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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
Which enzyme converts superoxide to peroxide?
Superoxide dismutase
26
What enzyme converts peroxide to bleach?
Myeloperoxidase
27
What are the characteristics of chronic granulomatous disease?
* Recurrent infection and Granuloma formation with catalase-positive organisms (S. Aureus, **Pseudomonas cepacia**, Serratia marcescens, Nocardia, and Aspergillus)
28
Which test screens for chronic granulomatous disease (CGD)?
Nitroblue tetrazolium test **NOTE:** Test terms blue if NAPDH oxidase can convert oxygen to superoxide
29
MPO deficiency results in increased risk for __________ infections.
Candida **NOTE:** This deficiency prevents the conversion of peroxide to bleach
30
When does O2-independent killing occre?
Via enzymes present in leukpcyte scondary granules (lysozyme in macrophages and major basic protein in eosinophils)
31
What are the antiinflammatory cytokines?
IL-10 and TGF-b
32
What are the four possible next steps to the acute inflammatory process?
1. Resolution and healing 2. continued acute inflammation 3. Abcess 4. Chronic inflammation **NOTE:** These steps are mediated primarily by macrophages
33
How is an abcess formed?
Acute inflammation surrounded by **fibrosis**. Macrophages mediate fibrosis via fibrogenic growth factors and cytokines
34
What is required for the activation of T cells?
* Binding of antigen/MHC complex * Additional 2nd signal * B7 binding CD28 * IL-2 from CD4 TH1 cell
35
What cytokine is secreted by TH1 and what is it's function?
**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
Which cytokines are secreted by TH2 and what are their functions?
**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
What are the defining characteristics of granulomas?
* **Epithelioid histiocytes** (macrophages with abundant pink cytoplasm) * Usually surrounded by giant cells and a rim of lymphocytes *
38
Noncaseating granuloma
* lack central necrosis * Common etiologies * Reaction to foreign material * Sarcoidosis * Beryllium exposure * Crohn disease * Cat scratch disease
39
Caseating granulomas
* 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
What are the steps involved in granuloma formation?
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
DiGeorge Syndrome
* 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
Severe combined Immunodeficiency
* 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
X-linked agammaglobulinemia
* 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
Common variable immunodeficiency
* Low immunoglobulin due to B-cell or helper T-cell defects * Increased risk for autoimmune disease and lymphoma
45
IgA deficiency
* Low serum and mucousal IgA * Increased risj for mucosal infection, especially viral * Risk for **Celiac disease**
46
Hyper IgM Syndrome
* Mutated **CD40L** * IL-4 and IL-5 not produced
47
Wiskott-Aldrich Syndrome
* Thrombocytopenia, eczema, and recurrent infections * Bleeding disorder is a major cause of death * Due to mutation in the **WASP gene; X-linked**
48
Patients with C5-C9 deficiences are susceptible to which infection?
Neisseria infection
49
C1 inhibitor deficiency
* Hereditary angioedema * Edema of the skin and mucosal surfaces **NOTE:** Overactivity of complement leads to vasodilation
50
\_\_\_\_\_\_\_\_\_\_mutations result in autoimmune polyendocrine syndrome
AIRE
51
\_\_\_\_\_\_\_\_\_\_\_ mutations lead to IPEX syndrome.
**FOXP3** * Immune dysregulation * Polyendocrinopathy * Enteropathy * X-linked
52
Deficency in what complement proteins result in SLE.
C1q, C4, and C2
53
What is the most common type of renal injury seen in SLE?
Diffuse proliferative glomerulonerphritis
54
Which antibodies are found in SLE?
* Antinuclear antibody (ANA)- not specific * Anti-dsDNA or anti-Sm antibodies - highly specific * Antiphospholipid antibody * Against proteins bound to phospholipids
55
\_\_\_\_\_\_ antibody is characteristic of drug induced lupus.
Antihistone **DRUGS:** Procainamide, hydralazine, and isoniazid **NOTE:** CNS and renal involvement are rare
56
Primary vs Seconday Sjogren Syndrome
**Primary** * Sicca syndrome **Secondary** * Rheumatoid arthritis
57
Diagnostic criterion for Sjogren syndrome
* Dry eyes * Dry mouth * Lymphocytic sialadenitis
58
Which antibodies are found in Sjogren Syndrome?
* 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
Mixed connective tissue disease
* Mixed features of SLE, systemic sclerosis, and polymyositis * ANA along with **serum antibodies to U1 ribonucleoprotein**
60
C2 and C4 defieciency
SLE
61
C3 deficiency
Recurrent infections
62
C5-C9 deficiency
Prone to Neisseria infections
63
C1 inhibitor deficiency
Hereditary angioedema
64
C55 and CD59 deficiency
Praoxysamal nocturnal hemoglobinuria

OSI (CAMELITA) (38 decks)

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