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MMMD 1 - QH > Immunodefiency > Flashcards

Immunodefiency Flashcards

1
Q

What are theories for allergy?

A

*rxns to parasite-like runs..when there is no parasites
-Genetic: no single gene
-Hygiene hypothesis: more allergic rxns if grow up too hygienic because body can’t swtich from Th2 bias to Th1bias
-Food: less fruits and veggies. Food preservatives affect gut flora.
(those with poor nutrition > immune compromised > less hypersensitvity)
-Occupational/urban lifestyle: more Th2 > mast cells, allergies
-Meds: ex - PPIs decrease acid > incomplete digestion > new rxn to food

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2
Q

What are 3 types of immediate hypersensitivity?

A
  1. IgE mediated
  2. non IgE mediated
  3. Non-immunologic (no mast cells, no IgE)
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3
Q

What is non-IgE immediate hypersensitivity rxns?

Ex?

A
  • direct activation of mast cells without IgE
  • no prior exposure needed
  • clinically presents similar to the IgE mediated rxns
    ex: drug rxns - relaxants, antibiotics, ASA, NSAIDS, radial contrast agents
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4
Q

What is non-immunologic immediate hypersensivitiy?

A
  • no mast cells, no IgE
  • complement-mediated (C3a, C5a)
    ex: rxns to blood products, dialysis membranes
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5
Q

What is IgE mediated immediate hypersensitivity?

A
  • prior exposure
  • B cells activated by CD40 and IL4 by Thelper > isotype switch to IgE
  • IgE binds mast cells via FCepsilonRI receptors (high affinity)
  • IgE sticks around for months
  • antigen again > crosslink IgE on mast cells > mast cell degranulation
  • similar antigen proteiin can cross react
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6
Q

What do mast cells secrete?

Effects? early vs late

A

Immediate: >sneezing, congestion, itchy nose, watery eyes

  • histamine
  • TNF-alpha
  • proteases
  • heparin

Minutes: >wheezing, bronchoconstrict

  • prostaglandins
  • leukotrienes

Hours: >mucus, eosinophils, inflammatory
-cytokines - IL4, IL13

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7
Q

Effects of histamine?

A

-from mast cells
-nonlife-threatening
-increase vascular perm, vasodilation, edema, bronchoconstriction, secretions, hives, conjuntivitis, rhinitis
(thick skin, eye, nose, lung)

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8
Q

Effects of Platelet Activating Factor?

A
  • from mast cells
  • life-threatening! > anaphylaxis (can be uni or biphasic. 1-72 hrs)
  • hypotension, increase vasc perm, bronchospasm, coagulopathy, impaired heart contraction
  • deficiency in PAF acetylhydrolase is seen in fatal peanut allergy
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9
Q

Clinical presentation of immediate hypersensitivity?

A
  • depends on route, dose, host

- systemic, wheel&flare, hay fever, bronchial asthma, GI for food allergies

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10
Q

How do skin tests work?

A
  • inject antigen

- look for wheal&flare (bump and red) indicative of IgE adn mast cell rxn.

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11
Q

Type of hypersensitivity reactions?

A

I: immediate (ex: IgE mediated)
II: mediated by antibodies binding antigens on membrane, basement, ECM
III: antibodies-antigen complex
IV: delayed-type - mediated by T cells. no antibodies

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12
Q

What is hypersensitivity?

A

immune-mediated tissue injury

-allergy + others

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13
Q

6 causes for hypersensitivity?

A
  1. allergic rxn
  2. infection
  3. autoimmune disease
  4. transplant rejection
  5. super antigen
  6. chronic inflammation unknown etiolog
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14
Q

Type II Hypersensitivity

ex?

A

Ex: autoimmune hemolytic anemia, autoimmune thrombocytopenic purpura, Goodpasture’s, acute rheumatic fever

  • cytotoxic antibody interact with CELL MEMBRANE component > attact other cells, complements > acute inflammation
  • organ specific
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15
Q

Type III Hypersensitivity

ex?

