Pathology MBBS > Cardiovascular System, vasculitis > Flashcards

Cardiovascular System, vasculitis Flashcards

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1
Q

Effects of ageing on heart

A
  1. Lipofuscin deposition
  2. Basophilic degeneration of cardiac myocytes
  3. Lambl’s excrescences
  4. Increased amount of epicardial fat
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2
Q

Causes of left heart failure

A
  1. Hypertension
  2. Ischaemic heart disease
  3. Valvular heart disease
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3
Q

Effects of left heart failure

A 
1. Lung:
Heart failure cells in lungs
2. Kidney:
 Acute tubular necrosis
3. Brain:
Hypoxic encephalopathy
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4
Q

Heart failure cells properties

A

Hemosiderin laden macrophages in lungs

Stained by Prussian blue

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5
Q

Common causes of right sided heart failure

A

M/C is left sided heart failure

M/C of isolated right heart failure is parenchymal lung disease

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6
Q

Effects of right sided heat failure

A

Organ congestion

  1. Liver: CVC, nutmeg liver
  2. Spleen: congestive splenomegaly, Gamna Gandy bodies
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7
Q

Ischaemic heart diseases

A
  1. Angina
  2. Myocardial infarction
  3. Chronic ischaemic heart disease
  4. Sudden cardiac death
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8
Q

Types of MI

A 
1. Transmural:
•Involves all 3 layers of heart
•most common
•ST elevation infarct 
2. Subendocardial:
•involves only subendocardial zone
•also called NSTEMI
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9
Q

M/C vessels affected by MI in decreasing order

A
  1. Left anterior descending artery
  2. Right coronary artery
  3. Left circumflex artery
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10
Q

Myocardial response to hypoxia

A 
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
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11
Q

Morphological changes in heat after MI in one day (dark mottling)

A 
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
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12
Q

Morphological changes in heat after MI after one day upto 1 week (mottling with yellow)

A

In 1-3 days:
• coagulation necrosis and interstitial infiltrate of neutrophils
In 3-7 days:
• disintegration of dead myofibres, dying neutrophils
• early phagocytosis, macrophages

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13
Q

Morphological changes in heart after MI after one week

A

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

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14
Q

MI less than 12 hours old can be detected by

A

TTC stain
Triphenyl tetrazolium chloride
Brick red- normal tissue
Yellow- infarct tissue

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15
Q

ECG changes in MI

A
  1. ST segment elevation
  2. T wave inversion
  3. Pathological Q waves
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16
Q

Biochemical markers of MI

A 
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
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17
Q

Complications of MI

A

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.
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18
Q

Dressler’s syndrome

A

Post MI fibrosuppurative pericarditis
Occurs within 2-3 days of MI
Autoimmune reaction

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19
Q

Ischaemia reperfusion injury

A

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

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20
Q

Types of carditis

A
  1. Pericarditis: acute or chronic
  2. Myocarditis
    M/C helminthic cause: Trichinella spiralis
    M/C virus: Coxsackie A & B, Herpes
  3. Endocarditis
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21
Q

Pericarditis

A 
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
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22
Q

