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STEP 1 > 05b: Immunology 2 > Flashcards

05b: Immunology 2 Flashcards

1
Q

Live vaccines induce (cell/humoral) immune response and are contraindicated in which populations?

A

Both cell and humoral;

Pregnant and immunodeficient patients

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2
Q

BCG vaccine is (live/killed). Rabies vaccine is (live/killed). Rotavirus vaccine is (live/killed).

A

Live; killed; live

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3
Q

Killed vaccines induce (cell/humoral) immune response. List some examples of killed vaccines.

A

“R.I.P. Always”

Rabies, Influenza (injection), Polio (salk), hep A

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4
Q

List the four types of hypersensitivity reactions:

A 
"ACID"
Type I: Anaphylactic/Atopic
Type II: Cytotoxic 
Type III: Immune complex
Type IV: Delayed
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5
Q

Which hypersensitivity reactions are antibody-mediated.

A

I, II, and IIII

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6
Q

Which key cells are playing role in anaphylactic reaction to bee sting?

A

Basophils and mast cells (releasing His) in response to IgE

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7
Q

One mechanism of type (I/II/III/IV) hypersensitivity reaction is opsonization of cell by Ab, leading to:

A

II

  1. Phagocytosis and/or complement activation
  2. NK cell killing (cytotoxicity)
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8
Q

(X)-mediated inflammation such as in Goodpasture syndrome is an example of type (I/II/III/IV) hypersensitivity reaction. List other examples like this.

A

X = Antibody;
II

Rheumatic fever, hyperacute transplant rejection

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9
Q

List examples of Type II HS reaction in which Ab mediates abnormal cell function by binding its receptors.

A

MG and Grave’s

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10
Q

Patient receives blood transfusion and 30 min later develops fever, chills, chest/flank pain. Urine is brown-colored. What type of hypersensitivity reaction?

A

Acute hemolytic transfusion reaction (ABO mismatch) is type II hypersensitivity (anti-ABO IgM bind donor RBCs and activate complement/lyse)

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11
Q

Hemolytic disease of newborn is what type of hypersensitivity reaction?

A

Type II

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12
Q

Serum sickness is Type (I/II/III/IV) hypersensitivity reaction and occurs (X) min/hour/days after (Y).

A

III (immune complex);
X = 5-10 days
Y = started drug (ex: infliximab)

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13
Q

Classic histology findings in serum sickness

A

Fibrinoid necrosis, PMN infiltration of small blood vessels

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14
Q

List the two mechanisms by which Type IV hypersensitivity reaction can be carried out.

A
  1. Direct cytotoxicity (CD8 T cells kill target)

2. Delayed-type: sensitized CD4 helper T cells see Ag, release cytokines, activate macrophages

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15
Q

List examples of Type IV hypersensitivity reactions.

A

3 T’s for the Th and Tc’s:

  1. Transplant rejections
  2. TB (and candida) skin tests
  3. Touching (contact dermatitis like poison ivy)
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16
Q

Patient that receives blood transfusion and has reaction (within 2-3 hours) involving urticaria, pruritus, and shock symptoms. Diagnosis must be:

A

Allergic/anaphylactic (can occur within minutes; Type I hypersensitivity)

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17
Q

Transfusion-related acute lung injury occurs within (X) min/hours/days. What’s the mechanism behind this?

A

X = 6 hours

Donor Anti-leukocyte Ab attack recipient PMNs and pulmonary endothelial cells

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18
Q

Anti glutamic acid decarboxylase Abs associated with which disease?

A

DM I

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19
Q

Antisynthetase (anti-Jo), anti-SRP, and anti-helicase Abs associated with which disease?

A

Polymyositis, dermatomyositis

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20
Q

Pt receives influenza injection vaccine. If exposed to virus through subsequent infection, (X) players of immune system will (stimulate/inhibit) viral (Y).

A

Killed vaccine:
X = neutralizing antibodies (humoral response) against hemagglutinin
Inhibit
Y = entry into cells

21
Q

Eosinophils fight off parasites via (X)-mediated cytotoxicity (degranulation).

A

X = antibody-dependent cell-mediated

IgG, IgE coat parasite and activate eos by binding Fc R

22
Q

T/F: Eosinophils play important role in Type I hypersensitivity reactions.

A

True, but in the LATE-PHASE type I HS (chronic allergic reactions)

23
Q

Bruton, aka (X), agammaglobulinemia: what’s the defect?

