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Pathology > Diseases of the Immune System > Flashcards

Diseases of the Immune System Flashcards

1
Q

What are the characteristics of an inflammatory response?

A
  • nonspecific/generalized process ot neutralize & eliminate foreign entity
  • acute/local inflammation
  • neutrophils, macrophages, T-lymphocytes
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2
Q

What are the characteristics of an immune response?

A
  • response to neutralize & eliminate specific foreign entity
  • identify & isolate antigens unique to a single pathogen
  • T-lymphocytes, B-lymphocytes, NK cells, APC
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3
Q

What are the cells of the immune system?

A
  • intravascular leukocytes: monocyte, eosinophil, basophil, neutrophil, lymphocyte
  • extravascular: histiocyte, plasma cell, mast cell
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4
Q

What are the myeloid cells?

A
  • nuetrophils: acute response
  • eosinophils: respond to parasitic infection
  • cytoplasmic granules
  • basophils: histamine, heparin, serotonin -> anaphylactic shock
  • monocytes: APC, chronic inflammation-> phagocytosis
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5
Q

What are the lymphoid cells?

A
  • T, B, NK
  • CD4+/CD8+ influences function
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6
Q

What is innate immunity?

A
  • major role by epithelial barriers, neutrophils, macrophages, NK cells
  • acute inflammation
  • stimulates adaptive immunity
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7
Q

What are natural killer cells in innate immunity?

A
  • CD8- or CD4-
  • important for immunoserveillance
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8
Q

What is the humoral response in adaptive immunity?

A
  • requires antigen-specific molecules
  • more effective than innate immunity
  • B lymphocyte
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9
Q

What are T lymphocytes?

A
  • thymus derived
  • 70% of lymphocytes in blood
  • recognize MHC-bound peptides on APC via TCR
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10
Q

What are the classes of T lymophocytes?

A
  • MHC class 2 -> CD4+ T cells
  • MHC class 1 -> CD8+ T cells
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11
Q

What is the role of CD4+ and CD8+ T cells?

A
  • CD4+: interact with B cells, macrophages,produce cytokines, eliminate extracellular pathogens
  • CD8+: cytotoxic T cells, destroy intracellular pathogens
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12
Q

What are B lymphoytes?

A
  • 20% of lymphocytes
  • undergo antigen stimulation in lymph nodes/organs
  • interact with CD4+ T cells
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13
Q

What are the characteristics of the Ig families?

A
  • 95% of circulating antibodies (IgG, IgM, IgA)
  • IgG: coats microbes, targets for phagocytosis, promotes passive immunity
  • IgG & IgM: activate complement system
  • IgA: mucosal secretions
  • IgE: tissue mast cells
  • IgD: surface on B cells; not secreted
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14
Q

What are aberrant inflammatory responses?

A

type 1, 2, 3, and 4 hypersensitivity

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15
Q

What are the immune disorders?

A
  • autoimmune disease
  • transplant rejection
  • immunodeficiency
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16
Q

What is type 1 hypersensitivity (IgE)?

A
  • allergy reaction; treated with anti-histamine
  • immediate hypersensitivity
  • Ab response to external antigen
  • IgE binds & activates mast cells (histamine) -> affinity for Fc of IgE heavy chain
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17
Q

When linked, what does IgE promote the release of?

A
  • histamine, prostaglandins,cytokines
  • results in vasodilation, mucus secretion, SM spasm, leukocyte activation
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18
Q

What are the 3 subtypes of type 2 hypersensitivity?

A
  1. opsinization & phagocytosis
  2. inflammation & complement mediated
  3. antibody mediated
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19
Q

What is opsonization & phagocytosis in type 2 hypersensitivity?

A
  • C3b-dependent
  • host cell opsonized with autoantibodies
  • typified by thrombocytopenia purpura
  • no association with inflammation
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20
Q

What is iodiopathic thrombocytopenia purpura in type 2 hypersensitivity?

A
  • low number of platelets in blood
  • < 5000 platelets per cubic mL
  • treated with platelet transfusion
  • bone biopsy shows megakaryocytic hyperplasia
  • pupura: 3-10mm hemorrhages
  • petachae: < 3mmhemorrhages
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21
Q

What is inflammation & complement mediation in type 2 hypersensitivity?

A
  • autoantibodies on host cells activate C3a/C5a
  • typified by Rh factor incompatibility, Goodpasture syndrome
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22
Q

What is Goodpasture syndrome?

A

autoantibodies to domain of alpha 3 chain of collagen 4 (basement membrane)

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23
Q

What is antibody mediated cellular dysfunction in type 2 hypersensitivity?

