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STEP 1 > Hypersensitivities > Flashcards

Hypersensitivities Flashcards

1
Q

Food, Drug, Bee sting allergies.
Asthma
Type __ HSR

A

1

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2
Q 
Autoimmune- hemolytic anemia
ITP
Hemolytic Disease of Newborn
Transfusion reactions
Type \_\_ HSR
A

2

Antibody dependent Cellular Cytotoxicity
NK cell killing

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3
Q

Good Pasture Syndrome
Rheumatic Fever
Hyperacute Transplant Rejection
Type __ HSR

A

2

Complement system & Fc receptor-mediated Inflammation

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4
Q

Myasthenia Gravis
Graves Disease
Pemphigus Vulgaris (IgG-Desmoglein)
Type __ HSR

A

2

ABs bind to cell surface receptor and block or activate downstream processes.

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5
Q 
SLE
Polyarteritis Nodosa (Hep. B association)
PSGN
Serum Sickness
Type \_\_ HSR
A

3

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6
Q

Poison Ivy
Nickel Allergy
Type __ HSR

A

4

Contact Dermatitis

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7
Q

Graft Vs Host Disease
PPD test for TB
Candida skin test
Type __ HSR

A

4

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8
Q

Hypersensitivity reaction does NOT involve Antibodies

A

Type 4

Delayed Type

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9
Q

What HSR is described?

Direct cell cytotoxicity via CD8+ T cells killing target

A

Type 4
Delayed Type

(+CD4+ releasing inflammatory cytokines)

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10
Q 
Immune complexes (antigen-antibody) activate complement and neutrophils release lysosomal enzymes.
Complexes are insoluble and may deposit onto tissue surfaces.
A

Type 3

Ag-Ab-C3 (3 things stuck together)

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11
Q

What HSR is described?

Antibodies bind to cell surface antigens causing cellular destruction, inflammation, and organ dysfunction.

A

Type 2

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12
Q

One mechanism is the cell is opsonized by antibodies leading to either, complement mediated phagocytosis or NK cell killing (ADCC).

A

Type 2

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13
Q

Detects Antibodies attached DIRECTLY to the RBC surface. + result means agglutination

A

Coombs

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14
Q

Detects the presence of unbound antibodies in the serum.

A

Indirect Coombs

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15
Q

ELISA blood test for allergen specific IgE to diagnose which HSR type?

A

Type 1

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16
Q

Anaphylactic & Atopic reactions occur in 2 phases:

The immediate reaction occurs in minutes when the antigen crosslinks ____ IgE on PRESENSITIZED Mast cells.

A

Pre-formed

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17
Q

Mast cell degranulation releases (2)

A

Histamine (increased permeability of capillary)

Tryptase

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18
Q

The second or delayed phase of Type 1 HSRs occur hours later when chemokines attract ___ and ___ causing inflammation and tissue damage.

A

Eosinophils

leukotrienes

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19
Q 
Describe 
Type 1 HSR 
Type 2 HSR
Type 3 HSR
Type 4 HSR
A

Mast cell/ IgE mediated (Immediate)
Antibody mediated
Immune Complex mediated
T Cell mediated (Delayed)

(MACT)

20
Q

This patient with recurrent episodes of abdominal pain and an episode of facial swelling likely has angioedema due to

A

C1 inhibitor (C1INH) deficiency

21
Q

C1 inhibitor (C1INH) deficiency causes increased cleavage of C2 and C4 and results in inappropriate activation of the complement cascade. C1INH also blocks ____-induced conversion of kininogen to bradykinin

A

kallikrein

22
Q

a potent vasodilator associated with angioedema due to increased permeability:

A

bradykinin

23
Q

Direct Mast Cell Activation can be done by ____ which caused pruritis & urticaria

A

Opioids

24
Q

Facial edema (without itchiness or rash) or laryngeal swelling caused by recent use of ACE-I is due to accumulation of _____

A

Bradykinin

25
Q

Excess Bradykinin resulting in edema can be caused by

A

C1 inhibitor deficiency

ACE-I

26
Q

Angiedema without urticaria or pruritis
Labs: low C4, High Bradykinin

indicative of

A

C1 inhibitor deficiency

High levels of activated C1
Low levels of C1 esterase inhibitor

27
Q

Kallikrein converts what to proteins

A

Plasminogen to Plasmin

Kininogen to Bradykinin

28
Q

Activated C1 inhibits what protein

A

Kallikrein

29
Q

____ inhibitor suppresses activation of the C1 complement component and therefore the rest of the classic complement pathway.

A

C1 esterase

30
Q

An erythematous area with indistinct margins over the skin. The area feels hot and indurated and is exquisitely tender.

A

Cellulitis

31
Q

Myeloperoxidase is found predominately in

A

neutrophils

32
Q

Drugs causing a nonimmunologic reaction that can cause itching, urticarial rash, wheezing, hypotension, and tachycardia that closely mimictrue IgE-mediated type 1 hypersensitivity (eg, anaphylaxis). (3)

A

Opioids
Vancomycin (red man syndrome)
radioiodine contrast

33
Q

Nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit cyclooxygenase, which leads to increased _____ activity. This effect can precipitate bronchoconstriction and wheezing due to increased production of leukotrienes (ie, NSAID-exacerbated respiratory disease)

A

5-lipoxygenase

34
Q

During initial allergen exposure, antibody class switching from IgM to IgE antibodies specific for the allergen occurs. IgE binds to high-affinity ____ on basophils and mast cells.

Re-exposure to the allergen results in cross-linking of bound IgE antibodies with subsequent degranulation and release of inflammatory mediators ( histamine, tryptase, leukotrienes, prostaglandins).

A

IgE Fc receptors

35
Q

TH1 cells are responsible for inducing macrophage and ____ inflammatory reactions.

A

cytotoxic T lymphocyte-mediated (type IV)

36
Q

__ is a cytokine produced by TH1 lymphocytes that increases proliferation and activity of helper, cytotoxic, and regulatory T cells as well as NK cells.

A

IL-2

37
Q

IL-4 is responsible for driving the production of TH2 cells, which promote antibody-mediated (humoral) immunity and facilitate type __ hypersensitivity.

A

I

38
Q

IL-4 is responsible for driving the production of __ cells

A

TH2

39
Q

Dyspnea, hypotension, and tachycardia soon after administration of β-lactam antibiotics are suggestive of

A

anaphylactic shock

*give epinephrine

40
Q

release of ___ causing widespread increased vascular PERMEABILITY aka Anaphylactic Shock

A

chemical mediators

histamine, prostaglandin, leukotrienes

41
Q

In response to anaphylaxis-induced hypotension, an intact ____ reflex leads to increased sympathetic activity, tachycardia, and compensatory vasoconstriction.

A

baroreceptor

42
Q

A toxin-mediated decrease in myocardial contractility and an increase in capillary permeability occur in

A

toxic shock syndrome (TSS)

43
Q

TSS toxin 1 is capable of nonspecifically activating T cells (superantigen). The subsequent dramatic release of inflammatory cytokines results in increased capillary permeability and hypotension, as well as high fever and a diffuse, erythematous rash. In addition, the exotoxin can directly inhibit myocardial function.

A

Anaphylactic Shock is due to CHEMIACAL mediators (like Histamine) not TOXIN mediators like TSS.

44
Q

Hypotension, Tachycardia, N/V, & Wheezing

are all signs of

A

Anaphylactic Shock

other signs: Edema, hoarseness, stridor, flushing, itchiness, rash, abdominal pain

45
Q

Erythema
Pruiritis
Urticaria
characteristic of Type __ HSR

A

1

STEP 1 (88 decks)

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