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Pathology Block 10 > Hypersensitivty Review And Skin Lesions > Flashcards

Hypersensitivty Review And Skin Lesions Flashcards

1
Q

ACID test

A

Anaphylactic/atopic - type I
Cytotoxic- type II
Immune complex - type III
Delayed (cell mediated)-type IV

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2
Q

What does the C stand for in ACID

A

Cytotoxic, NOT CELL MEDIATED

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3
Q

What does type II sensitivity do to cells

A

Activates them or kills them

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4
Q

Mechanism of action of type I HS

A
  • Allergen activates B cells, IGM class switched to IgE

- preformed IgE docks on mast cells (basophils)

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5
Q

Early-preformed mediators of type I HS

A

Histamine
Heparin
Eosinophils chemotactic factor of anaphylaxis (ECF-A)
Neutrophil chemotactic factor (IL-8_

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6
Q

Type I HS is ____ drive n

A

IgE

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7
Q

This is always a secondary immune response, never a primary response.

A

Type I HS

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8
Q

What drives the class switch of IGM to IGE?

A

IL-4

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9
Q

What are the 4 signs of inflammation driven by histamine

A

Tumor
Rubor
Calor

NOT DOLOR

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10
Q

Late-synthesized mediators in type I HS

A
  • prostaglandins
  • thromboxanes
  • LEUKOTRIENES (sloe reacting substance of anaphylaxis (SRS-A)
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11
Q

Where do steroids act

A

At the beginning of the arachidonic acid

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12
Q

Where do NSAIDs act

A

COX pathway

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13
Q

Leukotrienes and histamine

A

Leukotrienes 1000x potency of histamine

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14
Q

Late phase of type I HS

A

Infiltration of tissues with eos and segs

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15
Q

Drives IgM to IgE class switch

A

IL-4

And IgM to igg

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16
Q

Activates eosinophils

A

IL-5

Causes class switching to IgA

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17
Q

Massive IgE production, mucus secretion in epithelial cells, enhances smooth muscle contraction

A

IL-13

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18
Q

What are IL-4, IL-5, and IL-13 produced by

A

Activated TH2 cells

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19
Q

Historians release does what to blood pressure

A

Severely decreases it

-constricts the lungs a lot

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20
Q

Clinical manifestations of atopic/anaphylactic/immediate type I HS

A 
Anaphylaxis 
Atopy
Asthma 
Allergic rhinitis 
Urticaria 
Angiodema
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21
Q

What has a role in asthma (allergic and inflammation)

A

Leukotrienes

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22
Q

Cause of a type I reactions

A

Foods (peanuts, shellfish, red dye)
Drugs (penicillin)
Stinging insects (bees)

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23
Q

Why type of HS in penicillin reaction

A

Can have any of the 4 types of HS.

Most worried about type I

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24
Q

Eosinophils in parasites

A

Eosinophils collide with the parasite that has the IgE bound to it. It binds to the FC portion. Once eosinophils have cross linking, they release major basic protein and kills the parasite and causes tissue damage

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25
Q

Eosinophils in type I

A

IgE is already docked onto the mast cells. Waiting for antigen to demo and bind to it

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26
Q

Mechanism of type II HS

A

Cytotoxic/Ab dependent

-Ab bind to cell membrane and cause cellular destruction, inflammation, or cellular dysfunction

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27
Q

Cellular destruction in type II HS

A

Opsonization (scent trail) leads to activation of complement and phagocytosis, NK cell killing, inflammation

28
Q

What causes the complementary pathway in type II HS

A

IgG and IgM

29
Q

Cellular dysfunction in type II HS

A

Ab bind and cause abnormal blockade or activation

30
Q

In type II HS cellular dysfunction, is it destruction or activation

A

Either one

31
Q

Clinical manifestations of type II HS

A 
cytotoxic/Ab dependent 
destructive 
-autoimmune hemolytic anemia 
-immune thrombocytopenic purpura 
-transfusion reaction
-hyperacute transplant rejection 
Rheumatic fever 
Blocking or activating 
-myasthenia gravis 
-graves
32
Q

Difference between purpura and petechiae

A

Purpura is a larger bruise

Petechiae is smaller little red spots

33
Q

Autoimmune hemolytic anemia in type II HS

A

Auto antibody binding to RBC and can have lysing of these cells

34
Q

Lysing of platelets due to autoimmune reaction

A

Immune thrombocytopenic purpura

HS II

35
Q

Example of transfusion reaction in type II HS

A

Wrong blood type to someone. Start lysing then ew RBC because of preformed Ab around. Classical example

36
Q

Hyperacute transplant rejection in type II HS

A

Preformed Ab to organ. Occurs within minutes. Very small subset of transplant rejection types, most common is going to be either acute or chronic. In classical transplant rejection, it is cell mediate type IV.

