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112 Cards in this Set

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dd: honey-crusted lesions behind ears
S. epi
S. aureus
MCC of pelvic abcess following ruptured appendix
Bacteroides and microaerophilic strepococci
acid-fact bacilli with branching rods
Nocardia asteroides
diagnostic test for syphillis
Fluorescent treponemal ab absorbed test (FTA-ABS)
causative agent of Lyme disease
borrelia burgdorferi
high fever
swelling in armpits and groin
gm- rods w/ bipolar staining
yersinia pestis
spiral-shaped organism
Positive Fluorescent Ab test
Syphillis caused by treponema
where is yersinia perstis MC
southwest US
what is the infectious agent: child w/ weakness, droopy eyes, head lag.
endospore of clostridium botulinum (adult botulism = ingested preformed toxin)
what is the infectious agent: discoloration of buttock, blebs of skin --> shock and death
Description suggests myonecrosis caused by C.perfringens
lecithinase producer
C.perfringens
resevoir of Campy
poultry
what structure is found in gm- but not gm+
outer membrane
rose-colored spots, H2S
salmonella
what causes lymphocytosis, insulin secretion and histamine sensitization
pertussis toxin
what causes local edema in whooping cough
adenylate cyclase toxin
boy in NC goes hiking, rash that spread from extremities to trunk, conjunctivitis, proteinuria
Rocky Mountain spotted fever caused by Rickettsia rickettsiae
2 ways strep pyrogenes can be grouped
Lancefield
M proteins
mechanism of pertussis toxin
ADP ribosylation of Ginhibitory
mechanism of corynebacterium diptheriae
ADP ribosylation of EF2
mechanism of Pseudomonas toxin
ADP ribosylation of EF2
ADP ribosylation of GTP-binding protein
ETEC
Vibrio cholerae
Blocks release of ACh
Clostridium botulinum
Blocks release inhibitory transmitters GABA and glycine
Clostridium tetani
gm+ aerobic rod; toxin that inhibits protein synnthesis
C.diphtheriae
structure of V.cholera
gm- curved rod; toxin increases cAMP
metabolic requirements of H.plylori
microaerophilic
what protects gm+ organisms from osmotic damage
thick peptidoglycan layer
gm-
reduces nitrates to nitrites
E.coli
home-canned green beans
visual problems
Botulism
gm+cocci, cat+ grows in high salt
S.aureus
gm+ aerobic bacillus, sporulates
Bacillus cereus
gm+coccus, cat-, optochin-resistant
S.viridans
gm+ bacillus grown on low oxidation-reduction medium
Clost botulinum
what virulence factor in Mycobacterium inhibits phagosome-lysosomal fusion to allow it to survive intracellulary
sulfatides
clue cells
gardnerella vaginalis
gm- rod w/ bleach-like odor
Eikenella corrodens
organism that causes purulent conjunctivitis in a 15day old
Chlamydia
what form of chlamydia has ability to bind membranes and infect
elementary form
gelatinous, bloody sputum, PMNs
Klebsiella pneumoniae
MCC neonatal meningitis
GBS>E.coli
MCC meningitis in adults
S.pneumo
ecthyma gangrenosum (necrotic lesion w/ black center and erythematous margin)
Pseudomonas
complication of H.pylori infection
stomach cancer
cytokine involved in the differentiation of lymphoid cell line
IL-7
cytokine involved in the differentiation of myeloid cell line
GM-CSF, IL-3
lack of B cells
decreased T cells
early onset, failure to thrive, red rash, diarrhea, severe immune deficiency
Omenn syndrome (AR missense mutation in rag gene)
No B or T cells
SCID (mutation in rag gene)
Ag receptors of B cells involved in signal transduction
Iga, IgB, CD19, CD21
Ag receptors of T cells involved in signal transduction
CD3
one chromosome of a homologous pair will be inactivated --> one idiotype of ag-recognition molecule will be produced
allelic exclusion
cytokine: production of acute-phase proteins
IL6
stucture of MHC class I
a chain
B2 microglobulin (not coded within MHC)
CD56
NK cells
where do you find: CD4-CD8- T cells
Bone marrow
where do you find: maturing T cells ready to circulate
thymic medulla
splenic periarteriolar lymphoid sheaths
T-cell dependent areas of the spleen
what cells express tdt
T cells: prethymic and thymic cortex
B cells: pro-B, pre-B
tdt
MHCII
CD19,20
pro-B
tdt
MHCII
CD19,20
u+
pre-B
MHCII
CD19,20
IgM
immature B
MHCII
CD19,20
IgM, IgD
mature B
cytoplasmic Ig
plasma cell
what cell undergoes Ig heavy chain rearrangement
pro-B expressing tdt, MHCII, CD19,20
what cell undergoes light chain gene rearrangement
pre-B: tdt, MHCII, CD19,20,u+
order of lymph node filtration
