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Immune disorders Flashcards

1
Q

Immune Reactions

A

Immune system has numerous functions including
Prevention/defense from infection
Inactivation and clearance of foreign substances

Immune reactions can cause host tissue injury
Hypersensitivity reactions cause release of inflammatory mediators that lead to tissue damage and eventually can lead to scarring (repair)

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2
Q

Hypersensitivity Reactions

A

Type I – Immediate (anaphylactic)
Mediated by TH2 cell cytokines
Via IL-4 action on B cells get class switching to IgE
Via IL-5 get development and activation of eosinophils

Type II – Antibody-mediated
Secreted ***IgG and IgM antibodies participate directly in injury to cells

Type III – Immune complex mediated
IgG and IgM antibodies bind antigens and the antigen-antibody complexes deposit in tissues and induce inflammation

Type IV – Cell mediated
Sensitized T-lymphocytes (TH1, TH17 cells and CTLs)

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3
Q

hypersensitivity and granuloma

A

Type IV hypersensitivity

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4
Q

Type I Hypersensitivity Disorders

A

Anaphylaxis
Hypotension secondary to vasodilation that may lead to shock
Laryngeal edema that may lead to airway obstruction
Inflammation and tissue destruction leading to scarring

Asthma
Reversible bronchoconstriction
Mucous hyperplasia
Inflammation and tissue destruction leading to scarring

Urticaria
Dermal angioedema with wheals
Itching

Food allergies
Increased intestinal peristalsis
Inflammation and tissue destruction leading to scarring

Allergic rhinitis and sinusitis
Mucous hyperplasia
Inflammation and tissue destruction leading to scarring

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5
Q

Type I Immediate Hypersensitivity

A

Immediate phase: *** 5 to 30 minutes post exposure
for about an hour

Dilated leaky vessels –> edema
Contraction of smooth muscle
Increased mucus production

Late phase: **2 to 24 hours later and may lasts days

Inflammation with eosinophilia–> tissue injury

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6
Q

petechiae and echymoses, what do you start to think?

A

platelets and/or von Willebrandt’s

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7
Q

granulomas associated with?

A

Type IV- cell mediated hypersensitivity (activated T lymphocytes)

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8
Q

Type II hypersensitivity

A

Type II- antibody mediated. IgG or IgM binding

good pasture syndrome

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9
Q

Mechanisms of type I hypersensitivity

A

Early - TH2 activation  IgE class switch in B cells  IgE  release of mediators from mast cells

Later - TH2, epithelial and mast cells secrete IL-5 and eotaxin → eosinophils → enzyme (major basic protein and cationic protein) release → tissue destruction

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10
Q

signs/ symptoms of anaphylaxis

A 
lightheadedness
SOB, stridor
skin-- hives, itchiness, flushing
Heart-- fast or slow, low blood pressure
swelling of lips, tongue and/or throat
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11
Q

Mast cell secretagogues

A

IgE (via Fc receptors), Anaphylatoxins C5a, C4a and C3a –> Mast cell –> Eosinophil chemotactic factor

among many other things

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12
Q

Urticaria

A

dermal hyperpermeability & wheals

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13
Q

angioedema

A

edema of dermis, mucosae and deeper tissues

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14
Q

hereditary angioedema

A

autosomal dominant C1 inhibitor deficiency

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15
Q

asthma

A

reversible airway obstruction

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16
Q

autoimmunity

A

reactions against an individual’s own tissues and cells

types 2,3, and/or 4

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17
Q

Placental transfer in autoimmune disorders

A

Maternal igG antibodies

thyroid hormone receptor –> graves
RBCs–> hemolytic anemia
platelets–> thrombocytopenia
acetylcholine receptor–> myasthenia gravis
Ro & La–> Cutaneous lupus & heart block

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18
Q

HLA alleles and the diseases

A 
Rheumatoid arthritis- DR4
Type 1 diabetes DR3/DR4
Ankylosing spondylitis- B27
Postgonococcal arthritis-- B27
Autoimmune hepatitis- DR3
Primary Sjogren syndrome- DR3
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19
Q

Non-HLA genes associated with autoimmune diseases

A

PTPN22– protein tyrosine phosphatase
May affect signaling in lymphocytes
may alter activation of self-reactive T cells

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20
Q

Types II/III Antibody Mediated Hypersensitivity

A

Antibody-dependent complement-mediated cytotoxicity (Type II)
Classical complement cascade activation leads to lysis of cells
Direct lysis via membrane attack complex (C5b - C9), punches holes in cell
Mechanism normally used for killing Neisseria spp. bacteria
Antibody-dependent cell-mediated cytotoxicity (Type II)
Binding of antibody leads to activation of macrophages, neutrophils, eosinophils, natural killer cells, etc. that lead to cell injury and death
Mechanism normally used for killing other microorganisms, etc
Antibody-dependent cellular dysfunction (Type II)
Antibody binding causes abnormal cellular function (e.g. Graves disease)
No normal use for this mechanism
Antigen-antibody complex mediated attack on host tissues (Type III)
Antigen-antibodies complexes deposit or are initiated in tissue
Complement is activated (C5a attracts infl. Cells, C3a and C5a cause local vasodilation, etc.)
No normal use for this mechanism