A
  • autoantibodies impair host cell receptors without phagocytosis or inflammation
  • typified by Graves disease or myasthenia gravis
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24
Q

What is myasthenia gravis in type 2 hypersensitivity?

A
  • caused by defect in transmission of nerve impulses to muscles (usually in the face)
  • treated with pyridostigmine -> increase half-life of Ach
  • presents as ptosis (drooping eyelids), diplopia (double vision), dyasarthria (difficulty speaking)
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25
Q

What is Graves disease in type 2 hypersensitivity?

A
  • antibodies bind receptors on thyroid follicular cells
  • scalloping of colloid (thyroid gland)
  • hyperfunctional thyroid, exopathalmos
  • treated with immunosuppressants & radioactive iodine
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26
Q

What is type 3 hypersensitivity?

A
  • host antigen-autoantibody immune complex
  • circulation of immuno-complexes in blood vessels
  • depends on deposition of performed immuno-complexes
  • typified by systemic lupus & scleroderma
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27
Q

What is systemic lupus in type 3 hypersensitivity?

A
  • women > men
  • form antigen-antibody complexes
  • antinuclear antibodies: dsDNA
  • glomerulonephritis leads to renal failure & death
  • deposition of complexes causes malar (rash on skin)
  • cryoglobulins produce Raynaud’s phenomenon
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28
Q

What is systemic sclerosis in type 3 hypersensitivity?

A
  • common among older women
  • skin derived; progressive fibrosis
  • can lead to dysphagia
  • anitgen complexes
29
Q

What are the 2 subtypes of systemic sclerosis?

A
  • diffuse pattern: widespread skin, rapid progression, visceral involvement; Abs to DNA topoisomerase 1
  • limited pattern: lmited ksin & visceral involvement, slow progression; Abs to centromere
30
Q

What is CREST syndrome in systemic sclerosis?

A

associated with
* calcinosis
* Raynauds syndrome
* esophageal dysmotility
* scelrodactyly
* telangiectasia

31
Q

What is type 4 hypersensitivity?

A
  • delayed-type
  • T-cell mediated to external or self Ag
  • NO Abs
  • 12-48 hours after exposure
  • CD4+ T cells promotes cytokine secretion & tissue destruction
  • CD8+ T cells directly cytotoxic to Ag
  • TB and poison ivy reactions
32
Q

What are the characteristics of a poison ivy recation in type 4 hypersensitivity?

A
  • triggered by urushiol (external Ag)
  • treated with methotrexate
33
Q

What are the characteristics of a transplant rejection?

A
  • incompatibility b/w donor & host
  • autograft (donor=self)
  • allograft (donor=identical twin)
  • xenograft (donor=another species)
  • split ( dead organ divided b/w 2 patients)
  • domino ( mulitple transplants)
34
Q

What is a hyperacute transplant rejection?

A
  • occurs within minutes to hours
  • interaction of preformed host Abs
  • vascular disorders
  • acute fibrinoid necrosis in blood vessel walls precipitates occlusion
35
Q

What is an acute transplant rejection?

A
  • occurs within days-months in immunosuppressed patient
  • cellular/humoral based
  • require immunosuppressive therapy
  • acute cellular response: CD4+ and CD8+ T cells
36
Q

What 3 types of hypersensitivity are autoimmune?

A

types 2, 3, & 4

36
Q

What is a chronic transplant rejection?

A
  • over years
  • intimal hyperplasia develops in graft blood vessels
  • not retarded by immunosuppression
37
Q

What is a graft vs host transplant rejection?

A
  • occurs when donor lymphocytes respond to host MHC
  • common in bone marrow trans.
  • time onset varies
  • acute: days to week after trans.; destruction of liver
  • chronic: follows acute GvH or independ.
38
Q

What is congenital immunodeficiency?

A
  • severe immunodeficiency
  • 6 months-2 years as repeated infections
39
Q

What 3 types of hypersensitivity are autoimmune?

A

types 2, 3, & 4

39
Q

What is Brutons disease in the B cell lineage of congenital immunodeficiency?

A
  • X-linked recessive agammaglob.
  • absence of immature (IgD/IgM) B cells
  • depressed serum levels of all classes of IgGs
  • normal T cell repsonses
  • males > females
40
Q

What 3 types of hypersensitivity are autoimmune?

A

types 2, 3, & 4

41
Q

What is the B cell lineage of congenital immunodeficiency?

A
  • X-linked recessive agammaglob. (Bruton’s Disease)
  • absence of immature
42
Q

What is common variable immunodeficiency (CVID) in the B cell lineage of congenital immunodeficiency?

A
  • prone to autoimmune disorders
  • normal T cell responses
  • immature B-cells present
  • males=females
43
Q

What is hyper IgM syndrome in the B cell lineage of congenital immunodeficiency?

