Cardiovascular System, vasculitis Flashcards
Effects of ageing on heart
- Lipofuscin deposition
- Basophilic degeneration of cardiac myocytes
- Lambl’s excrescences
- Increased amount of epicardial fat
Causes of left heart failure
- Hypertension
- Ischaemic heart disease
- Valvular heart disease
Effects of left heart failure
1. Lung: Heart failure cells in lungs 2. Kidney: Acute tubular necrosis 3. Brain: Hypoxic encephalopathy
Heart failure cells properties
Hemosiderin laden macrophages in lungs
Stained by Prussian blue
Common causes of right sided heart failure
M/C is left sided heart failure
M/C of isolated right heart failure is parenchymal lung disease
Effects of right sided heat failure
Organ congestion
- Liver: CVC, nutmeg liver
- Spleen: congestive splenomegaly, Gamna Gandy bodies
Ischaemic heart diseases
- Angina
- Myocardial infarction
- Chronic ischaemic heart disease
- Sudden cardiac death
Types of MI
1. Transmural: •Involves all 3 layers of heart •most common •ST elevation infarct 2. Subendocardial: •involves only subendocardial zone •also called NSTEMI
M/C vessels affected by MI in decreasing order
- Left anterior descending artery
- Right coronary artery
- Left circumflex artery
Myocardial response to hypoxia
Onset of ATP deletion: second Loss of contractility: <2 min ATP reduced to 50% of normal: 10 min ATP reduced to 10% of normal: 40 min Microvascular injury: 1 hr
Morphological changes in heat after MI in one day (dark mottling)
Within 1/2 hr, injury is reversible: • relaxation of myofibrils • glycogen loss • mitochondrial swelling After 1/2 hr to 4 hr: • mitochondrial amorphous densities • variable weakness of fibres at border In first day: • early neutrophilic infiltrate • contraction band necrosis For first 4 hours, no gross change
Morphological changes in heat after MI after one day upto 1 week (mottling with yellow)
In 1-3 days:
• coagulation necrosis and interstitial infiltrate of neutrophils
In 3-7 days:
• disintegration of dead myofibres, dying neutrophils
• early phagocytosis, macrophages
Morphological changes in heart after MI after one week
In 7-10 days, granulation tissue at margins
In 10-14 days:
• well established granulation tissue
• collagen deposition
More than 2 months, dense collagenous tissue
MI less than 12 hours old can be detected by
TTC stain
Triphenyl tetrazolium chloride
Brick red- normal tissue
Yellow- infarct tissue
ECG changes in MI
- ST segment elevation
- T wave inversion
- Pathological Q waves
Biochemical markers of MI
1. LDH: 5 iso enzymes Normal LDH2>LDH2 LDH flip 2. Myoglobin Earliest to rise, but non specific 3. Troponin I and T: Most specific marker is Troponin I 4. CL-MB
Complications of MI
A. Aneurysm
C. Contractile dysfunction
T. Thrombus
R. Rupture of ventricular free wall A. Arrhythmia: • within 1 hr- ventricular fibrillation • after 1 hr- supraventricular tachycardia P. Pericarditis- Dressler syndrome I. D.
