Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Clinical Pathology > Diseases of the Cardiovascular System (29) > Flashcards

Diseases of the Cardiovascular System (29) Flashcards

1
Q

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

A

CVD
Cancer
Resp disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

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

A

Cancer
CVD
CHD
Resp

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Ischaemic heart disease

A

Inadequate blood supply to the myocardium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

IHD is due to

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Typical/stable angina

A

Fixed obstruction, predictable relationship to exertion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Crescendo/unstable angina

A

Often due to plaque disruption, red flag symptom

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Variant/prinzmetal angina

A

Coronary artery spasm (Ca channel blockers)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Acute coronary syndrome

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

IHD syndromes

A
  • Angina pectoris
  • Acute coronary syndrome
  • Sudden cardiac death
  • Chronic ischaemic heart disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Acute ischaemia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Diagnosis of acute ischaemia

A

Clinical, ECG, blood cardiac proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

MI morphology

A

Normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

MI morphology 1-2 days

A

Pale, oedema, yellow infarct, myocyte necrosis, neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

MI morphology 3-7 days

A

Yellow with haemorrhagic edge, myocyte necrosis, macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

MI morphology 1-3 weeks

A

Pale, thin, red/gray granulation tissue then fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

MI morphology 3-6 weeks

A

Dense fibrous scar (collagen)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Blood markers of cardiac myocyte damage

A
  • Troponins T & I
  • Creatine kinase MB
  • Myoglobin
  • Lactate dehydrogenase isoenzyme 1
  • Aspartate transaminase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Troponins T & I

A
  • Detectable 2-3hrs-7 days, peaks 12 hours

- Raised post MI, P.E, heart failure and myocarditis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Creatine kinase MB

A
  • Detectable 2-3hrs-3 days, peaks 10-24 hours

- Not very specific - skeletal muscle damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Myoglobin

A
  • Peaks at 2hr

- Released from damaged skeletal muscles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Lactate dehydrogenase isoenzyme 1

A

Peaks at 3 days, detectable until 14 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Aspartate transaminase

A

Present in liver - not v.useful

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Which is most useful marker of cardiac myocyte damage?

A

Troponins T & I

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Prognosis of MI

A

20% 1-2hr mortality - sudden cardiac death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Complications of MI (80-90%)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Common MI complications

A

Ventricular fibrillation, LV failure, DVT and PE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Chronic IHD

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Familial hypercholesterolaemia

A

Mutations in LDL receptor gene/apolipoprotein B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Familial hypercholesterolaemia heterozygotes

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Familial hypercholesterolaemia heterozygotes treatment

A

Statins (hydroxymethyglutaryl CoA reductase inhibitors)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Familial hypercholesterolaemia homozygotes treatment

A

More complex and less effective

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Blood pressure is physiologically regulated to

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Hypertension

A

140/90 mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What controls BP

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Renin

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Angiotensin 2

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Alodsterone

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Renal artery stenosis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Coarctation of aorta

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Treatment of coarctation of aorta

A

Surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Conn’s syndrome

A

Excess aldosterone secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Conn’s syndrome due to

A

Adrenocortical adenoma, micronodular hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Conn’s syndrome causes

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Low potassium

A

Muscular weakness, cardiac arrhythmias, paraesthesia, metabolic alkalosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Diagnosis of Conn’s syndrome

A

CT scan of adrenal glands and metabolic abnormalities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Phaeochromocytoma

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Phaeochromocytoma symptoms

A

Pallor, headaches, sweating, nervousness, hypertension

50
Q

Phaeochromocytoma diagnosis

A

24hr urine collection for adrenaline metabolites

51
Q

Cushing’s syndrome

A

Any steroid, caused by any source

52
Q

Cushing’s disease cause

A
  • Adrenocortical neoplasm (adenoma)
  • Pituitary adenoma
  • Paraneoplastic effect of other neoplasms producing adrenocorticotrophic hormone stimulates zona fasciculata cells on adrenal cortex
53
Q

Cushing’s disease

A

Overproduction of cortisol by adrenal cortex

54
Q

Cortisol’s effect

A

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

55
Q

Hypertensive effect on heart

A

Hypertensive heart disease, LV hypertrophy without dilataion > sudden death

56
Q

Hypertensive effect on kidney

A

Renal failure (arterial intimal fibroelastosis, hyaline arteriolosclerosis)

57
Q

Hypertensive effect on cerebrovascular

A

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

58
Q

Hypertensive crisis

A

BP >180/120 mmHg

Acute hypertensive encephalopathy, renal failure, retinal haemorrhages

59
Q

Acute hypertensive encephalopathy presentation

A

Confusion, vomiting, convulsions, raised ICP coma and death

60
Q

Pulmonary hypertension

A

Higher than normal pressure in pulmonary artery

61
Q

Pulmonary hypertension caused by

A
  • Loss of pulmonary vasculature
  • Secondary LV failure
  • Systemic to pulmonary artery shunting
  • Primary/idiopathic
    (Not high bp)
62
Q

