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Y3 > Cardiovascualr System 2 > Flashcards

Cardiovascualr System 2 Flashcards

1
Q

What is stenosis

A

Failure of a valve to open completely

This impedes the forward flow of blood

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2
Q

What is incompetent regurgitation

A

Failure of the valve to close completely

Allows the reverse flow of blood

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3
Q

What can valvular heart disease affect

A

Pure or mixed regurg or stenosis

Single or multiple valves

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4
Q

What is functional regurgitation

A

Valve becomes incompetent due to dilation of a ventricle

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5
Q

What does the clinical consequences of valvular heart disease depend on

A

Which valve
Degree of impairment
Rate of it’s development
Rate and quality of compensatory mechanisms
Can go from being physiologically unimportant to severe and rapidly fatal

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6
Q

What causes valvular incompetence

A 
Intrinsic disease of the valve cusps or damage to or distortion of the supporting structures 
Aorta 
Mitral valve annulus
Tendinous cords 
Papillary muscle 
Ventricular free wall 
\+/- underlying valve abnormality 
ACUTE OR CHRONIC
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7
Q

Valvular stenosis
Acute or chronic

Is the valve abnormal in this

A

Usually chronic

Almost always has an underlying valve abnormality

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8
Q

Where can valvular calcification occur

A

Calcific aortic stenosis
Calcification of a congenitally bicuspid aortic valve
Mitral annular calcification

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9
Q

What are heart valves subjected to

A

High repetitive mechanical stress especially at hinge points of cusp/leaflet
40 million cycles a year
Substantial tissue deformation
Transvalvular pressure gradients - aortic 120mmHg mitral 80mmHg
Cumulative damage is complicated by dystrophic calcification

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10
Q

Causes and epidemiology of calcific aortic stenosis

A

Age related wear and tear calcification
Clinically apparent 70-80 yo
Calcification of bicuspid valve occurs earlier

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11
Q

Most common cause of mitral stenosis

A

Rheumatic heart disease

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12
Q

Most common cause of mitral incompetence

A

Floppy mitral valve
Myxomatous degeneration
Mitral valve prolapse

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13
Q

Most common cause of aortic stenosis

A

Calcification of normal and congenitally bicuspid aortic valves

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14
Q

Most common cause of aortic incompetence

A

Dilation of ascending aorta related to hypertension and age

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15
Q

Mitral regurgitation facts

A

Most common form of valvular heart disease in the industrialised world
One or both mitral leaflets enlarged, hooded, redundant so prolapsed back into atrium during systole
Usually incidental finding on examination - mitral valve prolapse
Very rarely - sudden death

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16
Q

What is rheumatic fever

A

Acute immunologically mediated multisystem inflammatory disease
Occurs a few weeks after group A beta haemolytic streptococcal pharyngitis
Thought to be a hypersensitivity reaction induced by group A streptococci
Features:
Migratory polyarthritis of large joints
Carditis
Subcutaneous nodules
Skin rash
Syndenham chorea - neurological disorder (purposeless movements)

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17
Q

What is rheumatic heart disease

A 
Acute leads to pancarditis 
Endocardium --> vegetations
Myocardium --> Aschoff bodies 
Pericardium --> pericarditis 
Reactivation with subsequent pharyngeal infections 
--> cumulative damage
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18
Q

What is the most important complication of rheumatic fever

A

Chronic rheumatic heart disease
Characterised by
Deforming fibrotic valvular disease esp mitral stenosis
Fish mouth/button hole stenosis
Leaflet thickening, commissural fusion and shortening, thickening and fusion of chordea tendinea
Can cause permanent dysfunction
Most frequent cause of mitral stenosis
End stage of organisation of acute inflammatory damage

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19
Q

What is infective endocarditis

A

Serious infection
Colonisation/ invasion of the heart valves
Formation of friable bulky vegetations - composed of thrombotic debris and organisms
Often underlying tissue destruction
Most cases are BACTERIAL

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20
Q

Infective endocarditis types

A

Acute and subacute.

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21
Q

Characteristics of acute infective endocarditis

A 
High virulence 
Valve previously normal
Acute onset 
50% mortality days to weeks
Lesion is necrotising, ulcerative and invasive
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22
Q

Characteristics of subacute infective endocarditis

A

Low virulence
Insidious onset
Most recover weeks to months
Less destructive

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23
Q

What causes a predisposition to infective endocarditis

A 
Abnormal valve - 
Floppy mitral valve 
Degenerative calcific valvular stenosis 
Bicuspid aortic valve 
Artificial valve 
(Vascular graft) 
Host factors - 
Immunosuppression - neutropenia, immunodeficiency, therapeutic

Diabetes
Alcohol
IV drug use

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24
Q

What are the organisms involved in infective endocarditis

A

Alpha-haemolytic strep - abnormal valve 50-60%, subacute
Staph aureus (skin) high virulence, normal valve, IV drug users
Mouth commensals - most of rest
Staph epidermidis - prosthetic valves

