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96 Cards in this Set

  • Front
  • Back
most important component of complement
indiv w/ deficiencies in complement susceptible to what diseases:
1. pyogenic bacteria
2. illness involving the production of Ab's/IC's
potent inducers of inflammation
-C5a, C3a
-recruit inflammatory cells, activate effector mechanisms
C5a function/ effect
activator of all cell types of the myeloid lineage (phagocytes)
-neutrophils respond chemotactically, degranulate, release free O2 rads
-inc. surface expression of adhesion molecules
-macs secret IL5+6
-basophils+ mast degran=histamine
specific immunodeficiency
abnormalities of T + B cells (cells of adaptive immune system)
non-specific immunodeficiency
abnormalities in complement, phagocytes,
primary immunodeficiency
intrinsic defects in cells of immune system; genetic
X-linked agammaglobulinaemia
failure of Bcell maturation
-few or no Bcells in blood/lymphoid tissues
-no IgA, IgM, IgD, IgE
In immunodeficiency with increased IgM (HIGM)isotype, _______does not occur
isotype switching
-Bcells cannot make the switch from IgM to IgG and IgA (mutation of CD40 ligand)
common variable immunodeficiency (CVID)
defects in Tcell signaling to Bcells
-Bcells not defective but fail to receive signaling
-susceptible to pyogenic infec/ intestinal protozoa
transient hypogammaglobulinaemia of infancy
in some infants IgG synthesis delayed up to 36 mo. (don't have mom's anymore)
-Bcells normal but lack CD4 TH stimulus
-susceptible to pyogenic infx
Tcell deficiency
no Tcells or poor function = opportunistic infections
-results in Bcell deficiency since require Tcell help
severe combined immunodeficiency (SCID)
thymus never developed
-most profound
-treatment = bone marrow transplant
causes of SCID
1. defect on X chromosome (50%)- defective gene encodes the gamma chain of IL2 receptor- this also forms parts of IL-4,7,11,15 receps
2. other 50% due to recessive genes on other chromosomes= deficiency of ADA adenosine deaminase or PNP purine nucleoside phosphorylase - purines degredation enzymes = accum. of dATP and dGTP= toxic to lymphoid cells
MHC class II deficiency
TH cell deficiency results
-develop. of CD4+TH cells depends on positive selection by MHCII molecules
-auto recessive
-children have recurrent gastrointestinal infx
DiGeorge anomaly
defect in thymus embryogenesis
-Tcell deficiency variable depending upon effect on thymus
-wide eyes, low ears, upper lip shortened, cardiac malform
hereditary ataxia-telangectasia (AT)
-breaks in chromosome 7 and 14 at site of Tcell and Ig genes (auto recess)
-variable Tcell deficiency- some IgA def., others also IgG2 and IgG4
-infants develop ataxia @18 mo + sinus, lung infx
Wilscott-Aldrich syndrome (WAS)
-Tcell defects and abnormal Ig levels -> small+abnormal platelets, abnormal Tcells
-eczema, pyogenic, opp infx
increased susceptibility to pyogenic infections caused by deficiencies of C__ and Factor __or___
C3, factor H or I
(C3 plays a big role in opsonization)
-all inherited as auto recess
deficiencies in classical complement pathway results in development of ___
immune complexes (ie lupus)
-complement normally dissolves immune complxes)
hereditary angineurotic edema (HAE)
C1 inhibotor deficiency
*most important deficiency of complement
-C1 inhib responsible for dissociation of activated C1
-> swelling occurs in various parts of body
-auto dominant
chronic granulomatous disease (CGD)
defect in ox/red pathway:
defective NADPH oxidase that catalyzes red of O2 to O2-
phagocytes incapable of forming superoxide anions (O2-)so can't kill ingested microog- they stay alive->cell med response to persistant Ag = granuloma
Leukocyte adhesion deficiency (LAD)
complement receptor 3 (CR3) is deficient(normally binds C3b on opsonized organisms)
