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Clinical Pathology > Cardiovascular diseases 1 > Flashcards

Cardiovascular diseases 1 Flashcards

1
Q

What is the definition of ischaemic heart disease?

A

Inadequate blood supply to the myocardium

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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
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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)
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4
Q

What are the ischaemic heart disease syndromes?

A

Angina pectoris
Acute coronary syndrome
Sudden cardiac death
Chronic ischaemic heart disease

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5
Q

What are the different types of angina?

A
  • typical/stable
  • crescendo/unstable
  • variant/Prinzmetal
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6
Q

What is acute coronary syndrome?

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

- crescendo/unstable angina

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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
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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

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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
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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.

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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
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12
Q

What myoglobin levels woud you expect to see in MI?

A
  • peak at 2h but also released from damaged skeletal muscle
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13
Q

What lactate dehydrogenase levels would you expect to see in MI?

A
  • peaks at 3days, detectable to 14days
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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
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15
Q

What is the prognosis of MI?

A

20% 1-2h mortality – sudden cardiac death

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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
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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
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18
Q

When is blood pressure considered abnormal?

A
  • Abnormal: Sustained diastolic of 90mmHg

- Abnormal: Sustained systolic of 140mmHg

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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
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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
Q

How does coarctation of the aorta result in increased BP?

A

Hypotension in the kidneys leads to juxtaglomerular apparatus stimulation and renin release.

26
Q

What is Conn’s syndrome?

A

Caused by excess aldosterone secretion

27
Q

What are the possible causes of Conn’s syndrome?

A
  • Usually due to adrenocortical adenoma

- Possibly micronodular hyperplasia

28
Q

What are the signs and symptoms of Conn’s syndrome?

A
  • Renal sodium and water retention
    • Hypertension
  • Elevated aldosterone, low renin
    • Potassium loss
    • Muscular weakness, cardiac arrhythmias, parasthaesesia, metabolic alkalosis
29
Q

What diagnostic test can be used in Conn’s syndrome?

A

Diagnose by CT scan of adrenals in presence of these metabolic abnormalities

30
Q

What is a phaeochromocytoma?

A

Tumour of the adrenal medulla.

31
Q

What is pathogenesis of a phaeochromocytoma?

A

Presents due to secretion of vasoconstrictive catecholamines – adrenaline and noradrenaline.

32
Q

What are the signs and symptoms of a phaeochromocytoma?

A
  • Pallor
  • Headaches
  • Sweating
  • Nervousness
  • Hypertension
33
Q

What is the diagnostic test for phaeochromocytoma?

A

Diagnosed by 24hr urine collection for adrenaline metabolites.

34
Q

What is Cushing’s disease?

A

Overproduction of cortisol by adrenal cortex

35
Q

What are the consequences of Cushing’s disease?

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.

36
Q

What are the causes of Cushing’s disease?

A
  • 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
Q

What are the effects of hypertension?

A
  • Cardiovascular
    • Hypertensive heart disease
  • Renal
    • Renal failure
  • Cerebrovascular
    • Cerebrovascular accident
38
Q

What is hypertensive heart disease?

A
  • 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
Q

What are the renal effects of hypertension?

A

Vascular changes in essential hypertension

  • Arterial intimal fibroelastosis
  • Hyaline arteriolosclerosis

Slow deterioration in renal function leading to chronic renal failure

40
Q

What are the cerebral effects of hypertension?

A
  • Hypertensive encephalopathy
  • Increased risk of rupture abnormal arteries
    atheromatous (intracerebral haemorrhage)
  • berry aneurysm of the Circle of Willis (subarachnoid haemorrhage)
41
Q

What is a hypertensive crisis?

A
  • BP >180/120mmHg
  • Clinically signs & symptoms of organ damage
    • acute hypertensive encephalopathy
    • renal failure
    • retinal haemorrhages
42
Q

What is pulmonary hypertension?

A

Higher than normal pressure in the pulmonary artery

43
Q

What are the possible aetiologies of pulmonary hypertension?

A
  • 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
Q

What is the pathogenesis of pulmonary hypertension?

A
  • 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
Q

What risk factors are taken into account when calculating a Framingham risk score?

A 
Age
Gender
Total cholesterol mg/dl
HDL cholesterol mg/dl
Smoker y/n?
Systolic blood pressure mmHg
Currently taking antihypertensives y/n?
46
Q

What does your Framingham risk score tell you?

A

Your chance of having a heart attack within the next 10 years.

47
Q

What is typical/stable angina?

A

Fixed obstruction

Predictable relationship to exertion

48
Q

What is variant/Prinzmetal angina?

A

Coronary artery spasm

49
Q

What is crescendo/unstable angina?

A

Often due to plaque disruption

Clinical Pathology (65 decks)

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