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6. CP - Diseases of the Cardiovascular System > (1) Cardiovascular diseases 1 > Flashcards

(1) Cardiovascular diseases 1 Flashcards

1
Q

What proportion of deaths in women are caused by cardiovascular disease?

A

28%

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2
Q

What proportion of deaths in men are caused by cardiovascular disease?

A

29%

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3
Q

How much money was spent on treating cardiovascular disease in the NHS in England in 2012/2013?

A

More than £6.8 billion

63% in secondary care
21% in primary care

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4
Q

What is ischaemic heart disease?

A

Inadequate blood supply to the myocardium

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5
Q

Ischaemic heart disease is inadequate blood supply to the myocardium. What may it be due to?

A
  • reduced coronary blood flow, almost always due to atheroma +/- thrombus
  • myocardial hypertrophy, usually due to systemic hypertension
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6
Q

Describe the pathogenesis in ischaemic heart disease

A
  • acute and chronic ischaemia
  • autoregulation of coronary blood flow breaks down if >75% occlusion
  • low diastolic flow especially subendocardial
  • active aerobic metabolism of cardiac muscle
  • myocyte dysfunction/death from ischaemia
  • recovery possible if rapid reperfusion (15-20mins)
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7
Q

State the 4 many syndromes associated with ischaemic heart disease

A
  • angina pectoris
  • acute coronary syndrome
  • sudden cardiac death
  • chronic ischaemic heart disease
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8
Q

Describe the different types of angina pectoris

A
  • typical/stable
  • crescendo/unstable
  • variant/Prinzmetal
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9
Q

What is Prinzmetal angina?

A

Also known as variant angina

Angina at rest that occurs in cycles

Caused by vasospasm rather than directly by atherosclerosis

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10
Q

Describe the different types of acute coronary syndrome

A
  • acute myocardial infarction (+/- ECG ST elevation)

- crescendo/unstable angina

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11
Q

Describe the features of acute ischaemia

A
  • atheroma + acute thrombosis/haemorrhage
  • lipid rich plaques at most risk
  • regional transmural myocardial infarction
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12
Q

How may acute ischaemia be treated?

A

Thrombolysis - physiological and drugs

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13
Q

What is myocardial stunning?

A

The reversible reduction of heart contraction after reperfusion not accounted for by tissue damage or reduced blood flow

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14
Q

How is acute ischaemia diagnosed?

A
  • clinical
  • ECG
  • blood cardiac proteins
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15
Q

What are the 2 main types of acute myocardial infarction?

A
  • transmural

- subendocardial

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16
Q

What are acute transmural myocardial infarctions?

A

Associated with atherosclerosis involving a major coronary artery

Extends through the whole thickness of the heart muscle and are usually a result of complete occlusion of the area’s blood supply

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17
Q

What is seen on an ECG in acute transmural myocardial infarction?

A

ST elevation and Q waves are seen

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18
Q

What are acute subendocardial myocardial infarctions?

A

Involves a small area in the subendocardial wall of the left ventricle, ventricular septum, or papillary muscles

The subendocardial area is particularly susceptible to ischaemia

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19
Q

What is seen on an ECG in acute subendocardial myocardial infarction?

A

ST depression may be seen on ECG in addition to T wave changes

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20
Q

Describe the morphology in MI after less than 24 hours

A

Normal

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21
Q

Describe the morphology in MI after 1-2 days

A

Pale, oedema

Myocyte necrosis, neutrophils

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22
Q

Describe the morphology in MI after 2-4 days

A

Yellow with haemorrhagic edge, myocyte necrosis, macrophages

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23
Q

Describe the morphology in MI after 1-3 weeks

A

Pale, thin

Granulation tissue then fibrosis

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24
Q

Describe the morphology in MI after 3-6 weeks

A

Dense, fibrous scar

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25
Q

How well perfused is the subendocardial myocardium under normal conditions?

A

The subendocardial myocardium is relatively poorly perfused under normal conditions

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26
Q

Why might the subendocardial myocardium infarct without any acute coronary occlusion?

