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Pathology > Chapter 6- Diseases Of The Immune System > Flashcards

Chapter 6- Diseases Of The Immune System Flashcards

1
Q

What are the characteristics of innate immunity?

A

Elements are always present, ready to react before infections occur

No antigen specificity or memory

First line of defence

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2
Q

What are some elements of innate immunity?

A

Epithelial barriers

Phagocytes

NK cells

Complement

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3
Q

What are the characteristics of adaptive immunity?

A

Mechanisms stimulated by foreign substances

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4
Q

What makes up adaptive immunity?

A

Lymphocytes and their products

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5
Q

What are the two components of adaptive immunity?

A

Humoral (B cells)

Cell mediated (T cells)

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6
Q

What type of antigenic stimuli does each form of adaptive immunity protect against?

A

Humoral- extracellular, toxins

Cell mediated- intracellular

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7
Q

What is the most common APC?

A

Dendritic cells

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8
Q

What are the different immune cells and their functions?

A

B lymphs- Ab production

TH/CD4- recognizes Ag bound to APC, mac and lymph activation

TC/CD8- recognizes Ag on infected cells, kills cells

Treg- immune suppression

NK- kills infected cells

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9
Q

What tissues are involved in the production, maturation and storage of immune cells?

A

Generative lymphoid organs- BM and thymus

Peripheral lymphoid organs

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10
Q

What is a hypersensitivity reaction?

A

Excessive response to an Ag

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11
Q

What genes are often associated with hypersensitivity reactions?

A

Susceptibility genes (HLA/MHC)

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12
Q

What are the categories of hypersensitivity reactions?

A

Type I/immediate

Type II/Ab mediated

Type III/immune complex mediated

Type IV/T cell mediated

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13
Q

What are the characteristics of Type I hypersensitivity reactions?

A

Allergies

TH2 cells stimulate IgE production

IgE binds mast cells and releases histamine

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14
Q

What are the phases of Type I hypersensitivity reactions?

A

Immediate reaction- histamine release causes vasodilation, vessel permeability, etc

Second/delayed phase- eosinophils infiltrate tissues causing damage

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15
Q

What is systemic anaphylaxis?

A

Hypotensive shock associated with allergies (Type I)

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16
Q

What are the characteristics of Type II hypersensitivity reactions?

A

Abs on cell surfaces or ECM activate immune cells and lead to damage

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17
Q

What causes the pathology of Type II hypersensitivity reactions?

A

Opsonization and phagocytosis destroy cells

Inflammation

Complement activation

Cellular dysfunction

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18
Q

What diseases are caused by Type II hypersensitivity reactions? What are their characteristics?

A

Myasthenia gravis- Ab blocks ACh binding

Grave’s disease- Ab stimulates TSH receptor

Goodpasture’s disease- Ab causes tissue damage

AIHA- Ab binds RBCs, cells are lysed/cleared

Rh HDN- Ab binds and cells are lysed/cleared

ITP- Ab against platelets causes their destruction

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19
Q

What are the characteristics of Type III hypersensitivity reactions?

A

Ag-Ab complexes elicit inflammation at sites of deposition

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20
Q

What organs are involved in Type III hypersensitivity reactions?

A

Kidneys

Joints

Blood vessels

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21
Q

What are the phases of Type III hypersensitivity reactions?

A

Formation (1 week)

Deposition

Inflammation and tissue injury (10 days)

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22
Q

What diseases are associated with Type III hypersensitivity reactions? What are their characteristics?

A

SLE- deposition in kidney

Glomerulonephritis- deposition in glomerular BM

Polyarteritis- Hep B Ag causes systemic vasculitis

Reactive arthritis- bacterial Ags

Serum sickness- foreign protein causes arthritis, vasculitis, nephritis

Arthus reaction- localized necrosis, from vasculitis (large complexes ppt)

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23
Q

What are the characteristics of Type IV hypersensitivity reactions?

A

Stimulation of T cells leads to tissue injury

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24
Q

What test is prototypical of Type IV hypersensitivity reactions?

