Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathology MBBS > Cardiovascular System, vasculitis > Flashcards

Cardiovascular System, vasculitis Flashcards

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Causes of left heart failure

A
  1. Hypertension
  2. Ischaemic heart disease
  3. Valvular heart disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Effects of left heart failure

A 
1. Lung:
Heart failure cells in lungs
2. Kidney:
 Acute tubular necrosis
3. Brain:
Hypoxic encephalopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Heart failure cells properties

A

Hemosiderin laden macrophages in lungs

Stained by Prussian blue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Effects of right sided heat failure

A

Organ congestion

  1. Liver: CVC, nutmeg liver
  2. Spleen: congestive splenomegaly, Gamna Gandy bodies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Ischaemic heart diseases

A
  1. Angina
  2. Myocardial infarction
  3. Chronic ischaemic heart disease
  4. Sudden cardiac death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

ECG changes in MI

A
  1. ST segment elevation
  2. T wave inversion
  3. Pathological Q waves
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Dressler’s syndrome

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Most and least common valve affected by RHD

A

M/C valve: mitral valve

Least commonly affected valve: pulmonary valve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Common complications of acute and chronic RHD

A

Acute rheumatic fever: mitral regurgitation

Chronic rheumatic heart disease: mitral stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Revised Jones criteria

A 
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Morphology of heart in RHD

A
  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
Q

Aschoff bodies

A

Pathognomic for RHD

Consists of lymphocytes, plasma cross, giant cells, fibrinoid necrosis, collagen and caterpillar/ Antischkow cells

28
Q

Vegetations of RHD

A

Small warty, verrucous vegetation
Along lines of closure of valve leaflets
Sterile

29
Q

Acute infective endocarditis

A

Occurs in previously normal heat valves

Caused by Staphylococcus aureus

30
Q

Subacute infective endocarditis

A

Occurs in previously damaged heat valves

Caused by Streptococci

31
Q

Infective endocarditis

Diagnosis and features

A 
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
Q

Vegetation of infective endocarditis

A

Large, bulky, irregular, friable, destructive, infected vegetations along lines of closure

33
Q

NBTE - Non bacterial thrombotic endocarditis

A

Patients with debilitating diseases like metastatic carcinoma of pancreas, AML-M3
Small flat vegetations along lines of closure

34
Q

Libman Sachs endocarditis

A

Seen in SLE patients
Small- medium sized, sterile vegetations
Seen on both sides of valve leaflets (most commonly on under-surface)

35
Q

Types of cardiomyopathy

A
  1. Dilated cardiomyopathy
  2. Hypertrophic cardiomyopathy
  3. Restrictive cardiomyopathy
36
Q

Causes of dilated cardiomyopathy

A
  1. Idiopathic (>50%)
  2. Alcohol
  3. Post partum
  4. Myocarditis
  5. Drugs like adriamycin
  6. Haemochromatosis
  7. Genetic mutation of titin
37
Q

Dilatation of all four chambers of the heart is called as

A

Flabby hypocontracting heart

38
Q

Classification of vasculitis

A 
Chapel Hill classification
1. Large vessel
2. Medium vessel
3. Small vessel:
• immune complex mediated
• Pauci immune
39
Q

Large vessel vasculitis

A

Giant cell arteritis

Takayasu arteritis

40
Q

Medium vessel vasculitis

A
  1. Polyarteritis nodosa (PAN)
  2. Kawasaki disease
    (anti-endothelial antibody)
  3. Buerger’s disease
41
Q

Small vessel vasculitis

A 
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
Q

Antibodies involved in vasculitis

A 
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
Q

Anti-MPO ANCA or p-ANCA is seen in

A
  1. Microscopic polyangitis
  2. Churg Strauss syndrome
  3. Autoimmune diseases like SLE, ulcerative colitis
44
Q

Anti-PR3 ANCA or c-ANCA is seen in

A

Wegener’s granulomatosis

(c-ANCA > p-ANCA)

45
Q

Atypical ANCA is seen in

A

Autoimmune thyroiditis

Primary sclerosing cholangitis

46
Q

Giant cell arteritis / Temporal arteritis

A

Large vessels involved,
• M/C superficial temporal artery (ophthalmic artery, vertebral artery)
• M/C vasculitis in adults/elderly
Average age: >50 yrs

47
Q

Giant cell arteritis / temporal arteritis

Clinical features

A
  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
Q

Temporal arteritis/ Giant cell arteritis

Histopathology

A
  1. Giant cell
  2. Granulomatous inflammation
  3. Fragmentation of internal elastic lamina
49
Q

Takayasu arteritis/ aortic arch syndrome

A

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
Q

von Gielson staining

A

For elastin
Black and white
For tunica intima,…

51
Q

Polyarteritis nodosa

A

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
Q

Polyarteritis nodosa histopathology

A
  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
Q

Mucocutaneous lymph node syndrome/ Kawasaki disease

A 
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
Q

Thromboangitis obliterans

Buerger’s disease

A

Middle aged male smokers
• Associated with HLA B5, A9
• HLA B12 is protective
• can involve arteries, capillaries, nerves ➡️ painful lesions

55
Q

Thromboangitis obliterans

Clinical and histopathology

A 
Buerger’s disease 
Clinically:
1. Intermittent claudication 
2. Rest pain 
3. Gangrene
Histopathology:
1. Neutrophilic microabscesses
2. Granulomatous inflammation
56
Q

Leucocytoclastic vasculitis

Microscopic polyangitis

A 
Small vessel vasculitis
• p-ANCA +ve
• kidney and lung can be affected
• glomerulonephritis present
Clinically:
 GIT, kidney and skin problems
57
Q

Microscopic polyangitis

Histopathology

A

Histopathology:

  1. Segmental inflammation (rarely transmural)
  2. No granuloma
  3. All lessons are of the same age
58
Q

Granulomatosis with polyangitis or

Wegener’s granulomatosis

A 
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
Q

Limited Wegener’s granulomatosis

A

If only lung involvement of Wegener’s granulomatosis (granulomatosis with polyangitis)

60
Q

Allergic granulomatosis with angitis /

Churg Strauss syndrome

A 
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
Q

Henoch schonlein purpura

A

Type III hypersensitivity
• IgA mediated
• Normal platelet count, but purpura due to vasculitis
• M/C purpura in children

62
Q

Henoch Schonlein purpura

Clinically and histopathology

A 
Clinically:
1. Colicky abdominal pain
2. Arthralgia
3. Kidney disease
4. Non palpable purpura (M/C buttock)
Microscopy:
 IgA deposition in vessel wall
63
Q

Behçet’s disease

A

Small vessel vasculitis
Can be HLA B5, B-51 associated
Recurrent oral/ genital ulcers, uveitis
Neutrophilic vasculitis

64
Q

Granulomatous vasculitis

A
  1. Giant cell
  2. Takayasu
  3. Churg Strauss syndrome
  4. Wegener’s granulomatosis
  5. Buerger’s disease

Pathology MBBS (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions