Other cardiovascular pathology (cardiovascular system 2) Flashcards
(31 cards)
Valvular Heart disease
What is stenosis?
What is incompetence (regurgitation)?
What are the problems with valve regurgitation?
What is functional regurgitation?
STENOSIS - failure of the valve to open completely -> impedes the forward flow of blood
INCOMPETENCE (REGURGITATION) - failure of the valve to close completely allows the reverse flow of blood PURE OR MIXED, SINGLE OR MULTIPLE VALVES
FUNCTIONAL REGURGITATION - valve becomes incompetent due to dilation of a ventricle
Clinical consequences of valvular heart disease depend on?
Rheumatic mitral stenosis can lead to?
Clinical consequences depend on: Which valve, degree of impairment, rate of its development, rate and quality of compensatory mechanisms
physiologically unimportant -> severe and rapidly fatal
rheumatic mitral stenosis -> acute aortic incompetence, secondary to destruction of valve cusp from infection
Valvular incompetence
Happens due to?
Intrinsic disease of the valve cusps or damage to or distortion of the supporting structures - aorta, mitral valve annulus, tendinous cords, papillary muscles, ventricular free wall
+/- underlying valve abnormality. ACUTE OR CHRONIC
Valvular stenosis occurs almost always due to?
Is it usually chronic or acute?
Almost ALWAYS has an underlying VALVE ABNORMALITY
Usually CHRONIC
VALVULAR CALCIFICATION
Where is it commonly seen in?
What problems does it cause?
Calcific aortic stenosis • Calcification of a congenitally bicuspid aortic valve • Mitral annular calcification
The heart valves are subjected to high repetitive mechanical stresses especially at hinge points of cusp / leaflet 1. 40 million cardiac cycles / year 2. Substantial tissue deformation at each cycle 3. Transvavlular pressure gradients - Aortic 120mmHg Mitral 80mmHg CUMULATIVE DAMAGE COMPLICATED BY DYSTROPHIC CALCIFICATION
Calcific aortic stenosis?
What age is it clinically apparent?
Calcification of bicuspid aortic valves occur at what age?
What are the common causes of the following diseases:
1) Mitral stenosis
2) Mitral Incompetence
3) Aortic stenosis
4) Aortic incompetence
MITRAL STENOSIS - Rheumatic heart disease
MITRAL INCOMPETENCE - Floppy mitral valve (myxomatous degeneration) (mitral valve prolapse)
AORTIC STENOSIS - Calcification of normal and congenitally bicuspid aortic valves
AORTIC INCOMPETENCE - Dilation of ascending aorta related to hypertension and age
FLOPPY MITRAL VALVE
- Common
- Most common form of valvular heart disease in industrialised world
- One or both mitral leaflets enlarged, hooded, redundant
-> prolapse back into LA during systole
- Usually incidental finding on examination - mitral valve prolapse
- Very rarely -> sudden death
RHEUMATIC FEVER
What is it?
It occurs few weeks after what type of infection?
what are the features of the disease?
Acute rhematoid heart disease can lead to what?
- Acute immunologically mediated multisystem inflammatory disease
- Occurs a few weeks after group A B-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 •Sydenham chorea - neurological disorder (purposeless movements
Acute rheumatic heart disease -> pancarditis
- Endocardium -> Vegetations
- Myocardium Inflammatory -> foci with ASCHOFF BODIES
- Pericardium -> Pericarditis
- Reactivation with subsequent pharyngeal infections -> cumulative damage
What are the major and minor criteria of the Johnes criteria which is used for diagnosis of rheumatoid disease?
Chronic rheumatic heart disease - what is the most important consequence
Is it the most common cause of mitral stenosis?
The most important consequence of rheumatic fever is
CHRONIC RHEUMATIC HEART DISEASE
Characterised by
• deforming fibrotic valvular disease (especially mitral stenosis) FISH MOUTH / BUTTON-HOLE STENOSES
leaflet thickening, commissural fusion and shortening, thickening and fusion of the chordae tendinae. can -> permanent dysfunction
- most frequent cause of mitral stenosis (99% of cases)
- End stage of organisation of acute inflammatory damage
Infective endocarditis
What is it
Is it mostly a virus or bacterial?
What predisposes it?
What is the difference between acute and subacute infective endocarditis
Serious infection • Colonisation / invasion of heart valves • Formation of friable bulky vegetations - composed of thrombotic debris and organsims • Often underlying tissue destrudtion • Most cases are BACTERIAL
Things which predispose it
Abnormal valve: Floppy mitral valve, degenerative calcific valvular stenosis, bicuspid aortic valve, artificial valve (vascular graft).
Host factors: Immunosuppresion - neutropaenia immunodeficiency therapeutic, diabetes, alcohol, intravenous drug abuse
What organism is commonly involved in infective endocarditis?
What organism is seen in infective endocarditis in IV drug users?
What infection is seen in prosthetic valves?