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21
Q

Mechanisms of Antibody-mediated Injury

A

Antibody-dependent complement-mediated cytotoxicity
e.g. ABO incompatibility

Antibody-dependent cell-mediated cytotoxicity
e.g. killing virally infected cell

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22
Q

Autoimmune hemolytic anemia - mechanism

A

opsonization and phagocytosis of red cells

direct hemolysis via complement with ABO mismatch

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23
Q

Immunologic Thrombocytopenic Purpura

A

Spleen: normal size, congested sinusoids, prominent germinal centers, occasional megakaryocytes
Marrow: increased megakaryocytes
Peripheral blood: megathrombocytes

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24
Q

Goodpasture Syndrome

A

Diagnose = linear fluorescence

Antigen hidden in type collagen IV—exposed by smoking, solvents etc.

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25
antigen and manifestation: SLE
lupus nuclear antigens nephritis, skin lesions, arthritis
26
antigen and manifestation: poststreptococcal glomerulonephritis
streptococcal cell wall antigen nephritis
27
antigen and manifestation: polyarteritis nodosa
Hep B virus antigens (some cases) Systemic vasculitis pulmonary arteries are NOT involved
28
antigen and manifestation: Reactive arthritis
Bacterial antigens acute arthritis
29
antigen and manifestation: serum sickness
foreign serum protein arthritis, vasculitis, nephritis
30
antigen and manifestation: arthus reaction
injected foreign proteins cutaneous vasculitis
31
acute proliferative glomerulonephritis
can be post infectious (strepto, staphylo, virus) Immune complexes formed in circulation or on membrane, c3 deposited before others
32
Rheumatoid arthritis
citrullinated self proteins? chronic arthritis
33
MS
antigens to myelin basic protein myelin destruction by activated macrophages demyelination in CNS
34
Type 1 diabetes mellitus
antigens of pancreatic islet beta cells destruction of islet cells by CTLs insulitis, destruction of beta cells
35
inflammatory bowel disease
chronic intestinal inflammation Th1 and Th17 cytokines
36
psoriasis
plaques in the skin | Th17 cytokines
37
contact sensitivity
environmental antigens, poison ivy, etc. skin rash and blisters Th1/ Th17? cytokines
38
Guillain Barre Syndrome
Often begins after an infection or vaccination Ascending paralysis (also some sensory loss) 2-5 % mortality 20% disability Increased CSF protein Viral or bacterial disease or vaccination  T cell mediated peripheral nerve demyelination Segmental demyelination of peripheral nerves Axons damaged when severe Chronic inflammation—most intense in spinal and cranial nerve roots
39
Rheumatic fever
molecular mimicry
40
Acute Rheumatic Fever
Pericarditis Myocarditis; Aschoff bodies, Anitschkow cells Endocarditis
41
CREST syndrome associated with
centromeric (coarse speckled) staining
42
SLE, Drug-induced lupus associated with
Homogenous staining histone antigens
43
Fine speckled staining associated with
non specific
44
systemic sclerosis antigens
DNA topoisomerase I
45
autoimmune myosiis antigens
histidyl-tRNA synthetase
46
Sjogren syndrome antigens
RNP
47
SLE antigens
pretty much everything
48
how many criteria make SLE?
4 or more of the 11 photosensitivity, hemolytic anemia, anti-dna antibody, antiphospholipid antibodies, false-positive for syphilis, e.g.
49
prevalence of stuff in SLE
``` hematalogic 100 arthritis 80-90 skin 85 renal 50-70 raynaud 15-40 ```
50
SLE features
butterfly rash, fever, joint pain LE bodies or hematoxylin bodies cells that engulf these bodies are called LE cells In situ immune complex formation antigens probably the most important anti-phospholipid syndrome thrombotic microangiopathy recurrent miscarriages Nuclear antigens: nucleosomes- DNA and histones anti double stranded DNA Smith antigen Ro/SS-A, La/ SS-B Kidneys (75% of patients have renal involvement) Increased serum creatinine RBCs and RBC casts in the urine
51
Sjogren syndrome
Mikulicz syndrome - lacrimal and salivary gland enlargement from any cause Sicca syndrome Keratoconjunctivitis sicca  dry eyes with blurred vision, thick secretions in conjunctival sac Xerostomia  dry buccal mucosa, difficulty swallowing, buccal fissures Dry nasal mucosa SS-A (Ro) and SS-B (La) Lip biopsy Schirmer test
52
Systemic Sclerosis