A

Ex: animal serum sickness, vasculitis, SLE, Hep B persistent infection, farmer’s lung

  • antibody-antigen immune complex > activate complements > inflammation
  • systemic
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16
Q

Type IV Hypersensitivity

ex?

A

cell-mediated, delayed, T cell!

  • not antibodies
  • collateral damage from T cell response to:
  • underlying infection (TB, HepB)
  • autoimmune response
  • contact hypersensitivity/allergy (poison ivy)
  • chronic inflammatory disease (crohn’s, IBD, sarcoidosis)
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17
Q

What can happen with overproduction of TGF-beta?

A 
inhibitory cytokine
-from chronic inflammation > fibrosis 
>leukocyte chemotaxis
>angiogenesis
in cancer:
>early: growth inhibition 
>but late cancer: invasion, metastasis
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18
Q

Other causes of hypersensitivity not in the 4 classifications?
ex:

A

*superantigens > dysregulated polyclonal activation of T cells > cytokine storm
ex: Toxic shock syndrome
*inherited autoinflammatory syndromes > excessive cytokine production
ex: Familial Mediterranean fever: pyrin gene mutation > IL1 production > suddent inflamm attacks
»inflammation!

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19
Q

What are the immunologically privileged sites?

A
  • eyes
  • brain
  • testes
  • uterus
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20
Q

Central vs peripheral tolerance?

A

Central:
T - negative and positive selection
B - negative selection

Peripheral:

  • Regulatory cytokines: turn off cell (IL10, TGF beta)
  • Immunoinhibitory molecules
  • Treg
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21
Q

Etiologies of autoimmunity? (8)

A
  1. molecular mimicry
  2. Treg failure (foxp3 mutation)
  3. polyclonal activationof B or T cells
  4. Mutations to AIRE/Foxp3
  5. Tissue damage > release hidden antigens
  6. vit D def maybe?
  7. drugs, toxins
  8. cancer
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22
Q

Describe lupus.

cause, tx

A
  • systemic autoimmune disease (type 3 hypersensitivity)
  • anti-nuclear antibodies plus others
  • immune complex deposition > skin rash, glomerulonephritis, arthritis, vasculitis, endocarditis..

Cause: drugs, early complement def
Tx: immunosuppressive drugs

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23
Q

Which drugs can induce SLE?

A

hydralazine

procainamide

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24
Q

What is IPEX syndrome?

A

-Foxp3 mutation > decrease Treg > autoimmunity

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25
Q

what is scleroderma?

A

-systemic autoimmune disease; (type 3 hypersensitivity)
-fibrosis of skin adn internal organs due to ANAs
>occlusive vascular disease, renal disease, Raynaud’s

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26
Q

What is Rheumatoid Arthritis?

A

(type 3 hypersensitivity)
-inflammation of synovium, cartilage destruction
-RF = autoantibodies reactive to Fc of IgG
> joint deformities, vasculitis, lung issues

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27
Q

Describe how Type 1 DM is autoimmune?

A

-T cells recognize self peptides > kills beta cells of pancreas > no insulin
(mice models)

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28
Q

How is autoimmunity linked to cancer?

A
  • anti-cancer immunity is often autoimmune to block inhibitory signals
  • mutated tumour antigens > antigen mimicry > break tolerance
  • tumours secrete mediators > changing tolerance
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29
Q

What is Paraneiplastic anti-NMDA receptor encephlitis?

A
  • strange “exocist” symtoms associated
  • ovarian teratoma > autoimmune attack on NMDA receptor > encephalitis
  • young girls, early death
  • removed tumour, pt is better
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30
Q

Therapy for autoimmune diseases?
SLE
Arthritis
MS

A
  • not curative
  • SLE: corticosteroids, immunosuppresive drugs; mono antibodies
  • Arthritis: TNF-a IL6 blockade; monoantibodies
  • MS: IVIG, immunomodulation
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31
Q

Factors affecting microbiome?