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25
Q

How does the person get infected

A

Dental or surgical procedure
Dirty needle
Trivial injury

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26
Q

What should be done for those at risk

A

Prophylactic antibiotics

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27
Q

Morphology of infective endocarditis

A

Aortic and mitral valve most commonly affected
Tricuspid valve in IV drug users
Bulky friable vegetation
May involve more this one valve

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28
Q

Complications of infective endocarditis

A 
Myocardial abscess 
Valve rupture/perforation 
Systemic emboli- L sided body -kidney 
R sided - lungs 
Septic emboli
Immune complexes
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29
Q

What is non bacterial thrombotic endocarditis

A 
Deposition of fibrin/platelet thrombi on valve leaflets -SMALL 
Occur on either side of the heart 
Occurs on a previously normal valve 
Sterile
Non-destructive
Clinical importance = emboli
Occurs in hypercoagulable state -
Disseminated intravascular coagulation
Cancer sepsis
30
Q

What are the types of artificial valves

A

Mechanical
Bioprostheses
- homografts
- chemically treated animal (porcine) valves

31
Q

Complications of artificial valves

A

Thromboembolic - need long term coagulation
Infective endocarditis
Structural deterioration - esp bioprostheses

32
Q

What is a cardiomyopathy

A

Heart disease resulting from a primary abnormality in the myocardium

33
Q

What are the causes of a cardiomyopathy

A 
Inflammatory 
Immunological
Systemic metabolic disorders
Muscular dystrophies 
Genetic abnormalities of the cardiac myocytes 
- cardiac energy metabolism
- structural and contractile proteins
Idiopathic
34
Q

What are the 3 clinical pictures of cardiomyopathy

A

Dilated cardiomyopathy DCM 90%
Hypertrophic cardiomyopathy HCM
Restrictive cardiomyopathy least common
Within each group - spectrum of diversity and overlap of features between groups
Each pattern can be idiopathic , specific identifiable cause
Or secondary to extramyocardial disease
Diagnoses - endomyocardial biopsies of RV

35
Q

What is dilated cardiomyopathy characterised by

A 
Progressive -
Cardiac hypertrophy 
Dilation 
Contractile Dysfunction 
Leads to congestive cardiac failure
36
Q

Causes of dilated cardiomyopathy

A 
Most idiopathic 
Alcohol
Peripartum
Genetic (ox phos, beta ox FFA, dystrophin) 
Myocarditis 
Haemochromatosis
Chronic anaemia
Drugs - doxorubicin, adriamycin
Sarcoidosis
37
Q

What is the morphology of dilated cardiomyopathy

A 
Gross 
Heavy heart 2-3x normal
Large flabby
Dilation in all chambers
Mural thrombi common - thromboemboli
\+/- secondary mitral/tricuspid regurg
Normal coronary arteries
Histology - 
Non specific 
Hypertrophied fibres
Attentuated/ stretched fibres 
Interstitial and endocardial fibrosis
38
Q

Clinical features of dilated cardiomyopathy

A 
any age 20-60
Slowly progressive CCF 
But can be sudden compensated --> decompensated functional state 
EF 25% 
50% mortality in 2 years 
Death - progressive CCF 
- arrhythmia
Embolism
Treatment cardiac transplant
39
Q

What is hypertrophic cardiomyopathy characterised by

A

Myocardial hypertrophy
Abnormal diastolic filling
1/3 intermittent left ventricular outflow obstruction
Heavy muscular hyper contracting heart

40
Q

What is the gross morphology of hypertrophic cardiomyopathy

A

Massive myocardial hypertrophy
No ventricular disease
Asymmetric septal hypertrophy (10% symmetric)

41
Q

What is the histology of hypertrophic cardiomyopathy

A

Extensive myocyte hypertrophy
Myocyte disarray
Interstitial fibrosis

42
Q

What is the pathogenesis of hypertrophic cardiomyopathy

A 
50% genetic
50% sporadic 
Genetic autosomal dominant with variable penetrance
Many difference mutations in 4 genes that encode contractile proteins (sarcomeres) 
1) B- myosin heavy chain
2) cardiac troponin T 
3) alpha - tropomyosin
4) myosin binding protein C
43
Q

Clinical features of hypertrophic cardiomyopathy

A

Basic abnormality - Dec chamber size + poor compliance + Dec stroke volume

Clinical problems 
Angina
AF
Cardiac failure
Ventricular arrythmias
Sudden death
44
Q

What is restrictive cardiomyopathy

A

Primary Dec in ventricular compliance -> impaired ventricular filling

45
Q

What are the causes of restrictive cardiomyopathy

A

Idiopathic
Radiation fibrosis
Amyloidosis
Sarcoidosis
Metastatic tumour
Products of inborn errors of metabolism
Endomyocardial fibrosis (children in tropical areas)
Endocardial fibroelastosis (young children)
Many of these can be diagnosed by endomyocardial biopsy

