Pathology > Inflammation > Flashcards

Inflammation Flashcards

(55 cards)

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1
Q

Characteristics of the Immediate transient response of inflammation

  1. Cause
  2. Inducers
  3. Vessels most affected
A

A. Endothelial Contraction

B. Inducers:

  1. Histamine
  2. Serotonin
  3. Bradykinin
  4. Leukotrienes

C. Venules

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2
Q

Characteristics of the Immediate Sustained Response of inflammation

  1. Cause
  2. Vessels most affected
A

A. Damage (necrotizing injury, burns, microbes)

B. All vessels

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3
Q

Characteristics of the Delayed Prolonged Leakage of inflammation

  1. Cause
  2. Vessels most affected
A
  1. UV or thermal injury
  2. venules and capillaries
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4
Q

Characteristics of Neutrophil-mediated endothelial injury

  1. Cause
  2. Vessels most affected
A

A. Released enzymes or ROIs by neutrophils

B.

  1. Venules
  2. Pulmonary Capillaries
  3. Glomerular Capillaries
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5
Q

Which receptors/molecules are involved with leukocyte rolling in the inflammatory response?

A

“Speed-bump selectins”

  1. E and P selectins (Endothelium) – sialyl Lewis X glycoprotein (leukocytes)
  2. CD34 (Endothelium) – L selectin (leukocytes)
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6
Q

Which molecules are involved with activation of integrin affinity to leukocytes in the inflammatory response?

A

Cytokines:

  1. IL-1
  2. TNF

Chemokines:

  1. IL-8
  2. C5a
  3. LTB4
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7
Q

Which receptors/molecules are involved with leukocyte binding to endothelium in the inflammatory response?

A

ICAM-1 (endothelium) – CR3 and LFA-1

ICAM-2 (endothelium) – LFA-1

VCAM-1 (E) – VLA-4

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8
Q

Difference in fuction of VLA-4 vs VLA-2, -3, -6 in the inflammatory response

A

VLA-4: lymphocyte-endothelial interactions

VLA-2, -3, -6: lymphocyte – ECM interaction

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9
Q

Which receptors/molecules are involved with leukocyte emigration in the inflammatory response?

In which type of vessel does diapedesis occur?

A
  1. PECAM-1
  2. JAMs (junctional adhesion molecules) – Integrins

Diapedesis occurs in the venules

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10
Q

Timeline of Acute Inflammation

Order of infiltration

A
  1. Edema
  2. Neutrophils
  3. Macrophages

Exception: viral infection has only mononuclear infiltrate.

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11
Q

Activation of neutrophils occurs via which receptors?

A
  1. TLR binding to PAMPS (LPS)
  2. Mannose reeptor
  3. Fc or complement receptor
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12
Q

Function of NADPH oxidase in microbial killing

A

respiratory/oxidative burst

converts O2 to superoxide (O2-)

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13
Q

Function of Myeloperoxidase in Microbial killing

A

Convert H2O2 to Hypoclorite (HOCl radical)

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14
Q

Defect in Leukocyte Adhesion Deficiency 1

A

No expression of LFA-1

(No attachment to endothelium to prepare for transmigration)

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15
Q

Defect in Leukocyte Adhesion Deficiency 2

A

No sialyl-Lewis X (no selectin receptor)

(No rolling)

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16
Q

Defect in Chronic Granulomatous Disease?

A

No NADPH oxidase (no superoxide formation)

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17
Q

Defect in Chediak-Higashi syndrome

A

No fusion of lysosomes with phagosomes

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18
Q

Differences in initiation of:

Alternative pathway

Classical pathway

Lectin pathway

A
  1. C5 convertase: C3bBbC3b (spontaneous breakdown of C3b)
  2. Crosslinking leading to C5 convertase: C4b2a3b
  3. MBL binds mannose-containing structures of microbes, which initiates C4 hydrolysis; C5 convertase: C4b2a3b
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19
Q

Stimulus and Results of Kinin cascade

A

Stimulus: Hageman Factor (XIIa)

Results:

  1. Bradykinin synthesis (Pain, Increased vascular permeability, Vasodilation)
  2. Complement Cascade
  3. Fibrinolytic cascade (plasmin formation)
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20
Q

Stimulus and Results of Clotting Cascade

A

Stimulus: Hageman Factor (XIIa)

Result: Thrombin formation

  1. Acute inflammation
  2. Clotting (fibrin formation)
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21
Q

Function of Decay Accelerating Factor (DAF)

A

*Regulate complement*

  1. Block C2 binding to C4b
  2. Dissociation of C2a and C4b
  3. Block CD59 (inhibit C9 polymeration and MAC formation)
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22
Q

