Immuno Flashcards

1
Q

What are the characteristics of allergic asthma?

A

only leukotrienes (LTC4, LTD4, LTE4) and acetylcholines have pharmalogic receptor antagonists that offer clear therapeutic benefit

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2
Q

What are granulomatous conditions?

A
  • Langhans giant cells are characteristic
  • multiple nuclei peripherally organized in the shape of a horseshoe
  • the macrophages that form these giant cells are activated by CD4+ TH1 lymphocytes
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3
Q

What is a leukemoid reaction?

A

leukemoid reaction=benign leukocytosis (>50,000/mms)

  • in response to undelying condition
    • severe infection/hemorrhage
    • malignancy (leukemia)
    • acute hemolysis
  • Lab: increased/nml leukocyte alk phos levels
  • peripheral smear:
    • increased bands
    • early mature neutrophil precursors (myelocytes)
    • granules (Döhle bodies) in neutrophils
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4
Q

What is the job of the spleen?

A

2-fold

  1. blood filter=can remove circulating pathogens
  2. major site of opsonizing Ab synthesis
  • asplenic patients are prone to infections caused by encapsulated organisms:
    • S. pneumo
    • H. flu
    • N. meningitides
  • spleen=most commonly injured organ with blunt abdo trauma
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5
Q

Precursor proteins/peptides responsible for localized amyloidosis

A
  • cardiac atria: atrial natrieuretic peptide (ANP)
  • thyroid gland: calcitonin
  • pancreatic islets: islet amyloid protein (amylin)
  • cerebrum/cerebral blood vessels: beta-amyloid protein
  • pituitary gland: prolactin
  • immune globulin LC cause multi-organ ayloid deposition in primary systemic amyloidosis
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6
Q

Isotype switching

A
  • takes place in the germinal center of the lymph node
  • interaction of CD40R on B cells (activated) with CD40L (CD154) on T-cells
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7
Q

All of th CDs

A
  • CD4-recognize antigens presented by MHC2
    • on the surface of MHC2-restricted T-helper cells
  • CD7-multi-chain complex T-cell marker
  • CD8-transmembrane protein associated with T-cell receptor
    • recognizes antigenic peptide from MHC1
  • CD14-surface marker of monocyte-macrophage lineage
  • CD19,20,21=mature circulating B lymphocytes
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8
Q

HyperIgM Syndrome

A
  • inabiity of B-lymphocytes to undergo isotype switch from IgM to D,G,E,A
  • most commonly results in lymphoid hyperplasia and reurrent sinopulmonary infection
  • due to genetic absence of CD-40 ligand on T-lymphocytes OR genetic deficiency in the enzymes responsible for DNA modification
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9
Q

X-linked agammaglobulinemia

A
  • low/absent circulating CD19,20 pan B cells and pan-hypogammaglobulinemia
  • CP: increased susceptibility to pyogenic bacteria, enteroviruses, Giardia lambia (due to the absence of opsonizing and neutralizing Ab)
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10
Q

Passage of leukocytes into the inflamed tissue (MR.AT&T)

A
  • Margination
  • Rolling
  • Activation
  • Tight Adhesion and Crawling
  • Transmigration
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11
Q

Superantigen Activity

A
  • enterotoxins
  • oxfoliative toxins
  • toxic shock syndrome toxins (TSST-1)
  • super Ag interacts with MHC molecules on APC and the variable region of the TLR which causes non-specific, widespread activation of T-cells, resulting in release of IL-2 from T-cells and IL-1 and TNF from macrophages
  • TSS is due to the immune cascade
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12
Q

Reactive Arthritis

A
  • classic triad:
    1. non-gonococcal urethritis
    2. conjunctivitis
    3. arthritis
  • HLA-B27 associated arthropathy
    • within several weeks after GU or enteric infection
  • seronegative spondyloarthropathies
  • 20%->sacroiliitis
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13
Q

INF alpha and beta

A
  • produced by most human cells in response to viral infections
  • suppress viral replication by inhibiting protein synthesis and stimulating apoptosis of infected cells
    • limits the ability of viruses to spread through the tissues
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14
Q

Achondroplasia

A
  • AD gain of function in FGFR3 (fibroblast GFR3) gene
  • indiv: hetero and 50% chance of transmitting to their offspring
  • CP: short stature, disproportionately short upper and lower extremities, large head, prominent forehead
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15
Q

Chemotactics

A
  • macrophages make IL-8 which induces chemotaxis and phagocytosis in neutrophils
  • other chemotactics:
    • n-formylated peptides
    • leukotriene B4
    • 5-HETE
    • C5a
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16
Q

