(1) Cardiovascular diseases 1 Flashcards
(107 cards)
1
Q
What proportion of deaths in women are caused by cardiovascular disease?
A
28%
2
Q
What proportion of deaths in men are caused by cardiovascular disease?
A
29%
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
4
Q
What is ischaemic heart disease?
A
Inadequate blood supply to the myocardium
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
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)
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
8
Q
Describe the different types of angina pectoris
A
- typical/stable
- crescendo/unstable
- variant/Prinzmetal
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
10
Q
Describe the different types of acute coronary syndrome
A
- acute myocardial infarction (+/- ECG ST elevation)
- crescendo/unstable angina
11
Q
Describe the features of acute ischaemia
A
- atheroma + acute thrombosis/haemorrhage
- lipid rich plaques at most risk
- regional transmural myocardial infarction
12
Q
How may acute ischaemia be treated?
A
Thrombolysis - physiological and drugs
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
14
Q
How is acute ischaemia diagnosed?
A
- clinical
- ECG
- blood cardiac proteins
15
Q
What are the 2 main types of acute myocardial infarction?
A
- transmural
- subendocardial
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
17
Q
What is seen on an ECG in acute transmural myocardial infarction?
A
ST elevation and Q waves are seen
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
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
20
Q
Describe the morphology in MI after less than 24 hours
A
Normal
21
Q
Describe the morphology in MI after 1-2 days
A
Pale, oedema
Myocyte necrosis, neutrophils
22
Q
Describe the morphology in MI after 2-4 days
A
Yellow with haemorrhagic edge, myocyte necrosis, macrophages
23
Q
Describe the morphology in MI after 1-3 weeks
A
Pale, thin
Granulation tissue then fibrosis
24
Q
Describe the morphology in MI after 3-6 weeks
A
Dense, fibrous scar
25
How well perfused is the subendocardial myocardium under normal conditions?
The subendocardial myocardium is relatively poorly perfused under normal conditions
26
Why might the subendocardial myocardium infarct without any acute coronary occlusion?
If there is
- stable athermanous occlusion of the coronary circulation
- an acute hypotensive episode
27
Name 5 blood markers of cardiac myocyte damage ("cardiac enzymes")
- troponins T and I
- creatine kinase MB
- myoglobin
- lactate dehydrogenase isoenzyme 1
- aspartate transaminase
28
Describe how troponin levels can be used to detect cardiac myocyte damage
- raised post MI but also in pulmonary embolism, heart failure, and myocarditis
- detectable 2-3 hours, peaks at 12 hours, detectable to 7 days
29
Describe when creatine kinase MB levels are detectable (marker of cardiac myocyte damage)
- detectable 2-3 hours
- peaks at 10-24 hours
- detectable to 3 days
30
Describe how myoglobin can be used to detect cardiac myocyte damage
- peaks at 2 hours
| - but also released from damaged skeletal muscle
31
Describe when lactate dehydrogenase isoenzyme 1 is detectable (marker of cardiac myocyte damage)
- peaks at 3 days
| - detectable to 14 days
32
Is aspartate transaminase a useful blood marker for cardiac myocyte damage?
Also present in the liver so less useful as marker of myocardial damage
33
Describe the prognosis in MI
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
34
Describe the complications associated with MI (80-90%)
- 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
35
What is haemopericaridum?
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
36
What is cardiac tamponade?
Compression of the heart by an accumulation of fluid in the pericardial sac
37
What is chronic ischaemic heart disease?
Coronary artery atheroma producing relative myocardial ischaemia and angina pectoris on exertion
38
What is there a risk of in chronic ischaemic heart disease?
Risk of sudden death or MI
39
How is familial hypercholesterolaemia caused?
Mutation in genes involved in cholesterol metabolism
40
Familial hypercholesteraemia is caused by mutation in genes involved in cholesterol metabolism. Which genes are the commonest?
- low density lipoprotein receptor gene (1 in 500)
| - apolipoprotein B (1 in 1000)
41
What occurs in heterozygotes of familial hypercholesterolaemia genes?
Develop xanthomas - tendons, perioccular, corneal arcus - and early atherosclerosis
42
What treatment is given to heterozygotes of familial hypercholesterolaemia genes?
