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Clinical Pathology > cardiovascular disease 3 > Flashcards

cardiovascular disease 3 Flashcards

1
Q

define endocarditis

A

Inflammation of the endocardium of the heart.

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2
Q

2 main forms of endocarditis

A

– Infective endocarditis (Clinically important).
– Non-infective endocarditis
(Nonbacterial thrombotic endocarditis (NBTE)), Endocarditis of SLE (Libman-Sacks Disease)

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3
Q

what is contained within vegetations of infective endocarditis

A

– Mixture of thrombotic debris and organisms

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4
Q

where do vegetations of endocarditis occur

A

Aorta, aneurysmal sacs, blood vessels, prosthetic valves

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5
Q

what type of pathogen causes most endocarditis- bacterial,viral or fungal.

A

bacterial, although some can be fungal.

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6
Q

acute endocarditis is caused by

A

highly virulent organisms

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7
Q

lesions produced by acute endocarditis are typically

A

– Necrotizing, ulcerative, destructive

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8
Q

what is the prognosis of acute endocarditis

A

poor.

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9
Q

subacute endocarditis

A

low virulence organism

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10
Q

lesions produced by chronic endocarditis are typically

A

less destructive

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11
Q

what is the prognosis of subacute endocardditis

A

cured with antibiotics

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12
Q

risk factors of endocarditis

A

most common causes- mitral valve prolapse, valvular stenosis, prosthetic valves, unprepared congenital defects, bicuspid AV.
cardiac, valvular problems, rheumatic heart disease.

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13
Q

how does infection get to the heart and cause endocarditis

A

Dental abnormalities, IVDU, wounds, bowel cancer.
streptococcus viridans from mouth
S aurues from skin
coagulase negative staphylococci- from prosthetic valves
Strep. bovis- endocarditis should prompt investigations for bowel cancer.

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14
Q

vegetation from acute infective endocarditis have what features

A
  • Friable (soft), bulky, potentially destructive.
  • Single, multiple and often more than one valve.
  • Can erode— myocardium ——abscess (ring abscess).
  • Emboli contain large numbers of virulent organisms
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15
Q

clinical features of infective endocarditis

A

fever- rapidly developing, fever, chills and weakness.
weight loss
murmus- common in left sided endocarditis

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16
Q

complications of infective endocarditis

A

– Immunologically mediated conditions e.g. glomerulonephritis.
(micro-thromboemboli)
– Splinter(in nails) / subungual hemorrhages
– Janeway lesions- • Erythematous or haemorrhagic non-tender 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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17
Q

what does the pneumonic FROMJANE stand for in terms of the clinical presentation of infective endocarditis.

A
  • F – Fever
  • R – Roth spots
  • O – Osler’s nodes
  • M – Murmurs
  • J – Janeway Lesions
  • A – Anaemia
  • N – Nail (splinter) haemorrhage
  • E – Emboli (septic)
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18
Q

what are the 2 types of non-infective endocarditis

A

NBTE- non bacterial thrombolytic endocarditis

Libman sacks endocarditis

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19
Q

what is non bacterial thrombolytic endocarditis aka

A

marantic endocarditis

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20
Q

what group of patients is non bacterial thrombolytics endocarditis prevelanent in

A

chronically ill

people who are hypercoaguable

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21
Q

characteristics of vegetations in non-bacterial, thrombolytic endocarditis

A

small, non destructive, sterol thrombi on valve leaflets
single or multiple.
not invasive/no inflammatory reaction reaction- minimal local effect.
systemic emboli (infects into brain and heart)

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22
Q

what structures do non-bacterial, thrombolytic endocarditis affect

A

AV valves, chordae, valvular endocardium or mural endocardium of atria and ventricles.

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23
Q

what mediates rheumatic heart disease

A

immune system following group streptococcal infection.

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24
Q

what presentation is a diagnostic factor if rheumatic fever

A

Aschoff bodies- diagnostic of RHD.
distinctive cardiac leisons
foci- T cells, plasma cells and macrophages.
Can be found in all 3 cardiac layers-pancarditis

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25
Q

name of vegetations in rheumatic heart disease

A

veruccae.

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26
Q

which valve is typically affected in rheumatic heart disease and how is it affected

A

mitral valve stenosis
leaflet thickening
virtually always involved in chronic disease.

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27
Q

what name if given to the type of stenosis which occurs in rheumatic heart disease

A

fish mouth, buttonhole.

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28
Q

what is the aetiology of rheumatic fever/RHD

A

hypersensitivity reaction combines antibody and t cell mediated response.
– Antibodies directed against the M proteins of streptococci
– Cross-react with self antigens in the heart
– CD4+ T cells specific for streptococcal peptides
– Produce cytokines that activate macrophages (e.g. Aschoff bodies)

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29
Q

what criteria is used to diagnose a patient with rheumatic heart disease

A

Jones criteria.
Required criteria for diagnosis- 2 major
Required criteria- 1 major and 2 minor.