Dressler’s syndrome
Post MI fibrosuppurative pericarditis
Occurs within 2-3 days of MI
Autoimmune reaction
Ischaemia reperfusion injury
After stenting or treatment of patient for MI, when symptoms get worsened ➡️ ischaemia reperfusion injury
Because of free radicals, complement activation
On H & E, contraction band necrosis
Types of carditis
- Pericarditis: acute or chronic
- Myocarditis
M/C helminthic cause: Trichinella spiralis
M/C virus: Coxsackie A & B, Herpes - Endocarditis
Pericarditis
1. Acute: exudation of fluid • serous- SLE, RHD • M/C: fibrinous- RHD, MI • pus in bacterial, viral infection • caseous exudate- TB • hemorrhagic exudate- malignancy 2. Chronic: can cause fibrosis Chronic constrictive pericarditis
Rheumatic fever and rheumatic heart disease
Immunologically mediated multi system disease
• Type II hypersensitivity
• age: 5-15 years
• usually occurs 2-3 weeks after sore throat with βhaemolytic streptococci (strain: 1,3,5,6,18)
• Streptococcal M protein cross reacts with glycoprotein in heart and joints- molecular mimicry
Most and least common valve affected by RHD
M/C valve: mitral valve
Least commonly affected valve: pulmonary valve
Common complications of acute and chronic RHD
Acute rheumatic fever: mitral regurgitation
Chronic rheumatic heart disease: mitral stenosis
Revised Jones criteria
For RHD Major criteria: 1. Migratory polyarthritis: non erosive 2. Subcutaneous nodules- painless, extensor surface of palms and soles 3. Erythema marginatum except face 4. Sydenham’s chorea 5. Pericarditis Minor criteria: 1. Fever, polyarthalgia 2. Increased ESR, CRP, prolonged PR interval
Morphology of heart in RHD
- Aschoff bodies (caterpillar cells/ Antischkow cells)
- Bread and butter pericarditis
- McCallum plaques/ subendocardial jets- posterior wall of atrium
- In chronic cases:
• fish mouth stenosis
• button hole stenosis - Vegetation
Aschoff bodies
Pathognomic for RHD
Consists of lymphocytes, plasma cross, giant cells, fibrinoid necrosis, collagen and caterpillar/ Antischkow cells
Vegetations of RHD
Small warty, verrucous vegetation
Along lines of closure of valve leaflets
Sterile
Acute infective endocarditis
Occurs in previously normal heat valves
Caused by Staphylococcus aureus
Subacute infective endocarditis
Occurs in previously damaged heat valves
Caused by Streptococci
Infective endocarditis
Diagnosis and features
For diagnosis: Duke’s criteria Blood culture taken Clinically: 1. Fever and weight loss 2. Splenomegaly: Roth’s spots- retinal haemorrhage Osler’s modes Janeway lesions- painful M/C infected valves: mitral and aortic valve
Vegetation of infective endocarditis
Large, bulky, irregular, friable, destructive, infected vegetations along lines of closure
NBTE - Non bacterial thrombotic endocarditis
Patients with debilitating diseases like metastatic carcinoma of pancreas, AML-M3
Small flat vegetations along lines of closure
Libman Sachs endocarditis
Seen in SLE patients
Small- medium sized, sterile vegetations
Seen on both sides of valve leaflets (most commonly on under-surface)
Types of cardiomyopathy
- Dilated cardiomyopathy
- Hypertrophic cardiomyopathy
- Restrictive cardiomyopathy
Causes of dilated cardiomyopathy
- Idiopathic (>50%)
- Alcohol
- Post partum
- Myocarditis
- Drugs like adriamycin
- Haemochromatosis
- Genetic mutation of titin
Dilatation of all four chambers of the heart is called as
Flabby hypocontracting heart
Classification of vasculitis
Chapel Hill classification 1. Large vessel 2. Medium vessel 3. Small vessel: • immune complex mediated • Pauci immune
Large vessel vasculitis
Giant cell arteritis
Takayasu arteritis
Medium vessel vasculitis
- Polyarteritis nodosa (PAN)
- Kawasaki disease
(anti-endothelial antibody) - Buerger’s disease
Small vessel vasculitis
Immune complex mediated: 1. Henoch schonlein purpura 2. Goodpasteur syndrome 3. SLE Pauci immune: 1. Wegener’s granulomatosis (c-ANCA) 2. Microscopic polyangitis (p-ANCA) 3. Churg Strauss syndrome (“”)
Antibodies involved in vasculitis
1. Anti Neutrophilic Cytoplasmic Antibodies • c-ANCA: cytoplasmic Anti-PR3 ANCA, proteinase-3 • p-ANCA: peri nuclear Anti-MPO ANCA, MPO granules • atypical ANCA 2. Anti glomerular basement membrane GBM antibody: In Goodpasteur’s syndrome 3. Anti endothelial antibody: In Kawasaki disease