46
Q

Features of restrictive cardiomyopathy

A

Normal sized ventricles
Normal sized ventricular chambers
Both atria dilated
Firm myocardium

47
Q

What is myocarditis

A

Inflammatory process of the myocardium which results in injury to the cardiac myocytes

48
Q

Causes of myocarditis

A

Infection - esp viruses most common
Immune - post viral, post strep (rheumatic fever), SLE, drug hypersensitivity, transplant rejection
Unknown sarcoidosis

49
Q

Clinical features of myocarditis

A

Asymptomatic could lead to dilated cardiac myopathy years later
Or could lead to arrythmias, acute heart failure, sudden death

50
Q

Types of Pericardial disease

A

Pericardial effusion- fluid variety of compositions e.g. Transudate and exudate
Haemopericardium- blood
Purulent pericarditis - pus

51
Q

What is pericardial disease called when it is large and rapidly developing

A

Cardiac tamponade

52
Q

How can a haemopericardium form

A

Ruptured MI
Traumatic perforation
Ruptured aortic dissection

53
Q

What is pericarditis

A

Pericardial inflammation

Secondary to cardiac disease , thoracic or systemic disorders, or metastasis from distant site

54
Q

Causes of pericarditis

A 
Infection 
Virus
Bacteria
TB
Fungi
Immune mediated : 
Rheumatic fever
SLE
Scleroderma
Post MI dressier syndrome
Drug hypersensitivity 
Miscellaneous: 
MI
Uraemia
Post cardiac surgery.
Neoplasia
Trauma
Radiation
55
Q

What are the types of pericarditis

A 
Serous
Fibrinous
Purulent/suppurative
Haemorrhaging
Caseous
56
Q

What are the outcomes of pericarditis

A

Reabsorbed
Resolve
Organise -> obliterate pericardial space
+/- constructive pericarditis = heart is surrounded by dense fibrous scar that limits diastolic expansion of the heart and restricts cardiac output

57
Q

What is a neoplasm of the heart called and how common are they

A

Myxoma
Rare
5% of people dying from cancer
Most commonly a primary tumour

58
Q

Where is the most likely location of a myxoma

A

90% are located in the atria -most left

Called an atrial myxoma

59
Q

What is the gross morphology and what problems can it cause

A

Sessile or pedunculated

Cause
Half valve obstruction
Injury to the valve
Embolisation

60
Q

What is congenital heart disease

A

Abnormalities of the heart or great vessels present at birth

61
Q

What are the 3 main categories of congenital heart disease

A

1) left to right shunt
2) right to left shunt
3) obstructions

62
Q

What is a shunt

A

Abnormal connection between chambers or blood vessels

Blood flows from high to low pressure

63
Q

What is a right to left shunt and what are the consequences of this

A

Blood shunted from the pulmonary to the systemic circulation
Therefore the blood is less oxygenated -> cyanosis
Cyanosis congenital heart disease

64
Q

Conditions associated with right to left shunts

A

Tetralogy of fallot - most common
Transposition of the the great arteries
Persistent truncus arteriosus
Tricuspid atresia
Total anomalous pulmonary venous connection
Can get paradoxical embolus
Veins bypass lungs to systemic circulation

65
Q

What is a left to right shunt

A

Blood shunted from systemic to pulmonary army circulation

66
Q

Consequences of a left to right shunt

A

Increased pulmonary blood flow
-> pulmonary hypertension.
Reversible initially but need early treatment
With time -> reversal of shunt (high to low pressure)
-> late cyanosis (eisenmengers syndrome)
ASD
VSD- most common
PDA
AV septal defect

67
Q

What cause obstruction

A

Chamber
Valve blood
vessel
Abnormal narrowing

68
Q

What is vasculitis

A

Inflammation of wall of blood vessel

69
Q

Cause of vasculitis

A 
Immune :
Immune complex
Antineutrophil cytoplasmic antibodies
Direct antibody mediated 
Cell mediated
Inflammatory bowel disease
Paraneoplastic 
Infectious:
Unknown
Giant cell (temporal) arteritis-  most common
Takayasu arteritis 
Polyarteritis nodosum
70
Q

Consequences of vasculitis

A

affect specific blood vessels
Different patterns
Small vessel - skin - rash
Kidney glomerulonephritis

71
Q

Aetiology of vasculitis

A 
Infection - acute or chronic, bacterial viral fungal
Neoplasm benign, malignant 
Cardiovascular system
Haematological
Infiltrates e.g. Amyloid, sarcoid
Autoimmune
Drugs / chemicals
Unknown idiopathic

Y3 (22 decks)

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