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IMMUNO > Hypersensitivity Type II, III and IV > Flashcards

Hypersensitivity Type II, III and IV Flashcards

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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
type III hypersensitivity - mechanism
* immune complex (IC) formation * **IC = antibodies (IgG/IgM) + antigen + complement** * ICs deposit in lodge in blood vessels → tissue
26
what tissues are most likely affected in type III hypersensitivity?
* vasculature of the * kidneys * choroid plexus /ciliary artery of eye * joints
27
what diseases occur via Type III hypersensitivity reactions?
* post-streptococcal glomerulonephritis * serum sickness * arthus reaction * persistent infections * extrinsic allergic alveolitis * polyarteritis nodosa (PAN) * complement deficiency
28
post-streptococcal glomerulonephritis - mechanism
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
post-streptococcal glomerulonephritis - presentation
= type III hypersensitivity * presentation d/t glomerulonephritis: * **dark urine = first sign** * periorbital / facial edema
30
glomerulonephritis - diagnosis
ICs lodge in glomeruli → **lumpy-bumpy immunofluorescence**
31
glomerulonephritis (type III hypersensitivity reaction) - **lumpy-bumpy immunofluorescence**
32
serum sickness - mechanism
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
serum sickness - presentation
type III hypersensitivity * glomerulonephritis * arthritis/arthralgia * body rashes
34
serum sickness rash type III hypersensitivity
35
arthrus reaction - mechanism
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
arthrus reaction - presentation & complications?
type III hypersensitivity - * presentations: * **local area of edema +/- hemorrhage** w/ poorly defined edge * if IC causes platelet clumping clumping → **vascular occlusion / necrosis**
37
arthrus reaction (type III hypersensitivity) * **local area of edema +/- hemorrhage** w/ poorly defined edge * **vascular occlusion / necrosis** d/t platelet clumping on IC
38
extrinsic allergic alveolitis (occupational pneumonitis) * mechanism
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
chest radiograph with **chronic hypersensitivity pneumonitis** (= extrinsic allergic alveolitis, type III hypersensitivity) from (avian antigens → pigeon breeders)
40
what are the presentations of pneumonitis and their key differences?
* 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
**livedo reticularis -** d/t polyarteritis nodosa (type III hypersensitivity) reddish blue mottling of the skin following cold exposure
42
polyarteritis nodosa - mechanism
type III hypersensitivity * immune complexes → deposit throughout body in medium / muscular arteries → systemic necrotizing vasculitis
43
polyarteritis nodosa (PAN) - presentation
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
**livedo reticularis:** reddish-blue mottling of the skin - presentation of Polyarteritis Nodosa (PAN), a type III hypersensitivity
45
tx for PAN
* steroids * cyclophosphamide * plasmapheresis
46
complement deficiency - mechanism
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
what are the ways of diagnosing a Type III immune hypersensitivity?
* precipitation with polyethylene glycol (PEG) → IgG precipitates out * radioimmunoassay: * **using C1q** as ligand to bind IC * cryoglobulins * immunofluorescence for IC
48
stages of Type IV hypersensitivity
* sensitization * elicitation
49
outline the _sensitization phase_ of Type IV hypersensitivity
= 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
outline the elicitation phase of type IV hypersensitivity
= 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
what are the major variants of Type IV hypersensitivity?
* **contact dermatitis / eczema** * not to be confused w/ atopic eczema - IgE mediated * **tuberculin type hypersensitivity** * **granulomatous hypersensitivity**
52
contact dermatitis * mechanism/causes * presentation dx
* _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
tuberculin-type hypersensitivity * mechanism/cause * presentation * dx
* _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
what is considered a positive PPD (Mantoux) test?
demographic dependent * no known risk factors: **\>/= 15mm is +** * health care workers: **\>/= 10mm is +** * HIV/immunocompromised: **\>/= 5mm is +**
55
what can cause a false + mantoux (PPD test? how to r/o a false +?
* BCG vaccination can cause false + * if suspect false +. **Quantiferon-TB Gold** test can distinguish
56
+ Mantoux (PPD) test indurated, red, filled w/ Th1
57
identify & describe each reaction
* 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
granulomatous hypersensitivity * mechanism/cause * presentation * dx
* _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
m. tuberulosis * mechanism * presentation
* type IV * PPD rxn → red, indurated lesion * granulomatous → epithelioid clusters (multi-nucleated giant cells) + caseous necrosis
60
sarcoidosis * mechanism/cause * presentation
* type IV hypersensitivity * granulomatous variation: * presentation * LUNGS * hilar lymphadenopathy * pulmonary infiltrates * plus - **erythema nodosum**
61
granulomatous reaction (type IV)
62
granulomatous reaction (type IV)
63
IBD * mechanism * presentation * dx
* 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
compare & contrast IBDs in terms of * mechanism * location * gross presentation * clinical presentation * other manifestations * dx * tx
both: * _type IV_ hypersensitivity - granulomatous presentation * tx = TNF-a inhibitors * **adalimumab** * **infliximab**
65
tx of IBD
type IV (granulomatous) * TNF-a inhibitors * adalimumab * infliximab
66
p-ANCA: perinuclear anti-neutrophil cytoplasmic antibody ## Footnote **dx of ulcerative colitis**
67
ASCA - *anti-saccharomyces cerevisiae* antibodies ## Footnote **dx of crohn's disease**
68
berylliosis (chronic beryllium disease)
* mechanism: type IV hypersensitivity * **inhaled metal hapten + carrier lung protein** * haptens exposure to _industry elements_ * presentation * ground glass appearance * granuloma

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