASD

A

Between the 4th and 7th week of embryonic life septums form between the left and right atria. The septum primum has two defects but is covered by the septum secundum. In fetal life the septum secundum acts as a valve which allows blood to pass from the right to left atrium to bypass the lungs. When pulmonary circulation is established it closes, probe patent foramen ovale occurs when it doesn’t close properly.

84
Q

How are a patient’s heart sounds different if they have an ASD?

A

May have a diastolic rumbling murmur and a splitting of the second heart sound.

85
Q

What percentage of congenital abnormalities do ASD make up?

A

10%

86
Q

What percentage of congential abnormalities do VSD make up?

A

25%

87
Q

Why is there shunting through VSD?

A

Because the pressure in the left ventricle is larger than in the right

88
Q

What is the most prominent physical sign of a VSD?

A

Loud pansystolic murmur with an associated thrill

89
Q

What are the 5 causes of congenital heart diseases?

A 
Single genes associated (trisomy 21, Turner's syndrome X0, di-george syndrome)
Homeobox genes particularly associated
infections- rubella
Drugs- Thalidomide, alcohol
Diabetes
90
Q

What is a patent ductus arteriosus?

A

The ductus arteriosus allows blood to pass from the pulmonary artery to the aorta, it closes within the first few days of life. If it doesn’t occur then there is an abnormal shunt of blood from the aorta to the pulmonary artery

91
Q

What is coarctation of the aorta?

A

A congenital localised constriction in the diameter of the aorta.

92
Q

How do you treat a coarctation of the aorta?

A

Ablation of the stenosed segment

93
Q

What are the complications of coarctation of the aorta?

A

Cardiac failure, rupture of dissecting aneurysm, infective endarteritis, cerebral haemorrhage, stenosis of bicuspid aortic valve

94
Q

What is endocardial fibroelastosis?

A

Profound dense collagen and elastic tissue deposited on the endocardial aspect of the left ventricle. Causes cardiac failure due to stiffening.

95
Q

What is complete transposition of the great arteries (TGA)?

A

The aorta comes off the right ventricle and the pulmonary trunk came off the left ventricle.

96
Q

How do you treat TGA?

A

Arterial switch. Mortality is less than 10%

97
Q

What is dextrocardia?

A

The normal anatomy of the heart is completely reversed

98
Q

What is the tetralogy of fallot?

A

Four features:

  1. Pulmonary stenosis
  2. Ventricular septal defect
  3. Dextraposition/ over-riding ventricular septal defect
  4. Right ventricle hypertrophy
99
Q

What is pericarditis?

A

An inflammatory reaction involving the visceral and/ or parietal layers.

100
Q

What is the WHO classification of hypertension?

A

over 140/90 mmHg

101
Q

What is acute rheumatic fever?

A

An immune response to a group A Beta-haemolytic streptococcus infection. Antibodies cross react with cardiac myoctes

102
Q

What is infective carditis?

A

An infective process involving the cardiac valves

103
Q

What is myocarditis?

A

Inflammation of the myocardium usually associated with muscle cell necrosis and degeneration

104
Q

What is dilated cardiomyopathy (DCM)?

A

poorly generated contractile force leads to progressive dilation of heart with some diffuse interstitial fibrosis

105
Q

What are the common causes of primary DCM?

A

Autosomal dominant
Some recessive and x linked
Mutations in several genes

106
Q

What are the common causes of secondary DCM?

A

Alcohol, catecholamines, cocaine, pregnancy.

107
Q

What is hypertrophic cardiomyopathy?

A

Mutations involving beta-myosin, myosin binding protein C, troponin T
Force degeneration allowing progressive sarcomeric dysfunction

108
Q

What is restrictive cardiomyopathy?

A

Poor dilation of the heart restricts the eventual ability of the heart to take on blood and pass it onto the rest of the body

109
Q

What is malignant hypertension?

A

> 160/110mmHg

Fibrinoid necrosis of the vessel with local inflammation and focal smooth muscle cell proliferation.

110
Q

What is Raynaud’s phenomenon?

A

Intermittent bilateral ischaemia of digits/ extremities precipitated by motional cold temperature

111
Q

What is vasculitis?

