Cardiovascular diseases 1 Flashcards
1
Q
What is the definition of ischaemic heart disease?
A
Inadequate blood supply to the myocardium
2
Q
What are the possible causes of ischaemic heart disease?
A
- reduced coronary blood flow, almost always due to atheroma +/- thrombus
- myocardial hypertrophy, usually due to systemic hypertension
3
Q
What is the pathogenesis of IHD?
A
- acute & 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 rapid reperfusion (15-20min)
4
Q
What are the ischaemic heart disease syndromes?
A
Angina pectoris
Acute coronary syndrome
Sudden cardiac death
Chronic ischaemic heart disease
5
Q
What are the different types of angina?
A
- typical/stable
- crescendo/unstable
- variant/Prinzmetal
6
Q
What is acute coronary syndrome?
A
- acute myocardial infarction (+/- ecg ST elevation)
- crescendo/unstable angina
7
Q
What are the features of acute ischaemia?
A
- atheroma + acute thrombosis/haemorrhage
- lipid rich plaques at most risk
- regional transmural myocardial infarction
- thrombolysis - physiological & drugs
- myocardial stunning
- diagnosis - clinical, ecg, blood cardiac proteins
- subendocardial Mis are different
8
Q
What is a subendocardial MI?
A
The subendocardial myocardium is relatively poorly perfused under normal conditions
If there is
- stable athermanous occlusion of the coronary circulation
- an acute hypotensive episode
Then the subendocardial myocardium can infarct without any acute coronary occlusion
9
Q
What are the blood markers of cardiac myocyte damage?
A
Troponins T&I Creatinine kinase MB Myoglobin Lactate dehydrogenase isoenzyme 1 Aspartate transaminase
10
Q
What troponin levels would you expect to see in MI?
A
- detectable 2 – 3h, peaks at 12h, detectable to 7 days
- raised post MI but also in pulmonary embolism, heart failure, & myocarditis.
11
Q
What creatinine kinase MB levels would you expect to see in MI?
A
- detectable 2 – 3h, peaks at 10-24h, detectable to 3 days
12
Q
What myoglobin levels woud you expect to see in MI?
A
- peak at 2h but also released from damaged skeletal muscle
13
Q
What lactate dehydrogenase levels would you expect to see in MI?
A
- peaks at 3days, detectable to 14days
14
Q
What aspartate transaminase levels would you expect to see in MI?
A
- Also present in liver so less useful as a marker of myocardial damage
15
Q
What is the prognosis of MI?
A
20% 1-2h mortality – sudden cardiac death
16
Q
What are the possible complications of MI?
A
- arrhythmias, ventricular fibrillation (75-95%) & sudden death
- ischaemic pain
- left ventricular failure (60%) & shock (10-15%)
- pericarditis
- cardiac mural thrombus & emboli
- deep leg vein thrombosis & pulmonary embolus (15-40%)
- myocardial rupture - tamponade, ventricular septal perforation, papillary muscle rupture(1-5%)
- ventricular aneurysm
- autoimmune pericarditis (Dressler’s syndrome) +/- pleurisy 2 weeks to months post MI
17
Q
What are the features of chronic ischaemic heart disease?
A
- coronary artery atheroma produces relative myocardial
ischaemia & angina pectoris on exertion - risk of sudden death or MI
- possible previous occult MIs
- crescendo or unstable angina - evolving plaque
- variant angina - coronary arterial spasm
18
Q
When is blood pressure considered abnormal?
A
- Abnormal: Sustained diastolic of 90mmHg
- Abnormal: Sustained systolic of 140mmHg
19
Q
What causes primary hypertension?
A
- Cardiac baroreceptors
- Renin-angiotensin- aldosterone system
- Kinin-kallikrekin system
- Naturetic peptides
- Adrenergic receptor system
- Autocrine factors produced by blood vessels
- Autonomic nervous system
20
Q
What are the 4 groups of causes of secondary hypertension?
A
Renal
Endocrine
Neurologic
Cardiovascular
21
Q
What are the key features of the renin-angiotensin-aldosterone system?
A
- Renin
- Synthesized, stored in, and released from the juxtaglomerular apparatus in the wall of the afferent arterioles of the kidney
- Cleaves angiotensinogen to angiotensin I
- Angiotensin I is converted to active angiotensin II in many tissues
22
Q
What are the features of angiotensin II?
A
- Potent natural vasoconstrictor
- Very short half-life
- Stimulates adrenal cortex to produce aldosterone
23
Q
What are the features of aldosterone?