A

X = X-linked

Defective BTK (tyrosine kinase gene) leads to no B cell maturation

24
Q

IL-12 receptor deficiency: low (X) cell response with frequent (Y) infections.

A 
X = Th1
Y = disseminated mycobacterial/fungal infections
25
Q

IL-12 receptor deficiency: supplementation with (X) proves beneficial for these patients.

A

X = IFN-gamma

26
Q

Job, aka (X), syndrome is a deficiency of (Y).

A 
X = Autosomal dominant Hyper-IgE 
Y = Th17 cell (STAT3 mutation) so impaired PMN recruitment
27
Q

What are the key characteristics/symptoms of Job syndrome?

A

“FATED”

  1. course Face
  2. cold/non-inflamed staph Abscesses
  3. retained primary Teeth
  4. high igE
  5. Derm issues (eczema)
28
Q

SCID can be X-linked with defective (X) or AR with (Y) deficiency.

A 
X = IL-2 receptor (most common)
Y = adenosine deaminase
29
Q

Key issue/defect in Ataxia-telangiectasia, which is inherited in (X) fashion.

A

X = AR

Defect in ATM gene causes failure to detect DNA damage/halt cell cycle (accumulated mutations)

30
Q

Ataxia telangiectasia triad:

A

3 A’s

  1. cerebellar Ataxia
  2. spider Angiomas
  3. low IgA (recurrent sinopulm infections); IgG and IgE also low
31
Q

Hyper-IgM syndrome due to defective:

A

CD40L on Th cells (X-linked R); class switching impaired

32
Q

Wiscott-Aldrich syndrome: mutation in (X) causes defective (Y).

A 
X = WASp gene
Y = Ag presentation (WBCs, platelets can't reorganize actin cytoskeleton)
33
Q

Wiscott-Aldrich syndrome is inherited in (X) fashion and presents with low levels of which Ig?

A

X = X-linked R

IgG and IgM; high IgE, IgA

34
Q

Pt presents with recurrent skin/mucosal bacterial infections that are not purulent. Most likely diagnosis?

A

Leukocyte adhesion deficiency I

35
Q

Chédiak-Higashi syndrome is defect in (X) and is inherited in (Y) fashion.

A 
X = LYST (lysosomal trafficking regulator) causing microtubule dysfunction in phagosome-lysosome fusion
Y = AR
36
Q

Chédiak-Higashi syndrome: what would you expect to see on neuro/eye exam?

A

Nystagmus, peripheral neuropathy, neurodegeneration

37
Q

Chédiak-Higashi syndrome: what would you expect to see in histology?

A

Giant granules in granulocytes and platelets

38
Q

Chronic granulomatous disease is inherited in (X) fashion.

A

X = X-linked recessive

39
Q

Systemic candida infection is seen with low numbers of (X) cells whereas local candida infection is seen with low numbers of (Y) cells.

A 
X = granulocytes (also other systemic fungal infections)
Y = T cells
40
Q

Xenograft is graft from (X). Allograft is graft from (Y).

A 
X = different species
Y = same species, non-identical individual/twin
41
Q

Hyperacute transplant rejection is type (X) HS reaction

A

X = II (pre-existing Ab react to donor Ag)

42
Q

Patient develops chills, arthralgias a month after transplant. This is likely mediated by (X) cells.

A

X = CD8 (against donor MHCs; type IV HS) or by antibodies

43
Q

Chronic transplant rejection involves which components of immune response?

A

Both antibodies (type II HS) and CD4 T cells (type IV HS)

44
Q

Graft v host disease is type (X) HS reaction and occurs most commonly in which types of transplants?

A

X = IV

Liver and bone marrow (rich in lymphocytes)

45
Q

(X) drugs are calcineurin inhibitors that have which mechanism of action?

A

X = Cyclosporine and Tacrolimus

Immunosuppressants that block T cell activation by preventing IL2 transcription (in Th cell)

46
Q

Calcineurin inhibitors have which key side effect?

A

Nephrotoxicity

47
Q

Sirolimus is in (X) category of drugs and works by which mechanism?

A 
Sirolimus = Rapamycin
X = immunosuppressants (mTOR inhibitor)

Prevents IL-2 response in B and T cells

48
Q

Side effects of Sirolimus

A

Pancytopenia, insulin resistance, hyperlipidemia

49
Q

Basiliximab MOA

A

Blocks IL-2R (immunosuppressant)

STEP 1 (21 decks)

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