Lecture 3 - Acute Inflammation Flashcards

1
Q

What is Inflammation?

A

The response of living tissue to injury

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2
Q

What is the aim of acute inflammation?

A

Limits damage

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3
Q

What does it mean by referring to acute inflammation as stereotyped?

A

The response is the same regardless of the damage

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4
Q

What is the relative duration of acute inflammation?

A

Short lived

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5
Q

What are the 2 phases of acute inflammation?

A

Vascular Phase
Cellular Phase

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6
Q

Generally, what happens in the vascular phase of inflammation?

A

Change in blood flow and accumulation of exudate

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7
Q

Generally, what happens in the cellular phase of acute inflammation?

A

Delivery of neutrophils

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8
Q

What can cause inflammation?

A

Pretty much anything
Trauma
Micro-organisms
Hypersensitivity

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9
Q

What are the 5 clinical signs of acute inflammation?

A

Rubor
Calor
Tumor
Dolor
Functio laesa

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10
Q

What does Rubor mean?

A

Redness

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11
Q

What is Calor?

A

Heat

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12
Q

What is Tumor?

A

Swelling

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13
Q

What is Dolor?

A

Pain

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14
Q

What is Functio laesa?

A

Loss of function

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15
Q

What are the 3 changes that happen in the Vascular phase?

A

Vasoconstriction
Vasodilatation
Increased permeability

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16
Q

What signs does the vasodilation stage of the vascular phase of acute inflammation cause?

A

Calor
Rubor

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17
Q

What is Starlings Law?

A

The movement of fluid through the blood vessel is controlled by the balance of hydrostatic pressure and oncotic pressure

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18
Q

What is hydrostatic pressure?

A

The pressure exerted on a vessel wall by fluid

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19
Q

What is oncotic pressure?

A

The pressure exerted by proteins trying to draw fluid back into blood vessels.

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20
Q

What happens in the increased permeability stage of acute inflammation?

A

Plasma proteins move into interstital space
Increased interstitial oncotic pressure and decreased capillary oncotic pressure
Fluid is drawn out by the interstitial oncotic pressure and capillary hydrostatic pressure into interstitial space

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21
Q

What affect does the fluid being drawn out of the blood vessels have on the blood in acute inflammation?

A

Increased viscosity
Reduced blood flow through vessel

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22
Q

What is Stasis?

A

When blood flow is reduced/flows more slowly through vessels since its thicker

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23
Q

What is exudate?

A

Protein rich fluid

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24
Q

How is exudate produced?