A

An inflammatory and necrotic process centred on the blood vessels that may involve arteries, veins and capillaries.

112
Q

What is polyarteritis nodosa (PAN)?

A

affects medium and small muscular arteries. It is patchy arteritis with immune cells

113
Q

what is Hypersensitivity angiitis?

A

Fibrinoid necrosis and inflammation around small vessels. Affects smallest arteries and arterioles. Can be caused by a drugs and infections.

114
Q

What is churg-strauss syndrome?

A

Allergic granulomatosis and angiitis. Strongly associated with asthma.

115
Q

What is giant cell arteritis

A

Commonest type of vasculitis

Focal, chronic and granulomatous inflammation of temporal arteries

116
Q

What are the clinical features of giant cell arteritis?

A

Thickened blood vessel, often palpable
Granulomatous inflammation involving full thickness of the wall with macrophages, lymphocytes, plasma cells, neutrophils and occasionally eosinophils
Giant cells
Old areas of inflammation show up as focal scars.

117
Q

What is Wegner’s granulomatosis?

A

Vasculitis of the respiratory tract and kidney

118
Q

What is Takayasu’s arteritis?

A

Classically involves the aorta

119
Q

What is Kawaski disease?

A

Mucocutaneous lymph node syndrome. Arteritis principally affects the coronary arteries.

120
Q

What is buerger’s disease?

A

It is an inflammatory disease of medium and small arteries affecting the distal limbs

121
Q

What is an aneurysm?

A

Dilated areas of vasculature suggesting either congenita or acquired weakness of the wall of the vessels

122
Q

What is an abdominal aortic aneurysm defined as?

A

> 50% dilation of the aortic diameter

123
Q

Which size of abdominal aortic aneurysm is at an increased risk of explosion?

A

greater than 5-6cm

124
Q

What is a berry aneurysm?

A

berry-like vascular dilatation in the cerebral circulation

125
Q

What is a dissecting aneurysm?

A

A haematoma within the arterial wall with blood entering under pressure from the lumenal surface and dissecting along the length of the media

126
Q

What is a varicose vein?

A

An enlarged torturous vein which principally affects the superficial leg veins

127
Q

What are the risk factors for varicose veins?

A

Age, being female, hereditary, posture, obesity

128
Q

What is a haemangioma?

A

A benign proliferation of blood vessel tissue

129
Q

What is a haemangioendothelioma?

A

A vascular tumour of endothelial cells of low grade malignancy

130
Q

What is an angiosarcoma?

A

A highly aggressive malignant neoplasm of endothelial cells

131
Q

What does an odds ratio of greater than one represent?

A

Exposure is associated with a higher odds of outcome

132
Q

By what percentage does social isolation and loneliness increase the chance of a heart attack?

A

30%

133
Q

What is the population attributable factor?

A

The proportion of the incidence of a disease in the exposed and non-exposed population that is due to the exposure

134
Q

What is the number needed to treat?

A

The NNT offers a measurement of the impact of a medicine or therapy by estimating the number of patients that need to be treated over a given a period of time in order to have an impact on one person

135
Q

What is a psychosocial factor?

A

Factors influencing psychological responses to the social environment and pathophysiological changes.

136
Q

What is coronary prone behaviour pattern?

A

Someone who has a certain personality type which can be described as type A or someone who has competitive, hostile, impatient characteristics

137
Q

What are the 4 psychosocial factors which contribute to CHD?

A
  1. Coronary prone behaviour pattern
  2. Depression and anxiety
  3. Work stress
  4. Social support
138
Q

What is an epicardial vessel?

A

A vessel which lies on the surface of the heart

139
Q

What is angina?

A

A symptom which occurs as a consequence of restricted coronary blood flow.

140
Q

In normal physiology, how does the heart compensate when the resistance in the epicardial vessels is high?

A

The microvasculature dilates

141
Q

What happens when someone with angina starts to exercise?

A

The microvasculature is already dilated to try and compensate for the high resistance in the epicardial vessels so can not compensate for the exercise This person is decompensated.

142
Q

What are the 3 symptoms of typical angina?

