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IMMUNO > Hypersensitivity Type II, III and IV > Flashcards

Hypersensitivity Type II, III and IV Flashcards

1
Q

what is the mechanism behind type II hypersensitivity reactions?

A
  • IgG, IgM antibodies bind to antigens on pathogen cell surface
  • bound IgG / IgM are bound by other immune players that lead to
    • complement starting molecule→ complement cascade → MAC
    • NK cells → ADCC
    • PMNs → phagocytosis
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2
Q

what diseases are considered type II hypersensitivity reactions?

A
  • organ specific autoimmune diseases
    • goodpasture syndrome
    • grave’s
    • myasthenia gravis
    • Addison’s
    • pernicious anemia
  • others:
    • reactions against RBCs
      • transfusion rxns
      • erythroblastosis fetalis
      • autoimmune hemolytic anemias
    • thrombocytopenia
    • RF (rheumatic fever)
    • graft rejection
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3
Q

transfusion reactions against ABO antigens - mechanism?

A

a type II hypersensitivity rnx

  • humans possess natural Ab (IgM) against antigens not expressed by their own RBCs (based on blood type) .
    • if patient receives an incompatible blood type, IgM antibodies bind to the foreign antigens those RBCS → agglutinate those RBCs → complement cascade → MAC (red cell lysis)
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4
Q

which blood types are incompatible with which transfusions?

A

i.e., which blood types have antibodies against (would agglutinate with) which RBC antigens

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5
Q

which blood types are incompatible with which transfusions?

A

i.e., which blood types have antibodies against (would agglutinate) which RBC antigens?

type A - Type B, AB

type B- Type A, AB

type AB - none

type O - Type A, B, AB

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6
Q

what is the clinical presentation of a blood transfusion rxn?

A

= type II hypersensitivity reaction

  • fever
  • hypotension
  • nausea, vomiting
  • lower back pain
  • feelings of chest compression
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7
Q

erythroblastosis fetalis (HDNB) - mechanism

A

Type II hypersenstitivity rxn

  • the maternal IgG antibodies of a Rh- mother (who previously had a Rh+ pregnancies that created anti-Rh IgG antibodies) cross the placenta to bind Rh antigen on the baby’s Rh + erythrocytes
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8
Q

erythroblastosis fetalis (HDNB) - presentation

A

type II hypersensitivity rxn

  • hemolysis → anemia
  • fetal hydrops
  • accumulation of unconjugated bilirubin, leading to:
    • enlarged liver
    • kernicterus (CNS bilirubin)
    • jaundice
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9
Q

what is the treatment for erythroblastosis fetalis (HDNB)? how does it work?

A
  • Rhogam therapy: anti-Rh (anti-D) antibodies
    • mother injected immediately postpartum, which inhibits maternal anti-Rh IgG production by
      • neutralizing Rh+ RBC antigen
        • injected anti-Rh Abs bind attack baby’s RBCs so maternal anti-Rh IgG are not made
      • Ig mediated negative feedback
        • when injected anti-Rh Abs bind an RBC already bound by maternal anti-Rh IgG (who’s Fc portion is bound to a B-cell) , the Fc portion of the injected Ab binds CD32 (a B-cell marker) sending a negative signal to the B-cell → discontinued synthesis of anti-Rh igG
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10
Q

other than Rhogam, what treatments are available for erythroblastosis fetalis (HDNB)?

A

type II hypersenstivity rxn

  • fluorescent bili lights: tx of elevated bilirubin
  • exchange transfusion: baby’s blood removed, fresh compatible blood injected
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11
Q

in what situations should rhogam be given?

A
  • unsensitized Rh- women
    • 28-29 weeks gestation
    • 72 hours post delivery
  • ectopic pregnancy
  • abortion
  • placental abruption
  • amniocentesis
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12
Q

autoimmune hemolytic anemias - mechanism

A

type II hypersensitivity rxn

  • three variations
    • warm reactive autoantibodies (IgG) → erythrophagocytosis
    • cold reactive autoantibodies (IgM) → complement → lysis
    • drug-provoked (IgG) → complement → lysis
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13
Q

warm reactive autoantibodies - autoimmune hemolytic anemia

  • mechanism?
A

type II hypersensitivity

  • = erythrophagocytosis
    • IgG coated RBC removed by splenic & liver macrophages
      • temp is 37C
      • IgG auto-antibodies bind native RBCs
      • Fc portion of IgG binds macrophages in the spleen & liver → IgG coated RBCs removed
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14
Q

cold reactive autoantibodies - autoimmune hemolytic anemia

  • mechanism?
A

type II hypersensitivity

  • complement activation
    • temperature below 37 C
    • this triggers IgM against native RBCs
    • IgM binds RBCs → complement binds IgM → complement cascade → MAC (lysis)
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15
Q

what infection elicits cold reactive auto-antibodies (auto-immune hemolytic anemia)?

how does it work?

