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Flashcards in cardiovascular diseases 1 Deck (69):
1

what factors reduce blood supply to the myocardium resulting in ischameia

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

2

pathogenesis if acute and chronic ischameia.

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.

3

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

15-20 mins

4

4 common ischaemic heart disease syndromes

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

5

3 types of angina pectoris

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.

6

what is shown on an ECG in acute coronary syndrome

ST elevation

7

what are the main factors resulting in acute ischaemia

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

8

how is acute iscahemia diagnosed

ECG, cardiac proteins

9

what are the 3 categories of MI

transmural
subendocardial
regional

10

pathogenesis of a subendocardial MI

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)

11

what 2 factors cause the subendocardial to infarct

Stable athermanous occlusion of the coronary circulation
An acute hypotensive episode

12

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

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

13

what conditions is troponin raised in excluding MI

pulmonary embolism, heart failure, & myocarditis.

14

what damage does creatinine kinase show excluding MI

skeletal muscle damage

15

what damage does myoglobin show excluding MI

skeletal muscle damage

16

what damage does aspartate transaminase show excluding MI

liver damage

17

what is the mechanism of action of troponin.

binds to actin to prevent contraction,
Ca2+ ions allow troponin to release tropomyosin and therefore bind to actin.

18

most common prognosis post MI

cardiac death within 1-2 hrs.

19

complications of MI

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.

20

define mural thrombus

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

21

what cause chronic ischaemic heart disease

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

22

what type of genetic defect is familial hypercholesterolemia

autosomal dominant.

23

commonest gene mutations familial hypercholesterolemia

Low density lipoprotein receptor gene
Apolipoprotein B

24

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

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

heterozygous has a better prognosis.

25

symptoms of familial hypercholesterolaemia

xanthomas- tendons, perioccular, corneal arcus
atheroslerosis

26

treatment of familial hypercholesterolaemia

statins
Treatment of homozygotes is more complex and less effective

27

what is classed as abnormally high blood pressure

140/90

28

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

primary and secondary hypertension.

29

what are the main causes of primary hypertension (congenital)

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

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

salt.

31

pathogenesis of primary hypertension

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

Renal causes of secondary hypertension.

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

33

Endocrine causes of secondary hypertension

– 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

cardiovascular causes of secondary hypertension

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

35

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

BP is low

36

where is renin synthesised

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

37

what is the function of renin

cleaves angitensinogen to angiotensin 1.

38

in which organ is angiotensin I converted to angiotensin II

lungs

39

what is a major side effect of ACE inhibitors

chronic cough

40

main function of angiotensin II

Potent natural vasoconstrictor
stimulate aldosterone production.

41

main function of aldosterone

renal action cause sodium and water retention
circulating blood volume therefore increases

42

what are the consequences of renal artery stenosis

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

define co-arctation of the aorta

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

44

how is coarctation of the aorta detected.

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

45

how is coarctation of the aorta treated

surgically correctable

46

what is conn's syndrome

excessive aldosterone secretion

47

what is the most common cause of conn's syndrome

adrenocortical adenoma

48

how is conn's syndrome diagnosed

CT scan of adrenals in presence of these metabolic abnormalities

49

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

Renal sodium and water retention.
Potassium loss

50

what are the side effects of excessive potassium loss

Muscular weakness, cardiac arrhythmias, parasthaesesia, metabolic alkalosis

51

define phaechromocytoma

tumour of the adrenal medulla

52

common symptoms of phaechromocytoma

pallor, headaches, sweating, nervousness, hypertension

53

how is phaechromocytoma diagnosed

24hr urine collection for adrenaline metabolites

54

treatment for phaechromocytoma

remove adrenal medulla.

55

Cushing's disease.

Overproduction of cortisol by the adrenal cortex.

56

effects of cortisol overproduction

– Potentiating sympathetic nervous system activity.
– Mineralocorticoid action on the kidneys, thus causing hypertension.

57

Cause of Cushing's disease.

– 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

what 3 organs does hypertension severely effect

heart, renal and brain.

59

pathogenesis of hypertensive heart disease

– 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

what renal changes occur due to systemic hypertension

– 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

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

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

62

define hypertensive crisis

rapid rise in BP (increased risk of stroke).

63

what blood pressure reading shows hypertensive crisis

BP 180/120mmHg

64

clinical signs of hypertensive crisis

• Renal failure
• Retinal haemorrhages
• acute hypertensive encephalopathy

65

what are the clinical symptoms of acute hypertensive encephlopathy

confusion, vomitting, convulsions, coma and death

66

what are the causes of pulmonary hypertension

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

risk factors for cardiovascular disease

• 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

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

The Framingham Heart Study

69

risk assessment methods for cardiovascular disease include

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