Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathological Processes > Session 2 - Inflammation > Flashcards

Session 2 - Inflammation Flashcards

1
Q

What are the causes of inflammation?

A

Trauma
Hypersensitivity
Micro organisms
Other illnesses induce inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the 5 clinical signs of inflammation?

A 
Rubor - redness
Calor - heat
Tumour - swelling 
Dolor - Pain 
Loss of function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What happens in the vascular phase of inflammation?

A
  1. Vasoconstriction (seconds)
  2. Vasodilation (minutes), causing heat and redness
  3. Permeability increase, causing oedema
  4. Red cell stasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is Starlings Law?

A

Fluid movement controlled by balance between hydrostatic pressure (on vessel wall by fluid) and oncotic pressure (pressure exerted by plasma protein).
These pressures exist in the vessels and the interstitium.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What happens to Starlings Law during inflammation?

A

Vasodilation. - increased hydrostatic pressure in capillary.
More vessel permeability - Loss of plasma proteins into interstitium, increased interstitial oncotic pressure.
Causes tumour - oedema.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Why does stasis occur?

A

Movement of fluid out of the vessel, increases the viscosity of blood so reduced flow through vessel.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the two types of interstitial fluid?

A

Exudate - Occurs in inflammation, occurs due to increased vascular permeability so it is protein rich.
Transudate - Fluid loss due to increased capillary hydrostatic pressure or reduced capillary oncotic pressure. No change of vascular permeability.
- Occurs in heart failure/hepatic/renal failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the 4 mechanisms of increased vascular permeability?

A
  1. Endothelial contraction
  2. Endothelial cytoskeleton reorganisation
  3. Direct injury eg chemical, toxic burns
  4. Leucocyte dependent injury

Not f8nished

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the primary cell involved in the cellular phase?

Appearance?

A

Neutrophil - granulocyte, trilobed nucleus, eosinophilic.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How do neutrophils escape vessels?

A
  1. Margination - Statis causes neutrophils to line up at endothelium
  2. Rolling - Neutrophils roll along endothelium
  3. Adhesion - to endothelium
  4. Emigration - through blood vessel wall by diapedesis (collagenase digests basement membrane)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How to neutrophils adhere to endothelium?

A
  1. Selectins - endothelial surface, upregulated by chemical mediators.
  2. Integrins - On neutrophil surface, bind to receptors on endothelial surface. Can be made high affinity upon binding.
    Integrins bind to selectins.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How do neutrophils move through the interstitium?

A

Chemotaxis - Move along a chemical gradient of chemoattractants.
Eg Bacterial peptides
Neutrophil cytoskeleton changes and produces pseudopod towards the area.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How to neutrophils recognise what they should be phagocytosing?

A

Opsonisation
Toxin covered with C3b and Fc (opsonins)
Receptors for the opsonins on neutrophil surface.
If bacteria has been encountered before, IgG is used as the opsonin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does oedema limit damage?

A
  1. Dilutes toxins
  2. Delivers plasma proteins to area of injury eg fibrin mesh limits spread of toxin, immunoglobulins
  3. Increased lymphatic drainage to deliver antigens to lymph nodes, inducing adaptive immune response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Why are neutrophils beneficial?

A
  1. Removal of toxins and pathogenic organisms
  2. Removal of necrotic tissue
  3. Release of chemical mediators stimulates and regulates further inflammation
  4. Stimulates pain to limit risk of further damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the local complications of inflammation?

A
  1. Swelling - blockage of nearby tubes and ducts (intestines/bile duct)
  2. Compression of organs (pericarditis causes cardiac tamponade)
  3. Loss of fluid eg in burns
  4. Pain and loss of function eg muscle atrophy
17
Q

What are the systemic complications of inflammation?

A

Fever - Endogenous pyrogens act on hypothalamus to alter baseline temperature control
NSAIDs - Non steroidal anti inflammatory drugs block production of prostaglandins (important pyrogens)
Leucocytosis - More WBC’s by IL-1 and TNF, useful to measure blood vessels
Acute phase response - CRP from inflammatory cells increases - malaise, reduced appetite, altered sleep, tachycardia

18
Q

What is septic shock?

A

Widespread vasodilation due to an overwhelming infection. Huge release of chemical mediators.
Causes hypotension and tachycardia, multiple organ failure then death
Can be due to endotoxins produced by bacterial cells.

19
Q

What happens after acute inflammation?

A
  1. Complete resolution
  2. Continuation causing chronic inflammation, abscess
  3. Chronic inflammation and fibrous repair, some tissue degradation
  4. Death
20
Q

How does complete resolution occur?

A

All changes reverse - no margination of neutrophils, permeability and vessel calibre back to normal.

  1. Exudate drains away via lymphatics
  2. Fibrin degrades
  3. Neutrophils die, break up and get phagocytosed
  4. Damaged tissue regenerated
  5. Mediators are diluted/degraded
21
Q

What are 5 features of acute inflammation?

A
  1. Immediate
  2. Short duration
  3. Innate
  4. Stereotyped
  5. Limits damage
22
Q

What do neutrophils do?

A

Phagocytose pathogen and fuse with lysosomes, produce secondary phagolysosomes.

23
Q

What chemical mediators cause vasodilation?

A

Histamine
Serotonin
Prostaglandins
Nitrous Oxide

24
Q

What chemical mediators cause increase vascular permeability

A

Histamine
Bradykinins (vasoactive peptide)
Leukotrienes
C3a and C5a

25
Q

What chemical mediators cause chemotaxis?

A 
C5a and C3a
LTB4 (leukotriene B4 from leucocytes)
TNF - a 
IL - 1
Bacterial Peptides
26
Q

What chemical mediators cause a fever?

A

Prostaglandins
IL - 1
TNF - a
IL - 6

27
Q

What chemical mediators cause pain?

A

Bradykinins
Substance P
Prostaglandins

28
Q

How does appendicitis occur?

A
  1. Lumen blocks, commonly with a faecolith

2. Bacteria accumulates which increases pressure and reduces blood flow

29
Q

What is pneumonia?

A

A lung infection, commonly caused by streptococcus pneumoniae or haemophilus influenzae.

30
Q

How does bacterial meningitis occur?

A

Inflammation of the meninges caused by a pathogen.
Group B streptococcus
E. Coli
Neisseria Meningitides

31
Q

What are the clinical signs of meningitis?

A

Neck stiffness, fever, photophobia, altered mental state

Rapidly fatal

32
Q

What is an abscess?

A

An accumulation of dead and dying neutrophils, associated with liquefactive necrosis
Causes compression of surrounding structures and nerves.
Causes pain and blockage of ducts.

33
Q

What 3 inflammation of serous cavities can you get?

A
  1. ASCITES - abdominal distension
  2. Pleural effusion - Shortness of breath
  3. Pericardial effusion - Cardiac impairment
34
Q

What are histamine and serotonin?

A

Vasoactive amines which are the first mediators to occur in inflammation.
Histamine - Granules of mast cells, basophils and platelets.
Serotonin - From platelets.
Causes pain, arteriolar dilation and venular leakage.

35
Q

What are prostaglandins?

How can production be blocked?

A

Produced in inflammation from cell membrane phospholipids and cause vasodilation, pain and fever.
Can be blocked by NSAIDs and aspirin by inhibiting cyclo-oxygenase.

36
Q

What bacterial chemotoxin attracts neutrophils?

A

Endotoxin which is a lipopolysaccharide on the outer membrane on gram negative bacteria.

Pathological Processes (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions