Acute Inflammation Flashcards
1
Q
What is inflammation?
A
A complex reaction of vascularised connective tissue to local injury
2
Q
What are the purposes of inflammation? (3)
A
1) Contain/isolate injurious stimulus
2) Destroy/dilute/wall off agents to neutralise toxins
1 + 2 = LIMIT DAMAGE
3) Repair damage caused
3
Q
What is inflammation classified according to?
A
Time course
4
Q
What are the two types of inflammation?
A
- Chronic
- Acute
5
Q
What is acute inflammation?
A
Inflammation of relatively short duration. Quick response
6
Q
What is chronic inflammation?
A
Inflammation of relatively long duration
7
Q
What does acute inflammation response time depend on? (2)
A
- Pathogen causing injury
- Body ability to respond to injury
8
Q
What are the two parts that make up the name given to an infection?
A
- Name of organ/tissue
- Suffix “itis”
9
Q
What are the 5 signs of acute inflammation?
A
- Heat
- Redness
- Swelling
- Pain
- Loss of function
10
Q
What is heat and redness caused by in acute inflammation?
A
Hyperaemia (increased blood flow)
11
Q
What is swelling caused by in acute inflammation?
A
Increased amount of fluid in tissue (exudate)
12
Q
What 2 things is pain caused by in acute inflammation?
A
- Neural damage
- Chemical mediators e.g across gland
13
Q
Why is pain important in acute inflammation?
A
For awareness of event
14
Q
What can loss of function be caused by in acute inflammation?
A
Pain
-
15
Q
What does loss of function be caused in acute inflammation depend on?
A
Specific part affected by inflammation e.g reduced mobility in joint
16
Q
What are the 3 processes an injury triggers in acute inflammation?
A
- Vascular changes
- Cellular events
- Chemical mediators
17
Q
What is the first immediate vascular reaction in acute inflammation?
A
Rapid transient vasoconstriction of arterioles to reduce blood flow
18
Q
Why is there an initial rapid transient vasoconstriction of arterioles to limit blood flow in acute inflammation?
A
Limit pathogenic spread
19
Q
What is the change in vascular calibre after the initial transient vasoconstriction in acute inflammation?
A
Vasodilation to increase blood flow to capillaries
20
Q
What activates the vasodilation after initial transient vasoconstriction in acute inflammation?
A
Chemical mediators activated
Causes damaged tissues releasing INF and interleukins
- Nitric oxide released
- Dilates vessels
21
Q
What activates the vasodilation after initial transient vasoconstriction in acute inflammation? (4)
A
- Chemical mediators activated
- Causes damaged tissues releasing INF and interleukins
- Nitric oxide released
- Dilates vessels
22
Q
Why is there vasodilation after initial transient vasoconstriction in acute inflammation? (2)
A
- Dilute pathogenic agent
- Increases WBCS locally
23
Q
What changes occur in vascular calibre during acute inflammation?
A
Rapid transient vasoconstriction of arterioles followed by vasodilation
24
Q
What changes occur in blood flow during acute inflammation?
A
Initial reduction of blood flow followed by increased blood flow to capillaries
25
What changes occur in vascular permeability during acute inflammation?
Increased permeability of microvasculature
26
What is the purpose of increased permeability of microvasculature during acute inflammation? (4)
- Blood vessels leak fluid and protein
- Losing protein reduces oncotic pressure in vessels
- Favours fluid movement to interstitium
- Allows migration of WBCs from vessel to interstitium
27
What is exudate? (3)
- Protein rich fluid from plasma (similar protein levels)
- Inflammatory
- Extravascular
28
What is tissue swelling/oedema caused by in acute inflammation? (3)
- Increased hydrostatic pressure
- Decreased osmotic gradient
- Increased fluid in interstitium
29
Is swelling always a sign of inflammation?
No
30
What is the colour of exudate the same colour as?
Plasma
31
What is inflammatory swelling caused by?
