Inflammation Flashcards
1
Q
What are the characteristics of acute inflammation (4)?
A
- rapid course
- vasodilation
- increased vascular permeability
- accumulated neutrophils
2
Q
What is the dominant characteristic of chronic inflammation?
A
Scar tissue formation and proliferation
3
Q
Which kind of inflammation has predictable clinical manifestations, and which does not?
A
Predictable: acute
Unpredictable: chronic
4
Q
What are (5) benefits of inflammation?
A
- Localizes and dilutes damaging substances
- promotes antibody transport
- promotes fibrin clot formation
- stimulates immune response
- mobilizes phagocytes
5
Q
What are (4) risks of inflammation?
A
- release of lysosomal enzymes
- prolonged vascular pooling leading to hypoxia
- excessive swelling
Chronically can lead to excessive scarring
6
Q
What are the (5) cardinal signs of acute inflammation?
A
S.H.A.R.P.
- Swelling
- Heat
- A loss of function
- Redness
- Pain
7
Q
What is the triple response of Lewis?
A
- Flush (red line)
- Red flare
- Wheal
8
Q
When does the triple response of Lewis occur?
A
In the beginning of acute inflammation.
Common response to insect bites, minor skin trauma.
9
Q
How long does the triple response of Lewis tend to last?
A
15-30 minutes
10
Q
What is the flush, or red line stage, of Lewis response?
A
Local vasodilation - the result of histamine release
11
Q
What is the flare stage of Lewis response?
A
Dilation of arterioles adjacent to the injury site dilate, causing a red zone.
If local nerve fibers are cut, then no flare.
12
Q
What is the wheal stage of lewis response?
A
Local edema (swelling) caused by fluid accumulation. Fluid may persist, even if redness fades.
13
Q
What are the (3) stages of blood flow alteration that may occur during acute inflammation?
A
- transient vasoconstriction caused by short lived arteriole spasms in the SNS
- vasodilation (hyperemia) leading to increased flow (up to 10x)
- stasis (pooling) includes sludging (clumping of red blood cells)
14
Q
What are exudates and what do they contain?
A
Inflammatory fluids Contain: - fluid - plasma proteins - debris - leukocytes
15
Q
What are transudates?
A
Non-inflammatory fluids
16
Q
What kind of exudates are produced in mild (non-serious) injury?
What is their main component, and what color results?
A
Serous exudates
Consists of albumin
Thin, straw-colored fluid
17
Q
What are the (5) stages of leukocyte response to injury?
A
- Margination & rolling - move to edge of vessels
- Pavementing - adhere to vessel walls
- Diapedesis - exit vessels / enter tissue
- Migration (chemotaxis) - follow chemokines to injury site
- Phagocytosis & degranulation - ingestion and digestion of solid particles
18
Q
What are the (4) steps of phagocytosis?
A
- Adhesion of target to phagocyte
- Ingestion of particle via phagosome / lysosome (or phagolysosomes)
- Intracellular killing
- Digestion
19
Q
What immune cells are the first responders during acute inflammation?
A
Neutrophils
20
Q
Neutrophils do the best job with which kind of pathogens?
A
Bacteria
21
Q
Macrophages (monocytes) are most common with what kind of injury?
A
Chronic inflammation (all phases)
22
Q
Lymphocytes and plasma cells are most common with with kinds of pathogens?
A
Viruses
23
Q
When are eosinophils and basophils most common?
A
Parasitic infection (eosin)
Hypersensitivity (baso)
24
Q
What are the amine chemical mediators, and where are they found?
A
Histamine - mast cells, basophils, platelets
Serotonin - platelets, mast cells
25
What kinds of cells produce prostaglandins?
- leukocytes
- platelets
- endothelium
26
What action do histamines and serotonin have on vasculature?
Vasoconstriction
26
When are arachidonic acids released?
During every phase of acute inflammation
27
What (3) eicosanoids are the main derivatives of arachidonic acid?
- prostaglandins
- thromboxanes
- leukotrienes
28
When arachidonic acid is released from plasma membrane phospholipids, which (2) enzymatic pathways are activated?
- cyclooxygenase
| - lipoxygenase
29
What kind of hormones block the phospholipase pathway that activates arachidonic acid?
Corticosteroids
30
What are the (2) main actions of leukotrienes?
- attract neutrophils (chemotactic)
| - increase vessel permeability (leakier vessels)
31
Which inflammatory pathway is inhibited by NSAIDs?
Cyclooxygenase
32
Which enzymatic pathway produces leukotrienes?
Lipooxygenase
33
Which enzymatic pathway produces prostaglandins and thromboxanes?
Cyclooxygenase
34
What are the (5) main actions of prostaglandins and thromboxanes?
- increase vessel permeability
- increase vascular smooth muscle activity
- increase platelet activity
- contribute to fever
- potentiate pain
35
What effect do fish oils (eicosapentaetoic acids) have on the inflammation process?
Inhibit the production of leukotrienes by affecting the lipooxygenase pathway
36
What are the (6) categories of cell derived mediators of inflammation?
1. Lysosomal agents
2. Oxygen-derived free radicals
3. Platelet activating factor
4. Cytokines
5. Neuropeptides
6. Nitric oxide
37
What (2) plasma systems act as mediators of inflammation?
- kinin system
| - complement system
38
What do kinins (especially bradykinin) do?
- enhance permeability
- elicit pain
- fever
39
What is the classic activation pathway for the complement system?