Early primary treatment with statins (hydroxymethylglutaryl CoA) is effective
43
Is treatment for homozygotes of familial hypercholesterolaemia genes effective?
Treatment is more complex and less effective (than it is for heterozygotes)
44
Blood pressure is physiologically regulated for what reasons?
- 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
When is blood pressure high?
Sustained diastolic of 90mmHg
Sustained systolic of 140mmHg
46
95% of cases of high blood pressure are what?
Primary
aka "idiopathic", "benign", "essential"
47
What causes primary hypertension?
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
What is the hypothesis behind primary/essential hypertension?
Positive sodium balance as a common pathway (all inherited and acquired forms share increased net salt balance as a common pathway)
49
Why does increased net salt balance lead to primary hypertension?
- 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
The causes of secondary hypertension (5%) can be put under which categories?
- renal
- endocrine
- cardiovascular
- neurologic
51
What are the renal causes of secondary hypertension?
- acute glomerulonephritis
- chronic renal disease
- polycystic kidneys
- renal artery stenosis
- renal artery fibromuscular dysplasia
- renal vasculitis
- renin-producing tumour
52
What are the endocrine causes of secondary hypertension?
- adrenocortical hormones
- exogenous chemicals
- pheochromocytoma
- acromegaly
- hypothyroidism
- hyperthyroidism
- pregnancy
53
Give examples of adrenocortical hormone-causes of secondary hypertension
- Cushing syndrome
- primary aldosteronism
- congential adrenal hyperplasia
- liquorice ingestion
54
Give some examples of exogenous chemicals that can cause secondary hypertension
- glucocorticoids
- oestrogen inc. pregnancy and oral contraceptives
- monoamine oxidase inhibitors
- amphetamines
- cocaine
55
Pheochromocytoma can be an endocrine cause of secondary hypertension. What is it?
A neuroendocrine tumor of the medulla of the adrenal glands
56
Give some examples of cardiovascular causes of secondary hypertension
- coarctation of the aorta
- polyarteritis nodosa
- increased intravascular volume
- increased cardiac output
57
Give some examples of neurologic causes of secondary hypertension
- raised intracranial pressure
- acute stress (inc. surgery)
- sleep apnoea
- psychogenic
58
What does renin do?
Cleaves angiotensinogen to angiotensin I
59
Where is renin synthesised and stored?
Renin is synthesised, stored in, and released from the juxtaglomerular apparatus of the kidney
60
What is the active form of angiotensin I?
Angiotensin I is converted to active angiotensin II in many tissues
61
State the main characteristic of angiotensin II
- potent natural vasoconstrictor
- very short half-life
- stimulates adrenal cortex to produce aldosterone
62
State the main characteristic of aldosterone
- the physiological mineralocorticoid
- renal action causes sodium and thus water retention
- circulating blood volume increases
63
What does renal artery stenosis lead to?
- 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
Where is aldosterone produced?
By the zone glomerulosa cells in the adrenal cortex
65
What is coarctation of the aorta?
Congenital narrowing of the aorta, usually distal to the origin of the left subclavian artery
66
How does coarctation of the aorta lead to increased blood pressure?
Coarctation leads to hypotension in the kidneys which leads to juxtaglomerular apparatus stimulation and renin release (RAAS activation)
67
What are the features of coarctation of the aorta? (symptoms, detection, treatment)
- usually asymptomatic
- detected by difference in blood pressure between the arms and legs
- characteristic chest X-ray
- surgically correctable
68
What is Conn's syndrome?
Primary aldosteronism
Caused by excessive aldosterone secretion by the adrenal glands resulting in low renin levels
69
Conn's syndrome is caused by excessive aldosterone secretion. What causes this?
- usually due to adrenocortical adenoma
| - possibly micronodular hyperplasia
70
What are the resulting effects of excessive aldosterone secretion in Conn's syndrome?
- renal sodium and water retention = hypertension
- elevated aldosterone, low renin
- potassium loss = muscular weakness, cardiac arrhythmias, paraesthesia, metabolic alkalosis
71
How is Conn's syndrome diagnosed?
By CT scan of adrenals in presence of these metabolic abnormalities
72
Pheochromocytoma is a tumour of the adrenal medulla. What symptoms does it present with?