A
  1. Heavy, central, tight, radiation to arms, jaw, neck
  2. Precipitated by exertion
  3. Relieved my rest/ GTN
143
Q

What is the differential diagnosis of angina?

A
  1. pericarditis, myocarditis
  2. Pulmonary embolism/ pleurisy
  3. Chest infection/ pleurisy
  4. Dissection of the aorta
  5. Gastro-esophageal
  6. Musculo-skeletal
  7. Psychological
144
Q

How do you investigate angina?

A
  1. 12 lead ECG

2. Echo

145
Q

Which diagnostic investigations can you do to . investigate angina?

A

Anatomical: CT angiography, Invasive angiography
Physiological: Exercise stress treadmill, stress echo, SPECT, perfusion MRI

146
Q

Which three types of medicines are used for primary prevention of angina?

A 
Beta blockers (Beta 1 specific)
Nitrates
Calcium channel antagonists
147
Q

How do beta blockers reduce the likelihood of angina?

A

Antagonise the sympathetic nervous system. Reduce the heart rate and reduce contractility. -ve chronotrope and -ve inotrope

148
Q

What are the side effects of beta blockers?

A

Tiredness, nightmares, bradycardia, ED, cold hands and feet.

149
Q

What are contraindications of B blockers?

A

Excess bradycardia, severe heart block, severe bronchospasm, asthma, prinzmetal’s angina

150
Q

How nitrates prevent angina?

A

They are venodilators. Dilate systemic veins which reduces the venous return to the right side of the heart. Reduces preload on the heart

151
Q

How do calcium channel antagonists work to prevent angina?

A

They are primarily arterodilators. They dilate systejmic arteries which reduces the blood pressure. Reduce afterload on the heart

152
Q

How does aspirin work to prevent IHD?

A

Cyclo-oxygenase inhibitor. Reduces prostaglandin synthesis, reduces platelet aggregation

153
Q

How do statins help prevent IHD?

A

Reduce LDL-cholesterol

154
Q

What does CABG stand for?

A

Coronary artery bypass graft

155
Q

What is the clinical classification of unstable angina?

A

Cardiac chest pain at rest
Cardiac chest pain with a crescendo pattern
New onset angina

156
Q

How do you diagnose unstable angina?

A

History
ECG
Troponin (no significant rise in unstable angina)

157
Q

What is the chest pain like in an acute MI?

A 
Unremitting
Usually severe
Occurs at rest
Associated with sweating, breathlessness, nausea and vomiting
One third can occur in bed at night
158
Q

how do you initially manage an MI?

A

If there is ST elevation, contact primary PCI centre for treatment
Take aspirin 300mg immediately
Take pain relief

159
Q

How is an acute MI managed in hospital?

A 
Bed rest
Oxygen therapy if hypoxic
Pain relief
Aspirin
Consider beta blocker
Antianginal therapy
Consider urgent coronary angiography if the troponin is elevated or unstable
160
Q

What are 4 possible outcomes of atherogenesis?

A

MI, Ischaemic stroke, critical leg ischaemia, cardiovascular death.

161
Q

What is ACS?

A

Acute coronary syndrome. It includes unstable angina and MI.

162
Q

What is troponin?

A

A protein complex that regulates actin: myosin contraction

163
Q

Which two drugs are used together in dual antiplatelet therapy?

A

P2Y12 inhibitor and aspirin

164
Q

What are the three oral options of p2Y12 inhibitors?

A

Clopidogrel, prasugrel and ticagrelor

165
Q

Why are GPIIb/IIIa antagonists used selectively?

A

Because they increase the risk of major bleeding

166
Q

Which two anticoagulants are commonly used?

A

Fondaparinux or heparin

167
Q

What 6 factors affect the response to clopidogrel?

A
  1. Dose
  2. Age
  3. Weight
  4. Disease state
  5. Drug interactions
  6. CYP2C19 loss of function alleles
168
Q

How long should a patient be put on dual antiplatelet therapy?

A

P2Y12 inhibitor may be continued for longer than a year after ACS if there is a risk of ischaemic events.

