Theme 9: Cardiovascular Pathology III Flashcards

1
Q

What is peripheral vascular disease?

A

atherosclerosis of arteries supplying legs (or arms), leading to narrowing of the vessel lumen and restriction of blood flow

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

Who gets peripheral vascular disease? (epidemiology)

A
  • age > 40
  • obesity
  • smokers
  • family history
  • men (or post-menopausal women)
  • dyslipidaemia
  • those with a PMH including: diabetes, hypercholesterolaemia, hypertension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Why is the prevalence of peripheral vascular disease higher in men?

A

oestrogen is a protective factor so it protects women until menopause

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

Explain the process of atherosclerosis (5 steps)

A
  1. Normal artery
  2. Endothelial dysfunction
  3. Fatty streak formation
  4. Stable (fibrous) plaque formation
  5. Unstable plaque formation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Explain the pathogenesis of peripheral vascular disease

A
  1. Gradual artherosclerosis (chronic) or plaque rupture/ thrombus formation (acute)
  2. Narrows lumen
  3. Reduced blood flow
  4. Ischaemia
  5. Tissue damage/ death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the clinical features of acute peripheral vascular disease?

A
6 Ps:
Pale
Pulseless
Painful
Paralysed
Paraesthetic (pins and needles)
Perishingly cold
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the clinical features of chronic peripheral vascular disease?

A

Asymptomatic: reduced pulses
Symptomatic: intermittent claudication
Critical limb ischaemia: rest pain and tissue loss

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

What is giant cell artertitis? (temporal arteritis)

A

A type of vasculitis affecting the large arteries in the head. Considered a medical emergency as it can lead to blindness

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

Who is at risk of giant cell arteritis?

A
  • older individuals, VERY rare if < 50 years old
  • US/europe
  • F > M
  • PMH of polymyalgia rheumatica
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What causes giant cell arteritis?

A
  • autoimmune damage to blood vessels

- type IV hypersensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Explain the pathogenesis of giant cell arteritis?

A
  1. Chronic granulomatous inflammation
  2. Thickens wall of artery
  3. Narrows lumen
  4. Reduced blood flow
  5. ischaemia
  6. tissue damage and death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the clinical features of giant cell arteritis?

A
  • fatigue
  • weight loss
  • fever
  • tender superficial temporal artery
  • jaw claudication (when eating)
  • blurred vision
  • blind ness
  • stroke
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is infective endocarditis?

A

infection and inflammation of the endocardium (lining of the heart), mainly involving valves

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

Who is at risk of IE?

A

Patients with:

  • structurally abnormal valves (rheumatic heart disease, congenital heart disease, age-related calcification)
  • foreign material in heart (ICD, prosthetic valves)
  • immunosuppression
  • bacteraemia - IVDU, long term IV catheters

but can occur in healthy patients with virulent organisms e.g S.aureus

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

What causes IE?

A
  1. Streptococcus - viridans / bovis
  2. Staphylococcus - aureus / epidermis
  3. Fungi - candida, aspergillus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How does IE make you ill?

A
  1. Damage to endothelium over valve
  2. Fibrin deposition
  3. Circulating bacteria colonise this fibrin
  4. Vegetations form
    then either
    -vegetations damage valves–> HR, murmur
    -bacteria in vegetations form local abscess –> AV block
    -bits of vegetations break off –> emboli/ infarction
    -immune response to infecction - fever, weight loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the clinical features of IE?

A
  • splenic infarct
  • splinter haemorrhage
  • jane way lesions
  • osler’s nodes
  • roth spots (retinal haemorrhage)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is pericarditis?

A

inflammation of the pericardial sac

19
Q

how are the different types of pericarditis classified?

A
  1. Acute (<6 months): then further classified based on the type of fluid surrounding the cells - serofibrinous, caseous, haemorrhagic and purulent
  2. Chronic (>6 months): constrictive
20
Q

What can cause pericarditis?

A
  1. Infections - viruses (coxsackie B), bacteria, TB, fungi, parasites
  2. Autoimmune- rheumatic fever, SLE, scleroderma, drug hypersensitivity, post-MI
  3. Miscellaneous - uraemia, radiation, neoplasia, trauma
21
Q

How does chronic pericarditis make you ill?

