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Pathology MBBS > Immunity and amyloidosis > Flashcards

Immunity and amyloidosis Flashcards

1
Q

The cell mediated hypersensitivity reaction

A

Type 4 hypersensitivity

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2
Q

Type 1 hypersensitivity examples

A
  1. Bronchial asthma
  2. Hay fever
  3. Allergic reactions like…
  4. Casoni’s test
  5. Theobald smith reaction
  6. PK reaction
  7. Schultz Dale phenomenon
  8. Anaphylaxis
  9. Atopy (hereditary allergy)
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3
Q

Allergic reactions that cause Type 1 hypersensitivity

A
  1. Allergic dermatitis
  2. Allergic rhinitis
  3. Food allergy
  4. Pollen allergy
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4
Q

Pathogenesis of type 1 hypersensitivity reaction

A
  1. Antigen ➡️ APCs ➡️
  2. T cells which activates TH2 cells:
    A) IL-4:
    IgE antibody production ➡️
    B) IL-5 recruitment of eosinophils
  3. Degranulation of ‘sensitised’ mast cells by IgE:
    A) early phase reaction
    B) late phase reaction
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5
Q

Early phase reaction of type 1 hypersensitivity reaction

A

Due to release of preformed mediators like histamine from sensitised mast cells within 30 minutes

  1. Vasodilation
  2. Increased permeability
  3. Bronchospasm
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6
Q

Late phase reaction of type 1 hypersensitivity reaction

A 
Due to mediators that are formed later like leukotrienes, cytokines, chemokines
Between 2-24 hours
1. Epithelial damage
2. Tissue destruction
Most important cell is eosinophil
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7
Q

Stain for mast cell

A

Toluidine blue

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8
Q

Type 2 hypersensitivity

Example

A 
Antibody mediated
M. Myasthenia gravis 
B. Blood transfusion reactions 
G. Grave’s disease, Good Pasteur’s syndrome
I. ITP, Immune haemolytic anaemia, IDDM
R. Rheumatic fever
H. Hyper acute graft rejection
P. Pernicious anaemia, pemphigus vulgaris
My blood group is Rh positive
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9
Q

Mechanism of type 2 hypersensitivity reaction

A

Antibodies which are directed against fixed antigen (cell surface or ECM/ basement membrane-Good Pasteur’s syndrome)

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10
Q

When the antigen of type 2 hypersensitivity reaction is attached to basement membrane

A
  1. Antigen combines with Antibody on basement membrane
  2. Complement activation
  3. C3a, C5a
  4. Neutrophil recruitment
  5. Release of enzymes from neutrophil
  6. Destruction of basement membrane

Good Pasteur’s syndrome

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11
Q

When antigen of type 2 hypersensitivity reaction is fixed on cell membrane

A 
Antigen-Antibody complex can cause:
1. Destruction of target cells: 
 A) opsonisation
 B) complement fixation
2. Dysregulation of the function of target cells in myasthenia gravis, Graves’ disease (type 5 hypersensitivity reaction)
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12
Q

Type 3 hypersensitivity reaction

Examples

A 
Immune complex mediated
S. Serum sickness, SLE
H. HSP (Henoch Schonlein purpura)
A. Arthus reaction
R. Reactive arthritis (Yersinia)
P. PSGN (post streptococcus glomerulo nephritis), PAN (Poly arteritis nodusa)
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13
Q

SLE is which type of hypersensitivity reaction

A

Both type 2 and type 3 hypersensitivity reaction
The haematological lesions are type 2
Whereas the visceral lessons are type 3

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14
Q

Pathogenesis of type 3 hypersensitivity reaction

A 
The three phases:
1. Formation of immune complex
 5-7 days
2. Deposition of immune complex
3. Immune complex mediated tissue injury
 A) complement activation
 B) activation of Hageman factor

The entire process takes in 10-14 days

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15
Q

Most pathogenic immune complex are

A

Small, medium sized

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16
Q

Most common sites of deposition of immune complex

A

Kidney, blood vessels, skin

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17
Q

Type 4 hypersensitivity reaction

Examples

A 
Delayed type hypersensitivity reaction
Cell mediated (T cell)
1. Granuloma formation
2. Tuberculin test and Lepromin test
3. Contact dermatitis
4. Acute and chronic graft rejection
5. Rheumatoid arthritis
6. Multiple sclerosis
7. Inflammatory bowel disease
8. Psoriasis
9. GVHD (graft v/s host disease)
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18
Q