A
  • No flow
  • Skin, mucosal integrity: barrier, mucus, immune cells. opportunity for commensal bacteria to go inside.
  • gravity, mobility: keeps bugs on right side of gut
  • pH and chemicals (gastric acid, urinary chemicals, tears, saliva…)
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32
Q

Ex of altered flow problems > infection?

A
  • tumour > penumonia
  • prostatic hypertrophy > UTI
  • lyphedema > cellulitis
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33
Q

What is a bedsore?

A

-prolonged pressure > damage > fibrosis > necrosis > opportunity for infecton

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34
Q

Describe cdiff:

A

-anaerobic, gram + bacillus
-antibiotic resistant
-in colon normally, antibiotic use eradicate protective bacteria > alter the normal flora > cdiff proliferate
» diarrhea, colitis, death
-faecal-oral

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35
Q

Describe candida infection:

A

-yeasts
-normal flora : skin, GI, sputum, genitals
-antibiotic use > alter flora. yeast abnormally goes up.
» genital yeasts, oral thrush, cadidoemia

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36
Q

What is biofilm?

A
  • prosthetic devices, intravascular devices
  • introduce infection at time of insertion (usually old bacteria on skin)
  • usually: coag -ve staphylococci, staph aureus
    1. bacteria adhere to polymer material
    2. proliferate > multilayer cell clusers + ECM
  • hard to remove. need to take device out
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37
Q

What infection is late complement def associated with?

A

meningococcus

-but later onset, lower mortality because not responding

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38
Q

Neutropaenia vs neutrophil dysfunction

what are common infections at risk?

A

neutropaenia:
-low
-more common: inherited, acq, drug-induced, autoimmune, cancer
»sepsis

dysfunc:
-problems with adhesion, chemotaxis, opsonization, killing
»infection localized

*common infections with: staphylococci, gram -ve, Aspergillus fungi

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39
Q

What is febrile neutropaenia?

what happens when pts recover from FNP?

A
  • neutropeania syndrome
  • most common cause of neutropaenia = chemotherapy
  • FEVER. other symptoms subtle.
  • causes: sick, lying around, use of antibiotics, lines, catheters > risk of infection from own flora
  • granuloctyes decrease to 0.5x10^9/L
  • when neutrophils come back > robust immune response risking pulmonary infiltrates and hepatosplenic candidiasis (fungal infections)
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40
Q

Pts hospitalized have increased risk of which infections?

Why is this impt to know?

A
  • cdiff
  • UTIs
  • bacteraemia (from venous catheters)
  • MRSA
  • VRE
  • surgical site infections
  • infection control is impt!
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41
Q

Asplenia at risk of what infection?

infection precautions for these pts?

A

OPSI: overwhelming post-splenectomy infection
pathogens: s.pneumoniae, N.meningitidis, malaria, baesia
infection prev: vaccination, stay away from dogs, travel…

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42
Q

IgG def/dysfunction at risk of what infection?

A

> s.penumoniae

|&raquo_space;sinopulmonary, GI, skin infections

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43
Q

Cell-mediated immunocompromise at risk of what infection?

A

ALL

think HIV: viruses, mycobacteria, fungi, protozoa

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44
Q

Hypogammaglobulineamia vs dysgammaglobulinaemia?

A

-def in ALL Igs (hypo) is more common than def in some (dys)

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45
Q

What are common acquired causes of Ig def?

A
  • nephrotic syndrome > renal loss
  • GI malabsorption > loss
  • CLLeukaemia > lack of production
46
Q

Stem cell transplant: autologous vs allogenneic vs syngeneic?

A
  1. own stem cell
  2. matched donor
  3. twin
47
Q

What is Graft-vs-host-disease?