A

Mantoux/tuberculin test

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25
What cells are involved in Type IV hypersensitivity reactions and how do they function?
CD4- produce inflammatory cytokines (tissue damage) CD8- kill viral infected cells
26
What are the characteristics of autoimmune diseases?
Reactions against self Ags Breakdown in self tolerance
27
What are the two kinds of tolerance and where do they occur?
1. Central- BM and thymus | 2. Peripheral- peripheral tissues
28
How does tolerance occur?
Central- T and B cells that are self reactive are killed/inactivated Peripheral- self reactive lymphs are inactivated (anergy), suppressed or killed
29
What cell suppressed self reactive lymphs?
Tregs
30
What factors can lead to disruption of tolerance?
HLA genes Defective tolerance Abnormal self Ag displays Inflammation
31
How may infections cause autoimmune reactions?
Upregulation of a costimulator Molecular mimicry Injury leads to release of cryptic self Ags (no tolerance) Alteration of self Ag
32
What is molecular mimicry?
Microbes express Ags similar to self Ags and Abs cross react
33
What are the common autoimmune diseases?
SLE Sjögren syndrome Scleroderma/systemic sclerosis Mixed connective tissue disease Transplant rejection
34
What are the characteristics of SLE?
Systemic disease involving ANAs Can affect all organs
35
How does tissue injury occur in SLE?
Immune complex deposition (Type III) Ab mediated actions (Type II)
36
How does SLE affect various organ systems?
Vessels- necrotizing vasculitis Kidney- lupus nephritis Skin- butterfly rash, erythema Spleen- splenomegaly, capsular thickening Lungs- pleuritis and effusions, fibrosis, hypertension Serosal cavity- fibrinous exudate, effusions Cardiovascular- valve thickening (mitral and aortic), peri and myocarditis
37
What type of vegetations are associated with SLE?
Libman-Sacks/nonbacterial verrucous endocarditis On mitral and tricuspid
38
What are the characteristics of Sjögren syndrome?
Immune mediated salivary and lacrimal gland destruction Dry eyes (keratoconjunctivitis) and mouth (xerostomia)
39
How is Sjögren syndrome diagnosed?
Lip biopsy
40
What are patients with Sjögren syndrome at risk for?
B cell lymphoma
41
What are the characteristics of scleroderma?
Chronic inflammation Small vessel damage Interstitial and perivascular fibrosis (skin, GI tract) Claw-like fingers (autoamputation), drawn mask-like face
42
What types of scleroderma are there and what are their characteristics?
Diffuse- widespread skin involvement, early visceral involvement Limited- late visceral involvement
43
Mixed connective tissue disease includes features of what disorders?
SLE Scleroderma Polymyositis
44
Why does graft rejection occur?
The immune system recognizes the graft as foreign Triggered by foreign HLA histocompatibility molecules
45
What are the two classes of HLA molecules? What cells are they present on and what cells are they recognized by?
Class I- on all uncleared cells, CD8 recognition Class II- on APC, CD4 recognition
46
What are the two pathways of graft rejection?
Direct- donor APC activates host T cells Indirect- host APC presents donor Ag to T cells
47
What are the three types of graft rejection? What are their characteristics?
1. Hyperacute- previously sensitized, occurs in minutes to days, cyanotic/mottled organ 2. Acute- newly synthesized Abs, occurs in days to months, causes necrotizing vasculitis 3. Chronic- progressive dysfunction, occurs in months to years, allograft ischemic, immune suppression
48
What is graft vs host disease?
Donor lymphs (BM transplant) recognize host cells as foreign T cell injury
49
What host components are most affected by GVHD?
Immune cells Biliary epithelium Skin GI tract
50
How is infection differentiated from GVHD?
Biopsy
51
What types of immunodeficiency syndromes are there?
Primary/congenital Acquired/secondary
52
What are the characteristics of primary immunodeficiencies?
Genetically determined Detected early (6mo-2yr) Affects innate immunity and cellular components of adaptive immunity
53
Why are primary immunodeficiencies detected at 6mo?
Mom provides IgA (breastfeeding, drop off from in utero)
54
What are the common primary immunodeficiencies? What are their characteristics?
Defects in leukocyte function Defects in complement Severe combined immunodeficiency- defects in both immune responses X-linked/Bruton’s aggamaglobulinemia- no serum Ig Common variable immunodeficiency- hypogammaglobulinemia Isolated IgA deficiency- mucosal immunity affected Hyper IgM syndrome- no other Ig, can react with blood cells DiGeorge syndrome- thymic and parathyroid hyperplasia
55
What are common defects in leukocyte function?
Adhesion defects Phagylosome function defect (Chediak-Higashi) Microbicidal activity defect Defect in TLR signalling (recognition)
56
What deletion is common in DiGeorge syndrome?
22q11
57
What type of immunodeficiency is more common?
Secondary
58
What are common acquired immunodeficiency disorders? What are their characteristics?
HIV- CD4 depletion Cancer therapy- BM precursor depletion BM cancers- reduced leukocyte production Malnutrition- maturation and function inhibited Splenectomy- reduced microbial phagocytosis
59
What are the characteristics of AIDS?
Immunodeficiency retrovirus T cell suppression (CD4)- inactivation and death Opportunistic infections Tumours CNS disease
60
What are the phases of HIV?
1. Primary infection- virus dissemination 2. Chronic infection- latency 3. AIDS
61
What tumours are associated with AIDS?
Kaposi sarcoma- vascular, HHV8/KSHV Lymphoma- B cell NHL Squamous cell (HPV)
62
What infection increases the likelihood of CNS lymphomas in AIDS?
EBV
63
What are the characteristics of amyloidosis?
Extracellular deposits of fibrillation proteins result in damage and dysfunction Aggregations of insoluble misfolded proteins
64
How are proteins in amyloidosis misfolded?
Beta pleated sheets
65
What stain is used for amyloidosis and what does it look like?
Congo red Apple green birefringence with polarized light (red/pink with light mic)
66
What are the forms of amyloidosis?
1. Amyloid light chain (plasma cells) 2. Amyloid associated (chronic inflammation) 3. Beta amyloid (Alzheimer’s)
67
What are different amyloidosis disorders?
Primary- immunocyte dyscrasias with amyloidosis (light chain, tumour secreted) Secondary reactive- chronic inflammation Hemodialysis associated (60-80% of patients) Heredofamilial amyloidosis (familial Mediterranean fever) Localized- endocrine and aging
68
What is the morphology of amyloidosis?
Enlarged, waxy, form tissues Kidneys- glomerular hyalinization, tubular deposits, atrial wall thickening Sago spleen- tapioca granules in white pulp (follicles) Lardaceous spleen- red pulp deposits Hepatomegaly Heart- subendocardial droplets Macroglossia Carpal tunnel syndrome
69
What are the favoured biopsy sites for amyloidosis?
Kidney rectum Gingiva Abdominal fat pad (reduced sensitivity)

Pathology (25 decks)

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