Antigen-antibody complexes
40
What is the alternate activation pathway for the complement system?
Exposure to bacterial endotoxins
41
What are the (3) components of the clotting system?
- fibrinopeptides
- plasmin
- thrombin
42
In the clotting system, activation of plasmin produces what (2) effects?
- lysis of fibrin clots
| - activation of complement
43
In mild injury, how quickly does the immediate transient response start, and how long does it last?
Starts within 10 minutes
Lasts 30-60 minutes
44
When does a delayed-prolonged response to injury begin, and how long does it last?
Starts 2-3 hours post injury
Lasts several hours up to days
45
What are (3) common causes of the delayed-prolonged response to injury?
- sunburn
- radiation therapy
- moderate thermal burns
46
When does injury lead to an immediate-sustained response?
When endothelial cells are directly damaged and undergo necrosis
47
What are (3) main characteristics of chronic inflammation?
- prolonged (4-6 weeks)
- leukocytic infiltration
- fibrosis (scarring)
48
What are the clinical signs of chronic inflammation?
Highly variable
49
What is the most common fatal infectious disease?
TB
50
What are the (6) morphological patterns of inflammation?
1. Serous
2. Fibrinous
3. Catarrhal
4. Pyogenic
5. Granulomatous
6. Ulcer
51
What are some (3) mild injuries that give rise to serous inflammation?
- Rheumatoid arthritis
- Burn injury
- Herpetic sores
52
What is the main characteristic of pyogenic response?
Pus generation
53
What kind of inflammation leads to the formation of abscesses?
Pyogenic - pus formation
54
What is a furuncle?
A boil - small, pus filled abscess
55
What is a caruncle?
An enlarged furuncle - a pus filled boil with multiple points of discharge
56
What kind of inflammation is cellulitis, and what are its (3) main characteristics?
A type of pyogenic inflammation - subcutaneous
It is:
- acute
- diffuse
- spreading
57
What are erysipelas?
Cellulitis in the face
58
What are (2) common infections that lead to cellulitis?
- strep
| - staph
59
What is a special kind of chronic inflammation involving deposits of non-digestible materials?
Granulomatous
60
What are (2) infection types that lead to granulomatous inflammation?
- TB
| - autoimmune disorders like rheumatoid arthritis
61
What is the major cell type involved in granulomatous inflammation?
Modified macrophages
62
What is an acute ulcer?
A shallow crater in the surface of a tissue, resulting from sloughing of necrotic tissue
63
What is pyrexia?
Fever
64
What brain area regulates body temperature?
Hypothalamus
65
Besides increased body temperature, what happens during fever?
Increased metabolic rates due to increased energy and oxygen demand of cells
66
What are the (4) stages of fever?
1. Prodrome
2. Cold
3. Flush
4. Crisis
67
What happens in the prodrome stage of fever?
Pre-fever: the subject feels sick and achy, but no increase in temp
68
What happens in the cold stage of fever?
Fever begins - cutaneous blood flow is reduced to conserve heat, resulting in the skin feeling cold and possibly shivering
69
What happens in the flush stage of fever?
Higher body temperature has been achieved, blood flow increases to the skin
70
Patients may fluctuate between which two stages of fever?
Cold and flush
71
What happens in the crisis stage of fever?
Fever breaks, temperature returns to normal. Sweating occurs to release heat.
72
What is the upper temperature limit for non-neuronal cell function?
105-106 degrees
73
At what temperature do CNS disturbances start to appear?
103-105 degrees
74
At what temperature is death likely?
110 degrees
75
Systematic manifestations of inflammation, also called acute phase reactions include what (5) symptoms?
1. Somnolence
2. Fever
3. Poor appetite
4. Increased neutrophils (production, release, and activity)
5. Alterations in plasma proteins
76
What is leukocytosis?
Elevated levels of circulating WBC, usually neutrophils >10,000 mm3
77
What is leukopenia?
Reduced circulating WBC <3,000 mm3
78
What is the ideal outcome of inflammation?
Resolution - tissues completely restored to normal
- remove or inactive inflammatory stimulus
- reverse vascular changes
- remove exudates and debris
79
What is parenchymal regeneration?
Replacement of damaged tissues by normal cells of the same type
80
What is repair by connective tissue?
Replacement of damaged tissue with collagen
81
What is granulation tissue and what are it’s (3) major characteristics?
Immature, early scar tissue
Characteristics:
- cellular (macrophages)
- vascular
- edematous (fibroblasts)
82
What is a primary union in wound repair?
The margins of clean wounds are apposed under sterile conditions - the ideal healing (stitches)
83
What is secondary union in wound repair?
Repair of large wounds with separated edges - tissue loss has occurred and the resulting gap must be filled with granulation tissue
84
What are the (3) main factors to increase tensile strength in wound repair?
1. Type and quantity of collagen - Type III should be replaced by Type I
2. Orientation and size of fibers - initially random, should be realigned and reinforced along the direction of stress
3. Cross linkages - should form between the alpha chains of collagen
85
What is a keloid?
Hyperplastic scar tissue covered by intact skin - an excessive proliferation of scar tissue
86
When does repair by connective tissue take place?
When resolution or parenchymal regeneration is not possible, so damaged tissue is replaced with granulation tissue.
87
What is the maximum tensile strength of primary union restoration tissue?
80%
88
Can striated muscle fibers repair?
Limited repair capacity
89
Can the heart muscle repair?
Necrosis of heart muscle generally causes scarring; diffuse, non-lethal injury may be repairable