A

-donor lymphocyte attack host
-HLA not matched
-usually via GUT b/c conditioning meds damage gut>LPS of bacteria goes into tissue> inflammation > cells react like normal.
>dendritic cells take the antigen > lymph nodes > now DONOR cells react…to host

48
Q

What is conditioning for transplant?

A
  • meds to wipe immune system for transplant
  • chemo w+/out radiation
  • only in haematopoetic stem cell transplant
49
Q

What are common viruses that reactive if immunocompromised?

A
  • herpes
  • polyoma: BK, JC
  • HPV
50
Q

Infection prevention for transplant pts?

A
  1. Prophylaxis: vaccincation, handwash, low contact, meds
  2. Pre-emption: early treatment even if no infection yet (ex: antibiotic for CMV)
    * minimize exposure
51
Q

What is transplant pt at risk of pre engraft and post engraftment? what is risk based on?

A

-1 month pre-engraft: like chemo induced NFP
-30-100 days post engraft: risk of viral reactivation, fungal infection.
Risk depends on graft-vs-host-disease

52
Q

Difference bt HSCT and solid organ transplant?

risk over time for solid organ transplant?

A

solid organ: no conditioning, no graft-vs-host-disease
-infection risks over time come from own flora, transplanted organ, from procedure/equipment > reactivation opportunitistic infections > community acquired

53
Q

Public health and infection control where?

A
  • overcrowding
  • handwashing
  • safe practices
  • animals and humans
  • food
  • vaccination
  • travel
54
Q

What is anti-HLA antibodies? Why is this important?

A

-check recipient for presence of anti-HLA against donor
-caused by exposure to antigen: preg, blood transfusion, organ transplant OR cross-link from viral infection
>CROSSmatch test

55
Q

Tolerance in transplantation

-explain trial

A

-pt is immunologically competent but unresponsive to antigen of graft
-no T cell response, no donor-specific ab
-normal response to other antigens
TRIAL:
-get mix of donor and recipient lymphocytes in system
-immunosup before transplant > infuse donor bone marrow in addition to transplant > withdraw immunosup meds slowly post.
-mixed results - rejection at different stages. some ok after 2-5 yrs. don’t know if never rejection

56
Q

What is HLA? Why is it impt in transplant?

A
  • human leukocyte antigen is a MHC
  • on all cells: MHC1
  • gene on Chrom 6.
  • many loci for it so check match between donor and host. Usually 16 alleles (8 loci)
  • even if 0 mismatch, doesn’t mean genetic identity b/c there are other HLA loci, and non HLA loci.
  • aim for 0 mismatch >longer graft survival, less immunosup needed.
  • but diff between 1 and 2..onward is not major.
57
Q

What are Crossmatch Tests?

A
  • detect presence of anti-HLA antibodies against donor in pt before transplanting. test for T and B cell.
    1. Complement-Dependent Cytotoxicity (CDC) Test
  • add pt serum to donor sample with dye
  • if have antibodies: ab binds HLA antigen > fixes complements > MAC = holes, dye goes into cell > lights up = POSITIVE = bad!
    2. Flow Cytometry
  • more specific and sensitive
  • fluorescent tagged ab binds anti-HLA antibody > binds HLA antigen - see fluorescence in Coulter counter
  • no complements
  • may be different than CDC test
    3. Beads
  • most specific and sensitive
  • use comercial beads with HLA antigens, add host antibodies and check fluorescence through Coulter counter
58
Q

What is Hyperacute Rejection?

A

-antibody mediated rejection
-anti-HLA class 1 donor-specific ab present at transplant
>endothelial damage, thrombus, necrossi
=immediate graft loss

59
Q

What is antibody-mediated rejection?

A
  • 7 days post transplant
  • activation of memory cells > production of anti-HLA ab > complements > reaction
  • measure C4d for presence of complement reaction
60
Q

Why is crossmatch test impt?

when is a neg CDC but positive antiHLA ab?

