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MoD Session 2 Flashcards

0
Q

Why is acute inflammation initiated?

A

To limit tissue damage

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1
Q

What is acute inflammation?

A

Response of living tissue to injury

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2
Q

What characterises acute inflammation?

A

Innate
Immediate
Early
Stereotyped

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3
Q

How long does acute inflammation last?

A

Mins to a few days

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4
Q

How does the reaction of acute inflammation to a stimulus vary?

A

It does not, it is the same irrespective of frequency

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5
Q

What causes the accumulation of fluid exudate and neutrophils in tissues in acute inflammation?

A

Vascular and cellular reactions

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6
Q

What controls acute inflammation and is derived mostly from plasma cells?

A

Variety of chemical mediators

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7
Q

Even though acute inflammation is protective, what can it lead to?

A

Local complications

Systemic effects

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8
Q

What can cause acute inflammation?

A

Chemicals
Any tissue damage
Microbial infections by pyogenic organisms
Acute phase of hypersensitivity reactions
Physical agents

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9
Q

What are the five cardinal signs of acute inflammation?

A 
Redness
Swelling
Heat
Pain
Loss of function
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10
Q

Why is function lost in acute inflammation?

A

To prevent further damage

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11
Q

What are the 3 changes to tissues seen in acute inflammation?

A

Changes in blood flow
Exudation of fluid into tissues
Infiltration of inflammatory cells

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12
Q

What controls each of the three changes to tissues in acute inflammation?

A

Mediators for each step

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13
Q

How is blood flow increased in the vascular phase of acute inflammation?

A

Transient vasoconstriction of arterioles followed by vasodilatation of arterioles then capillaries

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14
Q

What changes do the increase in bloodflow seen in acute inflammation cause?

A

Heat

Redness

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15
Q

What are the effects of increasing BV permeability in the vascular phase of acute inflammation?

A

Exudation of protein-rich fluid into tissues

Slowing of circulation due to thicker blood from fluid loss to tissues

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16
Q

Why is stasis of blood seen in the vascular phase of acute inflammation?

A

Increased concentration of RBC in small vessels

Increased blood viscosity

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17
Q

What type of granulocyte/polymorphonuclear leucocyte is the primary type of WBCS involved in inflammation?

A

Neutrophils leucocytes

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18
Q

How is tissue oedema seen histiologically?

A

Pale neutrophils due to high fluid content

Margination and emigration of neutrophils visible

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19
Q

What determines the exudation of fluid into tissues?

A

Balance of hydrostatic and colloid osmotic pressure

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20
Q

What two pressure changes cause fluid to move out of the BV?

A

Increase hydrostatic pressure

Increase oncotic pressure of intersticium

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21
Q

Why does arteriolar dilatation increase hydrostatic pressure?

A

Lack of resistance to blood flow

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22
Q

What can cause pathological exudation of fluid into tissues?

A

Heart failure

Inflammation

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23
Q

What mechanisms of vascular leakage can be used?

