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2 Pathological Processes > 3 Acute Inflammation > Flashcards

3 Acute Inflammation Flashcards

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:

A
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
Q

What are NSAIDs?

A

Non-steroidal anti inflammatory drugs

–> block cyclooxygenase enzymes- involved in prostglandin production

26
Q

What happens in septic shock?

A
  1. Huge release of chemical mediators- overwhelming infection-widespread vasodilation
  2. Hypotension, tachycardia
  3. Multiple organ failure
27
Q

What are the 4 possible outcomes for acute inflammation?

A
  1. Resolution
  2. Absess: continued acute inflammation
  3. Chronic inflammation- fibrous repair
  4. Death
28
Q

How does complete resolution occur?

A
  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
Q

What causes appendicitis?

A

Blocked lumen

  • Accumulation of bacteria
  • Increased pressure
  • Reduced blood flow

DANGEROUS if perforation occurs

30
Q

What bacteria causes pneumonia?

A

Streptococcus pneumoniae

31
Q

What are some risk factors for Pnuemonia? (4)

A
  1. Smoking
  2. COPD
  3. Asthma
  4. Malignancy
32
Q

What are the signs and symptoms of pneumonia?

A
  1. Shortness of breath
  2. Coughing
  3. Fever
  4. Chest pain
  5. Sputum production
33
Q

What is bacterial meningitis?

A

Inflammation of meninges- 3 layers investing brain and spinal chord

Pathogens= e.coli, group 3 streptococcus

34
Q

What are the clinical signs of bacterial meningitis?

A
  1. Neck stiffness
  2. Fever
  3. Photophobia
  4. Altered metal state
35
Q

What is an absess?

A

= Accumulation of dead and dying neutrophils

=asssociated w./ liquefactive necrosis

36
Q

What complications can an absess cause?

A

Compression of surrounding tissues:

  • Pain
  • Blockage of ducts
37
Q

What can happen when there is inflammation in these serous cavities?

  • Abdomen
  • Lungs
  • Heart
A
  • Ascites- abdominal distension
  • Pleural effusion= shortness of breath
  • Pericardial effusion= cardiac impairment
38
Q

Name a rare disorder of acute inflammation:

A
  • Hereditary angio-oedema
  • Chronic granulomatous disease
  • Alpha-1 antitrypsin deficiency

2 Pathological Processes (12 decks)

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