A

-positive CDC T cell = absolute NO for transplant
-neg CDC T cell but anti-HLA ab may still be present if:
positive CDC B cell;
positive flow T or B cell;
single antigen bead detect anti-HLA;
risk of immediate rejection is low but memory response still an issue
-not as impt for all organs (ex: liver)

61
Q

What is Panel Reactive Antibody? What is used for?

A
  • use flow cytometry with beads
  • test host serum against multiple HLAs
  • % indicate having ab against % of HLA antigens
  • virtual cross-match
62
Q

What are the 2 signal pathways for T cell activation?

A
  1. donor antigen processed by APC > presented on MHC, binds TCR > signal pathway to make IL2 > #3
  2. Costimulation CD receptors bind > IL2 >#3
  3. IL2 and CD25 activates mTOR > cell replication
63
Q

What is acute cellular rejection?

A

-no immediate reaction but a few days after transplant:
antigen present > T CELLs mount a response > killing of cells with HLA antigens
>fibrosis of tissue; lympho infiltrate!
*needs immunosuppressive drugs to avoid this

64
Q

Cyclosporine?

A 
calcineurin inhibitor (CnI)> block cytokine production > inhibit T cell activation
-immuno sup
65
Q

Tacrolimus?

A 
calcineurin inhibitor (CnI)> block cytokine production > inhibit T cell activation
-immuno sup
66
Q

Abatacept/Belatacept?

A

block costimulation > inhibit T cell activation

  • immunosup
  • fusion protein: Fc of IgG and domain of CTLA4. binds B7 on APC so T cell CD28 cant bind.
67
Q

Basiliximab?

A

bind IL2> inhibit T cell activation

  • immunosup
  • monoantibody
  • use prophalytic not tx in transplant
68
Q

Azathiprine, mycophenolic acid, sirolimus?

A

act on mTOR > inhibit proliferation

-immunosup

69
Q

What is acute humoral rejection?

A
  • activation of B cells against donor HLA antigen > NEW anti-HLA ab post-transplant
  • complement deposits in graft!
  • can lead to graft rejection but can take yrs
  • unsure of med use to treat
70
Q

What are potential rejection issues with transplant?

A
  • hyperacute
  • antibody mediated
  • acute cellular
  • acute humoral
  • chronic (B and T)
  • rejection doesn’t not mean graft loss!
  • no acute rejection doesn’t mean longer term outcomes
71
Q

What is chronic graft rejection?

A
  • fibrosis!

- no treatment effective

72
Q

If we block B and T cell, are we safe from rejection?

A

NO: Monocyte mediated rejection!

73
Q

complications of transplant?

A
  • acute rejection
  • chronic loss of fnc
  • infection
  • recurrence of original disease
  • malignancy (bc of disease, immunosuppression)
  • htn, hyperlipid, DM > CVD
  • weight gain
  • acute renal failure
  • osteopenia, osteoporosis
  • teratogenic toxicity from drugs?
74
Q

What organs are transplanted?

A

heart, liver, lungs, kidneys, pancreas, bone marrow

QoL: s.intestine, keratolimbal stem cell, abdo wall, arms, hands, larynx, face

75
Q

What are some indications for heart transplant?

A
  • adv failure

- cardiomyopathy

76
Q

What are some indications for lung transplant?

A

COPD
pulmonary fibrosis
CF
1ry pulmonary hypertension

77
Q

What are some indications for kidney transplant?

A

end stage renal disease

78
Q

What are some indications for liver transplant?

A

decomp cirrhosis
fulminant hepaptic failure
heptocellular carcinoma

79
Q

What are some indications for pancreas transplant?

A

DM1

80
Q

What are some ex of contraindications for transplant?

A
  • infection
  • psychososial - psych, compliance with treatment
  • comorbities:
  • cancer - depends
  • adv heart disease in liver t
  • cirrhosis in lung t
  • renal in pancreas t
  • DM in heart t
  • age is not absolute contraindication
81
Q

What is pretransplant eval?