Pathogenesis of type 4 hypersensitivity reaction in brief

A 
Mediated by
1. CD4+ T cells
 Activation of T helper (TH-1) cells
2. CD8+ T cells
 Direct destruction of viral infected and tumour cells
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19
Q

Pathogenesis of type 4 hypersensitivity reaction through CD8+ T cells

A

Through:

  1. Fas-Fas ligand mechanism
  2. Perforin granzyme mechanism
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20
Q

Pathogenesis of type 4 hypersensitivity reaction through CD4+ T cells

A

Activation of TH1 cells
These T helper cells produce cytokines like:
1. IL-2
2. IL-12 (recruits lymphocytes)
3. IFN- gamma (Interferon-gamma)- granuloma formation

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21
Q

Components of innate immunity

A
  1. Epithelial barriers
  2. Phagocytic cells
  3. Dendritic cells
  4. Natural killer cells
  5. Other innate lymphoid cells
  6. Several plasma proteins like compliment system
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22
Q

MHC/ HLA

Their types and loci

A

Gene is located in chromosome 6 (short arm)
3 types:
1. A,B,C
3. (Encode for certain complement proteins like C2, C4, properdin, HSP)
2. DP, DQ ,DR

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23
Q

Difference between HLA class 1 and 2 on the basis of location in cells

A

Class 1 is located on all nuclear cells and platelets

Class 2 are only present on APCs (dendritic cells, endothelial cells, fibroblasts)

