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Clinical Pathology > Lecture 51 - Cardiovascular Pathology 3 > Flashcards

Lecture 51 - Cardiovascular Pathology 3 Flashcards

1
Q

What is peripheral vascular disease?

A

Narrowing of blood vessels (usually arteries) that restricts blood flow

mostly int he legs but sometimes in the arms

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2
Q

edimeiology of peripheral vascular disease

A 
smokers - common
obese, diabetics,
hypertension
hypercholesterolaemia
Age - increase with age over 40
sex - men more likely and post menopausual women
genetic factors
developed world
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3
Q

Aetiology of peripheral vascular disease

A

Agents that can damage the endothelium - lead to atherosclerosis

  • smoking
  • hypertension
    diabetes
    hypercholesterolaemic conditions
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4
Q

pathogenesis of peripheral vascular disease

A

Causative agents damage the endothelium - trigger cellular events - lead to eccentric wall thickening by atheroma +/- thrombosis

+/- embolism - narrow lumen - reduced blood flow
- narrows artery - ischaemia - cell damage

all symptoms and consequences of PVD are related to restricted blood flow

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5
Q

clinical features of peripheral vascular disease

A

progressive disease leading to increasing levels of tissue hypoxia

narrowed lumen - decreased perfusion (pain, cold, pale peripheries, loss of function, eventually can be cell death gangrene)

  • ruptured plaque - sudden increase in narrowing or emboli from plaque or thrombus (actute onset peripheral pallor and pain and loss of function - more gangrene)
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6
Q

6 P’s of acute ischaemia

A

Pale, pulseless, painful, paralysed, paraesthetic, perishing cold

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7
Q

Clinical consequences of chronic peripheral vascular disease

A

Symptoms vary depending on severity
Critical limb ischaemia

Asymptomatic - found during a physical exam

intermittent claudication - symptomatic = complaint of pain upon exertion

Critical limb ischaemia - Rest pain, tissue loss

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8
Q

Definition of giant cell arteritis

A

Chronic granulomatous inflammation of large to small sixed arteries principally int he head

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9
Q

Aetiology of giant cell arteritis

A

exact cause not known but end stage problems are immune mediated

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10
Q

Epidemiology of giant cell arteritis

A

most common form of vasculitis

older individuals in US/Europe over 50

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11
Q

Pathogenesis of giant cell arteritis

A

Chronic granulomatous inflammation - narrows artery - ischaemia - cell damage

esp in head - temportal arteries - aka temporal arteritis
also vertebral and ophthalmic arteries
ophthalmic arterial involvement
-permanent blindness
- giant-cell arteritis is a medical emergency requiring prompt recognition and treatment - vital

  • also occurs in other vessels
  • eg aorta - giant-cell aortitis
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12
Q

Morphology of giant cell arteritis

A

Intimal thickening - reduces the lumenal diameter

Med. granulomatous inflammation - elastic lamina fragmentation

Multinucleated giant cells - 75% of adequately biopsied

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13
Q

Key clinical features of giant cell arteritis

A

Rare - less than age 50, vague symptoms eg. fatigue, weight loss,

Facial pain or headache

  • Superficial temporal artery (painful to palpation)
  • Jaw claudication
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14
Q

Diagnosis of giant cell arteritis

A

Biopsy and histologic

  • segmental disease
  • hence 2-3 cm length of artery
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15
Q

Treatment of giant cell arteritis

A

Corticosteroids is generally effective

Anti TNF therapy in refractory cases

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16
Q

What is endocarditis

A

Inflammation of the endocardium - lining of the heart inflamed, mainly involves the valves

Typical lesion = Vegetation on valves

2 main forms

Infective endocarditis
- Clinically important

Non-infective endocarditis - not covered

  • Nonbacterial thrombotic endocarditis (NBTE)
  • Endocarditis of SLE (Libman-Sacks Disease)
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17
Q

Epidemiology of endocarditis

A

Can occur in normal heart - with highly virulent organisms

more common in background of

Structural abnormality of valves or myocardium
-With organisms of lower virulence (>Sub-acute infective endocarditis = not so nasty