169
Q

When would you start a patient on heart drugs?

A 
If they are at risk of:
Stroke
MI
Heart failure
Chronic renal diseases
Cognitive decline
Premature death
170
Q

What happens with each 2mmHg rise in systolic BP?

A

7% increased mortality from ischaemic heart disease

10% increased mortality from stroke

171
Q

What measurement of BP classifies hypertension?

A

above 140/90 mmHg

172
Q

What is ambulatory blood pressure monitoring?

A

A technique used on people suspected of high BP. The machine which is worn on their arm takes the BP throughout the day.

173
Q

How does an aldosterone agonist reduce BP?

A

Reduces salt retention

174
Q

When would you start a patient on heart drugs?

A 
If they are at risk of:
Stroke
MI
Heart failure
Chronic renal diseases
Cognitive decline
Premature death
175
Q

What happens with each 2mmHg rise in systolic BP?

A

7% increased mortality from ischaemic heart disease

10% increased mortality from stroke

176
Q

What measurement of BP classifies hypertension?

A

above 140/90 mmHg

177
Q

What is ambulatory blood pressure monitoring?

A

A technique used on people suspected of high BP. The machine which is worn on their arm takes the BP throughout the day.

178
Q

How does an aldosterone agonist reduce BP?

A

Reduces salt retention

Reduces tubular sodium resorption

179
Q

How does an ACE inhibitor reduce BP?

A

Inhibits the conversion of angiotensin I to angiotensin II. Prevents synthesis of aldosterone, prevents tubular sodium resorption

180
Q

How does a renin inhibitor reduce BP?

A

Stops renin being converted to angiotensin I which is converted to angiotensin II which stimulates the release of aldosterone.

181
Q

What does aldosterone cause?

A

Vascular growth (Hyperplasia and hypertrophy) and salt retention by tubular sodium reabsorption

182
Q

How do alpha blockers work?

A

Prevent noradrenaline from causing vasoconstriction. Reduces peripheral resistance

183
Q

How do beta blockers work?

A

Reduce cardiac output by preventing noradrenaline from stimulating the sympathetic nervous system

184
Q

How do calcium channel blockers reduce BP

A

They reduce the peripheral resistance

185
Q

What are 4 examples of ACE inhibitors?

A

Ramipril
Perindopril
Enalapril
Trandolapril

186
Q

What are the main 7 adverse effects of ACE inhibitors?

A
  1. Hypotension
  2. Acute renal failure
  3. Hyperkalaemia
  4. Teratogenic effects in pregnancy
  5. Cough
  6. Rash
  7. Anaphylactoid reactions
187
Q

What are five examples of angiotensin II receptor blockers (ARB)?

A 
Candesartan
Valsartan
Telmisartan
Losartan
Irbesartan
188
Q

What are the 6 main adverse effects of angiotensin II receptor blockers (ARB)?

A 
Hypotension
Hyperkalaemia
Potential for renal dysfunction
Rash
Angio-oedema
Contraindicated in pregnancy
189
Q

What are 6 examples of calcium channel blockers?

A 
Amlodipine
nifedipine
diltiazem
felodipine
lacidipine
verapamil
190
Q

Name 6 beta blockers

A 
Bisoprolol
carvedilol
propanolol
matoprolol
atenolol
nadolol
191
Q

Which beta blockers are B1 selective?

A

Metoprolol

Bisoprolol

192
Q

Which beta blocker is between B1 selective and non selective?

A

Atenolol

193
Q

Which beta blockers are not selective?

A

Propanolol
Nadolol
Carvedilol

194
Q

What are the main adverse effects of Beta blockers?

A 
Fatigue 
Headache
Sleep disturbance/ nightmares
Bradycardia
Hypotension
Cold peripheries
ED
Asthma worsening
Heart failure
195
Q

What are the 4 classes of diuretics?

A
  1. Thiazides and related drugs
  2. Loop diuretics
  3. Potassium-sparing diuretics
  4. Aldosterone agonists
196
Q

Name 3 thiazide and related diuretics

A

Bendroflumethazide
Hydrochlorothiazide
Chlorthalidone

Phase 2a (5 decks)

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