A
  • normal immature B cells
  • normal/overproduction of IgM; fail to Ig isotype-switch
  • X-linked recessive
  • increased infections
44
Q

What 3 types of hypersensitivity are autoimmune?

A

types 2, 3, & 4

45
Q

What is IgA deficiency in the B cell lineage of congenital immunodeficiency?

A
  • normal immature B cells
  • normal production of IgM; normal isotype switch to IgG & IgE NOT IgA
  • sinopulmonary infections and diarrhea
46
Q

What is DiGeorge syndrome in the T cell lineage of congenital immunodeficiency?

A
  • deficient T cell maturation
  • T cell receptor capable of Ag recognition
  • reduced T cell cytokine production
  • thymic hypoplasia
  • repeated infections
47
Q

What is MHC class 2 deficiency in the T cell lineage of congenital immunodeficiency?

A
  • inability to develop CD4+ T cells
  • B cell and serum Igs are indirectly affected
  • reduced T cell cytokine production
48
Q

What are the characteristics of HIV?

A
  • acquired immunodeficiency
  • targets CD4+ T cells; eventually depletes
  • surface protein gp 120 binds to Cd4+
  • changes in gp 41 promote gp 120 cellular entry
  • 7-12 years
49
Q

What is leukopenia in non-proliferative WBC disorders?

A
  • reduced lymphocytes
  • secondary to disease or therapy/drugs
50
Q

What is lymphopenia in non-proliferative WBC disorders?

A
  • reduced granulocytes
  • neutropenia as reduced neutrophils
51
Q

What is neutrophilic leukocytosis?

A
  • reactive proliferative disorder
  • result of bacterial infection or sterile inflammation
52
Q

What is eosinophilic leukocytosis?

A
  • reactive proliferative disorder
  • result of allergic recations & parasitic infections
53
Q

What is basophilic leukocytosis?

A
  • reactive proliferative disorder
  • associated with conditions like neoplastic disease
54
Q

What is lymphocytosis?

A
  • reactive proliferative disorder
  • associated with infections
  • increased lymphocytes
  • caused by EBV -> B ell proliferation
55
Q

What is lymphadenitis?

A
  • reactive proliferative disorder
  • associated with lymphadenopathy
  • acute: enlarged B cell germinal centers
56
Q

What are the types of chronic lymphadenitis?

A
  • follicular: activated B cells migrate into follicular zone
  • paracortical hyperplasia: activation of T cells thta proliferate and displace B cell germinal centers
  • sinus histiocytosis: distention of lymphatic sinusoids due to endothelial hypertrophy
57
Q

What are the 3 sets of words of neoplastic WBC disease?

A
  1. acute (fast/blastic) or chronic (slow)
  2. myeloid (RBC/granulocyte) or lymphoid (T/B cells)
  3. leukemia (bone marrow/thymus) or lymphoma (lymphoid tissues)
58
Q

What is contained in the bone marrow?

A
  • all hematopoietic stem cells
  • progenitor lymphoid cells
  • myeloid progenitor & differentiated cells
59
Q

What is contained in the thymus & lymph nodes?

A
  • thymus -> differentiated T cells
  • lymph nodes -> differentiated B cells, some T cells
60
Q

Any myleoid cancer has to be ….

A

a leukemia

61
Q

What are the 4 types of leukemia?

A
  1. ALL: acute lymphoblastic leukemia
  2. AML: acute myeloblastic leukemia
  3. CLL: chronic lymphocytic leukemia
  4. CML: chronic myeloid leukemia
62
Q

What is acute lymphoblastic leukemia (ALL)?

A
  • 80% of child leukemias
  • pre B/T cell origin
  • bone marrow involvement
  • cytopenia of normal mature hematopoietic cells
  • 80% cure rate in all
63
Q

What is acute myeloblastic leukemia (AML)?

A
  • proliferation of precursor myeloid cells
  • affects more adults (>50 years old)
  • contains auer rods
  • bone marrow involvement
  • 50-80% remission with treatment
64
Q

What is chronic myeloid leukemia (CML)?

A
  • mature but abnormal myeloid
  • associated with philadelphia chromosome
  • bcr-abl fusion protein
  • affects 25-60 year old
  • slow disease progression
65
Q

What is chronic lymphocytic leukemia (CLL)?

A
  • B cell lineage
  • asymptomatic
66
Q

What is Hodgkin’s lymphoma?

A
  • has Reed-Sternberg cells
  • bilobed (mirror image)
  • large cells meausre 15-45 um
  • express CD30 & CD15
  • B cell derived
  • contiguous spread
  • cured with chemo

Pathology (7 decks)

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