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Clinical Pathology > Cardiovascular Diseases 1 > Flashcards

Cardiovascular Diseases 1 Flashcards

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1
Q

Inadequate blood supply to the myocardium

A

Ischaemic heart disease

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2
Q

What degree of coronary artery stenosis is insufficient at rest?

A

> 90%

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3
Q

At what stage in the heart cycle does most perfusion occur?

A

During diastole

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4
Q

3 types of angina pectoris

A

Stable/typical
Variant/prinzmetal
Crescendo/unstable

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5
Q

What type of angina is a fixed obstruction, predictable and related to exertion

A

Stable

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6
Q

What type of angina is due to a coronary artery spasm?

A

Varient/prinzmetal

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7
Q

What type of angina is often due to plaque disruption?

A

Crescendo/unstable

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8
Q

3 causes of acute coronary syndrome?

A

Acute MI with ST elevation
Acute MI without ST elevation
Unstable/crescendo angina

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9
Q

Give 2 types of MI, based on what area of the heart is affected

A

Subendocardial

Transmural

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10
Q

Is subendocardial MI associated with ST elevation?

A

No

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11
Q

Causes of subendocardial MI

A

Stable atheromatous occlusion

Acute hypotensive episode

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12
Q

What type of MI is caused by a sudden blockage that kills the whole wall?

A

Transmural

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13
Q

How do transmural MIs heal?

A

By scarring and fibrosis- no regeneration of myocytes and no contractile function

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14
Q

Causes of transmural MIs

A

Coronary atheroma and thrombus

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15
Q

Gross appearance of heart tissue

A

Normal/dark

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16
Q

Gross appearance of heart tissue 1-2 days after an MI

A

Yellow, infarct centre

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17
Q

Gross appearance of heart tissue 3-7 days after an MI

A

Hyperaemic border, yellow centre

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18
Q

Gross appearance of heart tissue

A

Red/grey

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19
Q

Gross appearance of heart tissue 3-6 weeks after an MI

A

Scar

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20
Q

Microscopic appearance of heart tissue

A

Necrosis and neutrophils

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21
Q

Microscopic appearance of heart tissue 1-2 days after an MI

A

More necrosis and neutrophils

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22
Q

Microscopic appearance of heart tissue 3-7 days after an MI

A

Macrophages

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23
Q

Microscopic appearance of heart tissue 1-3 weeks after an MI

A

Granulation tissue

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24
Q

Microscopic appearance of heart tissue 3-6 weeks after an MI

A

Collagen scar

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25
At what point after an MI is the heart tissue the weakest?
3-7 days- infiltrated with macrophages
26
Name 3 blood markers of cardiac myocyte damage
Troponins T&I Creatinine Kinase Myoglobin
27
Name the blood markers of cardiac myocyte damage in order of their appearance in the blood post MI
Myoglobin, CKMB, Troponin
28
When do troponin levels peak post MI?
12 hours
29
When else can troponin levels be high in the blood, other than post MI?
Renal failure PE Heart failure Myocarditis
30
How does troponin prevent muscle contraction?
binds to actin and stops in binding to tropomyosin
31
What are the 3 sybtypes of creatinine kinase and which tissues are they found in?
CKMM-cardiac and skeletal muscle CKBB-brain, lung CKMB-mainly cardiac, also skeletal muscle
32
7 complications of MIs
``` Contractile dysfunction and chronic cardiac failure infarct extension pericarditis arrhythmias mural thrombus ventricular aneurysm myocardial rupture ```
33
In familial hypercholesterolaemia, what are the specific genes affected?
low density lipoprotein receptor gene | apolipoprotein B
34
What is the result when the LDL receptor gene is not functional?
LDLs are not taken in by the liver, so instead they are taken in by scavengers and settle underneath endothelial cells- contribute to atheroscerosis
35
What is the difference between primary and secondary hypertension
primary hypertension develops over a long period of time due to obestiy, diabetes etc. Secondary hypertension develops much more rapidly and is the result of a condition or disease within the body e.g. renal complications, endocrime
36
Which is more common, primary or secondary hypertension?
Primary (accounts for 95%)
37
Too much sodium in the blood results in an increase in intravascular volume. As the perfusion exceeds metabolic demand, the body responds by vasoconstriction, resulting in a steady state haemodynamic pattern. Describe this pattern
Increase in blood pressure Increase in systemic vascular resistance Normal cardiac output
38
What are the 3 main organs affected by hypertension?
Kidneys, heart and brain
39
Describe the pathogenesis of hypertensive heart disease
Sytemic hypertension, Increase in LV blood pressure, LV hypertrophy without dilation initially in response to an increase in work load. Long term-dilation of LV.
40
What is a normal LV thickness?
18mm
41
What BP categorises as a bypertensive crisis?
>180/120 mmHg
42
Dramatic, immediate complications requiring urgent treatment. Results from primary or secondary hypertension
Hypertensive crisis
43
What are the 3 main effects of a hypertensive crisis
Acute hypertensive encephalopathy Renal failure Retinal haemorrhages
44
Diffuse cerebral dysfunction; confusion, vomiting, convulsions, coma and death
Acute hypertensive encephalopathy
45
3 causes of pulmonary hypertension
COPD Fibrosis (interstitial lung diseases) Emboli or thrombosis
46
Pulmonary hypertension occurs secondary to what
LV failure
47
Longitudinal study to identify cardiovascular risk factors- calculates an individual risk
Framingham heart study
48
Where is renin synthesises, stored and released from?
The juxtaglomerular apparatus in the wall of the afferent arterioles in the kidney
49
What does renin do?
Cleaves angiotensinogen to angiotensin 1
50
WHere is angiotensin 1 converted to active angiotensin 2?
In many tissues, especially lung
51
Role of angiotensin 2
Potent natural vasoconstrictor. V.short half life. Stimulates adrenal cortex to produce aldosterone
52
What effect does aldosterone have on the body?
It is a physiological mineralocorticoid. It acts on the kidneys and causes Na+ and thus water retention. Circulating blood volume increases.
53
Excessive aldosterone secretion
Conn's syndrome
54
Causes of conn's syndrome
Adrenocorticol adenoma | Micronodular hyperplasia
55
What effects does conn's syndrome have on aldosterone and renin concentrations
Aldosterone increases, renin decreases to compensate.
56
Result of Conn's syndrome
Gain sodium, lose potassium- muscular weakness, cardiac arrhythmias, metabolic alkalosis
57
How do you diagnose conn's syndrome?
CT scan of adrenals in presence of metabolic abnormalities (increase in aldosterone, decrease in renin)
58
Tymour of the adrenal medulla, secretes vasoactive catecholamines- adrenaline and noradrenaline
Phaeochromocytoma
59
Effects of phaeochromocytoma
Pallor, headaches, sweating, nervousness, hypertension
60
How do you diagnose phaeochromocytoma?
24hr urine collection for adrenal metabolites
61
Treatment for phaeochromocytoma?
Surgery
62
Overproduction of cortisol by adrenal cortex- caused by oversecretion of ACTH
Cushing's disease
63
How is cushing's disease different from cushing's syndrome?
Cushing's syndrome- cotisol from any source. | Cusching's disease- cortisol from adrenal cortex
64
Causes of cushing's syndrome
Adrenocorticol neoplasm (usually an adenoma) Pituitary adenoma Paraneoplastic effect of other neoplasms

Clinical Pathology (53 decks)

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