Pulmonary hypertension leads to

A
  • Increased RV work
  • RV hypertrophy without dilatation
  • Dilatation and systemic venous congestion
  • RV failure
63
Q

Loss of pulmonary vasculature caused by

A
  • Chronic obstructive lung disease
  • Pulmonary interstitial fibrosis
  • Pulmonary emboli/thrombosis
  • Under ventilated alveoli
64
Q

CVD risk factors

A

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

65
Q

The Framingham Heart Study

A

Identifying risk factors for CVD (longitudinal population study)

66
Q

Other risk assessments

A
  • SCORE
  • QRISK2
  • Joint British Societies risk prediction charts
67
Q

Thomas Royle Dawber

A

First director of Framingham Heart Study

68
Q

Richard Doll

A

Link between smoking and lung cancer

69
Q

Austin Bradford Hill

A

Link between smoking and lung cancer

70
Q

James Black

A

Discovered B-blockers

71
Q

Akira Endo

A

Discovered statins in fungi

72
Q

Left sided failure leads to ….output

73
Q

LHF and kidneys

A

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

74
Q

Natriuretic peptides

A

Induces discharge of sodium through urine

75
Q

LHF and brain

A

Irritability, decreased attention, stupor > coma

76
Q

LHF and lungs (congestion)

A

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
Q

RHF causes

A

Left heart failure or cor pulmonale (enlarged RHS)

78
Q

RHF and liver and spleen

A

Passive congestion (nutmeg liver), congestive splenomegaly, ascites

79
Q

RHF and kidneys

A

Not enough blood - congested

80
Q

RHF and pleura/pericardium

A

Pleural and pericardial effusions and transudates

81
Q

RHF and peripheral tissues

82
Q

CHF autopsy

A

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

83
Q

Opening valvular HD

84
Q

Closing valvular HD

A

Regurgitation (incomplete/insufficiency)

85
Q

Aortic stenosis

A

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

86
Q

Mitral stenosis

A

Rheumatic HD

87
Q

Rheumatic HD

A

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

88
Q

Acute Rheumatic HD

A

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

89
Q

Chronic Rheumatic HD

A

Thickened valves, commisural fusion, thick, short chordae tendinae

90
Q

Mitral annular (ring) calcification

A

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

91
Q

Aortic regurgitation cause

A

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

92
Q

Mitral regurgitation cause

A

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

93
Q

Mitral Valve Prolapse (MVP)

A

Connective tissue weakening, ‘floppy’ valve

94
Q

MVP epidemiology

A

3% incidence, F>M

95
Q

MVP diagnosis

A

Echocardiogram

96
Q

MVP clinical

A

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

97
Q

MVP complications

A

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

98
Q

Congenital heart defects

A

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

99
Q

Incidence of malformations

A
  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
Q

Genetics of Congenital heart defects

A

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
Q

22q11.2 deletion

A

Conotruncus, brachial arch, face

102
Q

Environmental factors

A

Rubella and teratogens

103
Q

L > R shunt

A

No cyanosis, pulmonary hypertension (irreversible)

104
Q

Examples of L > R shunt

A

ASD, VSD, PDA, AVSD

105
Q

R > L shunt

A

Cyanosis, venous emboli become systemic (paradoxical)

106
Q

Obstructions

A

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

107
Q

Examples of R > L shunt

A

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

108
Q

ASD

A

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

109
Q

VSD

A

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

110
Q

Patent Ductal Arteriosus (PDA)

A

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

111
Q

Atrial ventricular septal defect (AVSD)

A

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

112
Q

Tetralogy of Fallot

A
  1. VSD
  2. RVH
  3. Overriding aorta
  4. Obstruction to RV outflow
113
Q

Transposition of great arteries (TGA)

A

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

114
Q

TGA shunt needed

A
  • PDA/PFO (65%)
  • VSD (35%)
  • RV>LV
115
Q

Truncus arteriosus

A

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

116
Q

Tricuspid atresia

A

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

117
Q

Total anomalous pulmonary venous connection (TAPVC)

A

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

118
Q

Coarctation of aorta

A

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

119
Q

Pulmonary stenosis/atresia

A

Hypoplastic RV with ASD

120
Q

Aortic stenosis/atresia valvular

A

Severe, hypoplastic LV > fatal

121
Q

Aortic stenosis/atresia sub-valvular (subaortic)

A

Aortic wall thick below cusps

122
Q

Aortic stenosis/atresia supra-valvular

A

Aortical wall thick above cusps in ascending aorta

Clinical Pathology (60 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions