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Session 2 Flashcards

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1
Q

What is acute inflammation?

A

The response of living tissue to injury

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2
Q

What are some characteristics of acute inflammation?

A

Innate
Stereotyped
Immediate/Early
Short Duration (mins, hours, days)

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3
Q

Acute inflammation is controlled by…

A

Chemical mediators

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4
Q

Acute inflammation serves to limit…

A

The tissue damage

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5
Q

Give 5 causes of acute inflammation

A 
Microbial infections 
Hypersensitivity reactions 
Physical agents (e.g. Heat, light, radiation)
Chemicals 
Tissue necrosis
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6
Q

What are 5 clinical features of acute inflammation?

A 
Rubor 
Tumour
Calor 
Dolor
Loss of function
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7
Q

What is rubor?

A

Redness

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8
Q

What is tumour?

A

Swelling

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9
Q

What is calor?

A

Heat

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10
Q

What is dolor?

A

Pain

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11
Q

Acute inflammation involves which 3 changes in tissues?

A

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

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12
Q

Describe the changes in blood flow seen in acute inflammation with regards to the size of the arterial/capillary lumen

A

Initially vasoconstriction of arterioles

Then vasodilation of arterioles and then capillaries

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13
Q

How long does the initial transient vasoconstriction of arterioles in acute inflammation last for?

A

First few seconds of acute inflammation

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14
Q

Vasodilation of arterioles and capillaries contributes to which symptoms of acute inflammation?

A

Calor

Rubor

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15
Q

How is the permeability of blood vessels affected in acute inflammation? What consequences does this have? What happens to the viscosity of the blood as a result of this?

A

Increased permeability

Exudation of protein rich fluid into tissues and tumour seen

Increased viscosity

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16
Q

Name an immediate early response chemical mediator seen in acute inflammation

A

Histamine

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17
Q

When does histamine begin its action in acute inflammation? Histamine is produced from which cells?

A

Immediately (first 30 mins)

Mast cells, basophils and platelets

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18
Q

Name 3 things that histamine causes…

A

Vascular dilatation
Increase in vascular permeability
Pain

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19
Q

Name some other chemical mediators of acute inflammation?

A

Leukotrienes, bradykinin

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20
Q

Fluid loss from vessels is determined by ___________ law - the balance of __________ and ___________ __________ pressures.

A

Starling’s

Hydrostatic
Colloid Osmotic

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21
Q

What effect will increased hydrostatic pressure in a vessel have on fluid flow to tissues?

What effect will increase colloid osmotic pressure in the interstitial have on fluid flow to tissues?

A

Increased fluid flow out of vessels

Increased fluid flow out of vessels

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22
Q

How does arteriolar dilatation seen in acute inflammation affect hydrostatic pressure in capillaries?

How does increased permeability of vessel walls seen in acute inflammation affect the protein content of the interstitial fluid?

What consequence can both of these factors result in?

A

Increased

Increased protein content (colloid osmotic pressure)

OEDEMA

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23
Q

The fluid in oedema can be either…

A

Transudate

Exudate

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24
Q

What is a transudate? What is an exudate?

Give an example of where each is seen.

A

Fluid in oedema that has the same protein content as plasma
Cardiac failure

Fluid in oedema that has a higher protein content than plasma
Only in inflammation