Oedema due to accumulation of exudate
32
What is the specific gravity of exudate?
More than 1.020
33
What is non inflammatory swelling caused by?
Oedema due to accumulation of transudate
34
What is transudate? (3)
- Ultrafiltrate of blood
- Low protein
- No inflammatory cells
35
What is the specific gravity of transudate?
Less than 1.012
36
What is transudate swelling often found in and why?
Pregnancy due to increased BP
37
List the cellular events that occur in acute inflammation (3)
- Leucocyte transmigration
- Leucocyte degranulation
- Phagocytosis
38
Why is leucocyte transmigration necessary in acute inflammation?
Leucocytes need to move from circulation to damage site
39
What are the two steps to leucocyte transmigration and degranulation in acute inflammation?
- Extravasation
| - Migration
40
What occurs in extravasation during leucocyte transmigration and degranulation in acute inflammation?
Endothelial cells and leuocytes express mutually recognising adhesion molecules
41
How do leucocytes migrate during leucocyte transmigration and degranulation in acute inflammation? (2)
Leuocytes "roll" from one adhesion molecule to another on endothelium
- Until eventually reach molecule enabling transmembrane WBC movement
42
What allows leucocytes to "roll" loosely during leucocyte transmigration and degranulation in acute inflammation?
Bonds to adhesion molecules are not very strong
43
What ensures leucocytes migrate towards the wound site in leucocyte transmigration and degranulation in acute inflammation? (2)
- More adhesion proteins closer to wound site
| - Follow conc. gradients of chemicals and inflammatory mediators (chemotaxis)
44
Define chemotaxis
Movement of a cell in direction due to gradient of increasing or decreasing concentration of a particular substance
45
What is phagocytosis?
Phagocytes binding to material to ingest in multistep process
46
Give 2 examples of material ingested in phagocytosis
- Bacteria
| - Necrotic tissue
47
What are the steps of phagocytosis? (3)
- Recognition and attachment
- Engulfment
- Killing/degradation
48
How does recognition and attachment occur in phagocytosis? (2)
- Through own cell receptor
| - Molecules released by other cells bound to agent to eliminate
49
How does engulfment occur in phagocytosis?
Pseudopodia surrounds agent producing a vacuole
50
What is the vacuole produced in phagocytosis engulfment called?
Phagosome
51
How does killing/degradation occur in phagocytosis? (2)
- Lysosomal granules fuse with phagosome
| - Activates destruction by releasing chemicals
52
What chemicals are released to activate killing/degradation in phagocytosis?
- Lysozymes
- Proteases
- Hydrolase (oxygen independent)
- Toxic superoxides (oxygen dependant)
53
What are the two types of chemical mediators released in acute inflammation?
- Plasma mediators
| - Cell mediators
54
What occurs when leucocytes reach the inflammation site after transmigration?
Release cytokines (degranulation)
55
What are plasma mediators?
Present in precursor form and need to be activated
56
What are the 3 types of plasma mediator?
- Cogulation system
- Kinin system
- Complement system
57
What are cell mediators?
- Normally sequestered in intracellular granules (released from cells in inflammatory process)
- Synthesised de novo
58
What is the life length of chemical mediators once released from cells and why?
Short lived because inflammatory process should be self contained
59
What are the 3 types of cell mediators?
- Mast cells
- Basophils
- Platelets
60
What is the coagulation system activated by?
Tissue damage
61
What is the end product of the coagulation system?
Fibrin
62
What is the purpose of fibrin in the coagulation system? (2)
- Mesh limiting site of infection in coagulation cascade
| - Provides clot to stop bleeding
63
What is the purpose of thrombin in the coagulation system? (2)
- Increases leukocyte adhesion
| - Increases fibroblast proliferation
64
What reaction does thrombin catalyse?
Degradation of fibrinogen into fibrin
65
What is the purpose of factor Xa in the coagulation system? (3)
- Increases vascular permeability
- Increases leukocyte exudation
- Modulates ability of WBCs to migrate externally
66
What is fibrin degraded to?
