Immune Flashcards
1
Q
Parts of immune sxs
A
- innate and adaptive immunity
2
Q
Active immunity
- naturally acquired
- artifically acquired
A
- you get sick and produce antibodies
- vaccine
3
Q
Passive immunity
- naturally acquired
- artificially acquired
A
- mother passes IgG through placenta to baby or IgA through breast milk
- IV Ig
4
Q
Innate immune system
- parts
- also called
A
- physical barrier, complement, phagocytes
- tissue immunity
5
Q
Acquired immune system
- parts
- also called
A
- B and T cells
- humoral immunity
6
Q
Complement system
- classic: pathway, part
- alternative: pathway, importance, part
- mannose binding lectin
A
- IgG/ M activates C1 esterase -> Splits C2 into C2a and b, and C4 into C4a and b -> C2b and C4b combine -> split C3 into C3a and B -> C2b/3b/4b combine to become c5 convertase -> turns c5 into c5a and b -> c5b goes to MAC complex; part of acquired
- C3 spontaneously splits into C3a and b -> c3b will become c3bBb -> splits C5 -> MAC complex forms; dont need Ig to be activated, part of innate
- mannose is displayed on cell surface and bound by MBL, turns C2 and C4 into their peice; candida, salmonella, cryptococcus, listeria, nisseria
7
Q
Complement deficiences
- C1 esterase def causes
- C3 def causes
- MAC def
- decay accelerating factor def
A
- angioedema
- sinus and resp track infections
- recurring nisseria infections
- Paroxsymal Nocturnal Hemoglobinuria
8
Q
C1 esterase def
- normally
- C1 esterase inhibitor normally
- c2 b other product
A
- splits C2 and C4
- regulates C1 esterase and prevents plaminogen to plasmin to cause fibrin split products which also activate C1
- can be turned into c2 kinin by plasmin -> vasoactive peptide -> vasodilation and capillary leak
9
Q
Paroxsymal Nocturnal Hemoglobinuria
- genetics
- pathogen
- why just night
- tx
A
- acquired mutation to PIG-A gene that encodes for GPI
- GPI anchors CD55 (decay accelerating factor) and 59 (MIRL) to RBC so complement can destroy RBC
- RBC getting destroyed while you sleep and collects in urine making it red
- eculizumab against complement
10
Q
Organs of immune sxs
- thymus
- spleen
- peyer patch
- bone marrow
- appendix
- LN
A
- produce T cells
- have B and T cells to filter blood
- immune cells of immune sxs live
- where B cells made
- lymph organ but idk
- where naive B and T cells reside and plasma cells
11
Q
Spleen
- size
- location
- most
- blood supply
- red pulp function
- white pulp function
- role in gestation
A
- 4 in
- LUQ, between 9-11 rib
- injured in intraabdominal blunt trauma
- splenic a off celiac trunk
- consists of sinusoids which filter blood and have macrophages that destroy RBC
- humoral immunity, T cells in PALS, B cells in follicles and APC in marginal zones
- helps make RBC until 5th month
12
Q
LN
- function
- route
- outer most part: called, consists of, function
- paracortex: contain
- medulla: contain
A
- proliferation and storage B and T cells
- mult afferent and 1 efferent
- cortex -> primary (dormant B cells) and secondary follicles (proliferating B cell)
- contains t cells
- B tells, t cells, plasma cells
13
Q
MCC leukocytosis
- stress demargination: what is it, when will it be fixed
- infection: what will you see
- leukemia: what will you see
- lymphoma
- myelodysplastic
- leukemoid
A
- when there is stress PMNs come off wall and go into circulation; should return to normal in about a day
- elevated WBC, left shift -> increase in PMNs and bands, fever, chills, etc
- elevated WBC and blasts, night sweat, weight loss, etc
- everything will be raised
- exaggerated stress demargination -> stressor has caused elevated WBC for weeks (DKA)
14
Q
Viruses that cause leukopenia
A
- Parvo, Hep E and C
15
Q
lymph development
- b cell: location dev, location maturation, differentiation
- t cell: location dev, location maturation, differentiation
A
- BM, spleen, LN
- BM, thymus, LN
16
Q
T cells in thymus
- positive selection: location
- negative selection
- t suppressor
- CD4 function
A
- cortex, makes sure it can bind to MHC; those that can bind to MHC II -> CD4, those that only bind MHCI -> CD8
- medulla, makes sure CD8 doesn’t bind to self antigen too tightly (want weakest) and CD4 binds to MHCII very tightly (want strongest)
- select few of CD8 cells that bind too tightly to MHCI that reg t cells
