Diseases of the Cardiovascular System (29) Flashcards Preview

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Flashcards in Diseases of the Cardiovascular System (29) Deck (122):
1

What's the most common cause of death in women in UK?

CVD
Cancer
Resp disease

2

What's the most common cause of death in men in UK?

Cancer
CVD
CHD
Resp

3

Ischaemic heart disease

Inadequate blood supply to the myocardium

4

IHD is due to

Reduced coronary blood flow, almost always due to atheroma +/- thrombus, myocardial hypertrophy - systemic hypertension

5

Pathogenesis

Auto-regulation of coronary blood flow breaks down if >75% occlusion, low diastolic flow (subendocardial), active aerobic metabolism of cardiac muscle, myocyte dysfunction, recovery possible if rapid reperfusion (15-20min)

6

Typical/stable angina

Fixed obstruction, predictable relationship to exertion

7

Crescendo/unstable angina

Often due to plaque disruption, red flag symptom

8

Variant/prinzmetal angina

Coronary artery spasm (Ca channel blockers)

9

Acute coronary syndrome

Acute MI (+/- ST elevation), crescendo/unstable angina

10

IHD syndromes

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

11

Acute ischaemia

Atheroma + acute thrombosis/haemorrhage, lipid rich plaques, transmural MI, thrombolysis, myocardial stunning (contractile abnormality)

12

Diagnosis of acute ischaemia

Clinical, ECG, blood cardiac proteins

13

Subendocardial MIs

Poorly perfused, can infarct without any acute coronary occlusion if acute hypotensive episode/stable athermanous occlusion of coronary artery, non-elevation, involves innermost layer of myocardium doesn't extend to epicardium

14

MI morphology

Normal

15

MI morphology 1-2 days

Pale, oedema, yellow infarct, myocyte necrosis, neutrophils

16

MI morphology 3-7 days

Yellow with haemorrhagic edge, myocyte necrosis, macrophages

17

MI morphology 1-3 weeks

Pale, thin, red/gray granulation tissue then fibrosis

18

MI morphology 3-6 weeks

Dense fibrous scar (collagen)

19

Blood markers of cardiac myocyte damage

- Troponins T & I
- Creatine kinase MB
- Myoglobin
- Lactate dehydrogenase isoenzyme 1
- Aspartate transaminase

20

Troponins T & I

- Detectable 2-3hrs-7 days, peaks 12 hours
- Raised post MI, P.E, heart failure and myocarditis

21

Creatine kinase MB

- Detectable 2-3hrs-3 days, peaks 10-24 hours
- Not very specific - skeletal muscle damage

22

Myoglobin

- Peaks at 2hr
- Released from damaged skeletal muscles

23

Lactate dehydrogenase isoenzyme 1

Peaks at 3 days, detectable until 14 days

24

Aspartate transaminase

Present in liver - not v.useful

25

Which is most useful marker of cardiac myocyte damage?

Troponins T & I

26

Prognosis of MI

20% 1-2hr mortality - sudden cardiac death

27

Complications of MI (80-90%)

Arrhythmias, ventricular fibrillation, sudden death, ischaemic pain, LV failure, shock, pericarditis, cardiac mural thrombus and emboli, DVT, P.E, myocardial rupture (tamponade, ventricular septal perforation, papillary muscle rupture), ventricular aneurysm, autoimmune pericarditis (Dressler's) +/- pleurisy 2 weeks-months post, haemopericardium

28

Common MI complications

Ventricular fibrillation, LV failure, DVT and PE

29

Chronic IHD

Coronary artery atheroma produces relative myocardial ischaemia and angina pectoris on exertion, risk of sudden death/MI, possible previous MIs, crescendo/unstable angina (evolving plaque), variant angina (spasm)

30

Familial hypercholesterolaemia

Mutations in LDL receptor gene/apolipoprotein B

31

Familial hypercholesterolaemia heterozygotes

Xanthomas (yellow nodules) in tendons, perioccular, corneal arcus and early atherosclerosis

32

Familial hypercholesterolaemia heterozygotes treatment

Statins (hydroxymethyglutaryl CoA reductase inhibitors)

33

Familial hypercholesterolaemia homozygotes treatment

More complex and less effective

34

Blood pressure is physiologically regulated to

Ensure perfusion of organs sufficient to maintain function, prevents higher flow (that exceeds metabolic demands and increases damage to blood vessels and organs)

35

Hypertension

140/90 mmHg

36

What controls BP

Cardiac baroreceptors, RAAS, Kinin-kallikrein system, Naturetic peptides, Adrenergic receptor system, Autocrine factors produced by blood vessels, Autonomic NS, Na balance

37

Renin

Synthesised, stored in, released from juxtaglomerular apparatus in wall of afferent arterioles of the kidney, cleaves angiotensinogen > angiotensin I

38

Angiotensin 2

Vasoconstrictor, short half-life, stimulates adrenal cortex to produce aldosterone