Rheumatic fever and rheumatic heart disease

A

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

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23
Q

Most and least common valve affected by RHD

A

M/C valve: mitral valve

Least commonly affected valve: pulmonary valve

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24
Q

Common complications of acute and chronic RHD

A

Acute rheumatic fever: mitral regurgitation

Chronic rheumatic heart disease: mitral stenosis

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25
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 ```
26
Morphology of heart in RHD
1. Aschoff bodies (caterpillar cells/ Antischkow cells) 2. Bread and butter pericarditis 3. McCallum plaques/ subendocardial jets- posterior wall of atrium 4. In chronic cases: • fish mouth stenosis • button hole stenosis 5. Vegetation
27
Aschoff bodies
Pathognomic for RHD | Consists of lymphocytes, plasma cross, giant cells, fibrinoid necrosis, collagen and caterpillar/ Antischkow cells
28
Vegetations of RHD
Small warty, verrucous vegetation Along lines of closure of valve leaflets Sterile
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Acute infective endocarditis
Occurs in previously normal heat valves | Caused by Staphylococcus aureus
30
Subacute infective endocarditis
Occurs in previously damaged heat valves | Caused by Streptococci
31
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 ```
32
Vegetation of infective endocarditis
Large, bulky, irregular, friable, destructive, infected vegetations along lines of closure
33
NBTE - Non bacterial thrombotic endocarditis
Patients with debilitating diseases like metastatic carcinoma of pancreas, AML-M3 Small flat vegetations along lines of closure
34
Libman Sachs endocarditis
Seen in SLE patients Small- medium sized, sterile vegetations Seen on both sides of valve leaflets (most commonly on under-surface)
35
Types of cardiomyopathy
1. Dilated cardiomyopathy 2. Hypertrophic cardiomyopathy 3. Restrictive cardiomyopathy
36
Causes of dilated cardiomyopathy
1. Idiopathic (>50%) 2. Alcohol 3. Post partum 4. Myocarditis 5. Drugs like adriamycin 6. Haemochromatosis 7. Genetic mutation of titin
37
Dilatation of all four chambers of the heart is called as
Flabby hypocontracting heart
38
Classification of vasculitis
``` Chapel Hill classification 1. Large vessel 2. Medium vessel 3. Small vessel: • immune complex mediated • Pauci immune ```
39
Large vessel vasculitis
Giant cell arteritis | Takayasu arteritis
40
Medium vessel vasculitis
1. Polyarteritis nodosa (PAN) 2. Kawasaki disease (anti-endothelial antibody) 3. Buerger’s disease
41
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 (“”) ```
42
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 ```
43
Anti-MPO ANCA or p-ANCA is seen in
1. Microscopic polyangitis 2. Churg Strauss syndrome 3. Autoimmune diseases like SLE, ulcerative colitis
44
Anti-PR3 ANCA or c-ANCA is seen in
Wegener’s granulomatosis | (c-ANCA > p-ANCA)
45
Atypical ANCA is seen in
Autoimmune thyroiditis | Primary sclerosing cholangitis
46
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
47
Giant cell arteritis / temporal arteritis | Clinical features
1. Headache (M/C) 2. Jaw pain 3. Jaw claudication (most specific symptom) 4. Blindness: ophthalmic artery involved 5. Maybe associated with Polymyalgia Rheumatica 6. Increased ESR
48
Temporal arteritis/ Giant cell arteritis | Histopathology
1. Giant cell 2. Granulomatous inflammation 3. Fragmentation of internal elastic lamina
49
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
50
von Gielson staining
For elastin Black and white For tunica intima,...
51
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
52
Polyarteritis nodosa histopathology
1. 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
53
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 ```
54
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
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Thromboangitis obliterans | Clinical and histopathology
``` Buerger’s disease Clinically: 1. Intermittent claudication 2. Rest pain 3. Gangrene Histopathology: 1. Neutrophilic microabscesses 2. Granulomatous inflammation ```
56
Leucocytoclastic vasculitis | Microscopic polyangitis
``` Small vessel vasculitis • p-ANCA +ve • kidney and lung can be affected • glomerulonephritis present Clinically: GIT, kidney and skin problems ```
57
Microscopic polyangitis | Histopathology
Histopathology: 1. Segmental inflammation (rarely transmural) 2. No granuloma 3. All lessons are of the same age
58
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 ```
59
Limited Wegener’s granulomatosis
If only lung involvement of Wegener’s granulomatosis (granulomatosis with polyangitis)
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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 ```
61
Henoch schonlein purpura
Type III hypersensitivity • IgA mediated • Normal platelet count, but purpura due to vasculitis • M/C purpura in children
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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 ```
63
Behçet’s disease
Small vessel vasculitis Can be HLA B5, B-51 associated Recurrent oral/ genital ulcers, uveitis Neutrophilic vasculitis
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Granulomatous vasculitis
1. Giant cell 2. Takayasu 3. Churg Strauss syndrome 4. Wegener’s granulomatosis 5. Buerger’s disease
Pathology MBBS
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