3 Acute Inflammation Flashcards

(38 cards)

1
Q

Define Inflammation

A

Response of living tissue to injury

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2
Q

What are the characteristics of Acute Inflammation? (4)

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

What accumulates in tissues as a result of inflammation?

A

Exudate

Neutrophils

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4
Q

What are the 4 cardinal signs of acute inflammation?

A

Rubor

Calor

Tumor

Dolor

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5
Q

What happens in vessels as a result of acute inflammation?

A
  1. Vasoconstriction- (seconds)
  2. Vasodilation​- (mins)
    1. Heat and redness
    2. Permeability increase
    3. Oedema formation- red cell stasis
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6
Q

Why does fluid move into tissues in acute inflammation?

A

Starling’s law: fluid movement - controlled by balance between:

  • Hydrostatic pressure-exerted on vessel wall by fluid
  • Oncotic pressure- exerted by plasma protein
  1. Vasodilation:
    1. Increases capillary hydrostatic pressure
    2. Increase vessel permeability- los of plasma protein
    3. Net fluid movement OUT of VESSELS- oedema

Blood viscosity increases- STASIS

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7
Q

What’s the difference between Exudate and Transudate?

A
  • Exudate=
    • Protein rich
    • in Inflammation
    • Increased vascular permeability
    • Injury site
  • Transudate=
    • Low protein content
    • Fluid loss
    • NO CHANGE in vascular permeability
    • Eg. Heart/hepatic/renal failure
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8
Q

How might vascular permeability of vessels be increased? (3)

A
  1. Endothelial contraction- gaps between endothelial cells
    1. Due to histamine, leukatrienes
  2. Endothelial Cytoskeleton reorganisation- cytokines, TNF(tumour necrosis factor)
  3. Direct injury- chemical/toxic burns
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9
Q

What is a neutrophil?

A
  • Primary WBC
  • Involved in acute inflammation
  • Trilobed nucleus
  • Granulocyte
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10
Q

What type of WBC is shown here?

A

Neutrophil

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11
Q

In 4 steps, outline the process by which neutrophils escape vessels.

A
  1. Margination: stasis- neutrophils line up on endothelium edge
  2. Rolling: sticking intermittently
  3. Adhesion: Stick avidly
  4. Emigration: through blood vessel wall (aka Diapedesis)
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12
Q

What is the adhesion molecule found on the neutrophil surface?

A

Integrins- bind to receptors on endothelial surface

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13
Q

What is the adhesion molecule found on the endothelial surface?

A

Selectins- on endothelial surface- upregulated by chemical mediators

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14
Q

How do neutrophils move through the interstitium?

A

Chemotaxis

Along chemical gradient of chemoattractants (eg bacterial peptides)

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15
Q

What do neutrophils do at the site of infection?

A
  • Phagocytosis
  • Opsonisation
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16
Q

What is opsonisation?

A

Molecules= modified so that they are more reconisable to WBCs

Eg: Toxin covered in opsonins (C3b & Fc)

For receptors on neutrophil surfaces

17
Q

Name some examples of chemical mediators of acute inflammation:

18
Q

What are the two types of neutrophil killing mechanisms?

A

Oxygen dependent: Using reactive oxygen and reactive nitrogen species

Oxygen independent: Lysozome- uses hydrolytic enzymes-defensins

19
Q

How does oedema limit damage?

A
  1. Dilutes toxins
  2. Delivers plasma proteins eg FIBRIN, inflammatory mediators, immunoglobulins
  3. Increases lymphatic drainage from areas- delivers antigens to lymph node
20
Q

What is the function of fibrin?

A

Mesh

-limits spread of toxin

21
Q

How do neutrophils limit damage?(4)

A
  1. Remove toxins and pathogenic substances
  2. Remove necrotic tissue
  3. Release chemical mediators
  4. Stimulate pain (encourage rest and reduce risk of further damage)
22
Q

Give soe examples of chemical mediators at the inflammatory response?

A

Vasodilation: histamine/serotonin

Increased vascular permeability: histamine/C3a&C5a

Chemotaxis: bacterial peptides

Fever: prostaglandins

Pain: prostaglandins, bradykinin

23
Q

What local complications can occur as a result of acute inflammation? (5)

A
  1. Blockages- nearby tubes and ducts- due to swelling
  2. Compression of organs eg cardiac tamponade
  3. Loss of fluid eg due to burns
  4. Muscle atrophy- pain and loss of function
  5. Psycho-social consequences- chronic pain
24
Q

What systemic complications can occur due to acute inflammation?

A
  1. Fever: endogenous pyrogens-act on hypothalamus-alter baseline
  2. Leucocytosis: increased production of white cell (due to IL-1 and TNF acting on bone marrow)
  3. Acute Phase response: release proteins from inflammatory cells eg C-reactive protein
    1. Reduced appetite
    2. Altered sleep
    3. Tachycardia
25
What are NSAIDs?
Non-steroidal anti inflammatory drugs --\> block cyclooxygenase enzymes- involved in prostglandin production
26
What happens in septic shock?
1. Huge release of chemical mediators- overwhelming infection-widespread vasodilation 2. Hypotension, tachycardia 3. Multiple organ failure
27
What are the 4 possible outcomes for acute inflammation?
1. Resolution 2. Absess: continued acute inflammation 3. Chronic inflammation- fibrous repair 4. Death
28
How does complete resolution occur?
1. Neutrophils- stop marginating 2. Vascular permeability returns to normal 3. Vessel diameter returns to normal 4. Exudate drained- lymphatics 5. Fibrin= degraded 6. Neutrphils die- phagocytosed 7. If tissue architecture preserved, may be able to regenerate 8. Mediators= diluted/degrade/inactivated
29
What causes appendicitis?
Blocked lumen * Accumulation of bacteria * Increased pressure * Reduced blood flow *DANGEROUS if perforation occurs*
30
What bacteria causes pneumonia?
Streptococcus pneumoniae
31
What are some risk factors for Pnuemonia? (4)
1. Smoking 2. COPD 3. Asthma 4. Malignancy
32
What are the signs and symptoms of pneumonia?
1. Shortness of breath 2. Coughing 3. Fever 4. Chest pain 5. Sputum production
33
What is bacterial meningitis?
Inflammation of **meninges**- 3 layers investing brain and spinal chord Pathogens= e.coli, group 3 streptococcus
34
What are the clinical signs of bacterial meningitis?
1. Neck stiffness 2. Fever 3. Photophobia 4. Altered metal state
35
What is an absess?
= Accumulation of dead and dying neutrophils =asssociated w./ liquefactive necrosis
36
What complications can an absess cause?
Compression of surrounding tissues: * Pain * Blockage of ducts
37
What can happen when there is inflammation in these serous cavities? * Abdomen * Lungs * Heart
* Ascites- abdominal distension * Pleural effusion= shortness of breath * Pericardial effusion= cardiac impairment
38
Name a rare disorder of acute inflammation:
* Hereditary angio-oedema * Chronic granulomatous disease * Alpha-1 antitrypsin deficiency