39

Alodsterone

Mineralcorticoid, causes sodium and water retention, circulating blood vol increase

40

Renal artery stenosis

Reduced bp in kidneys and afferent arterioles, juxtaglomerular apparatus stimulates renin, RAAS stimulates adrenal cortex zone glomerulosa cells > aldosterone

41

Coarctation of aorta

Congenital narrowing, distal to original of left subclavian artery, RAAS activated, asymptomatic, difference in bp between arms and legs, chest x-ray

42

Treatment of coarctation of aorta

Surgery

43

Conn's syndrome

Excess aldosterone secretion

44

Conn's syndrome due to

Adrenocortical adenoma, micronodular hyperplasia

45

Conn's syndrome causes

Renal sodium and water retention (hypertension), elevated aldosterone, low renin, potassium loss

46

Low potassium

Muscular weakness, cardiac arrhythmias, paraesthesia, metabolic alkalosis

47

Diagnosis of Conn's syndrome

CT scan of adrenal glands and metabolic abnormalities

48

Phaeochromocytoma

Catecholamine secreting tumour of adrenal medulla (Vasoconstrictors - adrenaline and noradrenaline)

49

Phaeochromocytoma symptoms

Pallor, headaches, sweating, nervousness, hypertension

50

Phaeochromocytoma diagnosis

24hr urine collection for adrenaline metabolites

51

Cushing's syndrome

Any steroid, caused by any source

52

Cushing's disease cause

- Adrenocortical neoplasm (adenoma)
- Pituitary adenoma
- Paraneoplastic effect of other neoplasms producing adrenocorticotrophic hormone stimulates zona fasciculata cells on adrenal cortex

53

Cushing's disease

Overproduction of cortisol by adrenal cortex

54

Cortisol's effect

Increases sympathetic NS, aldosterone-like action on kidney > hypertension

55

Hypertensive effect on heart

Hypertensive heart disease, LV hypertrophy without dilataion > sudden death

56

Hypertensive effect on kidney

Renal failure (arterial intimal fibroelastosis, hyaline arteriolosclerosis)

57

Hypertensive effect on cerebrovascular

Hypertensive encephalopathy, increased risk of rupture abnormal arteries (atheromatous > intracerebral haemorrhage/berry aneuyrm > SAH)

58

Hypertensive crisis

BP >180/120 mmHg

Acute hypertensive encephalopathy, renal failure, retinal haemorrhages

59

Acute hypertensive encephalopathy presentation

Confusion, vomiting, convulsions, raised ICP coma and death

60

Pulmonary hypertension

Higher than normal pressure in pulmonary artery

61

Pulmonary hypertension caused by

- Loss of pulmonary vasculature
- Secondary LV failure
- Systemic to pulmonary artery shunting
- Primary/idiopathic
(Not high bp)

62

Pulmonary hypertension leads to

- Increased RV work
- RV hypertrophy without dilatation
- Dilatation and systemic venous congestion
- RV failure

63

Loss of pulmonary vasculature caused by

- Chronic obstructive lung disease
- Pulmonary interstitial fibrosis
- Pulmonary emboli/thrombosis
- Under ventilated alveoli

64

CVD risk factors

Gender, hypertension, smoking, high blood cholesterol, low blood high density lipoproteins, diabetes, sedentary lifestyle, obesity, alcohol, ethnicity - S.Asian

65

The Framingham Heart Study

Identifying risk factors for CVD (longitudinal population study)

66

Other risk assessments

- SCORE
- QRISK2
- Joint British Societies risk prediction charts

67

Thomas Royle Dawber

First director of Framingham Heart Study

68

Richard Doll

Link between smoking and lung cancer

69

Austin Bradford Hill

Link between smoking and lung cancer

70

James Black

Discovered B-blockers

71

Akira Endo

Discovered statins in fungi

72

Left sided failure leads to ....output

low

73

LHF and kidneys

Pre-renal azotemia (N2), salt and fluid retention (RAAS and natriuretic peptides)

74

Natriuretic peptides

Induces discharge of sodium through urine

75

LHF and brain

Irritability, decreased attention, stupor > coma

76

LHF and lungs (congestion)

Pulmonary congestion and oedema, heart failure cells, dyspnea, orthopnoea, Paroxysmal Nocturnal Dyspnea, Blood tinged sputum, Cyanosis, Elevated pulmonary 'WEDGE' pressure (normal 2-15 mm Hg)

77

RHF causes

Left heart failure or cor pulmonale (enlarged RHS)

78

RHF and liver and spleen

Passive congestion (nutmeg liver), congestive splenomegaly, ascites

79

RHF and kidneys

Not enough blood - congested

80

RHF and pleura/pericardium

Pleural and pericardial effusions and transudates

81

RHF and peripheral tissues

Oedema

82

CHF autopsy

Cardiomegaly, chamber dilatation, hypertrophy of myocardial fibres (boxcar nuclei)