A

type II hypersensitivity reaction

  • mycoplasma pneumonia
  • awhile after infection, when temperatures drop below 37 C, anti-RBC IgM binds i/I antigen on RBC surface → complement → lysis
    • maximum RBC agglutination is seen at 4 C
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16
Q
A

type II hypersensitivity

  • cold-reactive IgM autoantibodies in autoimmune hemolytic anemia
    • below 37, IgM auto-Ab bind RBCs → agglutination (aggregation) → complement
    • at 37, IgM not activated. no agglutination
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17
Q
A

type II hypersensitivity

  • gangrene shown - cold reactive autoantibodies (hemolytic anemia)
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18
Q

drug provoked autoimmune hemolytic anemia

  • mechanism?
  • which drugs do this?
A

type II hemolytic anemia

  • mechanism:
    • drugs adsorb to RBC surface
    • anti-drug IgG are made & bind to RBCs
    • IgG bound by complement → complement cascade → lysis
  • drugs
    • penicillin
    • quinine
    • sulfonamides
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19
Q
  • thrombocytopenia - mechanism
A

type II hypersensitivity

  • two variations
    • drug induced thrombocytopenia - drugs bind to platelets to induce Ab
    • idiopathic - mechanism unknown
  • for both
    • auto-Ab bind platelets, leading to
      • complement cascade lysis, or
      • phagocytosis, or
      • ADCC
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20
Q

thrombocytopenia - presentation

A

type II hypersensitivity reaction

= purpura

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21
Q
A

purpura

seen in thrombocytopenia (type II hypersensitivity)

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22
Q

rheumatic fever (RF) - mechanism

A

type II hypersensitivity reaction

  • triggered by strep pyogenes (Group A strep) infection
    • streptococcal M-protein induces production of IgG / IgM auto-antibodies against host cardiac tissue (cardiac myosin) that resembles it
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23
Q

rheumatic fever - presentation

A

type II hypersensitivity reaction

  • myocarditis / rheumatic heart disease
    • inflammation of
      • brain
      • joints
      • kidneys
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24
Q

hyperacute graft rejection - mechanism

A

type II hypersensitivity reaction

  • transplant recipient has pre-formed antigens to ABO antigens present on the vascular endothelium of the graft
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25
Q

type III hypersensitivity - mechanism

A
  • immune complex (IC) formation
    • IC = antibodies (IgG/IgM) + antigen + complement
      • ICs deposit in lodge in blood vessels → tissue
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26
Q

what tissues are most likely affected in type III hypersensitivity?

A
  • vasculature of the
    • kidneys
    • choroid plexus /ciliary artery of eye
    • joints
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27
Q

what diseases occur via Type III hypersensitivity reactions?

A
  • post-streptococcal glomerulonephritis
  • serum sickness
  • arthus reaction
  • persistent infections
  • extrinsic allergic alveolitis
  • polyarteritis nodosa (PAN)
  • complement deficiency
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28
Q

post-streptococcal glomerulonephritis - mechanism

A

type III hypersensitivity reaction

  • triggered by strep pyogenes infection
    • forms immune complex (IC):
      • antigen (s. pyogenes) + antibodies (IgG/IgM) complement
      • IC lodges in glomeruli → glomerulonephritis → dark urine
29
Q

post-streptococcal glomerulonephritis - presentation

A

= type III hypersensitivity

  • presentation d/t glomerulonephritis:
    • dark urine = first sign
    • periorbital / facial edema
30
Q

glomerulonephritis - diagnosis

A

ICs lodge in glomeruli → lumpy-bumpy immunofluorescence

31
Q
A

glomerulonephritis (type III hypersensitivity reaction) - lumpy-bumpy immunofluorescence