Anti-MPO ANCA or p-ANCA is seen in
- Microscopic polyangitis
- Churg Strauss syndrome
- Autoimmune diseases like SLE, ulcerative colitis
Anti-PR3 ANCA or c-ANCA is seen in
Wegener’s granulomatosis
(c-ANCA > p-ANCA)
Atypical ANCA is seen in
Autoimmune thyroiditis
Primary sclerosing cholangitis
Giant cell arteritis / Temporal arteritis
Large vessels involved,
• M/C superficial temporal artery (ophthalmic artery, vertebral artery)
• M/C vasculitis in adults/elderly
Average age: >50 yrs
Giant cell arteritis / temporal arteritis
Clinical features
- Headache (M/C)
- Jaw pain
- Jaw claudication (most specific symptom)
- Blindness:
ophthalmic artery involved - Maybe associated with Polymyalgia Rheumatica
- Increased ESR
Temporal arteritis/ Giant cell arteritis
Histopathology
- Giant cell
- Granulomatous inflammation
- Fragmentation of internal elastic lamina
Takayasu arteritis/ aortic arch syndrome
Pulseless disease, loss of pulse of upper extremities
• M/C artery: subclavian artery
• Least common: coronary artery
• Age: <40 years
Histopathology:
1. Intimal thickening ➡️ luminal narrowing
2. Granulomatous inflammation and giant cells
von Gielson staining
For elastin
Black and white
For tunica intima,…
Polyarteritis nodosa
Type III hypersensitivity
• Most vessels can be affected except pulmonary
• Can involve: liver, kidney (but glomerulonephritis is not seen), heart, GIT
• M/C cause of death: renal failure
• M/C vasculitis which can lead to mononeuritis multiplex
• 30% patients are HBsAg +ve
• p-ANCA -ve
Polyarteritis nodosa histopathology
- Segmental transmural necrotising inflammation ➡️ fibrinoid necrosis
Inflammatory infiltrate seen in all 3 layers of blood vessel
All stages of disease can be seen in a vessel at the same time
Mucocutaneous lymph node syndrome/ Kawasaki disease
K. Conjunctivitis (bilateral, non suppurative) A. Age: <4 years W. Vasculitis A. Adenosine S. Strawberry tongue, skin rash, swelling A. Anti endothelial antibodies K. Coronary artery involvement ➡️ MI I. Increased platelets M/C vasculitis causing death in children Histopathology: transmural inflammation
Thromboangitis obliterans
Buerger’s disease
Middle aged male smokers
• Associated with HLA B5, A9
• HLA B12 is protective
• can involve arteries, capillaries, nerves ➡️ painful lesions
Thromboangitis obliterans
Clinical and histopathology
Buerger’s disease Clinically: 1. Intermittent claudication 2. Rest pain 3. Gangrene Histopathology: 1. Neutrophilic microabscesses 2. Granulomatous inflammation
Leucocytoclastic vasculitis
Microscopic polyangitis
Small vessel vasculitis • p-ANCA +ve • kidney and lung can be affected • glomerulonephritis present Clinically: GIT, kidney and skin problems
Microscopic polyangitis
Histopathology
Histopathology:
- Segmental inflammation (rarely transmural)
- No granuloma
- All lessons are of the same age
Granulomatosis with polyangitis or
Wegener’s granulomatosis
Triad: 1. Lesions of upper and lower respiratory tract: • sinusitis • otitis media • lung involvement 2. Vasculitis 3. Kidney involvement: • Focal necrotising glomerulonephritis • rapidly progressive glomerulonephritis (RPGN) c-ANCA > p-ANCA in 95% Granuloma with giant cells
Limited Wegener’s granulomatosis
If only lung involvement of Wegener’s granulomatosis (granulomatosis with polyangitis)
Allergic granulomatosis with angitis /
Churg Strauss syndrome
Associated with bronchial asthma, eosinophilia hence allergic • Clinically: GIT and skin problems • p-ANCA positive • M/C cause of death ➡️ cardiac failure • Microscopy: necrotising granulomatosis
Henoch schonlein purpura
Type III hypersensitivity
• IgA mediated
• Normal platelet count, but purpura due to vasculitis
• M/C purpura in children
Henoch Schonlein purpura
Clinically and histopathology
Clinically: 1. Colicky abdominal pain 2. Arthralgia 3. Kidney disease 4. Non palpable purpura (M/C buttock) Microscopy: IgA deposition in vessel wall
Behçet’s disease
Small vessel vasculitis
Can be HLA B5, B-51 associated
Recurrent oral/ genital ulcers, uveitis
Neutrophilic vasculitis
Granulomatous vasculitis
- Giant cell
- Takayasu
- Churg Strauss syndrome
- Wegener’s granulomatosis
- Buerger’s disease