A

If there is

  • stable athermanous occlusion of the coronary circulation
  • an acute hypotensive episode
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27
Q

Name 5 blood markers of cardiac myocyte damage (“cardiac enzymes”)

A
  • troponins T and I
  • creatine kinase MB
  • myoglobin
  • lactate dehydrogenase isoenzyme 1
  • aspartate transaminase
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28
Q

Describe how troponin levels can be used to detect cardiac myocyte damage

A
  • raised post MI but also in pulmonary embolism, heart failure, and myocarditis
  • detectable 2-3 hours, peaks at 12 hours, detectable to 7 days
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29
Q

Describe when creatine kinase MB levels are detectable (marker of cardiac myocyte damage)

A
  • detectable 2-3 hours
  • peaks at 10-24 hours
  • detectable to 3 days
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30
Q

Describe how myoglobin can be used to detect cardiac myocyte damage

A
  • peaks at 2 hours

- but also released from damaged skeletal muscle

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31
Q

Describe when lactate dehydrogenase isoenzyme 1 is detectable (marker of cardiac myocyte damage)

A
  • peaks at 3 days

- detectable to 14 days

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32
Q

Is aspartate transaminase a useful blood marker for cardiac myocyte damage?

A

Also present in the liver so less useful as marker of myocardial damage

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33
Q

Describe the prognosis in MI

A

20% = sudden cardiac death, 1-2 hour mortality

10-15% = early hospital mortality

7-10% = further 1 year mortality

3-4% per year in subsequent years

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34
Q

Describe the complications associated with MI (80-90%)

A
  • arrhythmias, ventricular fibrillation and sudden death
  • ischaemic pain
  • left ventricular failure and shock
  • pericarditis
  • cardiac mural thrombus and emboli
  • deep leg vein thrombosis and pulmonary embolus
  • myocardial rupture, tamponade, ventricular septal perforation, papillary muscle rupture
  • ventricular aneurysm
  • autoimmune pericarditis (Dressler’s syndrome) +/- pleurisy 2 weeks to months post-MI
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35
Q

What is haemopericaridum?

A

Blood in the pericardial sac of the heart. It is clinically similar to a pericardial effusion, and, depending on the volume and rapidity with which it develops, may cause cardiac tamponade

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36
Q

What is cardiac tamponade?

A

Compression of the heart by an accumulation of fluid in the pericardial sac

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37
Q

What is chronic ischaemic heart disease?

A

Coronary artery atheroma producing relative myocardial ischaemia and angina pectoris on exertion

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38
Q

What is there a risk of in chronic ischaemic heart disease?

A

Risk of sudden death or MI

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39
Q

How is familial hypercholesterolaemia caused?

A

Mutation in genes involved in cholesterol metabolism

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40
Q

Familial hypercholesteraemia is caused by mutation in genes involved in cholesterol metabolism. Which genes are the commonest?

A
  • low density lipoprotein receptor gene (1 in 500)

- apolipoprotein B (1 in 1000)

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41
Q

What occurs in heterozygotes of familial hypercholesterolaemia genes?

A

Develop xanthomas - tendons, perioccular, corneal arcus - and early atherosclerosis

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42
Q

What treatment is given to heterozygotes of familial hypercholesterolaemia genes?

A

Early primary treatment with statins (hydroxymethylglutaryl CoA) is effective

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43
Q

Is treatment for homozygotes of familial hypercholesterolaemia genes effective?

A

Treatment is more complex and less effective (than it is for heterozygotes)

44
Q

Blood pressure is physiologically regulated for what reasons?

A
  • ensure the perfusion of organs is sufficient to maintain function
  • prevents higher flow that exceeds metabolic demands, as this would lead to increased damage to blood vessels and thus to organs
45
Q

When is blood pressure high?

A

Sustained diastolic of 90mmHg

Sustained systolic of 140mmHg

46
Q

95% of cases of high blood pressure are what?

A

Primary

aka “idiopathic”, “benign”, “essential”

47
Q

What causes primary hypertension?