A 
Endothelial contraction
Cytoskeletal reorganisation 
Direct injury
Leukocyte dependent injury
Increased transcytosis
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24
What causes endothelial contraction?
Histamine and leukotrienes
25
What mediators are used in cytoskeletal reorganisation?
IL-1 | TNF
26
What is leukocyte dependent injury?
When inflammatory response causes tissue injury itself
27
What causes damage in leukocyte dependent injury?
Toxic oxygen species | Leucocyte enzymes
28
What is transcytosis?
Channels across endothelial cytoplasm not visible by light microscopy
29
What increases transcytosis?
Vascular endothelial growth factor - VEGF
30
Why are plasma proteins delivered to the site of injury in the vascular phase of acute inflammation?
Fibrin localises injury and prevents fluid loss
31
How is delivery of plasma proteins to site of injury in acute inflammation mediated?
Chemotactic FDPs
32
How long do chemical mediators take before they mount a response in the vascular phase of acute inflammation?
1/2 hour
33
What mediates the very early steps of acute inflammation and causes its symptoms?
Histamine
34
Where is histamine released from?
Mast cells Basophils Platelets
35
What stimuli can cause histamine release?
``` Trauma Immunologic reactions C3a, C5a IL-1 Neutrophils and platelet factors ```
36
What action does histamine have?
Acts in receptors in BV wall to cause vascular dilation causing transient increase in vascular permeability and pain
37
What effect does persistent response have on mediators (which is incompletely understood)?
Interlinks mediators | Histamine thought to interlink w/leukotrienes and bradykinin
38
What is neutrophil margination?
Neutrophils line up at the edge of the BV along the endothelium
39
How is neutrophil rolling achieved?
Neutrophils intermittently stick to endothelium whilst rolling
40
What is the name given to different receptors allowing neutrophils to stick during their infiltration?
Adhesion
41
What is neutrophil emigration?
Movement through BV wall
42
How does cell movement alter when blood velocity decreases?
Cells move towards endothelial edge
43
What do surface ligands bind to in the rolling phase of neutrophils migration?
Endothelial receptors Selectins sLc^x
44
What do neutrophils bind to in primary adhesion in neutrophil migration?
Integrins lCAM1 VAM MAdCAM
45
Which molecules are used in stable adhesion and aggregation in neutrophil migration?
Integrins PECAMI lCAM1
46
How are neutrophils found outside BV in neutrophil migration?
Transendothelial migration --> extravasation
47
How do neutrophils escape from vessels in the cellular phase of acute inflammation?
Relaxation of endothelial cell junctions Enzymatic digestion of vascular BM Neutrophils change shape to fit through vessels
48
How do neutrophils move?
Diapedesis and emigration by chemotaxis
49
What is chemotaxis?
Movement along a concentration gradient of chemoattractants
50
What attract receptor-binding ligands causing a rearrangement of the cytoskeleton leading to the production of a pseudopod?
Chemotaxins: C5a LTB4 Bacterial peptides
51
Describe the process of phagocytosis in the cellular phase of acute inflammation.
Contact --> recognition --> internalisation
52
What is phagocytosis facilitated by?
Opsonins Non-specific fixed component of antibodies C3b
53
How are secondary lysosomes formed in phagocytosis?
Cytoskeletal changes occur allowing phagosomes to fuse with lysosomes
54
What is oedema?
Increase in fluid in intersticium of any cause
55
What change does oedema cause to the lymphatic system?
Increases drainage
56
What are the two types of oedema?
Transudate | Exudate
57
What causes transudate oedema?
Cardiac failure Venous outflow obstruction Arterial dilation removing resistance Sluggish flow at venules --> high hydrostatic pressure
58
What characterises exudate oedema?
High protein content
59
What mechanism causes exudate oedema?
Leaky membrane --> increase capillary hydrostatic pressure due to arterial dilatation and oncotic pressure
60
What pathology can cause exudate formation?
Cancers | Inflammation
61
Which type of killing mechanism is the most efficient?
Oxygen dependent
62
What do oxygen dependent killing mechanisms produce?
Superoxide | Hydrogen peroxide
63
Which proteins are used in oxygen independent killing mechanisms?
Lysozyme Cationic proteins - defensins Bactericidal permeability increasing protein (BPI) Hydrolases
64
How do neutrophils cause host tissue damage?
Migrate to site of injury by chemotaxis --> phagocytose microorganisms --> may release toxic metabolites and enzymes
65
What molecules are chemical mediators of acute inflammation?
Cytokines/chemokines Prostaglandins/leukotrienes Proteases
66
How do cytokines/chemokines mediate acute inflammation?
TNF-alpha and interleukins are produced by WBCs for communication
67
Which chemical mediators act on neutrophil chemotaxis?
Bacterial peptides C5a Leukotriene B4
68
Which chemical mediators of acute inflammation act on phagocytosis?
C3b
69
Which chemical mediators of acute inflammation act to increase blood flow?
Prostaglandins | Histamine
70
Which chemical mediators of acute inflammation act on vascular permeability?
Histamine | Leukotrienes
71
Which proteases mediate acute inflammation?
Kinins Complement system - C3a/C5a Generally plasma proteins produced in liver Coagulation/fibrinolytic system
72
How are prostaglandins/leukotrienes formed?
Metabolites of arachidonic acid formed from tissue phospholipids
73
What does leukotriene B4 do to mediate acute inflammation?
Recruits and activates neutrophils, monocytes and eosinophils Can prolong inflammation
74
What is the hallmark of acute inflammation?
Exudate of fluid and infiltration of cells
75
How does exudation of fluid combat injury in acute inflammation?
Delivers plasma proteins, immunoglobulins, inflammatory mediators and fibrinogen to site of injury Dilutes toxins, increases lymphatic drainage, delivers microorganisms to phagocytes and antigens to lymph nodes
76
