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HDM Final Brett > 8 Hypersensitivities (1 Hour) > Flashcards

8 Hypersensitivities (1 Hour) Flashcards

1
Q

Type 1 hypersensitivities are mediated by

A

Ab

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2
Q

What hypersensitivity is atopic?

A

Type 1

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3
Q

What cells are immediately activated in Type I responses?

A

Mast, eosinophil, basophil

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4
Q

What receptors facilitate Type 1 hypersensitivity?

A

FC(epsilon)

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5
Q

Mast cells are found

A

In skin and mucosa

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6
Q

What is the high affinity Fc receptors for IgE found on Mast cells called?

A

Fc(epsilon)RI or CD23a

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7
Q

What do IL4 and IL13 stimulate?

A

Th2 response

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8
Q

What, from mast cells, stimulates and promotes eosinophil activation?

A

IL3, IL5, GM-CSF

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9
Q

What does CCL3 do?

A

Attracts monocytes, macrophages, and neutrophils

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10
Q

What does IL-5 induce on eosinophils?

A

FC(epsilon)RI

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11
Q

What is in high number during chronic allergic inflammation?

A

Eosinophils

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12
Q

What is the major contributor to tissue damage?

A

Eosinophils

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13
Q

What has the same mechanism as histamine but lasts longer and has stronger action? Who makes it?

A

Leukotrienes

Eosinophils

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14
Q

What is the most potent leukotriene? What do they do?

A

LTB4

They increase capillary permeability and increase mucus production

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15
Q

What causes class switching of B cells?

A

IL4

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16
Q

What does IL4 increase on cell surface of leukocytes?

A

VCAM-1 for adhesion

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17
Q

What cells have Fc(epsilon)R

A

Basophils and mast cells

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18
Q

What are the properties of allergens?

A

They require a tiny dose, they are very stable and can exist for a long period of time, small and highly soluble

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19
Q

What is the first exposure to an allergen? What happens?

A

Priming

No allergic reaction

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20
Q

How are allergens taken up?

A

They diffuse across mucosal epithelium and are processed and presented by Th2 and B cells make IgE against them

These IgE bind to Fc(epsilon)RI on mast cells

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21
Q

What happens immediately in an acute atopic response?

A

Cross linking of mIgE
Degranulation of mast cells
Sneezing, congestion, pruritis, rhinorrhea

22
Q

What happens in the late phase of atopic responses?

A

After 4-12 hours there is an influx and activation of eosinophils, neutrophils, basophils and Th2

10 fold increase of mast cells w/ increased Fce receptors

23
Q

What happens in atopic asthma?

A

Contraction and relaxation of smooth muscle in bronchioles

24
Q

What causes systemic anaphylaxis?

A

Allergens introduced directly into the blood, systemic act. of mast cells, increase in vascular perm., huge drop in BP

25
Q

What are Type 2 hypersensitivities called? What do they react against?

A

IgG or IgM against cell surface or ECM

26
Q

What causes damage in Type 2 HS?

A

Complement binding (binds to both IgG and IgM)

NK through ADCC

27
Q

In Type 2 HS, Ab against cell surface are ___________ but Ab against internal Ag are ____________

A

Pathogenic, non-pathogenic

28
Q

What causes the bystander damage during Type 2 HS?

A

Phagocytes want to connect to the cells and phagocytose them but they can’t so they release lytic particles “at” the cells causing widespread damage

29
Q

What is a penicillin “allergy?” What does penicillin bind to?

A

It is a Type 2 HS

the penicillin binds to the surface of RBC and gets lysed because it is recognized as non-self

30
Q

What type of HS are transfusion reactions?

A

Type 2

31
Q

What is given to protect fetal RBC from maternal Ab in second pregnancy?

A

Rhogam, it prevents B cell activation to Rhesus factor

32
Q

Anti CD20 is used in

A

B cell non-Hodgkin’s lymphoma

33
Q

What is anti-CD52 used in?

A

Chronic B & T cell leukemias

Immunosuppressants for BMT

34
Q

What are Type 3 hypersensitivities known as?

A

Immune complex

35
Q

What do Ab react to in Type 3 HS?

A

Soluble Ag

This happens when there is too much Ab and not enough Ag

36
Q

How do Type 3 cause acute inflammation repsonse?

A

Phagocytes can’t chew up complexes so they release enzymes at the cells and the cells are damage and release internal contents, this leads to DAMPs and resultant activation

37
Q

Rheumatic fever is caused by what? What does it react to?

A

Streptococcal cell wall Ag

This is similar to the heart wall and we get cross reactivity

38
Q

What causes myasthenia gravis?

A

Anti-Ach receptor Ab

39
Q

What causes grave’s disease (hyperthyroidism)?

A

Antibody stimulates TSH binding to receptor and you get overactivation of thyroid

40
Q

What causes SLE?

A

Ab against nucleic acids, nucleoproteins

41
Q

What does SLE cause?

A

Nephritis, arthritis, and vasculitis

42
Q

What causes serum sickness?

A

Type 3 HS against various components of whole blood

43
Q

What do Type 2 and 3 HS have in common?

A

They are both Ab mediated

Complement is major mediator in both

44
Q

What are Type 4 HS also called?

A

Delayed type HS

45
Q

What mediates DTH?

A

Ag-specific CD4

46
Q

What are the 3 types of DTH?

A

Contact (Ni, poison ivy, latex)

Tuberculin (Tb test)

Granulomatous (look for presence of granulomas)

47
Q

What are the two stages of DTH?

A

Sensitization

  • antigen uptake by DC
  • present on class 2 HLA

Elicitation

  • recruit CD4 T cells
  • pro-inflammatory cytokines
  • Th1 cells
48
Q

What is a quick and dirty way to measure cell mediated immunity?

A

Reaction of CD4 to something you know they were previously exposed to

49
Q

What causes granulomatous DTH? What T responds?

A

Intracellular organism able to resist macro killing, macro walls it off with several layers, can form necrotic center, associated with Th1 response

happens in Tb

50
Q

What causes MS

A

Type 4 HS against myelin proteins

51
Q

What causes RA?

A

Type 4 HS in joints

52
Q

What causes IDDM?

A

Type 4 HS against pancreatic islet ag

HDM Final Brett (11 decks)

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