- produce memory cells, activate CD8, activate B cells, produce inflamm mediators to bring PMN and macro to area
17
Q
NK cells
- express
- function
- how
- activation
A
- CD 16 and 56
- respond to MHC class I
- perforation, apoptosis or opsinozation
- normal cell expresses MHC1 and NK ligand which bind to activating receptor and inhibitory receptor normally but when infected the cell will stop expressing MHCI and onlt the activating recptor on NK cell will be bound causing it to kill the cell
18
Q
T helper cells
- Th1: how does it differentiate, cytokines secreted, function
- Th2: how does it differentiate, cytokines secreted, function
- Th17: how does it differentiate, cytokines secreted, function
- T reg: where is it made, what does it secrete, function
A
- IL12 -> IFN gamma, lymphotoxin A; viral/bacterial infection, AI
- IL4 -> 1L4, 5, 10, 13; parasite and asthma/allergy
- IL6, TGF beta -> IL 12, 21; fungal and AI
- made in thymus -> IL 10, TGF beta -> immunosuppression and AI
19
Q
Antigen processing Viral infected cell
- CD8
- macrophage
A
- CD8 cannot recognize as self and will destroy
- macrophage sees antigen -> processes it -> presents on MHC II, secretes IL1 (fever and recruit t cell), secretes IL6 -> MHCII binds to CD4 -> macrophage produced B7 and binds to CD28 on CD4 activating it -> CD4 will activate B cells and CD8 cells
20
Q
MHC
- made up of
- I
- II
A
- alpha subunit and beta subunit
- alpha has binding cleft, embedded in cell membrane
- alpha and beta make up binding cleft and both embedded in cell membrane
21
Q
IL
- 1
- 2
- 3
- 4
- 5
- 6
- 10
- 12
A
- 1: fever, non specific sxs of illness, recruits CD4
- 2: recruits CD8 and B cells; inhibited by cyclosporin
- 3: B cell proliferation
- 4: b cell diff, differentiate into Th2, role in class switching for cells
- 5: IgA class switching
- 6: acute phase reactants, diff to th17
- 10: supress cell mediated immune sxs
- 12: enhances cell mediated immune sxs
22
Q
antibody structure
- chains
- parts
- papain
- pepsin
A
- heavy and light
- FC -> constant, Fab -> variable, where antigen binding site located; connected by disulfide bonds
- cleave above disulfide bonds
- cleave below disulfide bond -> entire molecule will be non-functional
23
Q
Somatic Hypermutation
- what happens
A
- activated B cell has high mutation rate in variable domain and will get diff AA in variable section so will get slightly diff antibodies and some will be better to bind to antigen and others will be worse
24
Q
Affinity maturation
- what is it
A
- every generation of antibodies produced by b cell are more specific -> give better and better immune response
25
Q
Class switching
- first antibody produced
- then to what
- importance
- requires
A
- IgM
- IgG, IgA, or IgE
- allows antibody on mucousal membranes and in blood
- CD40 and IL4, 5, and gamma IFN
26
Q
Antibodies
- IgE: structure, used with
- IgA: structure, used
- IgM: structure, dx
- IgG: structure, function, 1, 2, 3, 4
A
- monomer, active with allergies and parasites
- monomer in blood and dimer on mucousal surface
- surface marker as monomer and pentamer in blood; fixes complement; waldenstraun macroglobinunemia (hyperviscosity of blood because of increase in IgM) and wiscott aldreich (elevated IgA and IgE, and IgM is low), hyper IgM (elevated IgM bc cant class switch)
- monomer; activates complement, highest affinity; 1: crosses placenta, 2: most common subclass def, 3: deficiency is related to chronic lung infections, 4: doesn’t activate complement, associated with membranous glomerulonephritis
27
Q
Primary immune response
- IgM: arrive, peak, last
- IgG
- kicks in
A
- 3 day, 2 weeks, 2 months
- 2 week, 2 months, 1 yr
- 6 months
28
Q
Seconday immune response
- mediated by
- arrive
- peak
- last
- kicks in
A
- IgG
- 3 day
- 5 years
- 10 yrs
- 12-15 months
29
Q
Strep Pneumo
- 0 -10 yrs
- 18 yrs
A
- ## 2 (IgM), 4 (IgM), 6 (IgG primary), 18 (IgG secondary) -> dont need until 11.5 but out of age group where affected
30
Q
Live Vaccine
- what is it
- lasts
- examples
A
- live agent modified in to render non pathogenic
- replicate longer and persist for longer than killed -> allow for more immune response to be made
- MMR, varicella, yellow fever, rotavirus, influ nasal
31
Q
Killed
- what is it
- benefits
- down falls
A
- killed product w/ antigen given
- cant revert back to more virulent form
- less effective
- better inflamm response but less Ig made