A
- The physiological mineralocorticoid
- Renal action causes sodium and thus water retention
- Circulating blood volume increases
24
Q
What are the consequences of renal artery stenosis and why is it relevant?
A
- Reduced blood pressure in kidney
- Reduced blood pressure in renal afferent arterioles
- Juxtaglomerular apparatus stimulated to produce renin
- Renin-angiotensin system stimulates adrenal cortex zona glomerulosa cells to produce aldosterone
- Blood pressure increases
25
How does coarctation of the aorta result in increased BP?
Hypotension in the kidneys leads to juxtaglomerular apparatus stimulation and renin release.
26
What is Conn's syndrome?
Caused by excess aldosterone secretion
27
What are the possible causes of Conn's syndrome?
- Usually due to adrenocortical adenoma
| - Possibly micronodular hyperplasia
28
What are the signs and symptoms of Conn's syndrome?
- Renal sodium and water retention
- Hypertension
- Elevated aldosterone, low renin
- Potassium loss
- Muscular weakness, cardiac arrhythmias, parasthaesesia, metabolic alkalosis
29
What diagnostic test can be used in Conn's syndrome?
Diagnose by CT scan of adrenals in presence of these metabolic abnormalities
30
What is a phaeochromocytoma?
Tumour of the adrenal medulla.
31
What is pathogenesis of a phaeochromocytoma?
Presents due to secretion of vasoconstrictive catecholamines – adrenaline and noradrenaline.
32
What are the signs and symptoms of a phaeochromocytoma?
- Pallor
- Headaches
- Sweating
- Nervousness
- Hypertension
33
What is the diagnostic test for phaeochromocytoma?
Diagnosed by 24hr urine collection for adrenaline metabolites.
34
What is Cushing's disease?
Overproduction of cortisol by adrenal cortex
35
What are the consequences of Cushing's disease?
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.
36
What are the causes of Cushing's disease?
- An adrenocortical neoplasm usually an adenoma
- A pituitary adenoma (Cushing’s syndrome – 80% of cases) or a paraneoplastic effect of other neoplasms (particularly small cell lung carcinoma) producing adrenocorticotrophic hormone that stimulates the zona fasciculata cells of the adrenal cortex to produce cortisol.
37
What are the effects of hypertension?
- Cardiovascular
- Hypertensive heart disease
- Renal
- Renal failure
- Cerebrovascular
- Cerebrovascular accident
38
What is hypertensive heart disease?
- Systemic hypertension leads to increased left ventricular blood pressure
- Left ventricle hypertrophy without dilatation initially in response to increased work needed to pump blood
- Recognized cause of sudden death
- When the pressure is too great the left ventricle fails to pump blood at a normal rate and dilates
39
What are the renal effects of hypertension?
Vascular changes in essential hypertension
- Arterial intimal fibroelastosis
- Hyaline arteriolosclerosis
Slow deterioration in renal function leading to chronic renal failure
40
What are the cerebral effects of hypertension?
- Hypertensive encephalopathy
- Increased risk of rupture abnormal arteries
atheromatous (intracerebral haemorrhage)
- berry aneurysm of the Circle of Willis (subarachnoid haemorrhage)
41
What is a hypertensive crisis?
- BP >180/120mmHg
- Clinically signs & symptoms of organ damage
- acute hypertensive encephalopathy
- renal failure
- retinal haemorrhages
42
What is pulmonary hypertension?
Higher than normal pressure in the pulmonary artery
43
What are the possible aetiologies of pulmonary hypertension?
- Loss of pulmonary vasculature
- Chronic obstructive lung disease
- Pulmonary interstitial fibrosis (interstitial lung diseases)
- Pulmonary emboli or thrombosis
- Under ventilated alveoli
- Secondary to left ventricular failure
- Systemic to pulmonary artery shunting
- Primary or idiopathic
44
What is the pathogenesis of pulmonary hypertension?
- Increased right ventricular work to pump blood
- Right ventricular myocardial hypertrophy initially without dilation
- Later dilatation and systemic venous congestion as right ventricular failure develops
45
What risk factors are taken into account when calculating a Framingham risk score?
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Age
Gender
Total cholesterol mg/dl
HDL cholesterol mg/dl
Smoker y/n?
Systolic blood pressure mmHg
Currently taking antihypertensives y/n?
```
46
What does your Framingham risk score tell you?
Your chance of having a heart attack within the next 10 years.
47
What is typical/stable angina?
Fixed obstruction
Predictable relationship to exertion
48
What is variant/Prinzmetal angina?
Coronary artery spasm
49
What is crescendo/unstable angina?
Often due to plaque disruption