-severe bacterial/gastro infx
secondary immunodeficiencies examples
chemo-toxic to Tcells
protein malnutrition- results in Tcell deficiency
diarrhea-lose Ig's
burns-lose Ig's
infections (AIDS)
proteins on HIV membrane
gp120, gp41
cells that carry CD4
dendritic cells, langerhans cells, microglia of CNS
HIV cycle
binds gp120 to CD4
enters CD+ cell, loses coat, ssDNA copy of viral RNA made by HIV reverse transcriptase, comp strand made and integrates
when Tcell activated, HIV particles made and released by budding
effect of steroids
dec. circ lymphocytes
dec. circ monocytes
inc. circ neutrophils
*inhibit synth of cytokines
overall= inhibition of TH cells and macrophages
-alkylates DNA- interferes with strand sep during repro
-B cells more affected than Tcells, dec. lymphocytes not PMN's
*good to manage auntoAb and allograft rejection
fraudulent base in DNA- affects synthesis
-active only on dividing (cytostatic) dec. T+B cells, suppress NK + K cell activity
analog of folic acid (essential for DNA synth)
dec. in all Ig isotypes
anti-inflam cause suppress PMN's
no effect on Tcells
cyclosporin, tacrolimus (FK506), rapamycin
-bind to class of cytoplas proteins
-inhib Tcells and Ag presentation
iron def.
reduced ability of neutrophils to kill bac. + fungus, impaired NK cell activ
selenium + copper def.
mutations in viruses= altered virulence
vitamin A def.
alters epith struc= increased bac binding
vit B6 and folate def.
reduced cell mediated immunity
decreased #s of CD4 cells, dec in opsonization
TH2 cells...
secrete cytokines IL13 and IL14 --> induce Bcell prolif, favor IgE production
Type I hypersensitivity
mast cells bind IgE via their Fc receptors, IgE induces degranulation of mast cell, releasing mediators (typical allergic rxn)
when allergen encounters sensitized mast cell bound w/ IgE...
cross-links surfacebound IgE-->inc. influx Ca, triggers release of PREFORMED histamine and proteases(tryptase,chymase) and NEWLY SYNTH mediators leucotrienes and prostaglandins
2 types of mast cells
MMC- mucosal mast cell
CTMC- connective tissue mast cell
the skin prick test produces...
a wheel and flare reaction
-suppress increase in mast cell #'s
-inhibit cytokine production incl. IL13 & IL4
sodium cromoglycate
prevents histamine release by inhibiting calcium influx into cell
cyclosporin A
inhibits expression of Il2 receptors = Bcells can't proliferate
block histamine after release
hyposensitization therapy
-increasing doses of allergen
-increase in allergen specific IgG and suppressor Tcell (suppress IgE response)
Hyp Type II
-Ab against own cells
-cytotoxic action by K cells or complement-mediated lysis
-ex. blood transfusions
Hyp Type III
-immune complexes deposited in tissues
-complement activated
-PMN's attracted to deposition site
-tissue damage, inflam
ex. lupus
Hyp Type IV
-Ag-sensitized Tcells release lymphokines when encounter the Ag a 2nd time
-Tcells activating macrophages
difference b/t Type II and Type III?
II is restricted to specific cells or tissues bearing the Ag, III is against soluble Ag's in the serum
major cause of HDN
Rhesus system
Goodpasture's syndrome
nephritis from Ab's to glycoprotein on glomerular basement membrane- severe necrosis of glomerulus
(type II)
blistering of skin and mucous membranes
-Ab's to a desmosome protein that forms junctions b/t epidermal cells
-breakdown of the epidermis
Myasthenia gravis
Ab's to Ach receptors on surface of muscle membranes
immune complexes of type III due to 3 possible causes:
1. persistent infection/weak Ab response
2. autoimmune disease (phagocytes that remove complexes become overloaded, start to deposit)
3. inhalation of Ag material (actinomyces fungi in hay, pigeon poop - IgG produced rather than IgE)
vasoactive amines released by platelets, basophils, and mast cells cause...
