[1] Inflammation Flashcards Preview

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Flashcards in [1] Inflammation Deck (83):
1

Neutrophils are attracted to these chemical attractants

IL8
C5a
LTB4
Bacterial components

2

Where do neutrophils migrate to exert their action?

Post-capillary Venule

3

Disease characterized by impairment in protein trafficking

Chediak-Higashi Syndrome

4

Clinical Features of Chediak-Higashi Syndrome

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

5

Most effective mechanism of killing phagocytosed materials?

O2-Dependent Killing Mechanism

6

What converts Oxygen to Superoxide

NADPH

(Also called oxidative burst)

7

What converts Superoxide to Hydrogen Peroxide?

Superoxide Dismutase

8

What converts Hydrogen Peroxide to HOCl (Bleach)?

Myeloperoxidase

9

What is defective in Chronic Granulomatous Disease

NAPDH Oxidase Defect

10

Patients with CGD have granuloma formation with these kinds of organisms

How come only these organisms can cause infections?

Catalase-positive

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

11

Test used to screen for CGD

How?

Nitroblue Tetrazolium Test

Turns blue if NADPH oxidase can convert O2 to O2-

12

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

Candida Infections

13

Neutrophils disappear after how many hours via what mechanism?

24 hours via apoptosis

14

What leukocyte predominates after the neutrophil phase?

Macrophage

15

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

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

16

How do macrophages recruit additional neutrophils?

Secrete IL-8

17

4 Possible Endpoints of the Acute Inflammatory Process

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

18

Chronic inflammation is characterized by?

Lymphocytes and plasma cells in tissue

19

T Cells are produced in?

Bone Marrow

20

TCR Complexes can only recognize antigen when presented by?

MHC

21

CD4 and CD8 T-Cells recognize which MHC Class

CD4 :: MHC II
CD8 :: MHC I

22

Immature B Cells are produced in?

Bone Marrow

23

Function of IL-4

Class Switching of IgG -> IgE

24

Function of IL-5

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

25

Function of IL-10

Inhibits TH1 Phenotype

26

How are CD8 TCells Activated?

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

27

Key enzyme that mediates apoptosis?

Caspases

28

How are B-Cells Activated?

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)

29

What is the defining characteristic of a granuloma?

Epithelioid histiocytes (macrophages with abundant pink cytoplasm)

30

How can you differentiate caseating from non-caseating granulomas?

Central Necrosis

31

Caseating granulomas are characteristic of these diseases

TB and Fungal Infections

32

Steps involved in Granuloma Formation

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

33

Function: IL-12

Induce CD4 to differentiate into TH1

34

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

IFN-Y

35

DiGeorge Syndrome is a developmental failure of?
This is due to a deletion of which chromosome?

3rd and 4th Pharyngeal Pouch

22q11 microdeletion

36

Presentation of DiGeorge Syndrome

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

37

Etiologies of SCID

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

38

Treatment for SCID

1. Sterile Isolation
2. Stem Cell Transplant

39

X-Linked Agammaglobulinemia is a defect in?

Complete lack of immunoglobulin

Due to disordered B-cell maturation

40

X-Linked Agammaglobulinemia is caused by which mutated gene?

Mutated Tyrosine Kinase

41

These infections are common in patients with X-Linked Agammaglobulinemia

Bacterial
Enterovirus
Giardia infections

(Mucosal infections: IgA deficiency)

42

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

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

43

What is the most common Ig deficiency?

IgA

44

Which GI disease is commonly associated with IgA deficiency?

Celiac Disease

45

What is the cause of Hyper IgM Syndrome?

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

46

Which Immunoglobulins would be low in patients with HyperIgM Syndrome?

IgA
IgG
IgE

47

Triad of Wiskott-Aldrich Syndrome

1. Thrombocytopenia
2. Eczema
3. Recurrent infections

48

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

Neisseria

49

Autoimmune diseases are caused by a loss of this defense mechanism

Self-tolerance

50

SLE causes systemic damage via which Hypersensitivity Reactions?

Type II (Cytotoxic)
Type III (Antigen-Antibody Complexes)

51

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

Diffuse proliferative glomerulonephritis

52

What is unique about Libman-Sacks endocarditis?

Presence of vegetation on both sides of the heart valves

53

What is characteristic of drug-induced SLE?

Antihistone Antibody

54

These drugs are common causes of drug-induced SLE?

Hydralazine
Procainamide
Isoniazid

55

Which antibodies are associated with Antiphospholipid Syndrome?

Anticardiolipin
Lupus Anticoagulant

56

Anticardiolipin interferes with this test

Leads to a false-positive syphilis test

57

Lupus Anticoagulant interferes with this diagnostic test

Elevated PT/PTT

58

Treatment for APAS

Lifelong anticoagulation

59

Sjogren Syndrome is associated with destruction of these glands

Lacrimal
Salivary

60

Classic antibody test for Sjogren Syndrome

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

61

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?

The patient has possibly developed a B-cell Lymphoma

62

Scleroderma is characterized by these antibodies

Anti-DNA Topoisomerase I Antibody (Scl-70)

63

Classic Presentation of Crest Syndrome

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

64

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

Mucosal Crypts

65

Where are the stem cells located in the skin?

Basal Layer

66

Where are the stem cells located in the bone marrow?

Hematopoietic Stem Cells

67

Where are the stem cells located in the lung?

Type II Pneumocytes

68

What is the marker for hematopoietic stem cells?

CD34

69

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

Skeletal Muscle
Neurons
Cardiac Muscle

70

What are the components of granulation tissue?

1. Fibroblasts
2. Capillaries
3. Myofibroblasts

71

What do fibroblasts do in the initial phase of repair?

Deposit Type III Collagen

72

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

Type III -> Type I Collagen

73

Type I Collagen is commonly seen in?

Bone

[b-ONE]

74

Type II Collagen is commonly seen in?

Cartilage

[Car-TWO-lage]

75

Type III Collagen is commonly seen in?

Blood vessels, granulation tissue, embryonic tissue

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

76

Type IV Collagen is commonly seen in?

Basement Membrane

77

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

Zinc

78

[Function]

FGF

Angiogenesis
Skeletal Development

79

[Function]

VEGF

Angiogenesis

80

[Function]

TGF-A

Epithelial and Fibroblast Growth Factor

81

[Function]

TGF-B

Inhibits Inflammation
Fibroblast Growth Factor

82

[Function]

PDGF

Endothelium, Smooth Muscle, Fibroblast Growth Factor

83

Differentiate healing via primary versus secondary intention

Primary: Wound edges brought together; minimizes scar formation

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