A

INCREASED VASCULAR PERMEABILITY produces protein rich fluid

Produced in inflammation

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25
What is transudate and when is it produced?
Fluid produced as a result of increased capillary hydrostatic pressure and reduced oncotic pressure VASCULAR PERMEABILITY DOESNT CHANGE
26
What conditions produce transudate?
Heart failure Hepatic failure Renal failure
27
How is transudate produced in heart failure?
Blood pools in blood vessels increasing hydrostatic pressure
28
How is transudate produced in hepatic failure?
Liver responsible for producing plasma proteins Hepatic failure = decreased oncotic pressure
29
What are the 3 ways by which blood vessels increase their permeability?
Endothelial cells retract (become smaller) Direct injury to endothelial cells Leukocyte Dependant injury to endothelial cells
30
What stimulates the retraction of endothelial cells?
Histamines Nitric oxide
31
How is the vascular phase effective to minimise damage?
Fluid in interstital spaces dilutes toxins Exudate delivers proteins (fibrin- mesh limits spread of toxin)
32
Where does the fluid released into the interstitial space drain to?
Lymph nodes
33
What is the main white blood cell involved in acute inflammation?
Neutrophil
34
What is a key feature of a neutrophil?
Tri-lobular nucleus
35
What affect does stasis have on the blood cells in the vessel?
Margination
36
What is margination?
When the cells migrate to the borders of the blood vessels
37
What are the 4 steps to neutrophils escaping vessels?
Margination Rolling Adhesion Emigration
38
What is another word for emigration?
Diapedesis
39
What are the 2 adhesion molecules important in the migration of neutrophils from blood vessels?
Selectins Integrins
40
Which adhesion molecules are responsible for rolling of neutrophils?
Selectins
41
What is the strength of the bonds formed between the Selectins on the endothelial cells and the neutrophils?
Weak bonds
42
Where are Integrins located?
Surface of neutrophil
43
What is the function of Integrins on neutrophils?
Adhesion when they are in the high affinity state
44
What is chemotaxis?
The movement of cells along an increasing chemical gradient of chemoattractants
45
Give some examples of chemical attractants:
Bacterial peptides Inflammatory mediators
46
What do neutrophils do?
Phagocytosis Release inflammatory mediators
47
Briefly describe how a neutrophil phagocytoses a pathogen:
Cytoplasm extends around pathogen Forms phagosome Lysosome fuses with phagosome forming phagolysosome Phagolysosome digests pathogen
48
How do neutrophils know what to target and destroy?
Pathogen covered in markers/labels called opsonins
49
What is opsoninisation?
When a pathogen is labelled by proteins for destruction
50
What are 2 examples of opsonins?
Fc (antibody) C3b (complement protein made as part of innate immunity) What produces complement proteins like C3b? Liver
51
What is the cellular phase?
The migration of neutrophils into the interstitsium and destroying the opsoninised pathogens
52
How is the cellular phase effective?
REMOVES: Pathogens Necrotic tissue RELEASES: Inflammatory Mediators
53
What are inflammatory mediators?
Chemical messengers that control and coordinate the inflammatory response
54
What inflammatory mediators trigger vasodilation?
Histamine Serotonin Prostaglandins
55
What inflammatory mediators trigger increased vascular permeability?
Histamine Bradykinin
56
What inflammatory mediators are chemoattractants triggering chemotaxis?
C5a IL-1 Bacterial peptides
57
What inflammatory mediators cause fever?
Prostaglandins IL-1 IL-6
58
What inflammatory mediators cause pain?
Bradykinin Prostaglandins Substance P
59
What are the 2 types of complications of acute inflammation?
Local Systemic
60
What is meant by a local complication?
Specific to 1 anatomical area
61
What is meant by a systemic complication?
Affecting the whole body
62
Why can acute inflammation cause acute local complications?
Swelling my compress tubes like airways/ intestines
63
Give an example of an acute inflammation that would restrict breathing:
Epiglottitis (Epiglottis)
64
How can acute inflammation cause cardiac tamponade?
Acute inflammation of pericardial sac will cause exudate to accumulate in pericardial space compressing the heart
65
Why do burns cause rapid dehydration?
Acute inflammation of area causes lots of exudate to be produced Exudate will be directly exposed to air so will rapidly evaporate
66
What is essential when treating a burns patient?
Aggressive IV rehydration
67
What are pyrogens?
Type of inflammatory mediator that act on the hypothalamus to alter the body’s temperature/thermostat
68
What are NSAIDS?
Non-steroidal Anti Inflammatory Drugs
69
What is a common systemic complication of acute inflammation? Why does this happen?
Fever Neutrophils produce pyrogens as an inflammatory mediator which go to the hypothalamus leading to the base thermostat being increased
70
What is the function of NSAIDs?
Reduce fever, pain and inflammation
71
How do NSAIDs reduce fever, inflammation and pain?
Stop production of Prostaglandins Block Cox enzymes needed for their production
72
What is Leucocytosis?
Increased production of white blood cells
73
How is Leucocytosis a systemic complication of acute inflammation?
Inflammatory mediators act on bone marrow (IL-1)
74
Which white blood cell is going to be elevated in a bacterial infection?
Neutrophils
75
Which white blood cell is going to be elevated in a viral infection?
Lymphocytes
76
What is the Acute phase response?
Series of vague signs and symptoms indicating infection, inflammation or trauma
77
What are the acute phase response signs/symptoms?
Malaise Reduced appetite Altered sleep Tachycardia
78
What are the acute phase proteins?
C-Reactive protein Fibrinogen
79
What is CRP used for in hospitals?
Tested as a marker of severity of acute inflammation/infection
80
What happens in septic shock?
Huge release of chemical mediators Widespread vasodilation Hypotension (BP drops as TPR drops) Multiple organ failure due to poor perfusion of organs
81
What happens after acute inflammation has been completely resolved? In terms of the: -Inflammatory mediators -vessel permeability -neutrophils -exudate
Mediators have short half life so degrade Vessel permeability back to normal Neutrophils undergo apoptosis and get phagocytose Exudate drained to lymphatics
82
What happens if substantial tissue damage has occured following acute inflammation?
FIBROSIS (Repair with connective tissue)
83
Where is the appendix?
Hangs of caecum which is a part of the large intestine of the right side of the body
84
How does appendicitis usually occur?
Lumen of appendix blocked by fecal matter (Faecolith) Bacteria accumulate and so does exudate
85
What are the concerns with appendicitis?
The increased pressure due tot build up of exudate and bacteria may lead to the burst of the appendix exposing contents of large intestine to abdomen
86
What organisms can cause Pneumonia?
Streptococcus pneumoniae Haemophilus influenzae
87
What is the normal process for pneumonia?
Infection of lungs Lungs fill with fluid (exudate) following inflammation
88
What are the signs and symptoms of Pneumonia?
Shortness of breath (Dyspnoae) Cough Sputum Fever
89
What are the risk factors for pneumonia?
Smoking Pre-existing lung condition (COPD, asthma, malignancy)
90
What occurs in bacterial meningitis?
Inflammation of the meninges
91
What are the meninges?
The protective layer between the brain and the skull
92
What are the signs and symptoms of bacterial meningitis?
Headache Neck stiffness (meninges on spinal cord) Photophobia Altered mental state
93
What is an abscess?
An accumulation of dead and dying neutrophils
94
Why are abscesses associated with liquefactive necrosis?
The neutrophils release all of their enzymes
95
What are the 3 serous cavities of the body? 3Ps
Pleural space Peritoneal space Pericardial space
96
What is accumulation of fluid (exudate) in the abdomen called?
Ascites
97
With a patient with pleura effusion, why would you test the fluid?
To check for exudate (protein rich) to see if acute inflammation is happening
98
What are some rare disorders of acute inflammation?
Hereditary angio-oedema Chronic granulomatous disease Alpha-1 antitrypsin deficiency
99
What is Alpha-1 antitrypsin deficiency? How does it present?
Low levels of alpha-1 antitrypsin Bad since it inhibits proteases released by neutrophils at tissues If absent the proteases can breakdown self tissues like in the lungs Emphysema and liver cirrhosis
100
How does Hereditary angio-oedema present?
Cutaneous anti-oedema Recurrent abdominal pain
101
If a patient has Haemoptysis and chest pain, what sort of diseases must be considered?
TB (Tuberculosis) Lung cancer
102
What is sarcoidosis? How does it present?
Condition where bodies immune system over reacts Enlarged lymph nodes Granulomas
103
How are prostaglandins produced?
From cell membrane phospholipids