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Year 2 clinical pathology > Week 8 Cardiovascular 1 > Flashcards

Week 8 Cardiovascular 1 Flashcards

1
Q

Define Ischaemic heart disease.

A

Inadequate blood supply to the myocardium

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2
Q

What causes ischaemic heart disease?

A

Most comminly due to reduced coronary blood flow, almost always due to atheroma +/- thrombus.

Less common cause are due to amyloid accumulation or due to surgical problems

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3
Q

what additional complications can occur with ischeamic heart disease?

A

myocardial hypertrophy, usually due to systemic hypertension–> mainly left ventricular hypertrophy

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4
Q

What is the pathogenesis of ischaemic heart disease?

A

Autoregulation of coronary blood flow breaks down if > 75% occlusion

> 90% stenosis may be insufficient at rest

low diastolic flow especially subendocardial

myocyte dysfunction/death from ischaemia

Active aerobic metabolism of cardiac muscle

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5
Q

What are the different type of angina pectoris?

A

typical/stable –. fixed obstruction, predictable relationship to exertion

crescendo/unstable –> often due to plaque disruption

variant/Prinzmetal –> coronary artery spasm

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6
Q

What type of angina pectoris is the most dangerous?

A

Unstable angina as the angina increasingly gets worse

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7
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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8
Q

What is acute coronary syndrome?

A

It refers to a group of conditions due to decreased blood flow in the coronary arteries such that part of the heart muscle is unable to function properly or dies.

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9
Q

Give examples of acute coronary syndrome

A

acute myocardial infarction (+/- ecg ST elevation)

crescendo/unstable angina

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10
Q

What occurs in subendocardial myocardial infarction?

A

The subendocardial myocardium is relatively poorly perfused under normal conditions

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11
Q

How can the subendocardial myocardium infarct without any acute cornary occlusion?

A

If there is:
Stable athermanous occlusion of the coronary circulation

An acute hypotensive episode

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12
Q

Where is it common to get coronary atheroma and thrombus?

A

Occur in bifurcation, junctions of the coronary arteries or if there is any abnormalitis.

Due to the shear pressures at the time

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13
Q

What is the morphology of heart after MI within the fisrt 24 hours? Explain both gross and microscopic appearance

A

Gross appearance –> Normal/dark

Microscopic appearance –> necrosis and neutrophils

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14
Q

What is the morphology of heart after MI within post 1-2 days? Explain both gross and microscopic appearance

A

Gross appearance – more necrosis and neutrophils

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15
Q

What is the morphology of heart after MI within post 3-7 days? Explain both gross and microscopic appearance

A

Gross appearance –> hyperaemic borderm, yellow centre

Microscopic appearance –> macrophages

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16
Q

What is the morphology of heart after MI within post 1-3 weeks? Explain both gross and microscopic appearance

A

Gross appearance –> red/grey

Microscopic appearance–> granulation tissue

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17
Q

What is the morphology of heart after MI within post 3-6 weeks? Explain both gross and microscopic appearance

A

Gross –> scar

Microscopic –> collagen scar

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18
Q

What are the different blood markers of cardiac myocyte damage? When can they be detected?

A

Troponins T & I
detectable 2 – 3h, peaks at 12h, detectable to 7 days
raised post MI but also in pulmonary embolism, heart failure, & myocarditis.

Creatine kinase MB
detectable 2 – 3h, peaks at 10-24h, detectable to 3 days

Myoglobin
peak at 2h but also released from damaged skeletal muscle

Lactate dehydrogenase isoenzyme 1
peaks at 3days, detectable to 14days

Aspartate transaminase
Also present in liver so less useful as a marker of myocardial damage

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19
Q

Why is creatine kinase not the best marker for MI?

A

Because creatine kinase is seen in muscles all around the body and not just in the heart.

CK Mb which is mainly found in cardiac is also found in skeletal

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20
Q

What is the prognosis of MI?

A

20% 1-2h mortality – sudden cardiac death

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21
Q

What are the complications of MI?

A

Mural thrombus and emboli
arrhythmias, ventricular fibrillation (75-95%) & sudden death

ischaemic pain

left ventricular failure (60%) & shock (10-15%)

Pericarditis

deep leg vein thrombosis & pulmonary embolus (15-40%)

ventricular aneurysm

autoimmune pericarditis (Dressler’s syndrome

Contractile dysfunction and chronic cardiac failure

Infarct expansion

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22
Q

What can be the possible cause 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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23
Q

What is familial hypercholesterolaemia?

A

A genetic disorder characterized by high cholesterol levels, specifically very high levels of low-density lipoprotein

24
Q

What are the common type of mutation in familial hypercholesterolaemia?

A

Low density lipoprotein receptor gene (1 in 500)

Apolipoprotein B (1 in 1000)

25
Q

What are the possible consequence of heterozygote familial hypwecholesterolaemia?

A

develop xanthomas – tendons, perioccular, corneal arcus – and early atherosclerosis

26
Q

What is the cause of familial hypercholesterolaemia?