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24
Q

Difference between HLA class 1 and 2 on the basis of which T cells they bind to

A

Class 1 binds with CD8+ T cells

Class 2 binds with CD4+ T cells

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25
Difference between HLA class 1 and 2 on the basis of structure
``` Class 1 MHC consists of: 1. Alpha 1,2,3 2. Beta 2 micro globulin Peptide binding site is between alpha 1 and alpha 2 Class 2 MHC consists of: 1. Alpha 1,2 2. Beta 1,2 The peptide binding site is between alpha 1 and beta 1 ```
26
Difference between HLA class 1 and 2 on the basis of detection test
Class 1 is detected by allo-antisera test | Class 2 is detected by mixed lymphocyte reaction
27
Difference between HLA class 1 and 2 on the basis of relation to graft
Class 1 is involved in graft rejection | Class 2 is involved in GVHD
28
Uses of MHC
1. Paternity testing 2. Autoimmune disorders, like HLA B-27 ankylosing spondylitis HLADR3, DR4 diabetes mellitus 3. Transplantation 4. Anthropological testing
29
Order of importance of different HLA wrt transplant matching
HLA DR > B > A | These 3 are the most important ones for matching
30
000 mismatch
No mismatch on A, B ,D
31
HLA matching is not required for which and all graft
1. Liver 2. Lung 3. Cornea
32
Graft rejection types
1. Hyperacute graft rejection 2. Acute graft rejection 3. Chronic graft rejection
33
Hyperacute graft rejection
Occurs within minutes of transplantation Type 2 hypersensitivity reaction caused by preformed antibodies Most commonly seen in kidney transplants
34
Causes of the presence of preformed antibodies in hyperacute graft rejection
1. Previous blood transfusion 2. Previous transplantation 3. Multiparous women 4. ABO and Rh incompatibility
35
Hyperacute graft rejection features
Gross: Kidney becomes cyanosed, mottled, flaccid Microscopic: 1. Microthrombi 2. Fibrinoid necrosis 3. Neutrophillic infiltrate in glomerular capillary plexus
36
Acute graft rejection
Two types: 1. Acute cellular rejection 2. Acute humoral rejection Occurs within days or months (less than 6 months) of transplantation
37
Acute cellular graft rejection
It can be caused by CD4+ T cells or CD8+ T cells Type 4 hypersensitivity reaction Responds to increasing dose of immunosuppressants
38
Acute humoral graft rejection
Caused by anti donor antibody Either type 2 (or type 3) hypersensitivity reaction Does not respond to increasing dose of immunosuppressants So treatment is B cell depleting agents
39
Acute cellular graft rejection microscopic features
Tubulointerstitial pattern (most common): 1. Tubulitis 2. Interstitial mononuclear inflammation Vascular pattern: Endothelitis
40
Acute humoral graft rejection microscopic features
1. Fibrinoid necrosis 2. Peritubular capillaries have a deposition of a complement breakdown product C4d Therefore C4d is used as a marker acute humoral graft rejection
41
Chronic graft rejection
Occurs within months to years of transplant Can be cell mediated (T cell) or antibody mediated Can be type 2 or type 4 hypersensitivity reaction
42
Chronic graft rejection microscopic features
Glomerulopathy 1. Duplication of glomerular basement membrane 2. Glomerulo sclerosis 3. Tubular atrophy 4. Interstitial fibrosis 5. Atherosclerosis of graft vessels
43
GVHD or grunt disease of animals
``` Usually seen after bone marrow transplant Type 4 hypersensitivity reaction Two types: 1. Acute 2. Chronic ```
44
Acute GVHD
``` Occurs within 6 months Affected organs: 1. Skin - rash (most affected) 2. GIT - bloody diarrhoea 3. Liver - cholestatic jaundice ```
45
Chronic GVHD
``` Occurs after 6 months Affects: 1. Skin - scleroderma 2. GIT - strictures 3. Liver - cholestatic jaundice ```
46
Eichwald Slimser effect is also called | Explain
Y-linked graft rejection Usually seen when a male gives a graft to a female Y chromosome has UT4 gene which encodes for a graft rejection protein
47
Complications of transplantation
``` 1. Infections like A. cytomegalovirus CMV infection: (owl’s eye inclusions) - most common B. BK polyoma virus infection (decoy cells- intranuclear basophilic inclusions in PCT) 2. GVHD 3. Graft rejection 4. Increased risk of malignancy A. Squamous cell carcinoma (HPV associated) B. Non Hodgkins’s lymphoma (EBV) C. Kaposi’s sarcoma (HHV-8) ```
48
Best diagnostic features of kidney allograft rejection
Kidney biopsy
49
Examples of immunodeficiency disorders
1. Bruton’s hypogammaglobulinemia 2. DiGeorge syndrome 3. Wiscott Aldrich syndrome 4. SCID 5. Common variable immuno deficiency CVID 6. Isolated IgA deficiency 7. Hyper IgE syndrome / JOB syndrome 8. Hyper IgM syndrome 9. Ataxia telangiactasia
50
Bruton’s hypogammaglobulinemia
X linked recessive disorder Bruton tyrosine kinase BTK gene affected (B cell areas) B cell defect Decreased IgG (defective opsonisation) Increased risk of infections (esp pneumococci)
51
DiGeorge syndrome or velocardial facial defect | Causes and basic features
CATCH22 Deletion in long arm of chromosome 22 (del 22q 11) ➡️ Defect in TBX1 gene ➡️ Defective development of 3rd and 4th pharyngeal pouches ➡️ Thymic and parathyroid hyperplasia
52
Velocardial defect DiGeorge syndrome clinical features