A
  1. pt meet criteria?
  2. assess short term risks
  3. assess immunologic risk of infection
  4. assess long term complications
    - assess psychosocial
    - screen for cancer
82
Q

What is living donation?

A
  • liver donor
  • ex: kidney, partial liver, rarely: pancreas, 1 lung, intestinal
  • no wait list
  • good health, normal fnc, no med hx
  • consent
83
Q

What are criteria for deceased donation?

A
  • after brain death determination
  • sometimes after cardiac death
  • time is impt!
  • cold flush the organ to slow down
84
Q

heterotopic vs orthotopic surgery?

A
  • h: kidney and pancreas put into new location. leave old one in body.
  • o: remove old, transplant new.
85
Q

Induction vs maintenance therapy? - drug class?

A
  • Induction: monoclonal/polyclonal antibody. use higher dose

- maintenance therapy: Calcineurin inhibitor; antiproliferative agent; steroid

86
Q

Monitoring graft post-transplant?

A
  • immunosup drugs
  • tests of fnc: creatinine, pft, liver enzymes, amylase
  • imaging: ultrasound, echocardio
  • biopsy if unsure
87
Q

What is chronic allograft disease?

what are causes?

A

-no acute rejection
-gradual fibrosis
-paraenchymal atrophy; obliterative arteriopathy
-3-6 months post transplant
Causes:
-quality of organ
-cold/warm ischemia duration
-antibody-mediated response
-infection
-htn, hlipid
-primary disease
-toxicity: alcohol, smoking, meds

88
Q

Cancer and transplant?

A

immunosuppression increases risk of cancer

  • (esp thymoglobulin)
  • greatest risk in viral-mediated cancers: cervix, lympho, kaposi’s sarcoma, non-melanoma skin
  • more aggressive cancer
  • Tx as per standard
  • SCREEN as per general population
89
Q

Why acute renal failure post transplant?

A
  • intra-operative hypotension
  • sepsis
  • meds are nephrotoxic: esp calcineurin inhibitors
  • volume loss
  • risk of chronic failure and death
90
Q

Why transplant?

A
  • curative treatment option
  • no other treatment available
  • improve survival
  • improve QoL
91
Q

Why use immunosuppressive drugs?

A
  • autoimmune
  • transplant
  • cancer
92
Q

Corticosteroids for immunosup?

ex?

A

-systemic immunosup and anti-inflamm
-bind glucocorticoid receptor and NKkappaB transcription factor
-wide effects on different immune cells
-cheap
-don’t use for long term
-side effects: infection, htn, hyperlipid, diabetes, wt gain, skin change, osteopenia, muscle weakness, cataracts poor wound healing, mood changes
ex: prednisone (oral), methylprednisolone (iv)
dexamethasone, hydrocortisone

93
Q

Antiproliferative agents for immunosupp?

ex?

A

ex: cyclophosphamide, azathiprine, mycophenolic acid, methotrexate
- purine analougues, block purine synthesis, block pyrimidine syn, block folic acid
- prevent DNA synthesis/proliferation of lymphocytes
- side effect: bone marrow suppression, neutropaenia, toxic to liver, GI, pancreas

94
Q

What are monoclonal antibodies?

A

-ab against 1 molecule (ex: receptors, cytokines…)

side effects: infection, cancer
ex: basiliximab
infliximab
adalimumab
alemtuzumab
rituximab
eculizumab
natalizumab
95
Q

Infliximab?

A
  • monoclonal antibody against TNF-alpha
  • induce apoptosis of TNFalpha expressing cells
  • $
  • used in: IBD, spondylitis
96
Q

Thymoglobulin?

A
  • polyclonal antibody (against 40+ antigens)
  • depletes T cell
  • can act on B cell, dendritic cells
  • use: post transplant
  • side effect: prolonged lymphopenia
97
Q

IVIG?