A

Mutation in genes involved in cholesterol metabolism

Autosomal dominant but variant in penetrance

27
Q

What is the treatment for heterozygote familial hypercholesterolaemia?

A

Early primary treatment with statins (hydroxymethyglutaryl CoA reductase inhibitors) is effective

28
Q

Why is blood pressure physiologically regulated?

A

To ensure the perfusion of organs sufficient to maintain function

Prevents higher flow that exceeds metabolic demands, increases damage to blood vessels and thus to organs

29
Q

When is blood pressure high?

A

Normal = 120/80mmHg”

Abnormal: Sustained diastolic of 90mmHg

Abnormal: Sustained systolic of 140mmHg

95% of cases are “primary”
aka “idiopathic”, “benign”, “essential”,

30
Q

Dysfunction over a long period of time of what physiological systems cause 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

31
Q

What is the pathway that net set balance causes increase in BP?

A

Increased intravascular volume and volume delivery to the heart augment cardiac output and therefore blood pressur.

Results in tissue perfusion exceeding metabolic demand –> autoregulation of blood flow which increases vascoconstriction to reduce blood flow.

This results in a steady-state hemodynamic pattern of elevated blood pressure with increased systemic vascular resistance and normal cardiac output.

32
Q

What are the possible effect of hypertension?

A

Cardiovascular –> hypertensive heart disease

Renal failure

Cerebrovascular accident

33
Q

What occurs in 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

When the pressure is too great the left ventricle fails to pump blood at a normal rate and dilates

34
Q

Whattypes of arterial rupture are consequence of hypertensive cerebrovascular disease?

A

atheromatous (intracerebral haemorrhage) –> weak vessels with atheroma can rupture

berry aneurysm of the Circle of Willis (subarachnoid haemorrhage)

35
Q

What is the BP of malignant hypertension?

A

BP > 180/120 mmhg

36
Q

What are the signs and symptoms of malignant hypertension?

A

acute hypertensive encephalopathy

renal failure

retinal haemorrhages

37
Q

What are the complications of acute hypertensive encephalopathy?

A

Diffuse cerebral dysfunction:

Confusion, vomiting, convulsions, coma and death

38
Q

What are the causes pulmonary hypertension?

A

Loss of pulmonary vasculature
Secondary to left ventricular failure
Systemic to pulmonary artery shunting
Primary or idiopathic in children

39
Q

What pulmonary vasculature diseases can cause pulmonary hypertension?

A

Chronic obstructive lung disease

Pulmonary interstitial fibrosis (interstitial lung diseases)

Pulmonary emboli or thrombosis

Under ventilated alveoli

40
Q

What can be the consequence 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

41
Q

What are cardiovascular 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
42
Q

What is the consequence of hypertension on the kidney?

A

Arterial intimal fibroelastosis

Hyaline arteriolosclerosis

Slow deterioration in renal function leading to chronic renal failure

43
Q

How does kidney produce aldosterone?

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

Angiotensin II stimulates adrenal cortex to produce aldosterone

44
Q

What are the effects of angiotensin 11 and aldosterone?

A

Angiotensin II
Potent natural vasoconstrictor
Very short half-life

Aldosterone
The physiological mineralocorticoid
Renal action causes sodium and thus water retention
Circulating blood volume increases

45
Q

What disease is caused by excess aldosterone secretion?

A

Conn’s syndrome

46
Q

What causes excess aldosterone secretion?

A 
Usually due to adrenocortical adenoma
Possibly micronodular hyperplasia
Renal sodium and water retention
Hypertension
Elevated aldosterone, low renin
Potassium loss
47
Q

How is Conn’s syndrome diagnosed?

A

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

48
Q

What is phaechromocytoma?

A

Tumour of the adrenal medulla

Presents due to secretion of vasoconstrictive catecholamines – adrenaline and noradrenaline

49
Q

What is phaechromocytoma usually presented with?

A 
Presents with:
Pallor
Headaches
Sweating
Nervousness
Hypertension
50
Q

How do you diagnose and treat phaeochromocytoma?

A

Diagnosed by 24hr urine collection for adrenaline metabolites

Surgical is the main treatment but usually bilateral so don’t want to take both of your adrenal glands

51
Q

What is Cushings disease?

A

Overproduction of cortisol by adrenal cortex

52
Q

What is the conseuqence of Cushings 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

53
Q

What causes Cushings disease?

A

An adrenocortical neoplasm usually an adenoma

A pituitary adenoma

A paraneoplastic effect of other neoplasms

54
Q

What is a common paraneoplastic effect of other neoplasm that causes Cushings disease?

A

Small cell lung carcinoma producing adrenocorticotrophic hormone that stimulates the zona fasciculata cells of the adrenal cortex to produce cortisol

55
Q

What is the consequence of renal artery stenosis?

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

56
Q

What is the cause of hypertrophic cardiomyopathy?

A

Muscle contractile protein gene mutations

Year 2 clinical pathology (21 decks)

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