``` C. Cleft lip and cleft palate A. Abnormal facies T. Thymic hyperplasia, T cell defect C. Cardiac abnormalities H. Hypocalcemia 22 ```
53
Wiscott Aldrich syndrome
``` X linked recessive disorder Defect in WASP gene ➡️ Decreased IgM ➡️ 1. Eczema 2. Recurrent infections 3. Thrombocytopenia (size, number, function defect) ```
54
SCID (first disorder to be successfully treated by gene therapy)
Both T and B cell defect ADA (adenosine deaminase) deficiency Accumulation of substrates Decreased level of IL-7, IL-15 cytokines ➡️: 1. NK cell proliferation (IL-15) 2. Decreased production/activation of T cells, B cells (IL-7) Increased risk of Candida, pneumococci,...
55
Common variable immuno deficiency CVID
Commonly seen in children Defect in BAFF (B cell activating factor) or ICOS (inducible costimulator) gene ➡️ B cell maturation defect ➡️ No immunoglobulin production (no plasma cell) ➡️ Increased risk of sinopulmonary infections, giardiasis, other auto-immune disorders (like rheumatoid arthritis) and malignancies
56
Isolated IgA deficiency
B cell can’t produce IgA So IgG4 is also reduced Increased risk of GIT, sinopulmonary, allergies, anaphylaxis and other auto immune disorders
57
Hyper IgE syndrome or the JOB syndrome
``` Autosomal dominant Defect in STAT3 gene Increased level of IgE Cold abscesses Course facial features ```
58
Hyper IgM syndrome
``` X linked recessive disorder Increased IgM Defective class switching ➡️ Decreased IgG, IgA, IgE ➡️ Recurrent infections like pneumocystis jeroveci IgM starts attacking blood elements ➡️ : 1. Autoimmune haemolytic anaemia 2. Autoimmune thrombocytopenia 3. Autoimmune leukopenia ```
59
Ataxia telangiactasia
ATM (DNA damage sensor) gene of chromosome 11 ➡️ | Increased risk of neoplasms and immune defects are present
60
Amyloid definition
Pathological proteinaceous amorphous extracellular eosinophilic substance deposited in various tissues or organs in various conditions Hyaline like pink substance Misfolded protein
61
Structure of amyloid on electron microscopy
Non branching fibrils of indefinite length | 7.5-10 nm in diameter
62
Structure of amyloid protein on X-ray crystallography or infrared spectroscopy
Cross beta pleated sheet structure which is responsible apple green birefringes of amyloid in Congo red under polarised light
63
Chemical nature of amyloid
95% fibrillar protein | 5% P component
64
Classification of amyloidosis
1. Localised: DAMP 2. Systemic/ generalised 3. Familial
65
Localised amyloidosis
1. Type II DM (AIAPP-islet associated pancreatic peptide) 2. Alzheimer’s disease (Aβ) 3. Medullary carcinoma of thyroid (ACal) 4. Prion disease (APr)
66
Generalised or systemic amyloidosis
1. Primary amyloidosis: Seen in light chain disorders (commonly λ) like multiple myeloma AL 2. Secondary amyloidosis /reactive systemic amyloidosis: 3. Chronic renal failure/ long term dialysis (Aβ2m-micro globulin) 4. Senile/ ageing amyloidosis: ATTR-normal transthyretin
67
Secondary amyloidosis /reactive systemic amyloidosis:
``` AA amyloid deposition Seen in A. Chronic inflammatory conditions: 1. Bronchiectasis 2. Rheumatoid arthritis (most common) 3. Tuberculosis (most common in India) ``` B. Chronic malignancies: 1. Hodgkin’s lymphoma 2. Renal cell carcinoma
68
Familial amyloidotic polyneuropathy
Autosomal dominant Deposition of mutant transthyretin ATTR
69
Familial Mediterranean fever
Example of familial amyloidosis Autosomal recessive AA Pyrin protein deposition (pyrexia-fever)
70
Diagnosis of amyloidosis
Best and most commonly used test- Abdominal fat pad aspirate Rectal biopsy Then tongue biopsy
71
Stains for amyloid
1. H and E: pink 2. PAS-magenta (per-iodic shift reaction) 3. Congo red-best stain: On light-salmon pink On polarised light-apple green birefringence 4. Methyl violet/ crystal violet- metachromatic stains 5. Thioflavin S and T- inflorescence Gross stain
72
Gross stain for amyloidosis
Cut surface with Lugol’s iodine- Mahogany brown ➡️ sulphuric acid is then added and if it then becomes blue Then to confirm Congo red is used
73
Most common organ affected by amyloid | What are the effects
Kidney It is also the most severely affected organ Initially in the glomeruli Usually affects the mesangium (can also affect the walls of capillaries and arterioles) Clinically presents as nephrotic syndrome Renal biopsy is done
74
Most common cause of death in primary amyloidosis
Heart disease
75
Most common cause of death in secondary amyloid
Renal disease
76
General gross features of amyloidosis
The organ is waxy Firm in consistency Usually organomegaly is present
77
Liver and amyloidosis
First affects Space of Disse (thin space between hepatocytes and sinusoids) ➡️ pressure atrophy of hepatic Clinically presented as cirrhosis
78
Heart and amyloidosis
``` The subendocardium is the most commonly affected part Clinically: 1. Arrhythmia 2. Right bundle branch block 3. Restrictive cardiomyopathy ```
79
Amyloidosis and GIT
Macroglossia | Can affect many other parts of GIT
80
Spleen and amyloidosis
1. Sago spleen Splenic follicles are affected 2. Lardaceous spleen Sinusoids are affected

Pathology MBBS (17 decks)

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