Including:
- RHD was major cause of

more common causes now

  • MV Prolapse
  • Valvular stenosis (calcification etc)
  • Artificial (prosthetic) valves
  • Unrepaired and repaired congenital defects
  • Bicuspid AV
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18
Q

Aetiology of endocarditis

A

Mouth - dental disease or procedures - alpha haemolytic viridans streptococci. 1/3 - 1/2 of cases - more in underdeveloped countries

gut and perineum - enterococci eg. E faecalis, can cause urinary sepsis

Bowel malignancy - strep. bovis (rare)

Prolonged indwelling vascular catheter - staph aureus and candida

Native and prosthetic valve endocarditis
Early - poor prognosis - occurring within 60 days of valve surgery and acquired in the theatre or soon in the theatre or soon thereafter perhaps n the intensive care unit

Late - occurring more than 60 days after valve surgery and presumed to have been acquired in the community

  • Strep viridans (50-70%)
  • Staph aureus (25%)
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19
Q

How does an infection get to the heart

A

Any route of bacteria into blood stream eg. dental abnormalities, IVDU, wounds, bowel cancer

  • Streptococcus viridans from the mouth
  • Endocarditis in native but damaged/ abnormal valves
  • 50-60% of cases

S. aureus from the skin
- 10-20% of cases overall esp. IVDU

Coagulase-negative staphylococci (e.g. epidermidis)
-Commonly infect prosthetic heart valves

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20
Q

Pathogenesis of infective endocarditis

A

Clinically serious infection

-colonization/invasion of heart valves or heart chamber endocardium by a microbe

Vegetations made of thrombus and organisms

  • Destroy underlying heart or vascular tissues (eg. aorta)
  • aneurysmal sacs
  • abscesses local and distant (emboli)
  • septic infarcts or mycotic aneurysms

Most cases bacterial
- Fungi/other classes can also cause

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21
Q

Clinical features of endocarditis

A

Fever

  • most consistent sign
  • rapidly developing fever, chills, weakness
  • can be slight or absent, particularly in the elderly

Non-specific symptoms

  • May be only presentation
  • Loss of weight/flu-like syndrome

Murmurs

  • 90% of patients with left-sided IE (infective endocarditis)
  • New valvular defect or represent a pre-existing abnormality
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22
Q

complications of infective endocarditis

A

immunologically mediated conditions - eg. glomerulonephritis

Clinical manifestations (micro-thromboemboli)
-splinter/sublngual haemorrhages
- Janeway lesions
Erythematous or haemorrhagic non-tended lesions on the palms or soles
-Osler’s nodes
subcutaneous nodules in the pulp of the digits
-Roth spots
Retinal haemorrhages in the eyes

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23
Q

Infective endocarditis symptoms

A

F - FEVER
R - ROTH SPOTS
O - OSLER’S NODES
M - MURMURS

J - JANEWAY LESIONS
A - ANAEMIA
N - NAIL (SPLINTER) HAEMORRHAGE
E - EMBOLI (SEPTIC)

24
Q

Rheumatic fever - definition

A

Acute, immunologically mediated, multi-system inflammatory disease

following group A - streptococcal pharyngitis

25
Q

Epidemiology of rheumatic fever

A

Rare in developed world because of improved diagnosis/treatment

  • 15 million in developing countries (Africa, Middle and Far East in particular)/ poor Western populations

Age - typically children 5-15

26
Q

Rheumatic fever aetiology

A

Group A Streptococcal pharyngitis

27
Q

Pathological features of rheumatic fever

A

veruccae = vegetations

Mitral valve changes are classical
- Virtually only cause of mitral stenosis
- Leaflet thickening
- Virtually always involved in chronic disease
MV only in most cases
Aortic valve in 25% of cases
Tricuspid valve /pulmonary valves - uncommon

  • Fibrous bridging of valvular commissures and calcification
    • FISH MOUTH or buttonhole stenoses
28
Q

Pathogenesis of rheumatic fever

A

Due to hypersensitivity reactions

  • Combined antibody and T- cell mediated response to self antigens in the heart

Group A strep (pharyngitis) - antibodies and T cells

  • which make cytokines that activate macrophages (e.g. Aschoff bodies)
  • Cross react with self protein in the heart
29
Q

