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OSI (CAMELITA) > Acute and Chronic Inflammation > Flashcards

Acute and Chronic Inflammation Flashcards

1
Q

_____________ on macrophages recognizes lipopolysaccharide on the outer membrane of gram-negative bacteria.

A

CD14

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2
Q

What is the main result of TLR activation?

A

Results in an upregulation of NF-kB, a nuclear transcription factor that activates immune response genes leading to production of multiple immune mediators.

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3
Q

Which prostaglandings mediate vasodilation and increased vascular permeability?

A

PGI2, PGD2, and PGE2

REMEMBER: Increased vascular permeability takes place at the post capillary venule

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4
Q

Role of PGE2

A

mediates pain and fever

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5
Q

Which of the leukotrienes attracts and activates neutrophils?

A

LTB4

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6
Q

What is the role of LTC4, LTD4, and LTE4?

A

Leukotrienes that mediate vasoconstriction, bronchospasm, and increased vascular permeability

NOTE: These leukotrienes are known as slow reacting substances of anaphylaxis

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7
Q

What substances mediate and activate neutrophils?

A

LTB4, bacterial products, C5a, IL-8

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8
Q

What events activate mast cells?

A
  • Complement proteins C3a and C5a
  • Cross-linking of IgE molecules
  • Tissue trauma
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9
Q

Compare and contrast the immediate and delayed mast cell responses.

A

IMMEDIATE

  • Preformed histamine

DELAYED

  • Arachodonic acid metabolites, particularly leukotrienes
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10
Q

Which complement components are anaphylaxotoxins?

A

C3a and C5a

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11
Q

Which substances are involved in opsonization?

A

C3b and IgG

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12
Q

When is hageman factor (factor XII) activates?

A
  • upon exposure to subendothelial or tissue collagen
  • In response to severe gram negative sepsis
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13
Q

What systems are activated post-hagemen factor activation?

A
  • Coagulation and fribrinolytic systems
  • Kinin system
    • Cleavage to bradykinin
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14
Q

Which factors are involved in pain?

A

PGE2 and bradykinin

NOTE: They sensitive sensory nerve endings

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15
Q

What are the cardinal signs of inflammation?

A
  • Redness (rubor)
  • Warmth (calor)
    • mediators: bradykinin, prostaglandin, and histamine
  • Swelling (tumor)
    • Mediators: histamine and tissue damage
  • Pain (dolor)
    • Bradykinin and PGE2
  • Fever
    • IL-1, PGE2 and TGF-a
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16
Q

Steps of neutrophil arrival and function

A
  1. Margination
  2. Rolling
  3. Adhesion
  4. Transmigration and Chemotaxis
  5. Phagocytosis
  6. Destruction of phagocytosed material
  7. Resolution
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17
Q

P-selectin release from __________ is mediated by histamine.

A

Wiebel-Palade bodies

NOTE: Wiebel- Palade bodies have proteins necessary for the fucntion of endothelial cells

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18
Q

What factors induce E-selectin?

A

IL-1 and TNF

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19
Q

Selectins bind _______ on leukocytes.

A

Siacyl Lewis X

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20
Q

Which factors upregulated adhesion molecules?

A

VCAM and ICAM (on endothelium) are upregulated by IL-1 and TGF

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21
Q

Which factors upregulate integrin?

A

Intergrins are upreguate on leukocytes (neutrophils) by C5a and LTB4.

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22
Q

What are the clinical features of LAD1?

A
  • Delayed seperation of the umbilivcal cord
  • Increased circulating neutrophils
  • Recurrent bacterial infections that lack pus formation
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23
Q

What are the clinical feautures of Chediak-higashi syndrome?

A
  • Increased risk of pyrogenic infectiosn
  • Neutropenia
  • Giant granules in leukocytes
  • Defective primary hemostatis
  • Albinism
  • Peripheral neuropathy
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24
Q

Which enzyme catayles the conversion of oxygen to superoxide?

A

NADPH oxidase

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25
Q

Which enzyme converts superoxide to peroxide?

A

Superoxide dismutase

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26
Q

What enzyme converts peroxide to bleach?

A

Myeloperoxidase

27
Q

What are the characteristics of chronic granulomatous disease?

A
  • Recurrent infection and Granuloma formation with catalase-positive organisms (S. Aureus, Pseudomonas cepacia, Serratia marcescens, Nocardia, and Aspergillus)
28
Q

Which test screens for chronic granulomatous disease (CGD)?

A

Nitroblue tetrazolium test

NOTE: Test terms blue if NAPDH oxidase can convert oxygen to superoxide

29
Q

MPO deficiency results in increased risk for __________ infections.

A

Candida

NOTE: This deficiency prevents the conversion of peroxide to bleach

30
Q

When does O2-independent killing occre?

A

Via enzymes present in leukpcyte scondary granules (lysozyme in macrophages and major basic protein in eosinophils)

31
Q

What are the antiinflammatory cytokines?

A

IL-10 and TGF-b

32
Q

What are the four possible next steps to the acute inflammatory process?

A
  1. Resolution and healing
  2. continued acute inflammation
  3. Abcess
  4. Chronic inflammation

NOTE: These steps are mediated primarily by macrophages

33
Q

How is an abcess formed?

A

Acute inflammation surrounded by fibrosis. Macrophages mediate fibrosis via fibrogenic growth factors and cytokines

34
Q

What is required for the activation of T cells?

A
  • Binding of antigen/MHC complex
  • Additional 2nd signal
    • B7 binding CD28
    • IL-2 from CD4 TH1 cell
35
Q

What cytokine is secreted by TH1 and what is it’s function?