A

Likely many physiological systems interactive over long period of time with minor dysfunctions

  • cardiac baroreceptors
  • RAAS
  • kinin-kallilrekin system
  • naturetic peptides
  • adrenergic receptor system
  • autocrine factors produced by blood vessels
  • autonomic nervous system
48
Q

What is the hypothesis behind primary/essential hypertension?

A

Positive sodium balance as a common pathway (all inherited and acquired forms share increased net salt balance as a common pathway)

49
Q

Why does increased net salt balance lead to primary hypertension?

A
  • increased intravascular volume and delivery to heart = augment cardiac output = augment blood pressure
  • tissue perfusion > metabolic demand = increased vasoconstriction to reduce blood flow
  • = elevated blood pressure with increased systemic vascular resistance and normal cardiac output
50
Q

The causes of secondary hypertension (5%) can be put under which categories?

A
  • renal
  • endocrine
  • cardiovascular
  • neurologic
51
Q

What are the renal causes of secondary hypertension?

A
  • acute glomerulonephritis
  • chronic renal disease
  • polycystic kidneys
  • renal artery stenosis
  • renal artery fibromuscular dysplasia
  • renal vasculitis
  • renin-producing tumour
52
Q

What are the endocrine causes of secondary hypertension?

A
  • adrenocortical hormones
  • exogenous chemicals
  • pheochromocytoma
  • acromegaly
  • hypothyroidism
  • hyperthyroidism
  • pregnancy
53
Q

Give examples of adrenocortical hormone-causes of secondary hypertension

A
  • Cushing syndrome
  • primary aldosteronism
  • congential adrenal hyperplasia
  • liquorice ingestion
54
Q

Give some examples of exogenous chemicals that can cause secondary hypertension

A
  • glucocorticoids
  • oestrogen inc. pregnancy and oral contraceptives
  • monoamine oxidase inhibitors
  • amphetamines
  • cocaine
55
Q

Pheochromocytoma can be an endocrine cause of secondary hypertension. What is it?

A

A neuroendocrine tumor of the medulla of the adrenal glands

56
Q

Give some examples of cardiovascular causes of secondary hypertension

A
  • coarctation of the aorta
  • polyarteritis nodosa
  • increased intravascular volume
  • increased cardiac output
57
Q

Give some examples of neurologic causes of secondary hypertension

A
  • raised intracranial pressure
  • acute stress (inc. surgery)
  • sleep apnoea
  • psychogenic
58
Q

What does renin do?

A

Cleaves angiotensinogen to angiotensin I

59
Q

Where is renin synthesised and stored?

A

Renin is synthesised, stored in, and released from the juxtaglomerular apparatus of the kidney

60
Q

What is the active form of angiotensin I?

A

Angiotensin I is converted to active angiotensin II in many tissues

61
Q

State the main characteristic of angiotensin II

A
  • potent natural vasoconstrictor
  • very short half-life
  • stimulates adrenal cortex to produce aldosterone
62
Q

State the main characteristic of aldosterone

A
  • the physiological mineralocorticoid
  • renal action causes sodium and thus water retention
  • circulating blood volume increases
63
Q

What does renal artery stenosis lead to?

A
  • reduced blood pressure in kidney
  • reduced blood pressure within renal afferent arterioles
  • juxtaglomerular apparatus stimulated to produce renin
  • renin-angiotensin system stimulates adrenal cortex zona glomerulosa cells to produce aldosterone
  • increases blood pressure
64
Q

Where is aldosterone produced?

A

By the zone glomerulosa cells in the adrenal cortex

65
Q

What is coarctation of the aorta?

A

Congenital narrowing of the aorta, usually distal to the origin of the left subclavian artery

66
Q

How does coarctation of the aorta lead to increased blood pressure?

A

Coarctation leads to hypotension in the kidneys which leads to juxtaglomerular apparatus stimulation and renin release (RAAS activation)

67
Q

What are the features of coarctation of the aorta? (symptoms, detection, treatment)

A
  • usually asymptomatic
  • detected by difference in blood pressure between the arms and legs
  • characteristic chest X-ray
  • surgically correctable
68
Q

What is Conn’s syndrome?

