• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/56

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

56 Cards in this Set

  • Front
  • Back
HLA B27
PSORIASIS, AS, IBD, REITER'S SYNDROME
HLA B8
GRAVES, CELIAC
HLA DR2
MS, hay fever, SLE, Goodpastures
HLA (general information)

Class I
Class II
Human Leukocyte Antigen (MHC in animals)

Class I: A, B, C
Class II: DR, DP, DQ

HLA genes were identified as a result of the ability to successfully transplant organs between HLA similar individuals.
HLA DR3
DM type 1
HLA DR4
RA, DM type 1
HLA DR5
Pernicious anemia, Hashimoto's
DR7
Steroid responsive nephrotic syndrome
AUTOANTIBODIES

Antihistone
Anti-IgG
Anticentromere
AntiSCL70
Antimitochrondrial
Antismooth muscle
Antigliadin
Anti-epithelial cell
Antimicrosomal
Anti-Jo1
Antihistone - drug induced lupus
Anti-IgG - Rheumatoid
Anticentromere - scleroderma (CREST)
AntiSCL70 - scleroderma (lung)
Antimitochrondrial - PBC
Antismooth muscle - autoimmune hepatitis
Antigliadin - celiac
Anti-epithelial cell - pemphigus vulgaris
Antimicrosomal - hashimoto's
Anti-Jo1 - polymyositis and dermatomyositis
Bruton's agammaglobulinemia
X linked recessive defect in BTK.

Infections after 6 months when maternal IgG declines.
DiGeorge syndrome
22q11. Thymus and parathyroid fail to develop because 3rd and 4th pouches fail to develop.

Presents with tetany owing to hypocalcemia. Recurrent viral and fungal infections due to T cell deficiency. Also congenital defects of heart and great vessels.
SCID
B and T cell damage.

Defect in early stem-cell differentiation owing to either MHCII failure, defective IL2 receptors, or ADA deficiency.

Presents with recurrent infections from all pathogens.
IL12 receptor deficiency
Disseminated mycobacterial infections owing to decreased T cell activation.
Hyper IgM syndrome
Defect in CD40L on CD4 Th cells leads to inability to class switch.

Presents early in life with severe pyogenic infections. High levels of IgM, low levels of IgG, A, and E.
Wiskott-Aldrich syndrome
X linked defect in WASP gene leading to defect in ability to mount an IgM response to capsular polysaccharides of bacteria.

Elevated IgA, normal IgE, and low IgM.

WIPE: Infections, thrombocytopenic purpura, and Eczema.

OTHER WASP defects: X linked thrombocytopenia, X linked neutropenia (allelic heterogeneity).
Job syndrome
Failure of IFN-gamma production by Th cells.

PMNs fail to respond to chemotactic stimuli. Presents with recurrent cold abscesses, eczema, coarse facies, retained primary teeth, and high IgE
Leukocyte adhesion deficiency syndrome
LFA-1 defect.

Severe pyogenic and fungal infections and delayed separation of umbilicus. Also leukocytosis.
Chediak-Higashi disease
AR, defect in microtubular function and lysosomal emptying of phagocytes.

Presents with recurrent pyogenic infections by staph and strep, partial albinism, and peripheral neuropathy.
CGD
Lack of NADPH oxidase activity.

Marked susceptibility to bacterial infections. Recurrent lung infections and granulomatous lesions.

Negative nitroblue tetrazolium dye reduction test.

Major organisms: Staph aureus, Burkholderia, Serratia, Nocardia , Aspergillus

Note: not all catalase + organisms have increased infectivity in CGD (TB, cryptococcus, corynebacterium are also catalase + but no increased risk)
Chronic mucocutaneous candidiasis
T cell dysfunction specifically against candida albicans.
Selective immunoglobulin deficiency
Deficiency in a specific class of Ig, due to a defect in isotype switching.

