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ABSITE > Immuno > Flashcards

Immuno Flashcards

1
Q

Hypersensitivity reactions

A

I: IgE-mediated. allergic asthma or anaphylaxis

II: cytotoxic, ab-dependent. Autoimmune hemolytic anemia, immune thrombocytopenia

III: Ag-Ab complex. Serum-sickness like syndrome of acute Hep B

IV: delayed rxn, T-cell mediated. Dermatitis, PPD test

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2
Q

Immune thrombocytopenia (ITP)

A

acquired thrombocytopenia
AutoAb-mediated destruction of PLTs

Tx:

  • PLTs >=30K, asxs, minor mucocutaneous bleeding: observe
  • PLT <30K, asxs, minor mucocutaneous bleeding: corticosteroids
  • Urgent mgmt bleeding or prior to urgent procedure: IVIG
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3
Q

High risk of postop complications in pts w/ IBD

A

pts on steroid therapy within 4 weeks before surgery
Greater incidence of infection-related complications (abscess)

5-ASA acts on bowel lining, different from aspirin, don’t need to be stopped before surgery

Anti-TNF in 3 months prior to surgery has not been shown to affect wound healing

Preop hypoalbuminemia is strong predictor of postop morbidity and mortality

Thiopurines (azathioprine) within 6 weeks of surgery have increased risk of postop morbidity, anastomotic leak/sepsis

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4
Q

Management of ITP

A

1st line: steroids
2nd line: IVIg
3rd line: Rituximab, romiplostim (after splenectomy failure); splenectomy if med mgmt fails

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5
Q

Factors associated with Radiation Resistance

A 
Hypoxia
Smoking status
Inherent tumor cell characteristics
Repopulation
Tumor location
Tumor grade
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6
Q

Management of Periop Steroids in pts at risk for HPA Axis suppression (20mg/day pred for >3 weeks)

A

Minor/ambulatory surgery (local anesthetic, hernia): Take normal AM dose of PO steroid day of surgery, no supplemental steroids

Mod stress (leg revascularization): Take normal AM dose of PO steroid day of surgery. Before induction: hydrocortisone 50mg IV. POD 0-2: hydrocortisone 25mg q8h x 24h, POD 2: PO outpt dose

Major stress (cardiac, abd, thoracic): Take normal AM PO dose day of surgery. Before induction: hydrocortisone 100mg IV, POD 0-2: hydrocortison 50mg q8h x24h, POD 2: hydrocortisone 25mg q8h, POD 3-4: outpt dose

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7
Q

Management of periop steroids in pts at intermediate risk for HPA axis suppression (5-20mg/d pred for >=3 weeks)

A

Eval of HPA axis suppression periop to determine need for additional stress dose steroids

Cortisol levels, ACTH stimulation test

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8
Q

Graft-versus-host disease (GVHD)

A

T-cell-mediated disease

3 steps:

1) damage to recipient tissue as part of conditioning process for stem cell transplant (circulating immune cells are destroyed) -> translocation of microbes and activation of innate immune system
2) Differentiation of donor T-cells into Th2 and Th17. Recognize host as foreign, activate JAK1/2, TLR, cause release of proinflammatory CKs (IL-6, IFG), cause host tissue destruction (donor NK cells targeting MHC-1 cells)
3) Tissue dysregulation from CKs -> host tissue failure (skin, gut), fail to regenerate after being destroyed

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9
Q

Transfusion-related acute lung injury (TRALI)

A

Recipient cells target donor cells

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10
Q

Chronic GVHD

A

Dysregulation of donor T regulatory cells, resultant fibrosis

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11
Q

Phases of wound healing

A

Inflammatory (1-3 days)
Proliferative (4 days - 3 weeks)
Remodeling (3 - 8 weeks)

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12
Q

MPs in wound healing

A

Arrive at wound w/in 3-5 days after injury.
Release growth factors, proliferation of immune cells, initiate angiogenesis
Phagocytize tissue/bacteria/other phagocytes
Participate in regeneration and are essential for found healing

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13
Q

First cells in wound

A

NPs

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14
Q

Hodgkin Lymphoma staging

A

Stage I: Dz located in single lymphatic site
Stage II: Dz in 2+ sites either above or below diaphragm
Stage III: Dz located above & below diaphragm
Stage IV: Disseminated dz. Involves non-lymph tissue

add “b” designation if patient also has B sxs: night sweats, weight loss, pruritus

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15
Q

Delayed immune hemolytic reaction

A

ABO-compatible RBCs containing a specific antigen, RhD Duffy or Kell, transfused in pts with preformed alloantibodies.
Development of new Ab from previous blood transfusions
Abs are to minor Age - Rh, Duffy, Kell
Prevent by retyping & screening pt’s blood to ID new Abs
Can occur up to 30 days after transfusion
Sxs appear in 3-10 days - fever, malaise, unconjugated hyperbilirubinemia, declining Hg/Hct

Dx: Direct Coombs test + peripheral smear

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16
Q

Tumor lysis syndrome

A

hematuria, leukocytosis, hyperkalemia, hyperphosphatemia, hyperuricemia, hypocalcemia, AKI