32
Q
Hypersensitivity Reactions
- Type 1: time frame, involves, trigger
- Type 2: type, involves, causes
- Type 3: type, involves
- Type 4: involves, ex
A
- immediate; mast cell degranulation with histamine (broncho spasm, vasodilation, cap leak), IgE; allergies, asthma
- antibody mediated; IgG attack self; AI dx
- immune complex deposition, IgG implants in tissue and binds to complement causing damage
- CD4 activate CD8 and macrophage; chronic graft, PPD, poison ivy
33
Q
crossmatch
- function
- how
A
- see if there are preformed antibodies to donors lymphocytes
- radiolabeled complement used to see if it attaches to antibodies made by recpient to donor lymphocytes
34
Q
Mixed lymphocyte reaction
- how does it work
A
- mix recipients lymphocytes with irradiated donor lymphocytes, only reason recipients lymphocytes replicate is because they have been activated, so when add radiolabeled thymidine it will be incorporated into replicated lynphocytes -> if no radiation then no replication so good match, if there is radiation then there is replication then not good match
35
Q
HLA typing
- importance
- good donors
- best; worse
A
- looks for similarties in MHC
- at least 60% matching
- sibling, worse
36
Q
Rejection
- hyperacute
- acute
- chronic
- graft vs host
A
- w/i 12 hr of transplant; preformed antibodies from recepient towards donor
- w/i 10 days transplant, reactivation of sensitized T cells; suppress immune sxs in order to keep kidney
- moths-to-years after graft; primary activation of T cells, fibrosis and calification
- happens in BM transplant, donor BM rejects host ; w/i 6 months after transplant; painful, maculopapular rash, anorexia, diarrhea, and liver failure
37
Q
Neutrophils
- located
- how do they work
A
- 9-% marginated, 10% periphery
- resp burst
38
Q
Chronic granulomatous dx
- what is it
- sxs
- organisms
- tests
A
- def of NADPH oxidase -> phagocytosed bacteria never get destroyed
- pneumonia, skin abcesses, osteomyelitis
- staph, pseudomonas, aspergillus, candida, enterobacter
- nito blue tetrizolium will not turn PMN blue, dihydrorhoamine meausures NADPH function
39
Q
Neutropenia
- what is it
- causes
- if they have fever
- if continue to have fever
A
- decreases in PMN
- drugs or viruses are MCC
- treat for staph and pseudomonas
- treat for fungus
40
Q
Eosinophils
- NAACP
- MCC for eosinophilia
- granules
A
- Neoplasia (hodgkins), allergies, asthma, collagen/vasc dx, parasites
- asthma or parasite
- major basic protein ( mast cell degranulation), eosinophili peroxidase (kill parasites), eosionophilic cationic protein (neurotoxin, helminth toxin, ribonucleotidic activity), eosinophil derived neurotoxin ( also kills viruses)
41
Q
Mast cells
- immediately release
- released 4-8 hrs later
- ECF-A
A
- histamine
- SRS-A: slow reacting substance for anaphylaxis -> leukotrienes (5000x more potent than histamine -> can cause massive broncho constriction)
- calls upon eosinophil to counter histamine molecules
42
Q
Histamine
- causes
- 1st gen anti: MOA, BBB, act as, last, most common, low sedation
- 2nd gen: MOA, benefits, examples w/ common names
A
- itching, swelling, redness, pain
- completely blocking H1; lipophilic cross BBB (cause drowsiness), strong anti-cholinergic, 4-6 hours, diphenhydramine; meclizine (vertigo)
- also block H1; much less sedating, last longer, less anticholinergic; cetirizine (zyrtec), loratadine (claritin), fexofenadine (allegra)
43
Q
Decongestants
- MOA
- phenylephrine
- pseudophed
A
- stimulate alpha 1 receptor causing vaso constriction
- in nasal spray, can cause rebound congestion
- in OTC cold med, can be used to make meth
44
Q
Phagocytic Diorders
- G6PDH def
- chronic granulomatous dx
- chediak-higashi syndrome
- leukocyte adhesion def
- Job syndrome
- myeloperoxidase def
A
- XR; mediterranean; HMP shunt enzyme def -> RBC lysed under stress; anemia, jaundice, fatigue, SOB, dark urine
- NADPH oxidase def; recurring catalase positive infections
- LYST gene mutation; impaired lysosomal trafficking; recurring bacterial infection, neuropathy (cant get NM into vesicles), albinism (cant get melanin into keratinocyte)
- CD18 absence; lack inflamm response with recurrent non perulent infections
- PMN fail to respond to chemotactic stimuli bc lack of gamma IFN production; FATED
- enzyme def of azurophilic granules of PMNs; severe cases will have fungal infections