Morphology of infective endocarditis -> which valve is commonly affected. Which valve commonly affects IV drug users?
a-haemolytic streptococcus abnormal valve (50-60%) subacute
Staph aureus (skin) high virulence normal valve IV drug users
Mouth commensals most of rest
Staph epidermidis prosthetic valves
SEEDING OF BLOOD WITH MICROBES (BACTERAEMIA) Dental or surgical procedure, dirty needle, trivial injury
PROPHYLACTIC ANTIBIOTICS IN THOSE AT RISK
Aortic and mitral valve most commonly affected
Tricuspid valve in IV drug users
Bulky friable vegetations, May involve more than one valve
Complications of infective endocarditis?
Non bacterial thrombotic endocarditis.
When does it normally occur?
What are the types of artificial valves?
What are the complications?
2 TYPES 1. Mechanical 2. Bioprostheses - homograft chemically treated animal (porcine) valves
COMPLICATIONS
Thromboembolic - need long term anticoagulation
Infective endocarditis
Structural deterioration - esp bioprostheses
CARDIOMYOPATHY
What is it?
What causes it?
Causes
Inflammatory
Immunological
Systemic metabolic disorders
Muscular dystrophies
Genetic abnormalities of the cardiac myocytes: Cardiac energy metabolism, Structural and contractile proteins
Idiopathic
What is the most common cardiomypathy and what is the least?
What is it a definitive way to diagnose them?
- Dilated cardiomyopathy (DCM) 90%
- Hypertrophic cardiomyopathy (HCM / HOCM)
- Restrictive cardiomyopathy least common
Within each group: spectrum of severity, overlap of features between groups
Each pattern can be: idiopathic, specific identifiable cause, secondary to extramyocardial disease
Diagnosis - endomyocardial biopsies of right ventricle
DILATED CARDIOMYOPATHY
What is it characterised by?
What are the different causes and what is the most common cause?
Characterised by progressive: cardiac hypertrophy, dilation, contractile dysfunction -> congestive cardiac failure
Causes: Most IDIOPATHIC, Alcohol, Peripartum, Genetic (Ox Phos, beta ox FFA, dystrophin), Myocarditis, Haemochromatosis, Chronic anaemia, Drugs - (doxorubicin, adriamycin), Sarcoidosis
Gross: Heavy heart 2-3 x normal, Large flabby, Dilation of all chambers, Mural thrombi common -> Thromboemboli +/- secondary mitral / tricuspid regurgitation, Normal coronary arteries
Histology: Nonspecific, Hypertrophied fibres, attenuated / stretched fibres, interstitial and endocardial fibrosis
Any age (20-60), Slowly progressive CCF But can -> sudden compensated to decompensated functional state, EF 25% (normal 50-65%), 50% mortality in 2 years, Death: progressive CCF, Arrhythmia, Embolism, Treatment - Cardiac Transplant
HYPERTROPHIC CARDIOMYOPATHY
What is it characterised by?
What is the gross structure?
What is the histological findings?
Pathogenesis?
What 4 genes encode for contractile protein?
What are the clinical problems and clincal features?
Characterised by: Myocardial hypertrophy, Abnormal diastolic filling, 1/3 intermittent left ventricular outflow obstruction
Heavy muscular hypercontracting heart
GROSS Massive myocardial hypertrophy, No ventricular dilatation, Assymetric septal hypertrophy (10% symmetric)
Histology: extensive myocyte hypertrophy, myocyte disarray, interstitial fibrosis
50% Genetic 50% sporadic
Genetic Autosomal dominant with variable penetrance
Many different mutations in 4 genes that encode contractile proteins (sarcomeres)
- beta- myosin heavy chain 2. Cardiac troponin T 3. alpha- tropomyosin 4. Myosin-binding protein C
Basic abnormality = smaller chamber size + poor compliance = smaller stroke volume
Clinical Problems: Angina, Atrial fibrillation, Cardiac failure, Ventricular arrythmias, Sudden death
RESTRICTIVE CARDIOMYOPATHY
What problem does it cause
What is the most common causes?
How is it diagnosed?
What are the sizes of the ventricles and atria?
Primary: decrease ventricular compliance -> impaired ventricular filling
Causes 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
Normal sized ventricles, Normal sized ventricular chambers, Both atria dilated, Firm myocardium
Myocarditis
Inflammatory process of the myocardium which results in injury to the cardiac myocytes.
Causes:
Infections: esp viruses MOST COMMON
Immune: Post-viral, Post-streptococcal (rheumatic fever), SLE, Drug hypersensitivity (methyldopa, sulphonamides), Transplant rejection
Unknown: Sarcoidosis
What is this device?
PERICARDIAL DISEASE
What is the difference between pericardial effusiom, haemopericardium and purulent pericaditis.
What is a cardiac tamponade?
Where can haemopericardium come from?
What is pericarditis?
PERICARDIAL EFFUSION - fluid of variety of compositions eg transudate and exudate
HAEMOPERICARDIUM - blood
PURULENT PERICARDITIS - pus large and rapidly developing -> cardiac tamponade
eg haemopericardium from ruptured MI traumatic perforation ruptured aortic dissection
