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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
Q

Difference between HLA class 1 and 2 on the basis of structure

A 
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
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26
Q

Difference between HLA class 1 and 2 on the basis of detection test

A

Class 1 is detected by allo-antisera test

Class 2 is detected by mixed lymphocyte reaction

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27
Q

Difference between HLA class 1 and 2 on the basis of relation to graft

A

Class 1 is involved in graft rejection

Class 2 is involved in GVHD

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28
Q

Uses of MHC

A
  1. Paternity testing
  2. Autoimmune disorders, like
    HLA B-27 ankylosing spondylitis
    HLADR3, DR4 diabetes mellitus
  3. Transplantation
  4. Anthropological testing
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29
Q

Order of importance of different HLA wrt transplant matching

A

HLA DR > B > A

These 3 are the most important ones for matching

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30
Q

000 mismatch

A

No mismatch on A, B ,D

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31
Q

HLA matching is not required for which and all graft

A
  1. Liver
  2. Lung
  3. Cornea
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32
Q

Graft rejection types

A
  1. Hyperacute graft rejection
  2. Acute graft rejection
  3. Chronic graft rejection
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33
Q

Hyperacute graft rejection

A

Occurs within minutes of transplantation
Type 2 hypersensitivity reaction caused by preformed antibodies
Most commonly seen in kidney transplants

34
Q

Causes of the presence of preformed antibodies in hyperacute graft rejection

A
  1. Previous blood transfusion
  2. Previous transplantation
  3. Multiparous women
  4. ABO and Rh incompatibility
35
Q

Hyperacute graft rejection features

A

Gross:
Kidney becomes cyanosed, mottled, flaccid
Microscopic:
1. Microthrombi
2. Fibrinoid necrosis
3. Neutrophillic infiltrate in glomerular capillary plexus

36
Q

Acute graft rejection

A

Two types:
1. Acute cellular rejection
2. Acute humoral rejection
Occurs within days or months (less than 6 months) of transplantation

37
Q

Acute cellular graft rejection

A

It can be caused by CD4+ T cells or CD8+ T cells
Type 4 hypersensitivity reaction
Responds to increasing dose of immunosuppressants

38
Q

Acute humoral graft rejection

A

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
Q

Acute cellular graft rejection microscopic features

A

Tubulointerstitial pattern (most common):
1. Tubulitis
2. Interstitial mononuclear inflammation
Vascular pattern:
Endothelitis

40
Q

Acute humoral graft rejection microscopic features

A
  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
Q

Chronic graft rejection

A

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
Q

Chronic graft rejection microscopic features

A

Glomerulopathy

  1. Duplication of glomerular basement membrane
  2. Glomerulo sclerosis
  3. Tubular atrophy
  4. Interstitial fibrosis
  5. Atherosclerosis of graft vessels
43
Q

GVHD or grunt disease of animals

A 
Usually seen after bone marrow transplant
Type 4 hypersensitivity reaction
Two types:
1.  Acute
2. Chronic
44
Q

Acute GVHD

A 
Occurs within 6 months
Affected organs:
1. Skin - rash (most affected)
2. GIT - bloody diarrhoea
3. Liver - cholestatic jaundice
45
Q

Chronic GVHD

A 
Occurs after 6 months
Affects:
1. Skin - scleroderma 
2. GIT - strictures
3. Liver - cholestatic jaundice
46
Q

Eichwald Slimser effect is also called

Explain

A

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
Q

Complications of transplantation

A 
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
Q

Best diagnostic features of kidney allograft rejection

A

Kidney biopsy

49
Q

Examples of immunodeficiency disorders

A
  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
Q

Bruton’s hypogammaglobulinemia

A

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
Q

DiGeorge syndrome or velocardial facial defect

Causes and basic features

A

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
Q

Velocardial defect DiGeorge syndrome clinical features

A 
C. Cleft lip and cleft palate 
A. Abnormal facies
T. Thymic hyperplasia, T cell defect
C. Cardiac abnormalities
H. Hypocalcemia
22
53
Q

Wiscott Aldrich syndrome

A 
X linked recessive disorder
Defect in WASP gene ➡️ 
Decreased IgM ➡️
1. Eczema
2. Recurrent infections
3. Thrombocytopenia (size, number, function defect)
54
Q

SCID (first disorder to be successfully treated by gene therapy)

A

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
Q

Common variable immuno deficiency CVID

A

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
Q

Isolated IgA deficiency

A

B cell can’t produce IgA
So IgG4 is also reduced
Increased risk of GIT, sinopulmonary, allergies, anaphylaxis and other auto immune disorders

57
Q

Hyper IgE syndrome or the JOB syndrome

A 
Autosomal dominant
Defect in STAT3 gene
Increased level of IgE
Cold abscesses
Course facial features
58
Q

Hyper IgM syndrome

A 
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
Q

Ataxia telangiactasia

A

ATM (DNA damage sensor) gene of chromosome 11 ➡️

Increased risk of neoplasms and immune defects are present

60
Q

Amyloid definition

A

Pathological proteinaceous amorphous extracellular eosinophilic substance deposited in various tissues or organs in various conditions
Hyaline like pink substance
Misfolded protein

61
Q

Structure of amyloid on electron microscopy

A

Non branching fibrils of indefinite length

7.5-10 nm in diameter

62
Q

Structure of amyloid protein on X-ray crystallography or infrared spectroscopy

A

Cross beta pleated sheet structure which is responsible apple green birefringes of amyloid in Congo red under polarised light

63
Q

Chemical nature of amyloid

A

95% fibrillar protein

5% P component

64
Q

Classification of amyloidosis

A
  1. Localised:
    DAMP
  2. Systemic/ generalised
  3. Familial
65
Q

Localised amyloidosis

A
  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
Q

Generalised or systemic amyloidosis

A
  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
Q

Secondary amyloidosis /reactive systemic amyloidosis:

A 
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
Q

Familial amyloidotic polyneuropathy

A

Autosomal dominant
Deposition of mutant transthyretin
ATTR

69
Q

Familial Mediterranean fever

A

Example of familial amyloidosis
Autosomal recessive
AA
Pyrin protein deposition (pyrexia-fever)

70
Q

Diagnosis of amyloidosis

A

Best and most commonly used test- Abdominal fat pad aspirate
Rectal biopsy
Then tongue biopsy

71
Q

Stains for amyloid

A
  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
Q

Gross stain for amyloidosis

A

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
Q

Most common organ affected by amyloid

What are the effects

A

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
Q

Most common cause of death in primary amyloidosis

A

Heart disease

75
Q

Most common cause of death in secondary amyloid

A

Renal disease

76
Q

General gross features of amyloidosis

A

The organ is waxy
Firm in consistency
Usually organomegaly is present

77
Q

Liver and amyloidosis

A

First affects Space of Disse (thin space between hepatocytes and sinusoids) ➡️ pressure atrophy of hepatic
Clinically presented as cirrhosis

78
Q

Heart and amyloidosis

A 
The subendocardium is the most commonly affected part
Clinically:
1. Arrhythmia
2. Right bundle branch block
3. Restrictive cardiomyopathy
79
Q

Amyloidosis and GIT

A

Macroglossia

Can affect many other parts of GIT

80
Q

Spleen and amyloidosis

A
  1. Sago spleen
    Splenic follicles are affected
  2. Lardaceous spleen
    Sinusoids are affected

Pathology MBBS (17 decks)

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