GvHD

A
  • occurs after allogeneic bone marrow transplantation, transplantation of organs rich in lymphocytes (liver) or transfusion of non-irradiated blood
  • pt usually severely immunodef due to primary dz or immunosuppressive meds
    • donor T cells from graft survive, migrate into host tissues, recog host MHC Ag ad foreign and become sensitized
    • on activation, donor CD4+ and CD8+ T cell (NOT B-cells) participate in host cell destruction
  • skin, liver, GI most freq affected
  • early s/s:
    • diffuse maculopapular rash-palms and soles, may desquamate
    • GI: diarrhea, intestinal bleeding, abdo pain
    • liver: abnml LFT
17
Q

Pus

A
  • thin, protein-rich fluid=liquid puris, and dead leukocytes, primarily neutrophils
  • during infection, macrophages and surrounding endothelial cells release cytokines (IL-8) that trigger neutrophils to enter the site of infection via chemotaxis
    • IL-8 also induces phagocytosis in neutrophils once they have arrived
  • other significant chemotactic agents:
    • n-formylated peptides, leukotriene B4, 5-HETE (leukotriene precursor), complement component C5a
18
Q

SCID

A
  • etiology: gene defect leading to failure of T cell development
    • also: B cell dysfxn due to absent T cells
  • inheritance: X-linked recessive, AR
  • CP:
    • recurrent, severe viral, fungal, or opportunistic (Pneumocystis) infxns
    • failure to thrive
    • chronic diarrhea
  • tx: stem cell transplant
19
Q

Lymphatic system of extremities

A
  • superficial lymphatic vessels-follow venous sytem
    • receive lymph from skin and subq tissues
    • in lower extremities divided into medial and lateral tracks
      • lesions on medial foot cause inguinal lymphadenopathy
      • lateral mesions more likely to cause lymphadenopathy in both the popliteal and inguinal areas
  • deep lymphatic vessels-follow arterial system
    • drain deep muscles and superficial vessels
20
Q

TNF alpha

A
  • TNF alpha inhibitors impair cell-mediated immunity
  • all pts beginning tx with TNF alpha inhibitors should be evlauated for latent TB
21
Q

What are the steps of leukocyte transmigration

A
  • margination
    • vascular leakage into microvasculature=hemoconcentration and DEC wall shear stress=improved contact of neutrophils with endolthelial lining
  • rolling
    • neutrophils roll on endothelium via losse binding of (sialylated) carb groups:
      • sialyl lew X/PSGL-1 –to– L-selectin on neutophils
      • E-selectin/P-selectin on endothelial cells
  • activation
    • slow roll=leikocytes sample chemokines=activate integrins via signaling cascade=conformation change in integrins needed for binding
  • tight adhesion and crawling
    • neutrophils firmly attached to endothelium via CD18 beta 2 integrins (Mac-1 and LFA-1) to intercellular adhesio moecule-1 (ICAM-1)
  • transmigration
    • PECAM-1, at peripheral intercellular junctions of endothelial cells
22
Q

poison ivy dermatitis

A
  • form of allergic contact dermaitis
  • type 4 HSR mediated primarily by T lymphocytes
  • CP:
    • intensely pruritic erythematous papules, vesicles, or bullae that often form linear patterns
  • PP: urushiol [allergenic substance, causes immune resp when attached to proteins (hapten)]
23
Q

what is the major adaptive immune mech that prevents re-infection with the influenza virus

A
  • anti-hemagglutinin Ab
    • -humoral resp with Ab directed against Hemagglutinin can neutralize virus and primarily block its binding to the host cells
24
Q

Calcineurin

A
  • essential protein (phosphatase) in the activation of IL-2 which promotes the growth and differentiation of T-cells
  • once ativated, dephosphorylates nuclear factor of activated T-cells (NFAT)..allows NFAT to enter ncleus and binf to IL-2 promoter
  • immunosuppresants such as cyclosporine and tacrolimus work by inhibiting calcineurin activation
25
Q

Rheumatoid arthritis

A
  • autoimune dz triggered by an unknown Ag
  • cartilage components=auto-Ag that activate CD4+ T-cells which in turn stimulate B-cells to secrete rheumatoid factor, an IgM Ab specific for the Fc component of self IgG
26
Q

IgA protease

A
  • produced by:
    • N. mening
    • N. gonorrhoeae
    • Strep pneumo
    • H. flu
  • cleaves secretory IgA at its hinge region, rendering it ineffective
  • secretory IgA exists on mucosal surface and in secretions
    • it acts to bind and inhibit the action of pili as well as other cell surface antigens that normally mediate mucosal adeherence and subsequent penetration
27
Q

DILE (drug induced lupus erythematosus)

A
  • abrupt pnset of lupus symptoms
    • fever, arthralgias, pleuritis with posittive anti-histone Ab
  • linked to drugs metabolized by N-aetylation in the liver:
    • procainamide, hydralazine, isoniazid
  • genetically predisposed individuals who are slow acetylators are at greater risk for developing DILE