Diseases of the Cardiovascular System (29) Flashcards
(122 cards)
1
Q
What’s the most common cause of death in women in UK?
A
CVD
Cancer
Resp disease
2
Q
What’s the most common cause of death in men in UK?
A
Cancer
CVD
CHD
Resp
3
Q
Ischaemic heart disease
A
Inadequate blood supply to the myocardium
4
Q
IHD is due to
A
Reduced coronary blood flow, almost always due to atheroma +/- thrombus, myocardial hypertrophy - systemic hypertension
5
Q
Pathogenesis
A
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
Q
Typical/stable angina
A
Fixed obstruction, predictable relationship to exertion
7
Q
Crescendo/unstable angina
A
Often due to plaque disruption, red flag symptom
8
Q
Variant/prinzmetal angina
A
Coronary artery spasm (Ca channel blockers)
9
Q
Acute coronary syndrome
A
Acute MI (+/- ST elevation), crescendo/unstable angina
10
Q
IHD syndromes
A
- Angina pectoris
- Acute coronary syndrome
- Sudden cardiac death
- Chronic ischaemic heart disease
11
Q
Acute ischaemia
A
Atheroma + acute thrombosis/haemorrhage, lipid rich plaques, transmural MI, thrombolysis, myocardial stunning (contractile abnormality)
12
Q
Diagnosis of acute ischaemia
A
Clinical, ECG, blood cardiac proteins
13
Q
Subendocardial MIs
A
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
Q
MI morphology
A
Normal
15
Q
MI morphology 1-2 days
A
Pale, oedema, yellow infarct, myocyte necrosis, neutrophils
16
Q
MI morphology 3-7 days
A
Yellow with haemorrhagic edge, myocyte necrosis, macrophages
17
Q
MI morphology 1-3 weeks
A
Pale, thin, red/gray granulation tissue then fibrosis
18
Q
MI morphology 3-6 weeks
A
Dense fibrous scar (collagen)
19
Q
Blood markers of cardiac myocyte damage
A
- Troponins T & I
- Creatine kinase MB
- Myoglobin
- Lactate dehydrogenase isoenzyme 1
- Aspartate transaminase
20
Q
Troponins T & I
A
- Detectable 2-3hrs-7 days, peaks 12 hours
- Raised post MI, P.E, heart failure and myocarditis
21
Q
Creatine kinase MB
A
- Detectable 2-3hrs-3 days, peaks 10-24 hours
- Not very specific - skeletal muscle damage
22
Q
Myoglobin
A
- Peaks at 2hr
- Released from damaged skeletal muscles
23
Q
Lactate dehydrogenase isoenzyme 1
A
Peaks at 3 days, detectable until 14 days
24
Q
Aspartate transaminase
A
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