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30
Q

define pericarditis

A

inflammation of the pericardial sac

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31
Q

main causes of pericarditis

A

infections- coxscakie virus
bacterial- TB, fungi, parasites

Immunologically mediated processes- Rheumatic fever, SLE, scleroderma, post-cardiotomy, Late post-MI = Dressler’s, drug hypersensitivity

miscellaneous conditions
Post-MI (early), uraemia, cardiac surgery, neoplasia, Trauma, radiation

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32
Q

4 different forms of pericarditis

A

acute, chronic, serous, serofibrinous.

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33
Q

what are the typical components which define acute pericarditis

A

serous, serofibrinos/fibronous, purulent, haemorrhagic, caseous.

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34
Q

what are the typical components which define chronic pericarditis

A

adheisve
adhesive mediastinopericarditus.
constructive mediastinopericarditus.

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35
Q

what does serous pericarditis produce

A

inflammtion causes serous fluid accumulation.

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36
Q

what causes serous pericarditis

A

Caused by non-infectious aetiologies (generally)
– Inflammation in adjacent structures can cause pericardial reaction
– Rarely by viral pericarditis (Coxsackie B / echovirus)

Immunologically mediated processes
– Rheumatic fever, SLE, scleroderma

Miscellaneous conditions
– Uraemia, neoplasia, radiation

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37
Q

which is the most common type of pericarditis

A

Serofibrinous/ fibrinous pericarditis.

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38
Q

common causes of serofibrinous/ fibrinous pericarditis.

A

dresslers syndrome, acute MI, uraemia, radiation, rheumatic fever, SLE, trauma and surgey.

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39
Q

features of serofibrinous/ fibrinous pericarditis.

A

dry granular, roughend surface, intense inflammatory response.

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40
Q

define dressle’s syndrome

A

secondary pericarditis

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41
Q

what clinical triad does dressler’s syndrome involve.

A

fever, pleuritic chest pain, pericardial effusion.

42
Q

what causes dresseler’s syndrome

A

Autoimmune reaction to antigens released following myocardial infarction

43
Q

how long post MI does dresser’s syndrome develop

A

delay of weeks

44
Q

causes of supparative pericarditis

A

infections.

45
Q

Features of purulent / suppurative pericarditis

A

Red, granular, exudate i.e. pus (can be unto 500mls)

46
Q

inflammation caused by supportive pericarditis can extend to where

A

mediastinal pericarditis.

47
Q

what is a consequence of supportive pericarditis

A

restrictive pericarditis.

48
Q

define haemorrhagic pericarditis

A

blood mixed with serous or supportive effusion

49
Q

common causes of haemorrhagic pericariditis

A

Neoplasia (malignant cells in effusion)

Infections (inc TB)Following cardiac surgery —- cardiac tamponade

50
Q

common causes of caseous pericarditis

A

TB or fungal

51
Q

3 main types of chronic pericadrditis.

A

adhesive pericarditis
adhesive mediastinopericarditis
constructive pericarditis.

52
Q

what are the features of adhesive pericardiatis.

A

glued together

fibrosis/stringy adhesions obliterates the pericardial cavity

53
Q

what are the features of adhesive mediastinopericarditis

A

obliterated pericardial activity with adherence to surrounding structures.

54
Q

what are the features of constructive pericarditis

A

Heart encased in fibrous scar – limits cardiac function

55
Q

clinical features of pericarditis

A

sharp central chest pain
percadial frictiona rub
Fever, leucocytosis, lymphocytosis, pericardial effusion

56
Q

what factors exacerbate pericarditis chest pains

A

exacerbated by: movement, respiration, laying flat

57
Q

what factors relieve pericarditis chest pains

A

sitting forwards

58
Q

where does pericardial chest pain radiate to

A

shoulders and neck

59
Q

2 complications of pericarditis

A

pleural effusion and cardiac tamponade

60
Q

4 types of cardiomyopathy

A

dilated, hypertrophic, restrictive, arrythmogenic right ventricular cardiomyopathy.

61
Q

pathogenesis of dilated cardiomyopathy

A

progressive dilation-contractile dysfunction, heart is enlarged, heavy flabby and cannot contract, myocyte hypertrophy.

62
Q

causes of dilated cardiomyopathy

A

genetic- autosomal dominate
alcohol and other toxins- chemotherapy.
SLE, scleroderma, thiamine def., acromegaly, thyrotoxicosis, diabetes

63
Q

clinical features of dilated cardiomyopathy

A

at any age
slow progressive signs
fatigue and poor exertional capacity

64
Q

treatment for dilated cardiomyopathy

A

cardiac transplant

long -term ventricular assistance.