``` polyarthralgia tight skin on hands and face telangiectasias difficulty swallowing morphea CD4+ lymphocytes stimulate fibroblasts and collagen formation ``` Anti-Scl-70- against nuclear topoisomerase anti-centromere 90% anti-centromere in CREST GI tract- esophagus most common kidneys- intimal proliferation and thickening of arteries --> ischemia
53
CREST
``` calcinosis raynaud phenomenon esophagal dysmotility sclerodactyly telangiectasias ``` ANTI-Centromere antibody
54
Dermatomyositis
heliotropic rash often associated with occult tumors anti-Jo-1
55
Polymyositis
Autoimmune disease involving skeletal muscle without skin involvement
56
Mixed connective tissue disease
Ill-defined autoimmune disease with overlapping features
57
Transplantation
Mechanisms of rejection T Cell related Cytotoxic T lymphoctes--> parenchymal & endothelial cell injury CD4+--> delayed hypersensitivity reactions CD4+--> activation of macrophages Antibody Mediated ``` Types of Rejection Hyperacute -preformed antidonor antibodies are present Acute cellular -(direct pathway) T cells of recipient recognize allogeneic (donor) MHC molecules on the donor’s APCs Acute humoral - (indirect pathway) exposure to the class I and class II HLA antigens of the donor graft may evoke antibodies and attack graft vessels (vasculitis) Chronic - (indirect pathway) recipient T cells recognize MHC antigens of the graft donor after they are presented by the recipient's own APCs and induce direct cell mediated inflammatory damage or production of circulating antibodies that cause vascular injury in graft ```
58
HIV phases
acute- similar to flu for a few weeks about 3-6 weeks post infection middle chronic: asymptomatic for years, prolonged by HAART AIDS fever, weight loss, diarrhea, generalized generalized lymphadenopathy, multiple opportunistic infections, neurologic disease, and secondary neoplasms or
59
transplant phases
0-3 days hyperacute 4 days to 6 months- acute more than 6 months- chronic rejection
60
bone marrow transplant rejection
graft vs host diseases
61
Bruton
x linked agammaglobulinemia ``` males after 6 months bruton tyrosine kinase mutation decreased B cells no plasma cells no intestinal IgA (giardia infections) No Igs for opsonization of organizms (encapsulated bacteria) ```
62
DiGeorge
Thymic Hypoplasia 22q11 abnormal 3rd & 4th pharyngeal pouches Thymus, parathyroids, some of the clear cells of the thyroid, and ultimobranchial body defects Hypoparathyroidism with hypocalcemia can lead to tetany Cardiac outlet defects Facial abnormalities Viral, fungal and protozoal infections T-cell deficiency
63
Hyper IgM
Inability of helper T cells to induce IgG, IgA, and IgE formation
64
Common Variable Immunodeficiency
Absent plasma cells (maturation blockage) No immunoglobulins Normal numbers of other B cells
65
Isolated IgA deficiency
Low levels of secretory and serum IgA Anaphylactic transfusion reactions to IgA in donor plasma Immune disorders such as SLE and RA
66
complement deficiencies
C1 inhibitor = hereditary angioedema induced by stress or trauma Episodes of edema affecting skin and mucosal surfaces Life-threatening asphyxia Nausea, vomiting, and diarrhea Rx - C1 inhibitor concentrates ``` C5, 6, 7, 8, or 9 (attack complex) Recurrent neisserial (gonococcal and meningococcal) infections ```
67
Wiskott-Aldrich Syndrome
WASP (Wiskott-Aldrich syndrome protein) gene mutation Thrombocytopenia, eczema & recurrent infections Petechiae or purpura, hematemesis or melena, epistaxis Recurrent infections, ending in early death
68
HIV immunity
1% of white Americans inherit two defective copies of the CCR5 gene and are resistant to infection
69
CDC AIDS-defining conditions
``` cervical cancer, invasive encephalopathy kaposi sarcoma lymphoma: burkitt, immunoblastic, primary of brain wasting syndrome ```
70
Major abnormalities of immune function in AIDS
selective loss of CD4+ helper T cell subset susceptibility to opportunistic infections susceptibility to neoplasms hypergammaglobulinemia and circulating immune complexes
71
aids-related malignancy
B cell lymphoma
72
Amyloidosis
cross beta pleated sheet conformation congo red stain apple green birefringence
73
Classification of amyloidosis
primary- monoclonal plasma cell proliferations (immunoglobulin light chains, chiefly delta) secondary- chronic inflammatory conditions (SAA) chronic renal failure (beta two microglobulin) alzheimer (APP) type 2 diabetes (islet amyloid peptide) systemic senile amyloidosis-- transthyretin medullary carcinoma of thyroid- calcitonin

Transition to Clinical Medicine (6 decks)

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