How does infiltration of cells combat injury in acute inflammation?
Removes pathogenic organisms and necrotic debris
77
What order do cells infiltrate in acute inflammation?
Neutrophils followed by macrophages
78
How does vasodilatation combat injury in acute inflammation?
Increases delivery and temperature to give a more efficient response
79
How does pain and loss of function in acute inflammation help combat injury?
Enforces rest and reduces the chance of further traumatic damage
80
What are local complications of acute inflammation?
Swelling Exudate Loss of fluid Pain and loss of function
81
How does swelling caused by acute inflammation cause complication?
Blockage of tube e.g. Bile duct, intestine, epiglottis in children
82
What determines the significance of response in exudate formation in acute inflammation?
Site
83
At what point does appendix inflammation need rapid treatment?
When perforation of the appendix causes peritonitis which will be fatal if not treated
84
When can exudate production be dangerous to the heart?
If it causes compression e.g. in cardiac tamponade
85
What causes circulatory failure due to lack of fluid in vessels from vasodilation and exudation?
Failure of initial inflammatory reaction to localise cause leading to acute phase response and subsequent spread of micro-organisms and toxins
86
What are systemic effects of acute inflammation?
Fever Leukocytosis Acute phase response
87
What causes fever in acute inflammation?
Endogenous pyrogens IL-1, TNF-alpha, and prostaglandins turn up thermostat in hypothalamus
88
How does acute inflammation cause leukocytosis?
IL-1 and TNF-alpha stimulate WBC release --> macrophages and T-lymphocytes produce CSF
89
How are viral and bacterial leukocytosis differentiated?
``` Bacterial = neutrophils Viral = lymphocytes ```
90
What is the acute phase response?
Decreased appetite Increased pulse Altered sleep patterns Changes in plasma concentration of: CRP, alpha 1-antitrypsin, haptoglobin, fibrinogen, serum amyloid A protein
91
What are the four acute inflammation sequelae?
Complete resolution Continued acute inflammation w/chronic inflammation causing abcess - effectively walled off and needs extra input to overcome Chronic inflammation and fibrous repair probably w/tissue regeneration Death
92
What happens to changes that have occurred gradually during acute inflammation?
They reverse
93
What takes place during resolution of acute inflammation?
Vascular changes stop Neutrophils no longer marginate Vessel permeability returns to normal Vessel calibre returns to normal
94
What happens to exudate formed by acute inflammation upon resolution?
Drains into lympahtics
95
What thrombolytic process occurs during resolution of acute inflammation?
Fibrin degraded by plasmin and proteases
96
What happens to neutrophils upon resolution of acute inflammation?
Die --> break up --> carried away/phagocytosed
97
What must happen for damaged tissue to be regenerated in resolution of acute inflammation?
Tissue architecture not destroyed
98
Which acute inflammation resolution mechanisms may be unstable?
Some arachidonic acid derivatives, esp. prostaglandins
99
Which inhibitors may bind to allow resolution of acute inflammation?
Various anti-proteases
100
Which specific inhibitors of acute inflammatory changes are used in acute inflammation resolution?
Endothelin | Lipoxins
101
What may inactivate mechanisms to resolve acute inflammation?
Degradation e.g. by heparhase
102
What common feature do all mediators of acute inflammation resolution share?
Short half life
103
What mechanism of acute inflammation resolution may be diluted in the exudate?
Fibrin degradation products
104
Give four clinical examples of acute inflammation.
Bacterial meningitis Lobar pneumonia Skin blister Abscess
105
Why can bacterial meningitis cause vascular thrombosis and reduce cerebral perfusion?
All BV to the brain transverse meninges so can be compromised by inflammation
106
What accumulates in bacterial meningitis?
Pus
107
What causes lobar pneumonia?
Streptococcus pneumoniae (pneumococcus) causes alveoli to contain exudate instead of air
108
What are the S/S of lobar pneumonia?
``` Worsening fever Prostration Hypoxaemia over a few days Dry cough Breathlessness ```
109
What is prostration?
No energy to get up
110
What can cause a skin blister?
Heat Sunlight Chemicals
111
What are the predominant features of a skin blister?
Pain due to high sensory function | Profuse exudate which can lead to large loss of fluid
112
What causes the overlying epithelium in a skin blister to strip off?
Collection of fluid
113
In what circumstance would the exudate of a skin blister not appear clear?
If bacterial infection develops due to few inflammatory cells
114
What are the sequelae of skin blisters?
Resolved | Scarring
115
Where are abscesses usually found?
In solid tissues
116
How do abscesses form?
Inflammatory exudate forces tissues apart w/liquefactive necrosis in the centre forming pus
117
Why do abscesses cause lots of pain?
They can cause high pressure
118
What can abscesses do to surrounding tissue?
Cause damage | Squash adjacent structures
119
What alternative treatment can be better than antibiotics in some cases when treating an abscess?
Surgery
120
How does acute inflammation in serous cavities cause ascites, pleural or pericardial effusion?
Exudate pours into the cavity
121
What can acute inflammation in serous cavities cause?
Respiratory of cardiac impairment | Localised fibrin deposition --> 'bread and butter' pericarditis
122
Why are disorders of acute inflammation rare?
Natural selection
123
Give four examples of acute inflammation disorders.
Hereditary angio-oedema (angioneurotic oedema) Alpha-1 antitrypsin deficiency Inherited complement deficiencies Defects in neutrophil function or numbers
124
What does hereditary angio-oedema predispose patients to?
Airway swelling
125
Which disorder of acute inflammation causes repeated infections?
Alpha-1 antitrypsin deficiency

Semester 2 (45 decks)

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