A

IFN-gamma

  • Activates macrophage
  • Promotes B cell class switiching from IgM to IgG
  • Promotes TH1 phenotype and inhibits TH2 phenotype

NOTE: IL-10 inhibits TH1

36
Q

Which cytokines are secreted by TH2 and what are their functions?

A

IL-4

  • Facilitates B-cell switching to IgE

IL-5

  • Eosinophil chemotaxis and activation, and class switching to IgA

IL-10

  • Antiinflammatory
  • Inhibits TH1

IL-13

37
Q

What are the defining characteristics of granulomas?

A
  • Epithelioid histiocytes (macrophages with abundant pink cytoplasm)
    • Usually surrounded by giant cells and a rim of lymphocytes
      *
38
Q

Noncaseating granuloma

A
  • lack central necrosis
  • Common etiologies
    • Reaction to foreign material
    • Sarcoidosis
    • Beryllium exposure
    • Crohn disease
    • Cat scratch disease
39
Q

Caseating granulomas

A
  • Exhibit central necrosis
  • TB and fingal infections
    • AFB stain to look for TB
    • GMS stain to look for fungal infections

NOTE: A viral infetion will never give you a granuloma

40
Q

What are the steps involved in granuloma formation?

A
  1. Macrophages oricess and present antigen via MHC class II to CD4 cells
  2. macrophages secrete IL-12, inducing CD4 to differentiate into TH1
  3. TH1 secretes IFN-gamma which converts macrophages to epithelioid histiocytes and giant cells
41
Q

DiGeorge Syndrome

A
  • Developmental failure of the third and fourth pharyngeal pouches
    • Due to 22q11 microdeletion
  • Presents with:
    • T- cell deficiency
    • Hypocalemia
    • Abnormalties of heart, great vessels, and face
42
Q

Severe combined Immunodeficiency

A
  • Deffective cell-mediated and humoral immunity
  • Adenosine deaminase deficiency (ADA)
    • Buildup of adenosine and deoxyadenosine is toxic to lymphocytes
  • MHC class II deficiency
  • Susceptibility to fungal, viral, bacterial, and protozoal infections
  • Treatment: sterile isolation and stem cell transplantation
43
Q

X-linked agammaglobulinemia

A
  • Complete lack of immunoglobulin due to disordered B- cell maturation
    • Mutated Bruton tyrosine kinase
  • ​X-linked
  • Presents with:
    • Giardia lamblia infections,recurrent bacterial, enterovirus
  • Live vaccines must be avoided
44
Q

Common variable immunodeficiency

A
  • Low immunoglobulin due to B-cell or helper T-cell defects
  • Increased risk for autoimmune disease and lymphoma
45
Q

IgA deficiency

A
  • Low serum and mucousal IgA
  • Increased risj for mucosal infection, especially viral
  • Risk for Celiac disease
46
Q

Hyper IgM Syndrome

A
  • Mutated CD40L
  • IL-4 and IL-5 not produced
47
Q

Wiskott-Aldrich Syndrome

A
  • Thrombocytopenia, eczema, and recurrent infections
  • Bleeding disorder is a major cause of death
  • Due to mutation in the WASP gene; X-linked
48
Q

Patients with C5-C9 deficiences are susceptible to which infection?

A

Neisseria infection

49
Q

C1 inhibitor deficiency

A
  • Hereditary angioedema
    • Edema of the skin and mucosal surfaces

NOTE: Overactivity of complement leads to vasodilation

50
Q

__________mutations result in autoimmune polyendocrine syndrome

A

AIRE

51
Q

___________ mutations lead to IPEX syndrome.

A

FOXP3

  • Immune dysregulation
  • Polyendocrinopathy
  • Enteropathy
  • X-linked
52
Q

Deficency in what complement proteins result in SLE.

A

C1q, C4, and C2

53
Q

What is the most common type of renal injury seen in SLE?

A

Diffuse proliferative glomerulonerphritis

54
Q

Which antibodies are found in SLE?

A
  • Antinuclear antibody (ANA)- not specific
  • Anti-dsDNA or anti-Sm antibodies - highly specific
  • Antiphospholipid antibody
    • Against proteins bound to phospholipids
55
Q

______ antibody is characteristic of drug induced lupus.

A

Antihistone

DRUGS: Procainamide, hydralazine, and isoniazid

NOTE: CNS and renal involvement are rare

56
Q

Primary vs Seconday Sjogren Syndrome

A

Primary

  • Sicca syndrome

Secondary

  • Rheumatoid arthritis
57
Q

Diagnostic criterion for Sjogren syndrome

A
  • Dry eyes
  • Dry mouth
  • Lymphocytic sialadenitis
58
Q

Which antibodies are found in Sjogren Syndrome?

A
  • Antiribonucleoprotein antibodies
    • Anti-SSA
    • Anti- SSB

NOTE: Pregnant women with anti-SSA are at risk for delivering babies with neonatal lupus and congenital heart block

59
Q

Mixed connective tissue disease

A
  • Mixed features of SLE, systemic sclerosis, and polymyositis
  • ANA along with serum antibodies to U1 ribonucleoprotein
60
Q

C2 and C4 defieciency

A

SLE

61
Q

C3 deficiency

A

Recurrent infections

62
Q

C5-C9 deficiency

A

Prone to Neisseria infections

63
Q

C1 inhibitor deficiency

A

Hereditary angioedema

64
Q

C55 and CD59 deficiency

A

Praoxysamal nocturnal hemoglobinuria

OSI (CAMELITA) (38 decks)

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