endothelial retraction = increased permeability allowing IC's to deposit on blood vessel wall
large immune complexes removed faster or slower?
faster because more effective at fixing complement
IC deposition occurs where BP is ____
3 variants of Type IV:
1. contact hypersensitivity (poison ivy)
2. tuberculin-type (72 hrs)
3. granulomatous (21-28 days)
granumolatous rxn at peripheral nerves (likes cooler areas)
lung- fibrosis and lesions
host becomes sensitized to ova of trematode worms = granulomas
tissues, lung, lymphs
Crohn's disease
ileum and colon
live vaccines produce ____ and _______ immunity
humoral, cell-mediated
attenuation achieved by...
mutations (large # mutations diminished virulence)
killed vaccines produce primarily ______ immunity
chemicals used to inactivate pathogen
formaldhyde = alkylating agents
most sucessful bacterial vaccines
inactivated toxins and toxoids
limitation of polysaccharide vaccines
inability to activate Th cells - activate B cells in a Tcell independent manner (not presenting Ag) = more IgM, low IgG , have to get every 4 to 5 years to boost Bcells
recombinant antigen vaccines
introduce gene encoding antigen of pathogen into attentuated virus or bacteria- organism serves as vector- replicates within host, expresses gene product of pathogen (also clone into yeast, ie. Hep B vx)
DNA vaccine
plasmid DNA encoding viral antigen injected into muscle of recipient, taken up by muscles cells and encoded protein is expressed
anti-idiotype vaccine
1.immunize mouse with Ag, Ab (idiotype) generated against Ag
2. immunize mouse with Ab, then anti-idiotype generated (this looks like original Ag)
3. anti-idiotype used as vaccine
-testing for HIV vaccine
living vaccine advantage
1. Ag challenge lasts for days or weeks
2. induces it at the right site
3. contains greatest # microbial Ag's
killed vaccine disadvantage
do not replicate in host
repeated boosters needed
enhance Ab production
-aluminum salts, added to Ag
1.concentrates Ag where lymphocytes exposed to it
2. induce cytokines
benefits from host- host does not benefit but is not harmed
pseudomembrane colitis
antibiotics kill normal flora of bowel
-excessive toxin released by clostridium which is normally just a minor resident --> diarrhea
characteristics of normal flora
1. adherence to host cells (proteins, polysacch's, pili) even thru desquamation
2.production of antimicrobial substance- inhibit other competing microbes
characteristics of skin that inhibit microorganisms
1. dryness
2. low pH (b/t 3 and 4 due to organic acids such as lactic acid)
3. inhibitory substances
(sweat glands secrete lysozyme, sebaceous secrete complex lipids that are degraded into inhibitory acids)
tears contain _____ which _____
lyzozyme, cleaves peptidoglycan
major cause of dental caries
streptococcus mutans
-produces glucan that acts like cement to stick bacterial cells together
residents of adult vagina
-break down glycogen to form lactic acid
aquried sufficient immunity but unable to eliminate pathogen from body
fimbriae, pili, cell-surface structure that bind to receptors on surface of host's cells
antiphagocytic mechanisms
-capsules (slippery)
-fimbriae (prevent close contact)
-siderophores- compete for iron = growth factor
breaks down hyaluronic acid= connective tissue glue = spread
activates plasmin, causes disolution of blood clots = spread
coag of plasma = fibrin layer around cell= Ab doesn't recognize
breakdown RBC = iron
enterotoxins 2 types:
1. stim cAMP causing electrolyte imbalance= H2O flows in
2.inhibit protein synth = kills epith cells
-spastic paralysis - block inhibitory nerve impulses so fire all the time
(botulism prevents Ach release)
pyrogenic toxins
= superantigens --> induce secretions of TNF alpha and IL-1 = inflam, shock, death
Lipid A portion of Gram - cells
lipid A binds to macs, causing synth of TNF alpha and IL-1
what prevents microbes from going deep into body (ie rhinovirus)
temperature- higher temp inhibits growth inside