Fibrinopeptide
67
What is the purpose of fibrinopeptide? (2)
- Acts as a chemotactic factor for leucocytes
| - Increases endothelial permeability
68
What is a chemotatic factor?
Acts as a chemical stimulus along a concentration gradient, attracting cells to a site of inflammation
69
What overall effect does fibrinopeptide/degradation of fibrin have? (2)
- More cells to damaged site
| - More blood flow to damaged site
70
What is the kinin system activated through?
Coagulation factor XII
71
What is the end product of the kinin system?
Bradykinin
72
What does kinin system cause? (2)
- Vasodilation
| - Triggers pain
73
What is the purpose of the complement system?
- Triggers expression of adhesion molecules on leucocytes
- Components accumulate on surface of pathogenic agent to promote recognition = phagocytosis
- Triggers other cells = intercellular mediator release e.g histamine
74
How many components are there in the complement system?
20
75
What is the complement system activated by?
Foreign substances
76
What are the 3 parts of the complement system?
- Opsonisation
- Binding
- Phagocytosis
77
What is opsonisation?
Invading particle e.g bacteria is identified to the phagocyte
78
List the chemical mediators involved in lysis of microbes (6)
- Membrane attack complex (MAC)
- C5
- C6
- C7
- C8
- C9
79
What chemical mediator acts as an opsonin?
C3b
80
What chemical mediator is a powerful chemotactic agent?
C5a
81
What chemical mediators increase permeability and cause vasodilation through histamine? (3)
- C3a
- C5a
- Anaphylatoxins
82
What hormone causes vasodilation with the aid of chemical mediators?
Histamine
83
What is histamine produced by? (3)
- Mast cells
- Basophils
- Platelets
84
What is histamine released in response to? (4)
- Physical injury
- Trauma
- Cold/heat
- Immune reaction
85
What does histamine increase? (3)
- Arteriole dilation
- Venule vascular permeability
- Activation of inflammatory cascade
86
What are the vasoactive amine chemical mediators of inflammation? (2)
- Histamine
| - Serotonin
87
What is serotonin produced by in inflammation? (2)
- Platelets
| - Enterochromaffin cells
88
What are the actions of serotonin similar to?
Histamine
89
List the chemical cell mediators of inflammation (7)
- Arachidonic acid metabolites
- Cytokines and chemokines
- Nitric oxide
- Platelet activating factor
- Lysosomal constituents of leukocytes
- Oxygen derived free radicals
- Neuropeptides
90
What are arachidonic acid metabolites also known as?
Prostaglandins
91
What is the purpose of arachidonic acid metabolites? (2)
- Arterior dilatation
| - Pain
92
What is the purpose of cytokines and chemokines? (2)
- Increase vascular permeability
| - Chemotaxis
93
What are cytokines and chemokines released by?
Blood cells
94
What does nitric oxide cause?
Vasodilation
95
What is the purpose of platelet activating factor? ()
- Platelet aggregation
- Increased vascular permeability
- Leucoyte activation (+adhesion molecules)
- Chemotaxis
96
What is the purpose of lysosomal constituents of leukocytes?
Phagocytosis
97
What is the purpose of neuropeptides?
Pain
98
List the systemic effects of acute inflammation (7)
- Fever
- Malaise/lethargy/sleppiness
- Pain
- Leucocytosis
- Tissue damage
- Hyperpyrexia
- Shock/Death
99
What 3 chemical mediators released by damaged tissue cause fever in acute inflammation?
- IL1
- IL6
- TNF
100
How do Il1, IL6 and TNF cause fever in acute inflammation?
Release prostaglandins resetting hypothalmic thermostat to increase set point temp
101
What is the purpose of fever in acute inflammation?
Destroys bacteria/virus
102
Why can acute inflammation fever be damaging?