A

intravenous Ig

  • inhibit ab, complements, B cells, adhesion molecules
  • use: autoimmune disease, transplantation to treat rejection
  • pooled Ig from blood donors
  • adv: well tolerated, no increase risk of infection/cancer, $
  • not evidence based
98
Q

What is a fusion protein?

ex?

A
  • receptor of target molecule bind to Fc of ab
  • competes with molecule from binding receptor
  • Fc part allows protein to stay in circulation instead of being metabolized
  • “-cept”
  • ex: Etanercept
99
Q

Etanercept?

A

TNFalpha blocker

  • fusion protein
    use: IBD
100
Q

What are sulfa drugs?

ex?

A

ex: Sulfasalazine/5-aminosalicylic acid
- mech of action unknown
- use: IBD
- side effects rare: hepatitis, nephritis, agranulocytosis

101
Q

hydroxychloroquine?

A
  • originally used for malaria, now for lupus, rheumatoid arthritis, Sjogren’s syndrome
  • unknown mech - maybe impair stimulation of CD4 T cells by MHC
  • side effect: macular (eyes) toxicity
102
Q

Which blood type is the universal donor?
what blood can they get? why?
what about plasma transfusion?

A
  • O = universal donor (no antigens)
  • only get O because have antibodies against A and B.
  • plasma transfusion is opposite = universal recipient
103
Q

Which blood type is the university recipient?
what blood can they get? why?
what about plasma transfusion?

A
  • AB = universal recipient (has A and B antigen) b/c no antibodies against anything
  • plasma transfusion is opposite - have no antibodies = universal donor
104
Q

Describe major blood groups - why A?B?

A

-antigen determined by glycosyltransferase enzyme adding sugars to RBC surface
A: N-acetyl-D-galactosamine
B: D-galactose

105
Q

why is ABO antigen impt to look at during blood transfusion?

-what do we see on slides?

A

attack > cytokines > inflammation > hemolysis

-IgM mediated > agglutination

106
Q

What are non ABO antibodies? why impt

ex:

A
  • more dangerous than ABO antibodies because less activators > more likely extravascular hemolysis
  • first exposure > ab formation. delayed response
  • IgG mediated - doesn’t agglutinate
  • misdiagnosed
  • tires fall over time
  • relevant in foreign blood exposure: transfusion, preg, transplant, needlestick

ex: *RhD - test babies and mothers
RhC, Kell, Duffy, Kidd - only test matching if high risk

107
Q

What is the Coomb’s Test?

DAT vs IAT?

A

antiglobulin test
-give ab to antibodies on RBCs
>agglutination = positive

Direct AT: antiIg mixed with RBC > positive = RBC had Ab
Indirect AT: plasma mixed with RBC > positive = plasma had Ab against RBC

108
Q

What is the compatibility testing?

A
  • Check for blood group: ABO, Rh, and antibodies in serum
  • screen for alloantibodies against minor blood group antigens by mixing pt plasma with panel RBCs and antiIg
  • crossmatch with donor blood sample
109
Q

If we don’t have time to check blood, what do we give under emergency?

A

Give O-RhD-ve RBCs

110
Q

Blood bank solution to

  1. clotting
  2. spoilage
  3. contamination
  4. supply
A
  1. small citrate to bind calcium in blood > coaugulation pathway inhibited
  2. additives to preserve RBC: glucose, adenine, phosphate
  3. aseptic collection, refridgerate
  4. good question!
111
Q

What are blood products?

A
  • whole blood
  • RBC
  • plasma - coag factors in cryoprepitate, Ig, albumin
  • platelets - don’t need to be ABO compatible
112
Q

What is apheresis?

A
  • collecting specific component of blood

- run donor blood through device, centrifuge, take adn return remaining into donor

MMMD 1 - QH (7 decks)

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