Phosphate binds calcium. CaPhos crystals precipitate in kidneys –> AKI

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17
Q

Pt w/ Crohn’s disease, on azathioprine, noted with TI mass, received treatment (chemo) then noted with hyperkalemia, AKI, hyperphosphatemia, hematuria

A

tumor lysis syndrome from aggressive lymphoma (non-Hodgkin B cell lymphoma)

18
Q

Howell-Jolly bodies

A

nuclear remnants in RBCs
usually cleared by spleen

Seen on peripheral smear after splenectomy

19
Q

Heinz bodies

A

aggregates of denatured Hg

Found in G6PD deficiency pts

20
Q

Pappenheimer bodies

A

Iron-containing blue granules in RBCs

Seen in pts w/ siderblastic anemia

21
Q

DIC

A

Acquired coagulopathy. Excessive thrombin, diffuse microthrombi generation. consumptive thrombocytopenia, depletion of coagulation factors.

Prolonged PT and PTT. High fibrin split products, Low fibrinogen.

22
Q

Thoracic duct

A

Originates at cisterna chyli at midline L1-L2
Course superiorly through aortic hiatus at T10-12 (to right of aorta)
Runs along right of midline, crosses R -> L at T4-6
Empties into junction of L subclavian and L IJ vein

Carries chylomicrons and LCFA.

23
Q

Renal transplant rejection types

A

Hyperacute: min - hrs. preformed Abs, complement activation. endothelial damage, inflammation, thrombosis. Prevent by pre-transplant crossmatch, ABO type match

AcuTe: weeks - months. T cell-mediated, acquired Ab response. Lymphocytic infiltration, complement deposition, parenchymal necrosis. Prevent by initial immunosuppressive T cell depletion following by tapered T-cell inactivation

Chronic: months - years. T & B cells, donor-specific Ab. parenchymal replacement with fibrous tissue, intimal smooth muscle proliferation leading to vessel occlusion. prevent acute rejection episodes, limit ischemia/reperfusion at transplant

24
Q

Neutropenic enterocolitis

A

CT: thick colon, no evidence of bowel perf
Diarrheal dz in HIV patients

MCC AIDS-related diarrhea = CMV
2/2 reactivation of latent infection
RFs: CMV viremia, advanced immunosuppression (CD4 <50)
Stool studies: viral inclusion bodies
Endoscopy: ulcers, erosions

Tx: noon NPO/IVFs, Abx, Antiretroviral, +ganciclovir or valganciclovir (if CD4<50).

25
Q

hemolytic vs nonhemolytic transfusion reactions

A

febrile non hemolytic: host ab against donor leukocytes. CKs from donor. stop transfusion. tx sxs

hemolytic: ABO incompatibility - host Ab against donor RBCs. tx stop transfusion, IVFs

26
Q

Source and Effects of IL-1

A

MPs, monocytes

T-cell & APC stimulation, B-cell growth, Ab production
Induces fever through activity on hypothalamus

27
Q

Source and Effects of IL-2

A

Activated T-cells

T-cell growth & proliferation (CD4 cell)

28
Q

Source and Effects of IL-4

A

T-cells, mast cells

B-cell proliferation
IgE production
Involved in asthma exacerbation

29
Q

Source and Effect of IL-5

A

T-cells, mast cells

Eosinophil growth and modulation
Involved in asthma exacerbation

30
Q

Source and Effect of IL-6

A

Activated T-cells

Induces inflammation
Lymphocyte differentiation

31
Q

Source and Effects of IL-8

A

MPs

NP stimulation/recruitment, demargination, degranulation
Inhibition of endothelial adhesion
Implicated in obesity, cystic fibrosis

32
Q

Source and Effects of IL-10

A

Activated T-cells, B-cells, monocytes

Type 1 T-helper cell suppression
Down-regulates MHC II Ags

33
Q

Source and Effects of IL-12

A

MPs, B-cells

NK cell stimulation
Enhances IFN-gamma expression of B-cells

34
Q

Source and Effects of IL-13

A

Type 2 T-helper cells

IgE production
Assoc w/ asthma and allergy exacerbation

35
Q

Cells that stain CD3+ and recognize HLA-1 molecules

A

CD8+ cytotoxic T-cell
Causes release of lysosomal granules containing perforin, holes in cell membranes, granzymes responsible for cell lysis, promote apoptosis through CD95 (Fas) rec

36
Q

Primary lymphoid organs

A

Generate lymphocytes from immature cells

Liver
Bone
Thymus

37
Q

Secondary lymphoid organs

A

Maintain current lymphocytes and initiate adaptive immune response

LNs
Spleen
Peyers patches
Tonsils
Adenoids
38
Q

Mechanisms of apoptosis

A

Extrinsic: binding death rec -> recruitment of Fas associated death domain protein -> activation of caspase 3

intrinsic: protein mediators (Bcl-2) -> increased mitochondrial membrane permeability -> release of mitochondrial cytochrome C -> activates caspase 3

39
Q

Caspase

A

mediates organized breakdown of nuclear DNA –> apoptosis

40
Q

Ipilimumab (Yervoy)

A

CTLA-4 inhibitor, upregulates CD4

41
Q

Nivolumab (Opdivo)

A

PD1 inhibitor, up regulates CD4

42
Q

Pembrolizumab

A

Tx of metastatic melanoma

PD1 inhibitor

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