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[Board Exam] Pathology > [1] Inflammation > Flashcards

[1] Inflammation Flashcards

1
Q

Neutrophils are attracted to these chemical attractants

A

IL8
C5a
LTB4
Bacterial components

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2
Q

Where do neutrophils migrate to exert their action?

A

Post-capillary Venule

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3
Q

Disease characterized by impairment in protein trafficking

A

Chediak-Higashi Syndrome

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4
Q

Clinical Features of Chediak-Higashi Syndrome

A
  1. Increased risk of pyogenic infections
  2. Neutropenia
  3. Giant granules in leukocytes
  4. Defective primary hemostasis
  5. Albinism
  6. Peripheral Neuropathy
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5
Q

Most effective mechanism of killing phagocytosed materials?

A

O2-Dependent Killing Mechanism

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6
Q

What converts Oxygen to Superoxide

A

NADPH

Also called oxidative burst

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7
Q

What converts Superoxide to Hydrogen Peroxide?

A

Superoxide Dismutase

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8
Q

What converts Hydrogen Peroxide to HOCl (Bleach)?

A

Myeloperoxidase

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9
Q

What is defective in Chronic Granulomatous Disease

A

NAPDH Oxidase Defect

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10
Q

Patients with CGD have granuloma formation with these kinds of organisms

How come only these organisms can cause infections?

A

Catalase-positive

Most bacteria produce hydrogen peroxide, which can be converted to HOCl, but those that produce catalase breakdown H2O2, therefore disrupting the pathway

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11
Q

Test used to screen for CGD

How?

A

Nitroblue Tetrazolium Test

Turns blue if NADPH oxidase can convert O2 to O2-

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12
Q

Patients with MPO deficiency are usually asymptomatic but do have an increased risk for these infections

A

Candida Infections

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13
Q

Neutrophils disappear after how many hours via what mechanism?

A

24 hours via apoptosis

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14
Q

What leukocyte predominates after the neutrophil phase?

A

Macrophage

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15
Q

Macrophages manage the next step of the acute inflammatory process of resolution and healing by secreting?

A

Resolution and Healing: IL-10 and TGF-B (Anti-inflammatory)

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16
Q

How do macrophages recruit additional neutrophils?

A

Secrete IL-8

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17
Q

4 Possible Endpoints of the Acute Inflammatory Process

A
  1. Resolution and Healing
  2. Continued Acute Inflammation
  3. Abscess Formation
  4. Chronic Inflammation
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18
Q

Chronic inflammation is characterized by?

A

Lymphocytes and plasma cells in tissue

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19
Q

T Cells are produced in?

A

Bone Marrow

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20
Q

TCR Complexes can only recognize antigen when presented by?

A

MHC

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21
Q

CD4 and CD8 T-Cells recognize which MHC Class

A

CD4 :: MHC II

CD8 :: MHC I

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22
Q

Immature B Cells are produced in?

A

Bone Marrow

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23
Q

Function of IL-4

A

Class Switching of IgG -> IgE

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24
Q

Function of IL-5

A
  1. Eosinophil chemotaxis and activation
  2. Maturation of B cells to plasma cells
  3. Class switching to IgA
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25
Q

Function of IL-10

A

Inhibits TH1 Phenotype

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26
Q

How are CD8 TCells Activated?

A
  1. Intracellular antigen is presented to MHC I
  2. IL-2 from CD4 TH1 Cells provide a 2nd activation signal
  3. Cytotoxic T-Cells activated for killing
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27
Q

Key enzyme that mediates apoptosis?

A

Caspases

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28
Q

How are B-Cells Activated?

A
  1. Antigen binding by surface IgM or IgD
  2. Becomes an IgM or IgD secreting Plasma Cell

or

  1. Antigen presentation to CD4 Helper T Cell via MHC II
  2. CD40 receptor on B-Cells bind CD40L on Helper T Cell providing 2nd activation signal (Secretes IL-4,IL-5)
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29
Q

What is the defining characteristic of a granuloma?

A

Epithelioid histiocytes (macrophages with abundant pink cytoplasm)

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30
Q

How can you differentiate caseating from non-caseating granulomas?

A

Central Necrosis

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31
Q

Caseating granulomas are characteristic of these diseases

A

TB and Fungal Infections

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32
Q

Steps involved in Granuloma Formation

A
  1. Macrophages present antigen via MHC II to CD4 Helper T Cells
  2. Macrophages secrete IL-12, inducing CD4 to differentiate into TH1 Subtype
  3. TH1 Cells secrete IFN-Y which converts macrophages to epitheliod histiocytes
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33
Q

Function: IL-12

A

Induce CD4 to differentiate into TH1

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34
Q

What do helper T Cells secrete to convert macrophages to granulomas?

35
Q

DiGeorge Syndrome is a developmental failure of?

This is due to a deletion of which chromosome?

A

3rd and 4th Pharyngeal Pouch

22q11 microdeletion

36
Q

Presentation of DiGeorge Syndrome

A
  1. T-Cell Deficiency (Lack of Thymus)
  2. Hypocalcemia (Lack of Parathyroids)
  3. Abnormalities of heart, great vessels, and face
37
Q

Etiologies of SCID

A
  1. Cytokine Receptor Defects
  2. Adenosine deaminase deficiency (Adenosine and Adenosine oxide are toxic to lymphocytes)
  3. MHC Class II Deficiency
38
Q

Treatment for SCID

A
  1. Sterile Isolation

2. Stem Cell Transplant

39
Q

X-Linked Agammaglobulinemia is a defect in?