Can increase risk of seizures
103
What drugs are needed to bring down fever in acute inflammation?
Non-steroidal anti-inflammatory drugs (NSAIDs)
104
What is malaise caused by in acute inflammation?
Cytokines affecting brain to reduce counterproductive behaviour
105
What 2 chemical mediators cause pain in acute inflammation?
- Prostaglandins
| - Bradykinin
106
Other than chemical mediators, what causes pain in acute inflammation?
Localised nerve damage
107
What is one of the first signs of acute inflammation?
Leucocytosis
108
What is leucocytosis? (2)
- Colony stimulating factors stimulate release of leucocytes from bone marrow
- Big increase in WBC in blood systemically
109
What 3 chemicals released in acute inflammation cause tissue damage?
- Neutrophil and macrophage lysosomal enzymes
- Oxygen metabolites
- Nitric oxide
110
Why is there often brain damage in acute inflammation?
Swelling in a confined space
111
What causes hyperpyrexia/shock/death in acute inflammation?
Too many cytokines
112
What is hyperpyrexia?
Extreme elevation in body temp (+40c)
113
What are the 4 types of acute inflammation?
- Serous inflammation
- Fibrinous inflammation
- Suppurative inflammation
- Ulcer
114
What does the type of inflammatory response depend on?
The organ
115
What is serous inflammation?
Exudation of transudate into space caused by
- Tissue damage (skin blister)
- Body cavities (effusion)
116
What are the causes of serous inflammation? (3)
- Increased BP
- Reduced oncotic pressure
- Mechanical trauma
117
What is exudation?
Fluid being emitted by organism through wound/pores
118
What is fibrinous inflammation?
Fibrinogen exits blood and accumulates as fibrin in extracellular space
119
What are the 2 causes of fibrinous inflammation?
- Increased vascular permeability
| - Procoagulant stimuli (tumours)
120
What occurs if fibrinolysis is not complete?
Scarring
121
What is purulent inflammation?
Production of pus
122
What does pus in purulent inflammation contain? (4)
- Neutrophils (dead/alive)
- Cellular debris
- Oedema
- Sometimes microorganisms
123
What common infection involves purulent inflammation?
Appendicitus
124
How does appendicitus progress to peritonitus?
If purulent exodate reaches the serosa
125
What is purulent exodate a type of?
Inflammatory infiltrate
126
Label the histology picture of appendicitus
See notes for diagram
127
What is pus a type of?
Inflammatory exudate
128
What is abscess?
Localised collection of pus surrounded by fibrous tissue, confined so can't be drained
129
What is the advantage of abscess?
Normally physiologically protective - contains infection
130
What is the disadvantage of abscess?
Doesn't allow antibiotics to permeate
131
How is abscess treated?
Surgery for drainage and debriment
132
What is debriment?
Removal of damaged tissue/foreign objects from a wound
133
What is empyema?
Pus (exudate) formation in existing body cavity
134
Give 4 examples of body cavities that empyema could occur in
- Pleura
- Joints
- Uterus
- Pericardium
135
Where is pus often found in the skin?
Acne - localised accumulation of pus in the skin
136
When is pus found in the gall bladder?
Cholecystitis (esp. after gall stones)
137
What does the outcome of acute inflammation depend on?
- Type of injury
| - Ability of body to respond
138
What are the 4 non death outcomes of acute inflammation?
- Complete resolution
- Healing by fibrosis
- Abscess formation
- Chronic inflammation
139
What is the advantage of healing by fibrosis?
Puts connective tissue patch on damage, resists further damage
140
What is the disadvantage of healing by fibrosis?
Area no longer functioning
141
In what 2 ways can acute inflammation cause death?
- Severe local damage
| - Uncontrolled infection
142
Give 2 conditions where severe local damage caused by acute inflammation leads to death
- Meningitus
| - Endocarditus
143
How does uncontrolled infection in acute inflammation lead to death?
- Sepsis
| - Shock