32
Q

serum sickness - mechanism

A

type III hypersensitivity

  • triggered by either
    • xenogenic Ig therapy, for example
      • horse sera - snake bite tx
      • murine monoclonal Ab - cancer/graft rejection tx
    • drugs
      • penicillin
      • NSAIDS
  • which cause immune complexes (IC), made of
    • antigen (xenogeneic Ig/drugs) + antibodies (IgG/IgM) + complement
      • ICs lodge in
        • kidneys → glomerulonephritis
        • joints → arthritis
33
Q

serum sickness - presentation

A

type III hypersensitivity

  • glomerulonephritis
  • arthritis/arthralgia
  • body rashes
34
Q
A

serum sickness rash

type III hypersensitivity

35
Q

arthrus reaction - mechanism

A

Type III hypersensitivity

  • IC complexes form when boosters are administered to people that already have high Ab titers from initial vax
    • location deposition in small vessels (usually in the skin)
36
Q

arthrus reaction - presentation & complications?

A

type III hypersensitivity -

  • presentations:
    • local area of edema +/- hemorrhage w/ poorly defined edge
    • if IC causes platelet clumping clumping → vascular occlusion / necrosis
37
Q
A

arthrus reaction (type III hypersensitivity)

  • local area of edema +/- hemorrhage w/ poorly defined edge
    • vascular occlusion / necrosis d/t platelet clumping on IC
38
Q

extrinsic allergic alveolitis (occupational pneumonitis)

  • mechanism
A

type III hypersensitivity reaction

  • inhaled antigens complex with specific IgG Ab in the alveoli of the lungs → IgG brings complement → immune complex
    • antigen
      • farmer’s lung: actinomycete fungi (moldy hay)
      • pigeon fancier’s: avian antigen
39
Q
A

chest radiograph with chronic hypersensitivity pneumonitis (= extrinsic allergic alveolitis, type III hypersensitivity) from (avian antigens → pigeon breeders)

40
Q

what are the presentations of pneumonitis and their key differences?

A
  • acute - flu like sx + chest tightness + dyspnea
    • cessation of exposure allows for sx to spontaneously resolve (in about 12 hours)
  • subacute - dyspnea + productive cough + fatigue + anorexia/weight loss
  • chronic - same as subacute
    • removing exposure only results in partial improvement
41
Q
A

livedo reticularis - d/t polyarteritis nodosa (type III hypersensitivity)

reddish blue mottling of the skin following cold exposure

42
Q

polyarteritis nodosa - mechanism

A

type III hypersensitivity

  • immune complexes → deposit throughout body in medium / muscular arteries → systemic necrotizing vasculitis
43
Q

polyarteritis nodosa (PAN) - presentation

A

type III hypersensitivity

  • system necrotizing vasculitis of medium & small muscular arteries →
    • hemorrhage → thrombosis → organ ischemia / infarction in the
      • skin - livedo reticularis: reddish-blue mottling of
      • joints, nerves, gut, kidney
44
Q
A

livedo reticularis: reddish-blue mottling of the skin - presentation of Polyarteritis Nodosa (PAN), a type III hypersensitivity

45
Q

tx for PAN

A
  • steroids
  • cyclophosphamide
  • plasmapheresis
46
Q

complement deficiency - mechanism

A

type III hypersensitivity

  • pts with deficiencies effecting C1, C2 and C4
    • immune complexes are exceptionally large, and bind poorly to RBCs that otherwise take them to the spleen for destruction
      • ICs deposit in tissues → inflammation
47
Q

what are the ways of diagnosing a Type III immune hypersensitivity?

A
  • precipitation with polyethylene glycol (PEG) → IgG precipitates out
  • radioimmunoassay:
    • using C1q as ligand to bind IC
  • cryoglobulins
  • immunofluorescence for IC
48
Q

stages of Type IV hypersensitivity

A
  • sensitization
  • elicitation
49
Q

outline the sensitization phase of Type IV hypersensitivity

A

= initial exposure to antigen

  • antigen is presented to T-cells by Langerhan’s cells (APCs of the skin)
    • CD4 binds MHC-II
    • induces clonal proliferation of Th1 cells over the next 14-20 days
50
Q

outline the elicitation phase of type IV hypersensitivity

A

= second exposure to antigen

  • sensitized Th1 cells encounter antigen for a second time, which induces production of
    • INF-y (primarily), which:
      • activates macrophages, which produce
        • ROS
        • TNF=a

this leads to local tissue inflammation & damage

51
Q

what are the major variants of Type IV hypersensitivity?