A

Primary aldosteronism

Caused by excessive aldosterone secretion by the adrenal glands resulting in low renin levels

69
Q

Conn’s syndrome is caused by excessive aldosterone secretion. What causes this?

A
  • usually due to adrenocortical adenoma

- possibly micronodular hyperplasia

70
Q

What are the resulting effects of excessive aldosterone secretion in Conn’s syndrome?

A
  • renal sodium and water retention = hypertension
  • elevated aldosterone, low renin
  • potassium loss = muscular weakness, cardiac arrhythmias, paraesthesia, metabolic alkalosis
71
Q

How is Conn’s syndrome diagnosed?

A

By CT scan of adrenals in presence of these metabolic abnormalities

72
Q

Pheochromocytoma is a tumour of the adrenal medulla. What symptoms does it present with?

A
  • pallor
  • headaches
  • sweating
  • nervousness
  • hypertension
73
Q

Pheochromocytoma presents with a number of symptoms. What causes these symptoms?

A

Secretion of vasoconstrictive catecholamines - adrenaline and noradrenaline

74
Q

How is pheochromocytoma diagnosed?

A

By 24 hour urine collection for adrenaline metabolites

75
Q

What is Cushing’s disease?

A

Increased secretion of adrenocorticotropic hormone (ACTH) from the anterior pituitary = increased synthesis of cortisol by the adrenal glands

76
Q

In Cushing’s disease, there is overproduction of cortisol by the adrenal cortex. What does this lead to?

A

Cortisol has several metabolic effects including potentiating sympathetic nervous system activity and it has a mineralocorticoid (aldosterone-like) action on the kidneys, thus causing hypertension

77
Q

What is overproduction of cortisol caused by? (Cushing’s disease)

A
  • an adrenocortical neoplasm, usually an adenoma
    OR
  • a pituitary adenoma or a paraneoplastic effect of other neoplasms
78
Q

Cushing’s disease can be caused by the paraneoplastic effects of other neoplasms. Such as what?

A

Particularly small cell lung carcinoma

  • producing ACTH that stimulates the zona fasciculata cells of the adrenal cortex to produce cortisol
79
Q

What are the systemic effects of hypertension?

A

Cardiovascular = hypertensive heart disease

Renal = renal failure

Cerebrovascular = cerebrovascular accident

80
Q

What is hypertensive heart disease?

A
  • systemic hypertension leads to increased left ventricular blood pressure
  • left ventricular hypertrophy without dilatation initially in response to increased demand
  • recognised cause of sudden death
  • when pressure is too great, left ventricle fails to pump blood at a normal rate and dilates
81
Q

What are the effects of hypertension on the kidneys?

A
  • vascular changes in essential hypertension - arterial intimal fibroelastosis - hyaline arteriolosclerosis
  • slow deterioration in renal function leading to chronic renal failure
82
Q

What are the effects of hypertension on the brain?

A
  • hypertensive encephalopathy
  • increased risk of rupture of abnormal arteries (atheromatous - intracerebral haemorrhage, berry aneurysm of circle of Willis - subarachnoid haemorrhage)
83
Q

A hypertension crisis (aka “malignant hypertension”} is when BP is what?

A

BP over 180/120mmHg

84
Q

What are the signs and symptoms of malignant hypertension/hypertensive crisis?

A

Clinically signs and symptoms of organ damage

  • acute hypertensive encephalopathy
  • renal failure
  • retinal haemorrhages
85
Q

What does hypertensive crisis/malignant hypertension require?

A

Requires urgent treatment to preserve organ function

86
Q

How does acute hypertensive encephalopathy present?

A

Diffuse cerebral dysfunction

  • confusion
  • vomiting
  • convulsions
  • coma
  • death
87
Q

What is required in acute hypertensive dysfunction?

A

Rapid intervention is required to reduce the accompanying raised intracranial pressure

88
Q

What is pulmonary hypertension?

A

Higher than normal pressure in the pulmonary artery

89
Q

What is pulmonary hypertension caused by?