37
Q

What transplant rejections are type II

A

Hyperacute transplant rejection

38
Q

What transplant rejections are HS type IV

A

Classical transplant rejection and corneal

39
Q

What HS is myasthenia gravis

A

II

Blockade

40
Q

What HS is graves disease

A

Type II

Activation

41
Q

What are two antiglobulin tests that detect RBC antibodies

A

Coombs, direct (DAT) and indirect (IAT)

42
Q

Direct antiglobulin test (Coombs)

A

Detects antibodies on RBCs

  • Ab that are bound to it, ther are auto antibodies that are stuck to the RBCs. Find cells that have Ab stuck to them
  • can see if RBCs are getting destroyed in someone with anemia
43
Q

Indirect antiglobulin tests (Coombs)

A

Detects plasma antibodies

  • Ab that might bind to the cell.
  • do this if you want to transfuse blood
44
Q

Which antiglobulin test detects antibodies on RBCS

A

Direct (DAT)

45
Q

What antiglobulin test detects plasma antibodies

A

Indirect (IAT)

46
Q

What is Coombs serum

A

Antihuman IgG-serum from a rabbit immunized with human IgG

47
Q

Examples of things to use a direct antiglobulin test (DAT) for

A

Hemolytic disease of newborn (HDN)

Autoimmune hemolytic anemia

48
Q

Examples of when to use IAT, indirect antiglobulin tests

A

Blood bank antibody screen detects unexpected antibodies to red blood cell antigens

49
Q

Mechanism of type III HS

A
  • circulating antigen-antibody complexes lodge in vessels and on tissues
  • complement is activated and phagocytes are recruited, producing tissue damage
  • do not have Ab that are directly bound to cells, Ab bound to antigen and it gets stick an causes complement and causes tissue damage
50
Q

Clinical manifestations of type III HS

A

-systemic and localized inflammation/damage

Classical is Arthus reaction

51
Q

Examples of type III HS

A
  • arthus (redness around arm after immunization)
  • serum sickness
  • RA
  • SLE
52
Q

Causes of serum sickness

A

Most common modern day cause: oral drugs. Drugs form haptins, these bind to proteins and have formation of immune complex. If they bind directly to the cells and cause lysis that is type II

53
Q

Difference between Arthus and serum sickness

A

Arthus is localized

Serum sickness if systemic

54
Q

These HS are Ab driven

A

I-III

55
Q

HS that is driven by cell

A

IV

56
Q

What immunoglobulin is type I

A

IgE

57
Q

What immunoglobulins for types II and III

A

IgG and IgM

58
Q

Mechanism of type IV HS

A
  • antigens bind to sensitized CD4 cells
  • CD4 cells release cytokines that attract/activate macrophages and CTLs (CD8) and cause tissue damage
  • Ab are not involved
59
Q

Examples of type IV HS

A
  • contact dermatitis
  • poison oak
  • TB skin test
  • corneal transplant rejection
60
Q

Key cells of type IV HS

A

T helper cells and macrophages

61
Q

Blister-forming keratoconjunctivitis that occurs due to a type IV HS reaction to antigens of bacterial origin

A

Phlyctenular Keratoconjunctivitis (PKC)

62
Q

What is PKC connected with

A

Secondary to blepharitis due to staph aureus

  • antigens from staph can cause type IV reaction on the eye.
  • conj scrape would show CD4 and CD8 and langerhans cells
63
Q

What is PKC an example of

A

Type IV HS

64
Q

Patient is given a TB skin test. Which HS is being tested and which cells are expected to mediate a positive test result

A

Type IV, TH1 cells

65
Q

A clinician is worried that an Rh negative mom is going to have an Rx positive baby. Which of the following she worried about

A

Type II HS

66
Q

Which of the following mediators are produced during the late phase of an IGE mediated allergicereaction

A

Leukotrienes

Pathology Block 10 (8 decks)

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