A

Complete lack of immunoglobulin

Due to disordered B-cell maturation

40
Q

X-Linked Agammaglobulinemia is caused by which mutated gene?

A

Mutated Tyrosine Kinase

41
Q

These infections are common in patients with X-Linked Agammaglobulinemia

A

Bacterial
Enterovirus
Giardia infections

(Mucosal infections: IgA deficiency)

42
Q

How come patients with X-linked Agammaglobulinemia only present with symptoms after 6 months of life?

A

They have their mother’s immunoglobulins (IgA) through breast milk

43
Q

What is the most common Ig deficiency?

44
Q

Which GI disease is commonly associated with IgA deficiency?

A

Celiac Disease

45
Q

What is the cause of Hyper IgM Syndrome?

A

Mutation of the CD40L or CD40 Receptor (Cannot use the alternate pathway of B-Cell Activation)

46
Q

Which Immunoglobulins would be low in patients with HyperIgM Syndrome?

47
Q

Triad of Wiskott-Aldrich Syndrome

A
  1. Thrombocytopenia
  2. Eczema
  3. Recurrent infections
48
Q

C5-C9 deficiencies would have an increased risk for what kind of infections?

49
Q

Autoimmune diseases are caused by a loss of this defense mechanism

A

Self-tolerance

50
Q

SLE causes systemic damage via which Hypersensitivity Reactions?

A 
Type II (Cytotoxic)
Type III (Antigen-Antibody Complexes)
51
Q

This is the most common type of renal damage in patients with SLE

A

Diffuse proliferative glomerulonephritis

52
Q

What is unique about Libman-Sacks endocarditis?

A

Presence of vegetation on both sides of the heart valves

53
Q

What is characteristic of drug-induced SLE?

A

Antihistone Antibody

54
Q

These drugs are common causes of drug-induced SLE?

A

Hydralazine
Procainamide
Isoniazid

55
Q

Which antibodies are associated with Antiphospholipid Syndrome?

A

Anticardiolipin

Lupus Anticoagulant

56
Q

Anticardiolipin interferes with this test

A

Leads to a false-positive syphilis test

57
Q

Lupus Anticoagulant interferes with this diagnostic test

A

Elevated PT/PTT

58
Q

Treatment for APAS

A

Lifelong anticoagulation

59
Q

Sjogren Syndrome is associated with destruction of these glands

A

Lacrimal

Salivary

60
Q

Classic antibody test for Sjogren Syndrome

A

ANA

Anti-ribonucleoprotein Antibodies (Anti-SS-A and Anti-SS-B)

61
Q

Patients with Sjogren syndrome usually present with bilateral parotid gland enlargement. What is the significance of a unilateral enlargement of a parotid gland late in the disease course?

A

The patient has possibly developed a B-cell Lymphoma

62
Q

Scleroderma is characterized by these antibodies

A

Anti-DNA Topoisomerase I Antibody (Scl-70)

63
Q

Classic Presentation of Crest Syndrome

A 
Calcinosis/Anti-Centromere Antibody
Raynaud Phenonemon
Esophageal Dysmotility
Sclerodactyly
Telangectasias of Skin
64
Q

Where are the stem cells located in the small and large bowels?

A

Mucosal Crypts

65
Q

Where are the stem cells located in the skin?

A

Basal Layer

66
Q

Where are the stem cells located in the bone marrow?

A

Hematopoietic Stem Cells

67
Q

Where are the stem cells located in the lung?

A

Type II Pneumocytes

68
Q

What is the marker for hematopoietic stem cells?

69
Q

Which tissues in the body have poor/no regenerative potential?

A

Skeletal Muscle
Neurons
Cardiac Muscle

70
Q

What are the components of granulation tissue?

A
  1. Fibroblasts
  2. Capillaries
  3. Myofibroblasts
71
Q

What do fibroblasts do in the initial phase of repair?

A

Deposit Type III Collagen

72
Q

When granulation tissue scars, this type of collagen is replaced with what type of collagen?

A

Type III -> Type I Collagen

73
Q

Type I Collagen is commonly seen in?

A

Bone

[b-ONE]

74
Q

Type II Collagen is commonly seen in?

A

Cartilage

[Car-TWO-lage]

75
Q

Type III Collagen is commonly seen in?

A

Blood vessels, granulation tissue, embryonic tissue

[Seen in tissues that are able to stretch. s-THREE-tch]

76
Q

Type IV Collagen is commonly seen in?

A

Basement Membrane

77
Q

During repair, collagenase removes Type III collagen, but requires what as a co-factor?

78
Q

[Function]

FGF

A

Angiogenesis

Skeletal Development

79
Q

[Function]

VEGF

A

Angiogenesis

80
Q

[Function]

TGF-A

A

Epithelial and Fibroblast Growth Factor

81
Q

[Function]

TGF-B

A

Inhibits Inflammation

Fibroblast Growth Factor

82
Q

[Function]

PDGF

A

Endothelium, Smooth Muscle, Fibroblast Growth Factor

83
Q

Differentiate healing via primary versus secondary intention

A

Primary: Wound edges brought together; minimizes scar formation

Secondary: Edges are not approximated, granulation tissue fills in the defect

[Board Exam] Pathology (5 decks)

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