Selective IgA deficiency is the most common. Presents with sinus and lung infections, milk allergies and diarrhea are common.
Ataxia telangiectasia
Defect in DNA repair enzymes with associated IgA deficiency. Presents with ataxia and telangiectasias.
Common variable immune deficiency
Normal numbers of circulating B cells, decreased plasma cells, decreased Ig; can be acquired in 20s-30s.
Type I

diseases
Allergic, anaphylactic. degranulative.

Anaphylaxis, rhinitis
Type II

diseases
Cytotoxic, antibody mediated

Hemolytic anemia
ITP
Erythroblastosis fetalis
Rheumatic fever
Goodpasture's
Bullous pemphigoid
Graves
Myasthenia
Type III

diseases
Immune complex mediated; antigen antibody complexes deposit and fix complement.

Lupus
RA
PAN
Post-strep glomerulonephritis
Serum sickness (more common than arthus)
Arthus reaction (skin)
Hypersensitivity pneumonitis
Type IV

diseases
Delayed, T cell mediated. Not transferable by serum.

Type I DM
MS
Guillain Barre
Hashimotos
GVHD
PPD
Contact dermatitis
What do we treat with passive immunity (recieving preformed antibody)
Tetanus, botulism, HBV, rabies,
most antivenoms.
Deficiency of C1 esterase inhibitor
Hereditary angioneurotic edema
Deficiency of C3
severe recurrent pyogenic sinus and respiratory infections
Deficiency of Factor I ("aye")
Results in immune deficiency by paradoxical depletion of complement due to excess, useless activation.
Deficiency C6-C8
Recurrent Neisseria bacteremia.
Deficiency of Factor P
Factor P stabilizes the alternative pathway.

Results in Neisseria infections.
Paroxysmal nocturnal hemoglobinuria
X linked mutation in an enzyme that is involved in the synthesis of GPI tails that link DAF and protectin (CD54) to host cells. This deficiency of DAF and protectin on host cells causes excessive MAC activation and host cell destruction.
Th cells, surface proteins
CD4, TCR, CD3, CD40L, CD28
CD8 cells, surface proteins
CD8, CD3, TCR
B cells, surface proteins
IgM, B7, CD19, CD20, CD40, MHCII
Macrophages, surface proteins
MHC II, CD14, FcR, C3b-R
NK cells, surface proteins
MHC1 R, CD16, CD56
What cells do not express MHC I
trophoblast, RBCs
Which Ig crosses the placenta?
IgG
IL1
Made by macrophages. Stimulates T, B, PMN, fibrobolasts, and epithelial cells.

Endogenous pyrogen.
IL2
Secreted by Th cells. Stimulates growth of Th and CD8 cells.
IL3
Secreted by activated T cells. Similar to GMCSF
IL4
Secreted by Th2 cells. Promotes B cells, class switching to IgE and IgG. Weakens Th1 cells.
IL5
Secreted by Th2 cells. Promotes B cells, class switching to IgA. Also stimulates production and activation of eosinophils.
IL 6
Secreted by Th cells and macrophages. Stimulates acute phase reactants and immunoglobulins.
IL8
Major chemotactic factor for neutrophils. Made by macrophages (?)
IL-10
Secreted by Th2, and stimulates Th2.
IL-12
Secreted by B cells and macrophages. Activates NK and Th1 cells. Also increases IFN-gamma production.
IFN-gamma
Produced by Th1 cells. Stimulates macrophages and inhibits Th2.
TNF-alpha
Secreted by macrophages. Increases IL2 receptor synthesis by Th cells. Increases B cell proliferation. Attracts and activates PMNs. Stimulates dendritic cell migration. Cachexin.
When do you treat with passive immunity?
Tetanus, botulism, HBV, rabies

any other poisonings, too.
Fever, urticaria, arthralgias, proteinuria, lymphadenopathy 5-10 days post "drug/antigen" exposure

What is that? What type of hypersensitivity?
Serum sickness

Type III
Which type of hypersensitivity is NOT transferable by serum?
Delayed type hypersensitivity.
what is muromonab?
OKT3: monoclonal antibody against CD3/TCR complex, blocking T cell activation.