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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
Inflammasome recognizes __ and found in ___
Dead cell products Cytoplasm
26
Dead cell products
Crystals Proteins DNA ATP
27
Granulocytes are involved in
Allergic reactions | Asthma, anaphylaxis, allergic rhinitis, atopic dermatitis
28
Eosinophils involved in
Parasitic infections and allergic reactions
29
Percentages of WBC
``` Neutrophils - 70% Basophils- 1% Eosinophils- 3% Monocytes/macrophages- 10% Lymphocytes- 25% ```
30
Examples of molecule secreted by sentinel cells
Pro-inflammatory cytokines
31
Anti-inflammatory mechanisms that aid in termination of acute inflammation
Lipoxins | IL-10
32
Pro-inflammatory mediators are ___ in end of acute inflammation
Inactivated
33
Anti-inflammatory mediates are ___ with end of acute inflammation
Activated
34
Stimuli for acute inflammation
``` Infection Trauma Ischemia Necrosis Hypersensitivity reactions ```
35
Major components of acute inflammation
Vascular changes | Leukocyte recruitment and activation
36
Vascular changes
Altered caliber and permeability 1. Vasoconstriction 2. Vasodilation 3. Increased vessel permeability
37
Margination
WBCs collect along vascular wall
38
3 mechanisms of vascular changes
1. Endothelial contraction 2. Endothelial necrosis 3. Angiogenesis
39
Endothelial contraction
Gaps in postcapillary venules due to histamine
40
Histamine causes vessel wall permeability due to
Endothelial contraction
41
Angiogenesis
New vessels have immature endothelial cells, resulting in leakiness
42
Exudate edema
Protein rich Inflammatory edema
43
Transudate edema
Protein poor Cause pitting edema
44
Edema develops when
Lymphatic drainage can’t keep up
45
Lymphadenopathy
MC General disorder of lymph nodes
46
Lymphadenitis
Inflamed nods, increases sizes and pain
47
Lymphangitis
Inflamed lymphatic channel
48
Steps for WBC Recruitment
1. Margination and Rolling 2. Firm adhesion 3. Transmigration (Diapedesis) 4. Chemotaxis
49
Margination and rolling is mediated by
Selectins
50
Firm adhesion is mediated by
Integrins
51
WBC migrate via
Pseudopodia stimulated by bacteria, cytokines, complement
52
Leukocyte activation stimulated by
Microbes, necrotic tissue, foreign bodies
53
Opsonization
Tag a cell for destruction via antibodies (IgG) and complement proteins
54
Opsonization enhances
Macrophages binding and breakdown
55
Once activated, WBC are
Indiscriminate
56
Activated WBC can cause inadvertent
Damage to normal cells | Secondary tissue injury
57
WBC- induced tissue injury can be caused by
Persistent infections (TB, HIV, VZV) Ischemia-reperfusion injury Hypersensitivity reactions
58
Outcomes of acute inflammation
Resolution Chronic inflammation Scarring (fibrosis)
59
Resolution
Regeneration and repair Returns to normal function
60
Chronic inflammation
Severe injury or little capacity for replication Failure to remove offending agent Frequent scarring
61
Scarring / Fibrosis
Severe injury Alters structure= loss of function
62
6 Patterns of Inflammation
1. Serous 2. Fibrinous 3. Suppurative (purulent) 4. Ulcerative 5. Pseudomembranous 6. Granulomatous
63
Serous inflammation
Serum accumulates within or below epidermis Cause blister Due to burns, viral infections, autoimmunity
64
Fibrinous inflammation
Severe injury = increase vessel permeability= large molecules out of circulation Fibrinous-rich exudate Severe fibrosis
65
Suppurative
Local infection with pus-forming organism (staph, aureus)
66
Pus
Neutrophils Necrotic cells Edema
67
Abscess
Walled off collection of pus accumulation
68
Ulcerative inflammation
Superficial area of tissue necrosis Ex. Peptic ulcers, aphthous ulcer
69
Pseudomembranous inflammation
Diphtheria C-Diff

Gen Path (10 decks)

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