Effects of C3a

A

Leukocyte activation

Mast cell degranulation

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23
Q

Effects of C5a

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A

Neutrophil chemotaxis

Leukocyte activation

Mast cell degranulation

24
Q

Effect of C3b

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A

Opsonization and phagocytosis

25
Effects of Histamine
Dilation of arterioles and Capillaries Contraction of endothelial cells (increased permeability of venules/caps)
26
Effects of Serotonin
Produced by platelets Dilation Endothelial contraction causeing increased vasc. perm.
27
COX 1 vs COX 2 function
COX 1: maintenance COX 2: Proinflammatory Both: Produce PGs and TXA2
28
Prostaglandins vs Leukotrienes Synthesis Function
Synthesis: PGs: COX LTs: Lipoxygenase Function: PGs: stimulate acute inflammation (vasodilation, (-) platelet aggregation) LTs: Vasocontstriction, increased vasc. perm.
29
Production and Function of Lipoxins
Production: Leukocyte-Platelet interaction Function: Resolution of acute inflammation 1. (-) selectins: (-) neutrophil chemotaxis 2. (+) monocyte chemotaxis
30
Functions of Platelet Activating Factor (PAF)
Low concentration: 1. vasodilation 2. increased vasc. perm. High concentration: 1. (+) platelet aggregation 2. Vasoconstriction 3. Bronchoconstriction 4. (+) leukocytes
31
Major source of IL-1 and TNF-alpha
Macrophages
32
C-X-C chemokines Function Example
Function: neutrophil (leukocyte) chemotaxis IL-8
33
Function of NO in acute inflammation
down-regulates acute inflammation through reduced leukocyte and platelet adherence
34
Steps of Complete Resolution of Acute Inflammation
35
What type of inflammation is pictured?
Serous Inflammation Source: plasma or mesothelial cells lining body cavities
36
What type of inflammation is pictured?
Fibrinous inflammation | (with adhesions)
37
What type of inflammation is pictured?
Suppurative
38
What type of inflammation is pictured?
Suppurative
39
What type of inflammation is pictured?
Fibrinous
40
Pseudomembranous Inflammation is a combination of what two types of inflammation?
Purulent and fibrinous Ex: Pseudomembranous entercolitis
41
What is pictured?
Ulcer
42
Silicosis ## Footnote 1. Type of inflammation 2. Cause 3. Type of Granuloma pictured
1. Chronic 2. inhalation of silica 3. Foreign body granuloma (Results in fibrotic scarring)
43
Characteristics of Chronic Inflammation 1. Infiltrate 2. Cell types 3. Morphology 4. Location of infiltration compared to acute
1. Mononuclear infiltrates 2. Epithelioid macrophages, giant cells, plasma cells 3. Granulomas, Signs of destruction, signs of healing (fibrosis) and angiogenesis 4. Interstitial (in acute, it accumulates in cavities)
44
What type of inflammation is pictured? What is the cell type shown?
Chronic inflammation (see granuloma) Langhans type giant cell
45
What type of inflammation is pictured? What is the cell type shown?
Chronic Inflammation Foreign Body Giant Cell (forms near foreign material)
46
Chemotactic stimuli for macrophages
1. MCP-1 2. C5a 3. PDGF 4. TGF-alpha 5. collagen
47
1. Cytokine that stimulates resolution and repair following inflammation 2. Cytokine that stimulates further inflammation and tissue injury
1. IL-4 (followed by TGF-ß) 2. IFN-gamma (from T cells)
48
What type of granuloma is pictured? What is the cause?
1. Immune granuloma 2. microbes that are poorly degraded (here, TB) This shows a central area of caseous necrosis
49
What type of granuloma is pictured? What is the cause?
Foreign body granuloma Silicosis
50
What is the function of C-reactive protein?
opsonize microbes Used as a marker for increased risk of MI
51
Increased erythrocyte sedimentation rate signals what?
Increased fibrinogen which causes increased RBC stacking and increased sedimentation \*\*Signals inflammation\*\*
52
Function of serum amyloid A protein
opsonization of microbes
53
Significance of elevated levels of band cells
Bacterial infections (release of immature neutrophils (band cells) from bone marrow postmitotic reserve pool)
54
Significance of neutrophilia
bacterial infection
55
Septic shock triad and stimulating cytokines
Triad: 1. DIC (expression of tissue factor, initiating coagulation) 2. Hypoglycemia (Liver damage and reduced gluconeogenesis) 3. Cardiovascular failure (overproduction of NO) Cytokines: IL-1 and TNF
Pathology
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