Clinical features of rheumatic fever

A

Left atrium dilates - mural thrombi form - embolise

Right ventricular hypertrophy

30
Q

Pericarditis

A

Inflammation of the pericardial sac

31
Q

Epidemiology of Pericarditis

A

depends on cause

32
Q

Aetiology

A

Infections - viruses (Coxsackie B), bacteria, TB, fungi, parasites

Autoimmune

  • Rheumatic fever, SLE, Scleroderma, post-cardiotomy
  • Late post - MI = Dressler’s drug hypersensitivity

Miscellaneous

  • Post - MI (early), uraemia, cardiac surgery, neoplasia,
  • Trauma, radiation
33
Q

Pathogenesis of Pericarditis

A

Acute Pericarditis (inflamed)

  • Serous
  • Serofibrinous/ fibrinous
  • Purulent /suppurative
  • Haemorrhagic
  • Caseous

Chronic pericarditis (stuck down)

  • Adhesive
  • Adhesive mediastinopericarditis
  • Constrictive pericarditis
34
Q

Serous pericarditis

A

Inflammation causes clear ‘serous’ fluid accumulation

Caused by non-infectious aetiologies (generally)

  • inflammation in adjacent structures can cause pericardial reaction
  • Rarely by viral pericarditis (Coxsackie B / echovirus)

Autoimmune
- Rheumatic fever, SLE, scleroderma

Other
- Uraemia, neoplasia, radiation

35
Q

Serofibrinous pericarditis

A

Serous fluid and / or fibrinous exudate in pericardial sac

This is the most common form of pericarditis!

Common causes

  • Acute MI, Dressler’s syndrome
  • Uraemia, radiation, rheumatic fever, SLE, trauma, surgery

Features of fibrinous pericarditis (without fluid)

  • Dry, granular, roughened surface
  • More intense inflammatory response -> sero-fibrinous
36
Q

Purulent pericarditis

A

infections

Features of purulent / suppurative pericarditis
Red, granular, exudate i.e. pus (can be up to 500mls!)

Inflammation can extend causing mediastino-pericarditis

Outcome – complete resolution is rare
Organisation by scarring  restrictive pericarditis – serious!

37
Q

Haemorrhagic pericarditis

A

Blood mixed with serous (watery) or suppurative (pus) effusion
Common causes
Neoplasia (malignant cells in effusion)
Infections (inc TB)
Following cardiac surgery  cardiac tamponade

Caseous (cheesy) pericarditis
TB or fungal

38
Q

chronic pericarditis

A

Adhesive pericarditis / Constrictive pericarditis

39
Q

Adhesive pericarditis / Constrictive pericarditis

A

Fibrosis / stringy adhesions obliterates pericardial cavity

Heart can become encased in fibrous scar – limits cardiac function

Treated by surgery to remove ‘shell’ around heart

40
Q

Key Clinical features of Pericarditis

A 
Sharp central chest pain…characteristics
Exacerbated by : movement, respiration, laying flat
Relieved : sitting forwards
Radiating : shoulders / neck
Differentials : angina, pleurisy

Pericardial friction rub

Fever, leucocytosis, lymphocytosis, pericardial effusion

Complications – pericardial effusion / cardiac tamponade

41
Q

Cardiomyopathy

A

Literally means “heart muscle disease” and strictly speaking is of uncertain cause (but see later…)

4 main types

-Dilated
-Hypertrophic
-Restrictive
-Arrythmogenic right ventricular
cardiomyopathy (dysplasia)

42
Q

Epidemiology of cardiomyopathy

A

depends on subtypes

43
Q

Aetiology of cardiomyopathy

A

Unknown…

(tho’ there is a genetic component in many really)

(NB need exclusion of commoner causes of myocardial failure - hypertension, IHD, valvular and congenital HD)

44
Q

Pathogenesis of cardiomyopathy

A

Main ways the pathological abnormality causes signs and symptoms:

Heart Failure (abnormal muscle cannot cope with workload)