A
  • loss of pulmonary vasculature (- COPD - pulmonary interstitial fibrosis - pulmonary emboli/thrombosis - under ventilated alveoli)
  • secondary to left ventricular failure
  • systemic to pulmonary artery shunting
  • primary or idiopathic
90
Q

What does pulmonary hypertension cause?

A
  • increased right ventricular work to pump blood
  • right ventricular myocardial hypertrophy initially without dilation
  • later dilation and systemic venous congestion as right ventricular failure develops
91
Q

What are the cardiovascular disease risk factors?

A
  • gender
  • hypertension
  • smoking
  • high blood cholesterol
  • low blood high density lipoproteins
  • diabetes
  • sedentary lifestyle
  • obesity - especially central obesity
  • high alcohol use
  • ethnicity (south Asian)
92
Q

What was the Framingham heart study?

A
  • longitudinal population student to identify risk factors for cardiovascular disease
  • started in 1948 with a cohort of 5029 adults aged 30-62
  • now in its third study cohort
  • many other studies have followed similar protocols with different populations
93
Q

What is the Framingham risk score?

A
  • calculates an individual’s risk of cardiovascular disease based on assessment of multiple risk factors
  • can be calculated using a computer algorithms or calculated manually using tables
94
Q

What kind of risk factors does the Framingham risk score take into account?

A
  • age
  • gender
  • total cholesterol
  • HDL cholesterol
  • smoker
  • systolic blood pressure
  • medication to treat high blood pressure
95
Q

What are the other CVD risk assessment systems, other than Framingham?

A
  • SCORE
  • QRISK2
  • joint British Societies risk prediction charts
96
Q

Briefly explain the SCORE CVD risk assessment system

A
  • European society of cardiology

- 12 counties, 250,000 patients, 7000 deaths

97
Q

Breifly describe the QRISK2 CVD risk assessment system

A
  • Egton medical information systems ltd (a GP IT service company based in Rawdon) and the university of Nottingham
  • 2.29 million UK GP records from 1993 to 2009
98
Q

What does the SCORE CVD risk assessment system take into account?

A
  • gender
  • age
  • systolic blood pressure
  • smoking status
  • total cholesterol
99
Q

Risk of CVD is multifactorial and so can be more complicated than just using charts. Risk may be higher than indicated in the chart in… (SCORE)

A
  • sedentary or obese subjects, especially those with central obesity
  • those with a strong family history of premature CVD
  • socially deprived individuals and those from some ethnic minorities
  • individuals with diabetes
  • those with low HDL cholesterol or increased triglyceride, fibrinogen, opoB and perhaps increased high-sensitivity CRP
  • asymptomatic subjects with evidence of pre-clinical atherosclerosis, for example plaque on ultrasonography
  • those with moderate to severe chronic kidney disease (GFR
100
Q

What does the QRISK2 CVD risk assessment system take into account?

A
  • age
  • sex
  • ethnicity
  • postcode
  • smoking status
  • diabetic
  • angina or heart attack in 1st degree relative
101
Q

What does the joint British societies risk charts tell you?

A

Risk of developing cardiovascular disease in the next 10 years

102
Q

Which cardiac diseases occur in those that are at low risk?

A

Likely to be a rare disease than at high end risk.

  • coronary artery atheroma due to familial hypercholesterolaemia
  • cardiomyopathy eg. hypertrophic cardiomyopathy due to muscle contractile protein gene mutations
  • cardiac arrhythmia due to a “channelopathy” eg. long QT syndrome and Brugada syndrome
103
Q

How has coronary heart disease mortality changed since 1970?

A

Decreased

104
Q

Who is Thomas Royle Dawber?

A

First director of the Framingham heart study

105
Q

Who were involved in discovering the link between smoking and lung cancer?

A

Richard Doll

Austin Bradford Hill

106
Q

Who is James Black?

A

Discovered beta blockers

107
Q

Who is Akira Endo?

A

Discovered hydroxymethylglutaryl-CoA reductase inhibitors (statins) in fungi

6. CP - Diseases of the Cardiovascular System (3 decks)

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