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Pathology > Inflammation > Flashcards

Inflammation Flashcards

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

A

Neutrophil chemotaxis

Leukocyte activation

Mast cell degranulation

24
Q

Effect of C3b

A

Opsonization and phagocytosis

25
Q

Effects of Histamine

A

Dilation of arterioles and Capillaries

Contraction of endothelial cells (increased permeability of venules/caps)

26
Q

Effects of Serotonin

A

Produced by platelets

Dilation

Endothelial contraction causeing increased vasc. perm.

27
Q

COX 1 vs COX 2 function

A

COX 1: maintenance

COX 2: Proinflammatory

Both: Produce PGs and TXA2

28
Q

Prostaglandins vs Leukotrienes

Synthesis

Function

A

Synthesis:

PGs: COX

LTs: Lipoxygenase

Function:

PGs: stimulate acute inflammation (vasodilation, (-) platelet aggregation)

LTs: Vasocontstriction, increased vasc. perm.

29
Q

Production and Function of Lipoxins

A

Production: Leukocyte-Platelet interaction

Function: Resolution of acute inflammation

  1. (-) selectins: (-) neutrophil chemotaxis
  2. (+) monocyte chemotaxis
30
Q

Functions of Platelet Activating Factor (PAF)

A

Low concentration:

  1. vasodilation
  2. increased vasc. perm.

High concentration:

  1. (+) platelet aggregation
  2. Vasoconstriction
  3. Bronchoconstriction
  4. (+) leukocytes
31
Q

Major source of IL-1 and TNF-alpha

A

Macrophages

32
Q

C-X-C chemokines

Function

Example

A

Function: neutrophil (leukocyte) chemotaxis

IL-8

33
Q

Function of NO in acute inflammation

A

down-regulates acute inflammation through reduced leukocyte and platelet adherence

34
Q

Steps of Complete Resolution of Acute Inflammation

A
35
Q

What type of inflammation is pictured?

A

Serous Inflammation

Source: plasma or mesothelial cells lining body cavities

36
Q

What type of inflammation is pictured?

A

Fibrinous inflammation

(with adhesions)

37
Q

What type of inflammation is pictured?

A

Suppurative

38
Q

What type of inflammation is pictured?

A

Suppurative

39
Q

What type of inflammation is pictured?

A

Fibrinous

40
Q

Pseudomembranous Inflammation is a combination of what two types of inflammation?

A

Purulent and fibrinous

Ex: Pseudomembranous entercolitis

41
Q

What is pictured?

A

Ulcer

42
Q

Silicosis

  1. Type of inflammation
  2. Cause
  3. Type of Granuloma pictured
A
  1. Chronic
  2. inhalation of silica
  3. Foreign body granuloma

(Results in fibrotic scarring)

43
Q

Characteristics of Chronic Inflammation

  1. Infiltrate
  2. Cell types
  3. Morphology
  4. Location of infiltration compared to acute
A
  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
Q

What type of inflammation is pictured? What is the cell type shown?

A

Chronic inflammation (see granuloma)

Langhans type giant cell

45
Q

What type of inflammation is pictured? What is the cell type shown?

A

Chronic Inflammation

Foreign Body Giant Cell (forms near foreign material)

46
Q

Chemotactic stimuli for macrophages

A
  1. MCP-1
  2. C5a
  3. PDGF
  4. TGF-alpha
  5. collagen
47
Q
  1. Cytokine that stimulates resolution and repair following inflammation
  2. Cytokine that stimulates further inflammation and tissue injury
A
  1. IL-4 (followed by TGF-ß)
  2. IFN-gamma (from T cells)
48
Q

What type of granuloma is pictured? What is the cause?

A
  1. Immune granuloma
  2. microbes that are poorly degraded (here, TB)

This shows a central area of caseous necrosis

49
Q

What type of granuloma is pictured? What is the cause?

A

Foreign body granuloma

Silicosis

50
Q

What is the function of C-reactive protein?

A

opsonize microbes

Used as a marker for increased risk of MI

51
Q

Increased erythrocyte sedimentation rate signals what?

A

Increased fibrinogen which causes increased RBC stacking and increased sedimentation

**Signals inflammation**

52
Q

Function of serum amyloid A protein

A

opsonization of microbes

53
Q

Significance of elevated levels of band cells

A

Bacterial infections

(release of immature neutrophils (band cells) from bone marrow postmitotic reserve pool)

54
Q

Significance of neutrophilia

A

bacterial infection

55
Q

Septic shock triad and stimulating cytokines

A

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 (27 decks)

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