Emboli (It’s that Virchow’s Triad again…)

Arrhythmias (Disruption of electrical conduction pathways)

45
Q

Dilated cardiomyopathy

A

Progressive dilation  contractile (systolic) dysfunction
Heart enlarged, heavy, flabby (dilation of chambers)
Myocyte hypertrophy with fibrosis
Associations
Genetic (20 – 50% cases)
Autosomal dominant (mainly)
Cytoskeletal proteins gene mutation
Alcohol (10-20%) and other toxins
E.g. chemotherapy
Others
SLE, scleroderma, thiamine def., acromegaly, thyrotoxicosis, diabetes….

46
Q

Epidemiology and prognosis for cardiomyopathy

A

Any age but commonly 20 – 50
Slow progressive signs / symptoms of CCF
SoB, fatigue, and poor exertional capacity

5 year survival = ~ 25% (like the ejection fraction…)
Death due to CCF, arrhythmia / embolism (intra-cardiac thrombus)

Treatment
Cardiac transplantation
Long-term ventricular assist (can induce regression)

47
Q

Hypertrophic cardiomyopathy

A

Defined by myocardial hypertrophy
Thick-walled, heavy, poorly compliant left ventricular myocardium
Diastolic dysfunction with preserved systolic function
Intermittent ventricular outflow obstruction (1/3 cases)
ie Stiff ventricle that doesn’t fill properly

If LVH, no Hypertension, no Valve Disease - think of this

100% genetic (so much for unknown cause…)
Mutations sarcomeric proteins, Can be sporadic

48
Q

Hypertrophic cardiomyopathy - clinical features

A

↓Stroke volume
Impaired diastolic filling - reduced chamber size / compliance of hypertrophied left ventricle

Obstruction to the left ventricular outflow
25% of patients

Exertional dyspnoea due to above
Systolic ejection murmur
Ventricular outflow obstruction
Anterior mitral leaflet moves toward the ventricular septum during systole.

49
Q

Complications/treatment of hypertrophic cardiomyopathy

A

Complications
Atrial fibrillation
Mural thrombus formation  embolization / stroke
Cardiac failure
Ventricular arrhythmias
Sudden death, especially in some affected families
Most common causes of sudden death in athletes

Treatment
Decrease heart rate and contractility - β-adrenergic blockers.
Reduction of the mass of the septum, which relieves the outflow tract obstruction

50
Q

Restrictive cardiomyopathy

A

Rare

Primary disease in ventricular compliance
- Impaired ventricular filling during diastole

Idiopathic or secondary (infiltration)
-Fibrosis, amyloidosis, sarcoidosis, metastatic tumours or deposition of metabolites (inborn errors of metabolism)

Morphology
-Ventricles normal size / slightly enlarged
chambers normal
- Myocardium is firm and noncompliant

51
Q

Arrythmogenic right ventricular cardiomyopathy

A 
AKA arrhythmogenic R.V. dysplasia
Genetic disease (A.D.), ~1 in 5000
RV dilation / myocardial thinning
Fibrofatty replacement of RV
Disorder of cell-cell desmosomes
Exercise -> cells detach and die
Silent, syncope, chest pain, palpitations
Sudden cardiac death – young / exercise
52
Q

myocarditis

A

inflammation of myocardium

53
Q

epidemiology of myocarditis

A

Varies depends on cause

54
Q

Aetiology of myocarditis

A 
INFECTIONS
viruses
bacteria
fungi
protozoa
helminths
chlamydiae
rickettsiae
IMMUNE MEDIATED
post - viral
post - streptococcal
SLE
Drugs
transplant rejection

OTHERS
Sarcoidosis
Giant cell myocarditis

55
Q

Pathogenesis of myocarditis

A

Infection or inflammatory trigger 

cytokines, cytotoxic damage, damage myocytes 

myocytes +/or endothelium malfunction 

electrical problems / mechanical problems / clotting problems

56
Q

Clinical features of myocarditis

A 
Broad spectrum of changes
Asymptomatic
Chest pain
CHF
Arrhythmias
Sudden death

Clinical Pathology (16 decks)

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