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CMOD-Block 2 Path > Hypersensitivity Reactions (additions to Dr. Miller) > Flashcards

Hypersensitivity Reactions (additions to Dr. Miller) Flashcards

1
Q

What are the two phases to a Type I Immediate Hypersensitivity Reaction?

  • Time frame?
  • Cells?
A 
Early phase (minutes): 
- Mast Cells

Late phase (2-8 hours):

  • Eosoinophils
  • T cells
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2
Q

Define the role of the following in the type I hypersensitivity reaction, including what phase you see them in.

  • IL-4
  • IL-5
  • IL-13
A 
Early Phase: 
IL-4 - B cell class switching to IgE

Late Phase:
IL-5 - Eosinophil recruitment to late phase rxn
IL-13 - Epithelial Cell Mucus Secretion

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3
Q

What is the role of eotaxin?

- type of hypersensitivity reaction that its associated with?

A
  • Recruits Eosinophils and T-cells

- This is in the LATE PHASE of type I hypersensitivity reaction

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4
Q

What mast cell mediators induce Vasodilation and increased vascular permeability?

A
  • Histamine
  • PAF
  • Leukotrienes
  • Neutral Proteases that activate complement kinins
  • Prostaglandins D2
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5
Q

What mast cell mediators induce smooth muscle spasm?

A
  • LTC-4, D-4, E-4
  • Histamine
  • Prostaglandins
  • PAF
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6
Q

What is the most important prostaglandin that induces bronchospasm?

A

Prostaglandin D2

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7
Q

What mast cell mediators induce cellular infiltrations?

A
  • TNF, Chemokines
  • Leukrotriene B4
  • Eosinophil and Neutrophil Chemotactic factors
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8
Q

What is the ultimate effect of the mediators that induce cellular infiltrates in type I hypersensitivity reactions?
- what do the cellular infiltrates consist of?

A

SUSTAIN AND AMPLIFY THE RESPONSE EVEN IN THE ABSENCE OF AN ALLERGEN

  • TH2 cells and Eosinophils
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9
Q

How do you differntiate between acute and chronic rhinitis on H and E stain?
- cellular as well as other things

A
  • Chronic will show Eosinophil Presence

- Eosinophil granules may combine to make SHARP LIPIN crystals that are also eosinophilic

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10
Q

What is intrinsic factor?

- what does a IgG binding this cause?

A

Intrinsic Factor:
- secreted by the stomach and is necessary for B12 absorption

Lack of Intrinsic Factor:
- Pernicious Anemia

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11
Q

Why does lacking intrinsic factor cause anemia?

A

B12 is necessary for thymidylate synthetase function, without it you get slowed DNA synthesis

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12
Q

What is a common problem associated with given too much antivenom?

  • what type of reaction is this?
  • describe why it causes issues.
A

Too much antivenom = Serum Sickness

Rxn:
- Type III hypersensitivity Reaction

Issues:
- Abs from the anti-venom create small immune complexes that can’t be cleared, this causes inflammation, joint pain, vascularitis, and glomerulonephritis

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13
Q

What are the steps leading to vasculitis?

A
  1. Ab (endogenous or exogenous) binds Antigen
  2. Immune complex deposits in the endothelium and complement binds it
  3. C5a and C3a released from complement attract neutrophils that then degranulate on your vessels leading to their death
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14
Q

What is the Arthus Reaction?

A
  1. Non-self substance is injected into a person who has made IgG Abs. against the substance
  2. Local immune-complex forms and activates complement and C5a is released
  3. 5a binding to a C5a receptor on a mast cell
  4. Binding of Immune compex to FcgammaRIII on mast cell induces degranulation
  5. Granules induce inflammatory reaction
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15
Q

Suppose you do a lung biopsy on a patient with caseating granulomas showing Mycobacterium TB and they come back 5 years later and you do a TB test and they don’t test positive.

  • Explain.
  • Cells involved?
A

Patient could have aquired HIV in the past 5 years

  • Immunosuppressed individuals will not respond to a TB skin test because they lack CD4 T cells (SPECIFICALLY TH1 cells that are needed to form granulomas)
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16
Q

Stimulation by what hormone can cause the formation of Giant cells (epitheloid histiocytes).

A

IFN-gamma

17
Q

T or F: a positive test for anti-nuclear antibody (ANA) is a definitive test for the presence of lupus.

A

False, other disorders also show the presence of anti-ANA antibodies

**Additionally, about 20% of the population tests positive for ANA

18
Q

In what years and in what group of people is lupus most likely to manifest?

A
  • Reproductive Years

- African American FEMALES

19
Q

What are some of the Clinical Criteria for Lupus?

- which of these is typically the MAIN (lethal) problem lupus patients have?

A
  1. Acute Cutaneous Lupus
  2. Chronic Cutaneous Lupus
  3. Oral or Nasal Ulcers
  4. Arthritis
  5. Serositis
  6. Renal****
  7. Neurologic
  8. Leukopenia
  9. Non-scarring alopecia
20
Q

What are some of the imuunologic Criteria for Lupus?

A
  1. ANA
  2. Anti-DNA
  3. Anti-Sm
  4. Antiphospholipid Ab*****
  5. Low complement (C3, C4, CH50)
  6. Direct Coomb’s
21
Q

What antibodies lead to the following aspects of systemic lupus erythema?

  • Cytopenias
  • Thrombosis
  • Neuropsychiatric complications
A

Cytopenias:
- Autoantibodies for Red Cells, White Cells, and Platelets

Thrombosis:
- Autoantibodies against phospholipids (e.g. CARDIOLIPIN)

Neurophsychiatric:
- Autoantibodies against Neurotransmitters

22
Q

What are LE bodies?

- what causes them to form?

A

Neutrophils where nucleus is pushed to the edge of the cells because they have engulfed a lymphocyte that has been damaged so that their chromatin in homogenous

  • Homogeneous chromatin of Lymphocytes is causes by ANAs (anti-nuclear antibodies)
23
Q 
What causes the wire loop appearance of in the glomerulus of SLE patients? 
- What level/class of damage does this represent?
A

Loop appearance caused by SUBENDOTHELIAL deposits of DNA-ANTI-DNA-COMPLEXES

  • Class IV damage is classified by this wire loop pattern
24
Q

What causes Libman-Sacks endocarditis?

  • how is this related to SLE?
  • Relationship to bacteria?
A
  • Mononuclear Infiltrates attack heart valves causing Warty and Bumpy Lesions
  • SLE patients sometimes have this as a side Effect
  • NO RELATIONSHIP TO BACTERIA, it is a NONBACTERIAL VERRUCOUS ENDOCARDITIS
25
Q

What is the most common cause of death in SLE patients?

A

1 Renal Failure

  • Cardiovascular Disease also Plays a role
26
Q

What is the Difference between a primary and secondary Amyloidosis?
- Examples given in class?

A

Primary amyloidosis arises because of monoclonal plasma cell proliferation (AL - light chain amyloidosis)

Secondary Amyloidosis - arises from long term inflammatory processes and/or tissue damage
(IL-1 and IL-6 induced SAA formation leading to AA deposits in tissue)

27
Q

What is Transthyretin?

A

Binds and Transports Thyroxine and Retinol

28
Q

What is a plasmacytoma?

- location

A
  • It is a discrete solitary Mass of Neoplastic MONOCLONAL plasma cells

Found in:

  • Bone
  • Soft tissue

CMOD-Block 2 Path (22 decks)

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