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25
How does oedema affect lymphatic drainage?
Results in increased lymphatic drainage
26
Give 5 mechanisms by which vessels can become 'leaky'
``` Contraction of endothelial cells Cytoskeletal reorganisation Direct injury - e.g. Sunburn, chemicals Leukocyte dependent injury Increased transcytosis ```
27
How does contraction of endothelial cells and cytoskeletal reorganisation result in leaky vessels? Give an example of a chemical that causes contraction of endothelial cells Give an example of a chemical that causes cytoskeletal reorganisation
Leads to gaps in the walls of vessels Histamine, leukotrienes Cytokines IL-1 and TNF
28
How does leukocyte dependent injury make blood vessels leaky?
Leukocyte produce toxic oxygen species and enzymes which damage the vessels
29
Give an example of a chemical that results in increased transcytosis?
VEGF
30
What is an important protein component of the protein rich exudate seen in acute inflammation?
Fibrin
31
What is the role of fibrin in the protein rich exudate seen in acute inflammation? Where is this particularly important?
Forms a sticky meshwork to localise inflammation Serosal surfaces - e.g. Pleural cavity, pericardium - so whole cavity isn't filled with fluid
32
What is another term for a neutrophil? What is the appearance of these cells under the microscope?
Polymorph Come in multiple shapes with multi-lobed nuclei
33
What type of blood cell is a neutrophil?
White blood cell - type of granulocyte
34
What is a granulocyte?
A WBC with secretory granules in its cytoplasm
35
What is the main inflammatory cell?
Neutrophil
36
How do neutrophils get from within blood vessels to tissues to combat acute inflammation? (4 step process)
Margination Rolling Adhesion Emigration
37
Describe the margination process of neutrophils
Stasis causes neutrophils to line up at the edge of blood vessels along the endothelium
38
What happens to neutrophils after their margination around a blood vessel?
Rolling - roll along the endothelium, sticking to it intermittently Adhesion - stick more avidly Emigration of neutrophils into the tissue through the vessel wall
39
What two things make it possible for the emigration of neutrophils through the blood vessel wall?
Relaxation of inter-endothelial junctions | Digestion of the vascular basement membrane
40
How doe neutrophils move once inside the tissues?
By chemotaxis
41
What is chemotaxis?
Movement along concentration gradients of chemoattractants
42
Give 3 examples of chemotaxins for neutrophils? How do they work?
C5a LTB4 Bacterial peptides They bind to receptors on the neutrophils, resulting in rearrangement of cytoskeleton, production of pseudopod and movement.
43
What do neutrophils do once in the tissue?
Primarily phagocytosis
44
How are microorganisms recognised by neutrophils for phagocytosis?
Through the action of opsonins
45
Give an example of an opsonin
C3B | Fc (fixed component of antibodies)
46
Internalisation of a microorganism during phagocytosis is a result of what changes in the cell?
Changes to the cell cytoskeleton
47
How is a secondary lysosome formed?
Fusion of phagosome with lysosome
48
Phagocytosis can take place in neutrophils by which two mechanisms?
Oxygen dependent Oxygen independent
49
How does the oxygen dependent mechanism of phagocytosis in neutrophils work?
Produces superoxide and hydrogen peroxide | Produces HOCl*
50
How does the oxygen independent mechanism of phagocytosis in neutrophils work?
Enzymes such as lysozyme and hydrolases Bactericidal permeability increasing protein (BPI) Cationic proteins
51
What are some chemical mediators of acute inflammation, excluding neutrophils?
Proteases Prostaglandins Leukotrienes Cytokines
52
Where are proteases produced?
In the liver
53
Prostaglandins and leukotrienes are both metabolites of...
Arachidonic acid
54
Which cells produce chemokines/cytokines? Give an example of a cytokine/chemical?
WBCs Interleukins, TNF-a
55
What chemical mediators result in increased blood flow in vessels?
Histamine | Prostaglandins
56
Which chemical mediators result in increased vascular permeability?
Histamine | Leukotrienes
57
Which chemical mediators are important in neutrophil chemotaxis?
C5a, LTB4, bacterial peptides
58
What are some important chemicals for opsonisation?
C3B, Fc
59
How does exudation of fluid combat injury? (3)
Delivers plasma proteins (e.g. Inflammatory mediators) to area of injury Dilutes toxins Increases lymphatic drainage
60
How does increased lymphatic drainage as a result of exudation of fluid combat injury?
It delivers microorganisms to phagocytes and antigens to the immune system
61
How does infiltration of cells in acute inflammation combat injury?
Removes pathogenic organisms and necrotic debris
62
How does vasodilation in acute inflammation help combat injury?
Increases delivery to the area and increases temperature
63
How does pain and loss of function in acute inflammation combat injury?
Enforces rest and reduces chance of further traumatic damage
64
What complications can result due to the swelling seen in acute inflammation?
Blockage of tubes - e.g. Bile ducts/small intestine
65
What complications can result due to the exudate seen in acute inflammation?
Compression - e.g. Cardiac tamponade
66
In what instances of acute inflammation is fluid lost from the body?
Burns
67
What are some systemic consequences of acute inflammation?
``` Fever Leukocytosis Acute phase response Changes in plasma concentration of acute phase proteins Shock ```
68
What causes fever in acute inflammation?
Production of endogenous pyrogens e.g. IL-1 and TNF-a
69
Give an example of an endogenous pyrogen? Which household drug can be given to reduce fever?
IL-1, TNF-a, prostaglandins Aspirin
70
What is leukocytosis?
A high WBC level in FBC
71
Bacterial infections are associated particularly with which types of WBC? Viral infections are more associated with...
Neutrophils Lymphocytes
72
What causes the leukocytosis commonly seen in acute inflammation?
IL-1 and TNF-a which produce an accelerated release of WBCs from marrow
73
What are features of the acute phase response?
Decreased appetite Raised pulse rate Altered sleep patterns
74
Give an example of two acute phase proteins whose concentration changes in acute inflammation?
CRP | Fibrinogen
75
What is shock? What causes it?
A clinical syndrome of systemic circulatory failure The spread of microorganisms and toxins in the body
76
What are 4 different outcomes after the development of acute inflammation?
Complete resolution Continued acute inflammations with chronic inflammation Chronic inflammation and fibrous repair Death
77
What happens to the exudate in resolution from acute inflammation? What happens to vessel permeability? What happens to fibrin produced? What happens to the neutrophils?
Drains into lymphatics Returns to normal Degraded by plasmin Die, break up and carried away or phagocytosed
78
Describe the half-life of mediators of acute inflammation?
Short half lives
79
Bacterial meningitis can cause vascular __________ and reduce cerebral ____________ What part of the body does it affect?
Thrombosis Perfusion Meninges of the brain
80
What is the causative organism for lobar pneumonia? List some symptoms. Can it be resolved?
Streptococcus pneumoniae Worsening fever, dry cough, hypoxaemia, breathlessness Yes completely if treated
81
Why does the exudate seen in skin blisters appear relatively clear? What can cause skin blisters?
Inflammatory cell levels are low Heat, sunlight, chemicals
82
What are two other terms for an autopsy? Name three types of autopsy.
Post-mortem Necropsy Medicolegal Forensic Consent
83
For which type of autopsies is no consent required?
Medicolegal | Forensic
84
Name 4 parts of the body that are common causes of sudden death.
Head Heart Blood vessels Lungs
85
What is involved in an autopsy? (3)
History External examination Internal examination

Pathological Processes (10 decks)

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