83

Opening valvular HD

Stenosis

84

Closing valvular HD

Regurgitation (incomplete/insufficiency)

85

Aortic stenosis

Calcification of a deformed valve/Rheumatic heart disease, 2x gradient pressure, LVH (no hypertension), ischaemia, cardiac decompensation, angina, CHF

86

Mitral stenosis

Rheumatic HD

87

Rheumatic HD

Follows group A strep infection, decrease in 'developed' countries, pancarditis (endocarditis, myocarditis, pericarditis)

88

Acute Rheumatic HD

Inflammation, Aschoff bodies, Anitschkow cells, pancarditis, vegetations on chordae tendinae at leaflet junction

89

Chronic Rheumatic HD

Thickened valves, commisural fusion, thick, short chordae tendinae

90

Mitral annular (ring) calcification

No dysfunction, or regurgitation (stenosis), more common in females

91

Aortic regurgitation cause

Rheumatic, infectious, aortic dilatations (syphilis, RA, marfan)

92

Mitral regurgitation cause

Mitral valve prolapse, infectious, fen-phen, papillary muscles, chordae tendinae, calcification of mitral ring

93

Mitral Valve Prolapse (MVP)

Connective tissue weakening, 'floppy' valve

94

MVP epidemiology

3% incidence, F>M

95

MVP diagnosis

Echocardiogram

96

MVP clinical

Asymptomatic, mid-systolic 'click', holosystolic murmur (regurgitation), chest pain, dyspnea

97

MVP complications

(3%) Infective endocarditis, mitral insufficiency, arrythmias, sudden death

98

Congenital heart defects

Faulty embryogenesis (week 3-8), mono-morphic, not evident until adult life (coarctation, ASD), 1% incidence

99

Incidence of malformations

1. VSD
2. ASD
3. Pulmonary stenosis
4. PDA
5. Tetralogy of Fallot
6. Coarctation of aorta
7. ASD
8. Aortic stenosis
9. Transposition of GA
10. Truncus arteriosus
11. Total anomalous pulmonary venous connection
12. Tricuspid atresia

100

Genetics of Congenital heart defects

10%, trisomies 21, 13, 15, 18, XO, mutations of genes which encode for transcription factors TBX5 (ASD, VSD), NKX2.5 (ASD), region of chromosome 22 important in heart development

101

22q11.2 deletion

Conotruncus, brachial arch, face

102

Environmental factors

Rubella and teratogens

103

L > R shunt

No cyanosis, pulmonary hypertension (irreversible)

104

Examples of L > R shunt

ASD, VSD, PDA, AVSD

105

R > L shunt

Cyanosis, venous emboli become systemic (paradoxical)

106

Obstructions

Coarctation of aorta, pulmonary stenosis/atresia, aortic stenosis/atresia

107

Examples of R > L shunt

Tetralogy of Fallot, TGA, Truncus arteriosis, Tricuspid atresia, TAPVC

108

ASD

Defective fossa ovalis (secundum 90%), next to AV valves, mitral cleft (primum 5%), sinus venosus - next to SVC (5%)

109

VSD

Only 30% isolated (teralogy of fallot), 90% membranous septum, muscular septum multiple holes - small close spontaneously, large > pulmonary hypertension

110

Patent Ductal Arteriosus (PDA)

90% isolated, associated with VSD, coarctation of aorta, pulmonary or aortic stenosis, continuous harsh, machinery-like murmur

111

Atrial ventricular septal defect (AVSD)

Defective, inadequate AV valves, partial/complete (all chambers), more than 1/3rd with complete - down's

112

Tetralogy of Fallot

1. VSD
2. RVH
3. Overriding aorta
4. Obstruction to RV outflow

113

Transposition of great arteries (TGA)

Abnormal formation of truncal and aortopulmonary septa, needs shunt for survival, fatal in first few months, surgical 'switching'

114

TGA shunt needed

- PDA/PFO (65%)
- VSD (35%)
- RV>LV

115

Truncus arteriosus

Pulmonary artery and aorta don't separate, associated with VSD, cyanosis, increased pulmonary blood flow

116

Tricuspid atresia

Hypoplastic RV, need shunt (ASD, VSD, PDA), high mortality

117

Total anomalous pulmonary venous connection (TAPVC)

Pulmonary veins go into LV/coronary sinus, need PFO/VSD, hypoplastic LA

118

Coarctation of aorta

M>F, common in XO's, infant - proximal to PDA (serious), adult - no PDA, bbicuspid aortic valve 50% of time

119

Pulmonary stenosis/atresia

Hypoplastic RV with ASD

120

Aortic stenosis/atresia valvular

Severe, hypoplastic LV > fatal

121

Aortic stenosis/atresia sub-valvular (subaortic)

Aortic wall thick below cusps

122

Aortic stenosis/atresia supra-valvular

Aortical wall thick above cusps in ascending aorta

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