45
Q
T lymphocyte defects
- MHC class 1 def
- MGC class 2 def
- DiGeorge
A
- failure of peptide transfer to ER; decreased CD8 -> recurrent viral infections
- MHC class 2 expression failure; def CD4 cells
- 3rd/4th pharyngeal puch don’t develop: CATCH 22 (cardiac - tetra of fallot, abnormal faces, thymic aplasia, cleft palate, hypoCa/PTH)
46
Q
B cell defects
- IgA def
- Bruton x-linked hypogammaglobulinemia
- X-linked hyper IgM
- common variable hypogamma
- transient hypogamma
A
- recurring GI and sinopulm infections
- TYK def -> B cells cant mature; recurrent bact infections and susceptible to viral infections
- CD40 is def -> can’t class switch; IgM is increased
- unknown defect but decreased Ig levels and increase AI activity
- IgG synthesis delay -> pyogenic infections from 5-6 months but gone by 15-10 months
47
Q
Def T and B cells
- ataxia telangectasia
- SCID
- Wiskott-Aldrich syndrome
A
- cell cycle kinase def; ataxia, telangiectasia, IgA and IgE def
- adenosine deaminase def IL-2 receptor defect, Rag 1 or 2 gene mutations; absence of B and T cells, GI and derm findings
- cytoskeletal glycoprotein defect; eczema, thrombocytopenia, high risk of AI and CA
48
Q
HIV
- CD4 count: normal vs AIDS
- attaches to; location
- attachment
- replication cycle
- time to sxs
- Dx Aids
- MC CA associated
- immunity
- rapid progression
- screening
A
- 800-1200; under 400
- CD4 receptors; cervix, vessels, macrophages, t helper, CNS, testes
- Gp 120 and 41
- Gp120 attaches to CD4 -> GP41 allows RNA to be injected into host -> reverse transcriptase injected into host and turns RNA into DNA -> DNA goes into nuclease and uses integrase to get incorporated into host cell genome -> protease processes proteins for viral assembly -> HIV will bud from cell
- get flu like sxs right after infected and then nothing until CD4 count drops low enough
- low or equal to 200
- cervical, kaposi, testicular lymphoma, CNS lymphoma
- CCR5 mutation -> inhibit attachment of HIV; homo = immune, hetero= will develop AIDS at slower pace
- CXCR1 mutation
- look for p24 antigen -> if positive will distinguish between HIV1 and 2 with antibody differentiation assay -> if neg must do nucleic acid test
49
Q
HIV Tx
- started on
- Reverse transcriptase inhibitors
- Zidovudine
- integrase inhibitors
- protease inhibitors: MOA, examples, side effects
- fusion inhbitors
A
- anti-retroviral, usually combo of protease inhibitors, reverse transcriptase inhibitors, integrase inhibitors
- have nucleoside and non-nucleoside; inhibit DNA from being replicated
- decreases vertical transmission from mother to baby; BM suppression, neuropathy, pancreatitis
- prevent DNA from being put into host genome
- prevent virus from being assembled; asinovir, amdinovir (kidney stones), retinovir; all inhibit cyto p450, buffalo hump, hyperglycemia
- prevent virus from fusing with cell
50
Q
When to begin prophylaxis
- anti-retroviral
- PCP
- Toxo
- MAC
- alt: trimetrexate, atovoquone, dapsone
A
- as soon as diagnosed
- less than 200; TMP sulfa
- less than 100; TMP sulfa
- 50; azithromycin
- dihydrofolate reductase inhibitor for those no responding to TMP; dihydrofolate reductase inhibitor and blocks ETC in parasites; blocks PABA
51
Q
Immunosuppressants
- cyclosporine: MOA, indication, AE
- tacrolimus: MOA, indicationm AE
- azathioprine: MOA, indication, AE
- cyclophosphamide: MOA, indications, AE
- glatiramer: indication, AE
- IFN beta: MOA, indication, AE
- Rhogam: what is it used for
A
- decrease IL-2 -> inhibit T cell mediated immunity; prevent graft vs host dx and rejection; neuro, nephrom hepato tox
- supress t-lymph activity; prevent rejection; neuro and nephro tox
- inhibit purine synthesis; prevent organ transplant; infections, mild leukopenia/ thrombocytopenia
- alkylating agent; severe RA, AI disorder; hemm cystitis, GI distress, alopecia
- relapsing-remmitting MS; post injection reaction, CP
- balance pro-inflam and anti-inflam in brain; relapsing remitting MS; fever, sweating, weakness, injection sit pain
- given to Rh- mothers who have Rh + babies; prevents erythroblastosis fetalis
52
Q
Immunostimulant
- IFN: MOA, AE
- IL 2: MOA, AE
A
- enhances cytotoxic T cell , NK cells, PMNs; CA; mild myalgia, fever headaches
- enhance t cell production, gamma inf production, activation NK cells; fever, chills, hypotension, rigor
