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USMLE Step 1 flashcards > Immunology > Flashcards

Flashcards in Immunology Deck (22)
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1
Q

What is IκB kinase (IKK)?

A

is an enzyme complex —propagating the cellular response to inflammation, is part of the upstream NF-κB signal transduction cascade.

2
Q

Leukocyte adhesion deficiency

A

Defect in LFA-1 integrin (cd18)
impaired phagocytosis and migration-chemotaxis
AR
recurrent skin and mucosal bacterial infections
no pus
markedperipehral leukocytosis and neutrophilia

3
Q

Active vs passive immunity

A

Passive: receiving preformed abs
Active: exposure to foreign antigens

4
Q

C1 inhibitor deficiency

A

C1INH prevents C1 mediated clevage C2 and C4
also inhibited kallirein that converts kininogen to bradikinin.
Angioedema and GI manifestations

5
Q

Delayed hypersensitivity reactions

A
  • tuberculin skin test, contact dermatitis, candida extract skin test
  • mediated by T cells CD4: 2 days after exposure
  • dendritis cells presents the antigen to Th1 cd4 t lymphocytes through MCH- II
  • T cells secreted INF gamma, and recluted mos.
6
Q

The role of ubiquitine proteasome pathway in immune response?

A

ability to degrade foreign intracellular proteins

7
Q

Heavy chain

A

determine isotypes in immunoglobulins

8
Q

TNF- alpha

A

mediates septic shock

causes cachexia in malignancy

9
Q

which is the reason of polyssacharide conjugated vaccine?

A

example: Hib + tetanus toxoid (indicated in children less than 2 years)
induced T cell response, memory

10
Q

Wiskott Aldrich syndrome

A

Mutation in WAS gene
T cell unable to recognize actin cyrosjeleton
WATER: Wiskott Aldrish, Thrombocytopenia, Eczema, Recurret infections
increased the risk of autoimmunity and malignancy
Increased or normal IgM and IgG
Decreased IgA and IgE

11
Q

Rabies vaccine

A

inactivated vaccine

12
Q

Attenuated vaccines

A

herpes zoster, varicella and yellow fever

13
Q

Chediak higashi syndrome

A
  • Defect in LYST gene
  • Microtubule dysfunction in phagosoma - lysosome fusion
  • AR
  • recurrent pyogenic infections
  • albinism
  • peripheral neuroathy
  • progressive neurodegeneration
  • Pancytopenia
14
Q

Wiskott Aldrish syndrome

A
  • mutation in WAS gene
  • T cells unable to recognize actin cytoskeleton
  • X linked
  • WATER: Wiskott aldrish, Thrombocytopenia, Eczema and Recurrent infections.
  • Neutrophilia
15
Q

Which kind of vaccines causing better immune activation?

A

live attenuated vaccines produce stronger immune responses tthan killed vaccines by acting a persistent stimulus that better activates helper and cytotoxic T cells.

16
Q

Which cytokine is exclusively produce by lymphocytes

A

IL-2—— stimulates T lymphocyte: autocrine fashion

17
Q

ELISA

A

indirect enzyme linked immunosorbent assay
identify antibodies against a known target antigen
1. antigen
2. add patient serum: removed other thinks— only shows antibodies
3. aggregates antihumen immnumoglobin antibodies to recognized the antibodies: detectable signal (color change)

18
Q

Acute serum sickness

A

Tissue deposition of a circulating immune complexes
(Type III hypersensitivity)
fever, pruritic skin rash and artharlgias
begin 7-14 days to exposure an antigen (ex, administration of monoclonal antibodies or non human immunoglobulins)
small vessel vasculitis
hypocomplementemia
Serum like reaction (relacted with administration ofnon protein drugs)— penicillin, cefaclor and TMP/SMX

19
Q

MCH II, MHC I

A

MHCII: In antigen presenting cells

MHC I: all nucleated cells and platelets

20
Q

PD1

A

programmed death receptor 1
expressed on surface of activated T cells
in cancer downregulating the immune response against tumor
similar to CTLA4 (cytotoxic T lymphocyte associated protein 4)
** MONOCLONAL ANTIBODIES AGAINST PD1: promoting apoptosis———–used in advanced melanoma and certain types of lung cancer

21
Q

Main protein associated with MCH-I

A

Beta 2- microglobulin

22
Q

fab Region

fc Region

A

recognizes antigen

complement binding