- pallor
- headaches
- sweating
- nervousness
- hypertension
73
Pheochromocytoma presents with a number of symptoms. What causes these symptoms?
Secretion of vasoconstrictive catecholamines - adrenaline and noradrenaline
74
How is pheochromocytoma diagnosed?
By 24 hour urine collection for adrenaline metabolites
75
What is Cushing's disease?
Increased secretion of adrenocorticotropic hormone (ACTH) from the anterior pituitary = increased synthesis of cortisol by the adrenal glands
76
In Cushing's disease, there is overproduction of cortisol by the adrenal cortex. What does this lead to?
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
What is overproduction of cortisol caused by? (Cushing's disease)
- an adrenocortical neoplasm, usually an adenoma
OR
- a pituitary adenoma or a paraneoplastic effect of other neoplasms
78
Cushing's disease can be caused by the paraneoplastic effects of other neoplasms. Such as what?
Particularly small cell lung carcinoma
- producing ACTH that stimulates the zona fasciculata cells of the adrenal cortex to produce cortisol
79
What are the systemic effects of hypertension?
Cardiovascular = hypertensive heart disease
Renal = renal failure
Cerebrovascular = cerebrovascular accident
80
What is hypertensive heart disease?
- 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
What are the effects of hypertension on the kidneys?
- vascular changes in essential hypertension - arterial intimal fibroelastosis - hyaline arteriolosclerosis
- slow deterioration in renal function leading to chronic renal failure
82
What are the effects of hypertension on the brain?
- hypertensive encephalopathy
- increased risk of rupture of abnormal arteries (atheromatous - intracerebral haemorrhage, berry aneurysm of circle of Willis - subarachnoid haemorrhage)
83
A hypertension crisis (aka "malignant hypertension"} is when BP is what?
BP over 180/120mmHg
84
What are the signs and symptoms of malignant hypertension/hypertensive crisis?
Clinically signs and symptoms of organ damage
- acute hypertensive encephalopathy
- renal failure
- retinal haemorrhages
85
What does hypertensive crisis/malignant hypertension require?
Requires urgent treatment to preserve organ function
86
How does acute hypertensive encephalopathy present?
Diffuse cerebral dysfunction
- confusion
- vomiting
- convulsions
- coma
- death
87
What is required in acute hypertensive dysfunction?
Rapid intervention is required to reduce the accompanying raised intracranial pressure
88
What is pulmonary hypertension?
Higher than normal pressure in the pulmonary artery
89
What is pulmonary hypertension caused by?
- 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
What does pulmonary hypertension cause?
- 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
What are the cardiovascular disease risk factors?
- 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
What was the Framingham heart study?
- 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
What is the Framingham risk score?
- 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
What kind of risk factors does the Framingham risk score take into account?
- age
- gender
- total cholesterol
- HDL cholesterol
- smoker
- systolic blood pressure
- medication to treat high blood pressure
95
What are the other CVD risk assessment systems, other than Framingham?
- SCORE
- QRISK2
- joint British Societies risk prediction charts
96
Briefly explain the SCORE CVD risk assessment system
- European society of cardiology
| - 12 counties, 250,000 patients, 7000 deaths
97
Breifly describe the QRISK2 CVD risk assessment system
- 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
What does the SCORE CVD risk assessment system take into account?
- gender
- age
- systolic blood pressure
- smoking status
- total cholesterol
99
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)
- 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
What does the QRISK2 CVD risk assessment system take into account?
- age
- sex
- ethnicity
- postcode
- smoking status
- diabetic
- angina or heart attack in 1st degree relative
101
What does the joint British societies risk charts tell you?
Risk of developing cardiovascular disease in the next 10 years
102
Which cardiac diseases occur in those that are at low risk?
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
How has coronary heart disease mortality changed since 1970?
Decreased
104
Who is Thomas Royle Dawber?
First director of the Framingham heart study
105
Who were involved in discovering the link between smoking and lung cancer?
Richard Doll
Austin Bradford Hill
106
Who is James Black?
Discovered beta blockers
107
Who is Akira Endo?
Discovered hydroxymethylglutaryl-CoA reductase inhibitors (statins) in fungi