A
  • contact dermatitis / eczema
    • not to be confused w/ atopic eczema - IgE mediated
  • tuberculin type hypersensitivity
  • granulomatous hypersensitivity
52
Q

contact dermatitis

  • mechanism/causes
  • presentation dx
A
  • type IV: Langerhans cells Th1 → INF-y → macrophages → ROS/TNF-a)
  • causes
    • poison ivy - m/c
    • haptens
      • metals = nickel, chromate
      • latex
  • presentation - eczema + blister formation
  • dx
    • DNCB (dinitrochlorobenzene)
    • skin patch test
53
Q

tuberculin-type hypersensitivity

  • mechanism/cause
  • presentation
  • dx
A
  • type IV: Langerhans cells Th1 → INF-y → macrophages → ROS/TNF-a)
    • PPD/Mantoux test: antigen, tuberculin (from mycobacterium tuberulosis) injected into skin
  • presentation
    • area of firm red swelling
      • induration (raised area)
      • redness
      • filled w/ cellular infiltrate - mostly Th1 cells
54
Q

what is considered a positive PPD (Mantoux) test?

A

demographic dependent

  • no known risk factors: >/= 15mm is +
  • health care workers: >/= 10mm is +
  • HIV/immunocompromised: >/= 5mm is +
55
Q

what can cause a false + mantoux (PPD test? how to r/o a false +?

A
  • BCG vaccination can cause false +
  • if suspect false +. Quantiferon-TB Gold test can distinguish
56
Q
A

+ Mantoux (PPD) test

indurated, red, filled w/ Th1

57
Q

identify & describe each reaction

A
  • type I - allergens
  • type III - arthrus rxn, d/t booster administration to somebody w/ high Ab titers
  • type IV - contact eczema / PPD (Mantoux) test
58
Q

granulomatous hypersensitivity

  • mechanism/cause
  • presentation
  • dx
A
  • type IV: Langerhans cells Th1 → INF-y → macrophages → ROS/TNF-a)
    • causes
      • infectious - m. tuberculosis m/c
      • sarcoidosis
      • berylliosis
      • IBD - Crohn’s, UC
  • presentation
    • microscopic - accumulating macrophages → epithelioid cells clusters → multinucleate giant cells
    • gross - caseous, “cheesy” necrosis
59
Q

m. tuberulosis

  • mechanism
  • presentation
A
  • type IV
    • PPD rxn → red, indurated lesion
    • granulomatous → epithelioid clusters (multi-nucleated giant cells) + caseous necrosis
60
Q

sarcoidosis

  • mechanism/cause
  • presentation
A
  • type IV hypersensitivity
    • granulomatous variation:
  • presentation
    • LUNGS
      • hilar lymphadenopathy
      • pulmonary infiltrates
    • plus - erythema nodosum
61
Q
A

granulomatous reaction (type IV)

62
Q
A

granulomatous reaction (type IV)

63
Q

IBD

  • mechanism
  • presentation
  • dx
A
  • type IV hypersensitivity - granulomatous variation
  • presentation = diarrhea / abdominal pain / cramping
    • crohn’s
      • gross
        • can occur anywhere on GI tract
        • patchy distribution (cobblestone appearance)
        • transmural → deep ulcers
      • clinical
        • pain in RLQ
        • +/- bloody stool
        • fistulas, abscesses, fissures
      • dx - ASCA
    • UC
      • gross
        • limited to distal LI + rectum
        • continuation distribution
        • mucosal layer only → shallow ulcers
      • clinical
        • pain in LLQ
        • blood common in stool
      • dx -p-ANCA
64
Q

compare & contrast IBDs in terms of

  • mechanism
  • location
  • gross presentation
  • clinical presentation
  • other manifestations
  • dx
  • tx
A

both:

  • type IV hypersensitivity - granulomatous presentation
  • tx = TNF-a inhibitors
    • adalimumab
    • infliximab
65
Q

tx of IBD

A

type IV (granulomatous)

  • TNF-a inhibitors
    • adalimumab
    • infliximab
66
Q
A

p-ANCA: perinuclear anti-neutrophil cytoplasmic antibody

dx of ulcerative colitis

67
Q
A

ASCA - anti-saccharomyces cerevisiae antibodies

dx of crohn’s disease

68
Q

berylliosis (chronic beryllium disease)

A
  • mechanism: type IV hypersensitivity
    • inhaled metal hapten + carrier lung protein
      • haptens exposure to industry elements
  • presentation
    • ground glass appearance
    • granuloma

IMMUNO (4 decks)

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