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Clinical Pathology > cardiovascular diseases 1 > Flashcards

cardiovascular diseases 1 Flashcards

1
Q

what factors reduce blood supply to the myocardium resulting in ischameia

A

reduced coronary flow
myocardial hypertrophy
vasculitis, amyloid deposition, coronary artery dissection.

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2
Q

pathogenesis if acute and chronic ischameia.

A

auto-regulation of coronary blood flow which breakdown in occlusion.
low diastolic flow- especially subendocardial.
Active aerobic metabolism of cardiac muscle- reduced
Myocytes dysfunction and eventually will lead to cell death.

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3
Q

what is the time frame for recovery via repercussion of a oxygen starved heart

A

15-20 mins

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4
Q

4 common ischaemic heart disease syndromes

A

angina pectoris
acute coronary syndrome
sudden cardiac death
chronic ischaemic heart disease

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5
Q

3 types of angina pectoris

A

typical/stable- luminal narrowing and manifestation upon stress.

Crescendo/unstable plaque- disrupted so thrombus or emboli form, resulting in pain in an uncontrollable fashion.

Variant/prinmetal- fixed obstruction but effects are not predictable.

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6
Q

what is shown on an ECG in acute coronary syndrome

A

ST elevation

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7
Q

what are the main factors resulting in acute ischaemia

A 
atheroma and thrombosis.
lipid rich plaques.
Transmural MI
Thrombolysis
Myocardial stunning- contractility of the heart is abnormal
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8
Q

how is acute iscahemia diagnosed

A

ECG, cardiac proteins

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9
Q

what are the 3 categories of MI

A

transmural
subendocardial
regional

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10
Q

pathogenesis of a subendocardial MI

A

At the surface the epicardial has a direct supply of blood and the endocardial has a supply of blood from smaller infiltrating arteries and diffusion, however the space in-between is poorly perfused (subendocardial region)

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11
Q

what 2 factors cause the subendocardial to infarct

A

Stable athermanous occlusion of the coronary circulation

An acute hypotensive episode

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12
Q

what are the main blood markers of myocytes damage and which ones are used rottenly in clinic

A

Raised Troponin-most common measure- detectable from 3 hrs and peaks at 12hrs- present for unto 7 days.

Creatine Kinase
detectable from 2-3hrs and parks between 10-24hrs- present for 3 days, 3 subtypes

Myoglobin peak at 2hrs

LDH peaks at 3 days and is detectable for 14 days

Aspartate transminase

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13
Q

what conditions is troponin raised in excluding MI

A

pulmonary embolism, heart failure, & myocarditis.

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14
Q

what damage does creatinine kinase show excluding MI

A

skeletal muscle damage

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15
Q

what damage does myoglobin show excluding MI

A

skeletal muscle damage

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16
Q

what damage does aspartate transaminase show excluding MI

A

liver damage

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17
Q

what is the mechanism of action of troponin.

A

binds to actin to prevent contraction,

Ca2+ ions allow troponin to release tropomyosin and therefore bind to actin.

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18
Q

most common prognosis post MI

A

cardiac death within 1-2 hrs.

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19
Q

complications of MI

A

Arrhythmias, ventricular fibrillation, Ischaemic pain, Left ventricular failure, shock, pericarditis, cardiac mural thrombus or emboli, DVT, PE, myocardial rupture, ventricular aneurysm, autoimmune pericarditis (dressler’s syndrome), pleurisy, ventricular wall rupture, infarct extension, haemopericardium, mural thrombus.

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20
Q

define mural thrombus

A

layers of organised fibrin in the wall of the myocardium, which are unstable and can dislodge into circulation.

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21
Q

what cause chronic ischaemic heart disease

A

Coronary artery atheroma produces relative myocardial ischemia & angina pectoris on exertion

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22
Q

what type of genetic defect is familial hypercholesterolemia

A

autosomal dominant.

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23
Q

commonest gene mutations familial hypercholesterolemia

A

Low density lipoprotein receptor gene

Apolipoprotein B

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24
Q

what is the difference between homozygous and heterozygous familial hypercholesterolaemia
and which has a better prognosis

A
  • Homozygous- no functioning liver LDL receptors.
  • Heterozygotes – Still have some functioning liver LDL receptors

heterozygous has a better prognosis.

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25
Q

symptoms of familial hypercholesterolaemia

A

xanthomas- tendons, perioccular, corneal arcus

atheroslerosis

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26
Q

treatment of familial hypercholesterolaemia

A

statins

Treatment of homozygotes is more complex and less effective

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27
Q

what is classed as abnormally high blood pressure

A

140/90

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28
Q

what are the 2 types of hypertension and which is more common

A

primary and secondary hypertension.

29
Q

what are the main causes of primary hypertension (congenital)

A 
cardiac baroreceptors don't function.
RAS breakdown
kinin-kallikrekin system breakdown
Naturetic peptides
adrenergic receptor system
autocrine factor produced by blood vessels
autonomic nervous system.
30
Q

pathogenesis of all primary hypotension involves a increased net balance of what chemical/food

A

salt.

31
Q

pathogenesis of primary hypertension

A

increased intravascular volume due to renal salt absorption, increased cardiac output.
tissue perfusion exceeds metabolic demands, leading to auto-regulation of bloodflow in tissues. this results in steady state haemodynamic pattern of elevated blood pressure with increased systemic vascular resistance and normal cardiac output.

32
Q

Renal causes of secondary hypertension.