65
Q

what defines hypertrophic cardiomyopathy

A

myocardial hypertrophy.

66
Q

what causes a poorly compliant left ventricular myocardium.

A
  • Diastolic dysfunction with preserved systolic function

* Intermittent ventricular outflow obstruction (1/3 cases)

67
Q

clinical features of hypertrophic cardiomyopathy

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.

68
Q

complications of hypertophic cardiomyopathy

A

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

69
Q

treatment for hypertophic cardiomyopathy

A

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

70
Q

in restrictive cardiomyopathy what is the primary cause.

A

decrease in ventricular compliance.

– Impaired ventricular filling during diastole- decreased ventricular compliance so it cannot fill

71
Q

in restrictive cardiomyopathy what is the secondary cause.

A

– Fibrosis, amyloidosis, sarcoidosis, metastatic tumours or deposition of metabolites (inborn errors of metabolism)

72
Q

define arrythmogenic right ventricular cardiomyopathy

A

defect in cell adhesion which falls apart when we exercise.

73
Q

pathogenesis of arrythmogenic right ventricular cardiomyopathy

A
  • RV dilation / myocardial thinning
  • Fibrofatty replacement of RV
  • Disorder of cell-cell desmosomes.
  • Exercise causes the cells detach and die
74
Q

symptoms of arrythmogenic right ventricular cardiomyopathy

A

• Silent, syncope, chest pain, palpitations

75
Q

define myocarditis

A

• Infective (or inflammatory) process àmyocardial injury

76
Q

causes of myocarditis

A

• Infections - most cases

– Coxsackie A&B viruses most common

77
Q

primary cause of arrythmogenic right ventricular cardiomyopathy

A

genetics

78
Q

clinical features of myocarditis

A

– Asymptomatic
– Heart failure, arrhythmias and sudden death
– Non-specific symptoms - fatigue, dyspnea, palpitations, precordial discomfort, and fever
– Can mimic acute MI

79
Q

define vaculitis

A

• Inflammation of the vessel walls

80
Q

what is the most common form of vasculitis

A

giant cell arteritis

81
Q

pathology of giant cell arteritis

A

– Chronic granulomatous inflammation
– Large to medium-sized arteries
– Esp. in the head (e.g. temporal arteries – AKA temporal arteritis)
– Also vertebral and ophthalmic arteries

82
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
83
Q

clinical features of giant cell arteritis

A

• Rare

84
Q

treatment of giant cell arteritis

A

– Corticosteroids is generally effective
– anti-TNF therapy in refractory cases
Aneurysms

85
Q

define aneurysm

A

Localised, permanent, abnormal dilatations of a blood vessel

86
Q

what classifies a anyrsysm

A

shape- saccular berry, fusiform

87
Q

what are the different types of anyersyms.

A 
atherosclerotic
dissecting
 berry
 microanyersym
 syphilitic
mycotic and false
88
Q

what is the most common for of anyersysm in the elderly

A

atherosclerotic

89
Q

what are the pain complications of an anyersym

A

– Rupture causing retroperitoneal haemorrhage

– Embolisation causing limb ischaemia.

90
Q

define dissecting aneurysms

A

tear in the wall, blood tracks between intimal and medial layers,

91
Q

symptoms of a dissecting anyersysm

A

– Tearing pain in chest radiating to upper left shoulder

92
Q

define berry anyersym

A
  • Small, saccular lesions that develop in the Circle of Willis
  • Develop at sites of medial weakness at arterial bifurcations
93
Q

what does rupture of a berry anyeursym cause

A

subarachnoid haemorrhage

94
Q

what does micro and syphilitic aneurysms cause

A 
intracerebral haemorrhage
(stroke)
95
Q

where do charcot-bouchard aneurysms occur

A

intracerebral capillaries in hypertensive disease.

96
Q

define mycotic anyersyms

A

weakening of the arterial wall secondary to bacterial and fungal infections.

97
Q

what infection is mostly likely going to cause mycotic anyersyms

A

sub acute endocarditis

98
Q

which arteries are commonly affected in mycotic anyersym

A

AAA

cerebral arteries

99
Q

define false anyeursym

A

Blood filled space around a vessel, usually following traumatic rupture or perforating injury

100
Q

the puncture of which artery commonly presents with a false aneurysm

A

femoral artery

101
Q

Peripheral vascular disease can lead to what major consequence

A

limb ischaemia.

102
Q

what 6 P’s define ischaemia

A

pale, pulseless, painful, paralysed, paraesethtic, perishingly cold.

Clinical Pathology (45 decks)

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