A
  • collagen deposition
  • fibrosis and thickening of pericardium
  • fibrosis reduces filling of heart
  • HF
22
Q

Acute pericarditis is further named based on what type of fluid surrounds the cells. What is it called if:

  1. Fibrin
  2. Neutrophils
  3. RBCs
  4. Caseous necrosis
A
  1. Serofibrinous
  2. Purulent
  3. haemorrhagic
  4. TB
23
Q

what are the clinical features of pericarditis?

A
  • central chest pain
  • pericardial friction rub
  • fever
  • pericardial effusion (may lead to tamponade)
  • HF
24
Q

What is myocarditis?

A

inflammation of the myocardium

25
What are the possible causes of myocarditis?
1. Infections viruses, bacteria, fungi, protozoa, helminths 2. Immune mediated - post group A streptococcus - SLE - drugs - rejection of heart transplant other: sarcoidosis
26
Explain the pathogenesis of myocarditis
- inflammation of myocardium - dysfunctional myocardium - electrical dysfunction = arrhythmias/ sudden death mechanical dysfunction = heart failure
27
What is the definition of rheumatic fever?
a rare complication of group A streptococcal pharyngitis that affects the heart (and other parts of the body)
28
Who gets rheumatic fever?
- children - developing countries (rare in UK now) - often have recent Hx of core throught
29
What causes rheumatic fever?
untreated group A streptococcus infection (streptococcus pyogenes) + immune cross reactivity
30
Explain the pathogenesis of rheumatic fever
1. group A strep infection 2. Antibodies made against M protein on the surface of the strep pyogenes bacteria 3. Antibodies also recognise proteins on surface of cells (self antigens) in the heart, skin, joints and CNS Type II hypersensitivity = antibody
31
What are the clinical features of rheumatic fever
Heart – endocarditis, myocarditis, pericarditis (pancarditis when all together) * Endocarditis – mitral valve stenosis “fish mouth” most common valve lesion, vegetations “verrucae” * Skin – subcutaneous nodules, erythema marginatum * Joints – arthritis * CNS – sydenhams chorea * General symptoms – fever, malaise
32
What is a cardiomyopathy and what are the 4 main types?
= heart muscle disease 1. Dilated 2. Hypertrophic 3. Restrictive 4. Arrythmogenic right ventricular cardiomyopathy
33
What is the epidemiology and aetiology of hypertrophic cardiomyopathy?
Epidemiology: all ages and genders Aetiology: Genetic
34
Explain the pathogenesis of hypertrophic cardiomyopathy
- impaired ventricular filling as wall of heart is v thick so chambers are small - +/- left ventricular outflow obstruction - relative ischaemia
35
What are the clinical features of hypertrophic cardiomyopathy?
- HR - arrhythmias and sudden death - mural thrombus formation +/- embolization - relative ischaemia --> coronary arteries are still same magnitude so cannot supply hypertrophic muscle
36
What is the epidemiology and aetiology of dilated cardiomyopathy?
``` Epidemiology: any age but commonly males aged 20-50 Aetiology: -often unknown -AD genetic -alcohol -catecholamines -pregnancy -haemachromatosis -infection ```
37
How does dilated cardiomyopathy make you ill?
dilated and thin walled ventricular chambers --> impaired ventricular pumping i.e decreased LVEF
38
What is the aetiology of restrictive cardiomyopathy?
- idiopathic - secondary: - amyloidosis - sarcoidosis - metastatic tumours - deposition of metabolites
39
How does restrictive cardiomyopathy make you ill?
impaired ventricular filling
40
What is the epidemiology and aetiology of arrythmogenic RV cardiomyopathy?
Epidemiology: most common in young males Aetiology: genetic AD 1 in 5000
41
Explain the pathogenesis of arrythmogenic RV cardiomyopathy
-RV myocyte adhesion impaired due to mutation in desmosome proteins --> cells detach --> fibrofatty tissue forms in attempt to repair damage --> interferes with muscle contraction and electrical conduction
42
What are the clinical features of RV Arrythmogenic cardiomyopathy??
- palpitations - syncope - HR - thrombus - arrhythmias and sudden cardiac death
43
Which valve does rheumatic fever tend to affect?
mitral valve --> and causes regurgitation more than stenosis