A 
–	Acute glomerulonephritis
–	Chronic renal disease
–	Polycystic kidneys
–	Renal artery stenosis
–	Renal artery fibromuscular dysplasia
–	Renal vasculitis
–	Renin – producing tumour
33
Q

Endocrine causes of secondary hypertension

A

– Adrenocortical hormones (Cushing syndrome, primary aldosteronism, congenital adrenal hyperplasia, liquorice ingestion)
– Exogenous chemicals (glucocorticoids, oestrogen including pregnancy and oral contraceptives, monoamine oxidase inhibitors, amphetamines, cocaine)
– Phaeochromocytoma
– Acromegaly
– Hypothyroidism
– Hyperthyroidism
– Pregnancy – preeclampsia if severe

34
Q

cardiovascular causes of secondary hypertension

A

– Coarctation of the aorta
– Polyarteritis nodosa
– Increased intravascular volume
– Increased cardiac output

35
Q

when is the renin angiotensin system activated, when BP is low or high.

A

BP is low

36
Q

where is renin synthesised

A

juxtaglomerular apparatus in the wall of the afferent arterioles of the kidney

37
Q

what is the function of renin

A

cleaves angitensinogen to angiotensin 1.

38
Q

in which organ is angiotensin I converted to angiotensin II

A

lungs

39
Q

what is a major side effect of ACE inhibitors

A

chronic cough

40
Q

main function of angiotensin II

A

Potent natural vasoconstrictor

stimulate aldosterone production.

41
Q

main function of aldosterone

A

renal action cause sodium and water retention

circulating blood volume therefore increases

42
Q

what are the consequences of renal artery stenosis

A

reduced blood pressure in the kidney
Juxtaglomerular apparatus stimulated to produce renin
Renin-angiotensin system stimulates adrenal cortex zona glomerulosa cells to produce aldosterone

43
Q

define co-arctation of the aorta

A

Congenital narrowing of the aorta, usually distal to the origin of the left subclavian artery

44
Q

how is coarctation of the aorta detected.

A
  • Detected by difference in BP between the arms and legs- low BP in legs but normal in arms.
  • Characteristic chest X-ray
45
Q

how is coarctation of the aorta treated

A

surgically correctable

46
Q

what is conn’s syndrome

A

excessive aldosterone secretion

47
Q

what is the most common cause of conn’s syndrome

A

adrenocortical adenoma

48
Q

how is conn’s syndrome diagnosed

A

CT scan of adrenals in presence of these metabolic abnormalities

49
Q

what chemicals are retained and which chemicals are lost in Conn’s syndrome

A

Renal sodium and water retention.

Potassium loss

50
Q

what are the side effects of excessive potassium loss

A

Muscular weakness, cardiac arrhythmias, parasthaesesia, metabolic alkalosis

51
Q

define phaechromocytoma

A

tumour of the adrenal medulla

52
Q

common symptoms of phaechromocytoma

A

pallor, headaches, sweating, nervousness, hypertension

53
Q

how is phaechromocytoma diagnosed

A

24hr urine collection for adrenaline metabolites

54
Q

treatment for phaechromocytoma

A

remove adrenal medulla.

55
Q

Cushing’s disease.

A

Overproduction of cortisol by the adrenal cortex.

56
Q

effects of cortisol overproduction

A

– Potentiating sympathetic nervous system activity.

– Mineralocorticoid action on the kidneys, thus causing hypertension.

57
Q

Cause of Cushing’s disease.

A

– Adrenocortical neoplasm usually an adenoma.
– A pituitary adenoma
–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

58
Q

what 3 organs does hypertension severely effect

A

heart, renal and brain.

59
Q

pathogenesis of hypertensive heart disease

A

– Systemic hypertension leads to increased left ventricular blood pressure
– Initially left ventricular hypertrophy- recognized cause of cell death.
– When the pressure is too great the left ventricle fails to pump blood at a normal rate and dilates.

60
Q

what renal changes occur due to systemic hypertension

A

– Vascular changes- arterial intimal fibroelastosis, and hyaline arteriosclerosis.
– Slow deterioration in renal function leading to chronic renal failure- due to damage and scarring in the intima.

61
Q

what are the common conditions which occur in the brain due to hypertension

A
  • Athermanous plaque can rupture.(intracerebral haemorrhage)
  • Berry aneurysm (inherited) of the Circle of Willis (subarachnoid haemorrhage)
  • Massive basal ganglia haemorrhage
  • Lacunar infarct.
62
Q

define hypertensive crisis

A

rapid rise in BP (increased risk of stroke).

63
Q

what blood pressure reading shows hypertensive crisis

A

BP 180/120mmHg

64
Q

clinical signs of hypertensive crisis

A
  • Renal failure
  • Retinal haemorrhages
  • acute hypertensive encephalopathy
65
Q

what are the clinical symptoms of acute hypertensive encephlopathy

A

confusion, vomitting, convulsions, coma and death

66
Q

what are the causes of pulmonary hypertension

A

loss of pulmonary vasculature- Chronic obstructive lung disease, pulmonary interstitial fibrosis, pulmonary emboli and thrombosis, under ventilated alveoli
secondary to left ventricular failure
Systemic to pulmonary artery shunting
Primary or idiopathic

67
Q

risk factors for cardiovascular disease

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
68
Q

what study calculates an individual’s risk of cardiovascular disease based on assessment of multiple risk factors.

A

The Framingham Heart Study

69
Q

risk assessment methods for cardiovascular disease include

A
  • SCORE
  • QRISK2
  • Joint British societies risk prediction charts.

Clinical Pathology (45 decks)

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