afferent lymphatics-->subcapsular sinus-->cortex-->medula-->medullary cords-->efferent lymphatics
what type of infections are asplenic pt (sickle cell) more likely to get
encapsulated bacteria + blood-borne pathogens eg. Babesia microti
leukocyte surface molecule that mediates binding to high endothelial venules of lymph nodes
L-selectins
endothelial cell molecule that mediates binding to lymphocytes
addressins
what molecules mediate the following steps of phagocyte extravasation:
1. rolling
2. activation by chemoattractants
3. arrest and adhesion
1. E-selectin
2. IL8, C5a, leukotriene B4, fibribnopeptides
3. Integrams, Ig-CAMS
omphalitis
recurrent, chronic bacterial infections
No abscess or pus formation
Leukocyte adhesion deficiency (absence of CD18)
def of opsonization
enhancement of phagocytosis with IgG and C3B
what type of infections do people with CGD suffer
catalase positive (staph, klebsiella, serratia, aspergillus)
test for CGD
nitroblue tetrazolium reduction test (tests phagocytic cell's ability to generate oxygen radicals)
function of invariant chain
prevents any normal cellular peptides from being bound to MHC class II
cytokine: T cell proliferation
IL-2 is most important (IL1,6, TNFa)
Cosstimulatory molecules in Tcell activation
CD4--MHCII
CD8--MHCI
LFA1--ICAMI
CD2--LFA3
CD28--B7
mild SCID
CD8+, CD4-
don't develop graft-vs. host disease
hypogammaglobulinemia
Bare lymphocyte syndrome (MHCII deficiency)
what cytokines do TH1 produce
IFNgamma
TNFB
IL2
what cytokines do TH2 produce
IL2,4,5,6,10
1. what stimulates TH1
2. what inhibits TH1
1. innate immune response (intracellular bacteria, parasites that infect macrophages)--> IL12, IFNgamma
2. IL4,10 produced by TH1
1. what stimulates TH2
2. what inhibits TH2
1. extracellular pathogens --> IL4
2. IFN-gamma
superag
cross-link variable B (tcell) to a (MHCII) --> polyclonal activation of T cells
2 ex of thymus-independent ag
Ag w/ no peptide structure:
1. lipopolysaccharide from cell envelope of gm-
2. polysaccharide capsular Ag
Ab with lowest affinity and highest avidity
IgM
Ab in breast milk
IgA
what activates the alternative complete pathway
bacterial polysaccharides and lipopolysaccharides of cell envelope of gm-
what activates the classic complete pathway
Ag/Ab complexes (IgM and IgG)
Inappropriate activation of the complement cascade is controlled at the level of _____
C1,3,5
what does tx with pepsin produce
divalent F(ab)2 fragment
destruction of Fc
what does tx with papsin produce
two monovalent Fab fragments
destroys Fc
when do neonates start to make Ab
they make IgM immediately
all others after 1yr
they get IgG from mom
child who can't make IgG, IgA, IgE
hyper-macroglobulinemia
Absence of CD40 (can't isotype switch)
child who can't make genetic rearrangements necessary to form the idiotype of the Ab molecule. Would not affect isotype
absence of Tdt
child with no secretory IgA
monomeric IgM
normal IgA,IgE, IgG
Absence of J chains
Most important complement component in clearing extracellular pathogens
3b
how do CD8+ T-cells kill
perforins
cytokines
granymes
Fas/FasL
CD8+ T-cells:
what enhances their function
what inhibits
IFNa, IFNB, IL-12
MHC class I
CD14
macrophage
cytokine: increase expression of MHC class I and II
IFNgamma
risks of passive immunization (3)
IgE production
Type III hypersensitivity
Anti-allotype Ab
what kind of vaccine is HIB
T-cell dependent
Response type:
1. Live vaccines
2. Killed
1CMI, HMI
2. Ab
minor AA variations in constant domain of heavy and light chains. Expression is genetically determined.
allotype
3D shape of the Ag-combinding site of an Ab or TCR
idiotype
what immunoglobulin marker should be use in paternity tetxt
allotype
recurrent infection with bacteria
chemotactic and degranulation defects
absent NK activity
partial albinism
chediak-higashi syndrome (granule structural defect)
recurrent infections w/ catalase+ bacteria
anemia
G6PD deficiency
Low IgG of all classes
no circulating B cells
disease with B cells stoped at pre-B cell stage
normal CMI
Bruton X-linked hypogammaglobulinemia (deficiency of tyrosine kinase)
marked increase in immune complex disease, increased infecitons with pyogenic bacteria
deficiency in classic complement pathway (C1q, C1r, C1s, C4, C2)
Increased Neisseria infection
deficiency in alternative pathway (factor B, properdin) or C5,6,7,8
loss of humoral and cellular responses
thrombocytopenia
eczema
Wiskott-Aldrich Syndrome (defect in cytoskeletal glycoprotein)