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Gen Path > Section 2 Inflammation > Flashcards

Section 2 Inflammation Flashcards

1
Q

Inflammation needed to:

A
  1. Kill/eliminate microbes
  2. Remove debris
  3. Initiates repair
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2
Q

Types of WBC

A 
Lymphocytes
Monocytes
Neutrophils
Eosinophils
Basophils
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3
Q

MC granulocyte

A

Neutrophils

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4
Q

WBC that phagocytize microbes

A

Neutrophils

Macrophages

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5
Q

Types of lymphocytes

A

T cells
B cells
NK cells

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6
Q

Monocytes evolve into ___ when they encounter inflammation

A

Macrophages

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7
Q

WBC in chronic inflammation

A

Lymphocytes

Monocytes

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8
Q

WBC in acute inflammation

A

Neutrophils
Eosinophils
Basophils

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9
Q

Granulocytes

A

Neutrophils
Eosinophils
Basophils

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10
Q

Agranulocytes

A

Lymphocytes

Monocytes

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11
Q

Inflammation attracts

A

WBC and plasma proteins to target tissue

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12
Q

Injury to normal tissues is worse with:

A

Chronic infections
Virulent microbes
Allergies/autoimmunity

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13
Q

Cells that initiate inflammation

A

Macrophages
Dendritic cells
Mast cells

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14
Q

Cardinal signs of acute inflammation

A 
Rubor
Calor
Tumor
Dolor
Functio laesa
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15
Q

5 R’s of inflammation

A 
Recognize injury/microbes
Recruit WBC
Remove agent 
Regulate response
Resolution
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16
Q

Erythema

A

Redness

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17
Q

Inflammation is typically

A

Short lived and self limited

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18
Q

Hallmarks of acute inflammation

A

Rapid onset
Local and systemic signs
No fibrosis
Neutrophils

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19
Q

Hallmarks of chronic inflammation

A 
No obvious start 
Few signs
Angiogenesis
Fibrosis
Macrophages, lymphocytes
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20
Q

Neutrophils no longer present in inflammation ___ hours after injury

A

48 hours

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21
Q

First sign of inflammation is

A

Edema

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22
Q

Acute inflammation recognizes

A

Non-self

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23
Q

Acute inflammation receptors

A
  1. Toll-like receptors

2. Inflammasome

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24
Q

Toll-like receptors recognize ___ and found in ___

A

All types of infectious pathogens

Plasma membrane

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25
Q

Inflammasome recognizes __ and found in ___

A

Dead cell products

Cytoplasm

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26
Q

Dead cell products

A

Crystals
Proteins
DNA
ATP

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27
Q

Granulocytes are involved in

A

Allergic reactions

Asthma, anaphylaxis, allergic rhinitis, atopic dermatitis

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28
Q

Eosinophils involved in

A

Parasitic infections and allergic reactions

29
Q

Percentages of WBC

A 
Neutrophils - 70%
Basophils- 1%
Eosinophils- 3%
Monocytes/macrophages- 10%
Lymphocytes- 25%
30
Q

Examples of molecule secreted by sentinel cells

A

Pro-inflammatory cytokines

31
Q

Anti-inflammatory mechanisms that aid in termination of acute inflammation

A

Lipoxins

IL-10

32
Q

Pro-inflammatory mediators are ___ in end of acute inflammation

A

Inactivated

33
Q

Anti-inflammatory mediates are ___ with end of acute inflammation

A

Activated

34
Q

Stimuli for acute inflammation

A 
Infection
Trauma
Ischemia
Necrosis
Hypersensitivity reactions
35
Q

Major components of acute inflammation

A

Vascular changes

Leukocyte recruitment and activation

36
Q

Vascular changes

A

Altered caliber and permeability

  1. Vasoconstriction
  2. Vasodilation
  3. Increased vessel permeability
37
Q

Margination

A

WBCs collect along vascular wall

38
Q

3 mechanisms of vascular changes

A
  1. Endothelial contraction
  2. Endothelial necrosis
  3. Angiogenesis
39
Q

Endothelial contraction

A

Gaps in postcapillary venules due to histamine

40
Q

Histamine causes vessel wall permeability due to

A

Endothelial contraction

41
Q

Angiogenesis

A

New vessels have immature endothelial cells, resulting in leakiness

42
Q

Exudate edema

A

Protein rich

Inflammatory edema

43
Q

Transudate edema

A

Protein poor

Cause pitting edema

44
Q

Edema develops when

A

Lymphatic drainage can’t keep up

45
Q

Lymphadenopathy

A

MC

General disorder of lymph nodes

46
Q

Lymphadenitis

A

Inflamed nods, increases sizes and pain

47
Q

Lymphangitis

A

Inflamed lymphatic channel

48
Q

Steps for WBC Recruitment

A
  1. Margination and Rolling
  2. Firm adhesion
  3. Transmigration (Diapedesis)
  4. Chemotaxis
49
Q

Margination and rolling is mediated by

A

Selectins

50
Q

Firm adhesion is mediated by

A

Integrins

51
Q

WBC migrate via

A

Pseudopodia stimulated by bacteria, cytokines, complement

52
Q

Leukocyte activation stimulated by

A

Microbes, necrotic tissue, foreign bodies

53
Q

Opsonization

A

Tag a cell for destruction via antibodies (IgG) and complement proteins

54
Q

Opsonization enhances

A

Macrophages binding and breakdown

55
Q

Once activated, WBC are

A

Indiscriminate

56
Q

Activated WBC can cause inadvertent

A

Damage to normal cells

Secondary tissue injury

57
Q

WBC- induced tissue injury can be caused by

A

Persistent infections (TB, HIV, VZV)

Ischemia-reperfusion injury

Hypersensitivity reactions

58
Q

Outcomes of acute inflammation

A

Resolution
Chronic inflammation
Scarring (fibrosis)

59
Q

Resolution

A

Regeneration and repair

Returns to normal function

60
Q

Chronic inflammation

A

Severe injury or little capacity for replication

Failure to remove offending agent

Frequent scarring

61
Q

Scarring / Fibrosis

A

Severe injury

Alters structure= loss of function

62
Q

6 Patterns of Inflammation

A
  1. Serous
  2. Fibrinous
  3. Suppurative (purulent)
  4. Ulcerative
  5. Pseudomembranous
  6. Granulomatous
63
Q

Serous inflammation

A

Serum accumulates within or below epidermis

Cause blister

Due to burns, viral infections, autoimmunity

64
Q

Fibrinous inflammation

A

Severe injury = increase vessel permeability= large molecules out of circulation

Fibrinous-rich exudate

Severe fibrosis

65
Q

Suppurative

A

Local infection with pus-forming organism (staph, aureus)

66
Q

Pus

A

Neutrophils
Necrotic cells
Edema

67
Q

Abscess

A

Walled off collection of pus accumulation

68
Q

Ulcerative inflammation

A

Superficial area of tissue necrosis

Ex. Peptic ulcers, aphthous ulcer

69
Q

Pseudomembranous inflammation

A

Diphtheria

C-Diff

Gen Path (10 decks)

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