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Pathology > Acute inflammation > Flashcards

Acute inflammation Flashcards

1
Q

How long does acute inflammation take to respond to cell injury or agent? What dominates it?

A

Immediate response

Vascular changes

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2
Q

What is the first inflammatory cell at the site of acute inflammation? What do lots of neutrophils suggest about the infectious agent?

A

Neutrophils

Lots of neutrophils suggest bacterial infection

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3
Q

What happens to blood vessels and blood flow during acute inflammation?

A

Increased blood flow

Increased vascular permeability

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4
Q

What structural changes happen in blood vessels?

A

Increased vascular permeability

Allows leakage of plasma and WBCs

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5
Q

What are the 3 mechanisms that caused increased vascular permeability?

A

Chemical mediators - e.g. histamine, causes gap formation between endthelial cells
Direct injury - e.g burns damage endothelial cells
Leukocyte mediated injury – leukocytes release proteolytic enzymes

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6
Q

In acute inflammation, the predominating WBC changes over time. Which cells originally predominate? What takes over?

A

Neutrophils - short life span

Taken over by monocytes/macropages

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7
Q

Chemotaxis is the movement of a cell due to a chemical gradient. What are the 2 types of chemoattrctants? Give an example of each?

A

Exogenous - bacterial toxins/products

Endogenous - complement system, cytokines, leukotrienes

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8
Q

What proteins cause chemotaxis, angiogenesis and collagen production? Are they produced by a particular cell?

A

Chemokines

Produced by almost all cells

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9
Q

Where do chemokines bind to to create a chemical gradient?

A

Components of ECM

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10
Q

How do chemoattractants cause a cell to move in chemotaxis?

A

Chemoattractants bind to cell receptor
Cause mobilisation of intracellular calcium
Causes assembly of contractile elements and allows cell to move

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11
Q

Leukocytes move in response to chemoattractants. How do leukocytes move?

A

Move pseudopodia

Pull remainder of the celling that direction

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12
Q

What cells are the 2 major phagocytes?

A

Macrophages (monocytes in blood)

Neutrophils

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13
Q

What are the 3 stages of phagocytosis?

A

Recognition and attachment
Engulfment
Killing or degradation

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14
Q

During phagocytosis, what on the target cell do they bind to?

A

Pathogenic associated molecular patterns (PAMPs)

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15
Q

What is osponisation? What molecule causes it?

A

Adherence of opsonins to cell to mark an antigen

Osponin is a chemoattractant - attracts immune cells

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16
Q

How do phagocytes engulf a cell/pathogen?

A

Extend pseudopodia
Form a phagosome
Phagosome fuses with lysosome to form phagolysosome

17
Q

How do phagocytes usually kill cells?

A

Oxygen mechanisms - free radicals, relative O2 species

18
Q

What degrades bacteria after phagocytosis? What pH does this work at?

A

Acid hyrdolases

Work at low pH

19
Q

What are neutrophil extracellular traps?

A

Fibrous networks that prevent spread of microbes after phagocytosis

20
Q

Extracellular nuclear traps can go wrong and cause injury to the tissue, possibly more severe than the original stiulus. What are the 3 ways they caused damage?

A

Regurgitation during phagocytsosis
Frustrated phagocytosis - attempt phagocytosis of a material bound to a flat surface
Exocytosis

21
Q

What are the 4 outcomes of acute inflammation?

A

Complete resolution
Progression to chronic inflammation
Healing by fibrosis (scar)
Abscess formation

22
Q

What happens when acute inflammation leads to complete resolution?

A

Return to normal vascular permeability
Drainage of fluids, proteins, cells
Phagocytosis of degenerate neutrophils and debris
Disposal of phagocytes

23
Q

Why does acute inflammation progress to chronic inflammation?

A

Acute inflammation cannot be resolved

24
Q

What are the types of inflammation?

A 
Serous 
Fibrinous 
FIbrino-necrotising
Suppurative (purulent)
Haemorrhagic 
Necortising
25
Q

What is acute serous inflammation? Where can this happen?

A

Inflammation with outpouring of exudate

Skin (blisters), serial surfaces, mucosa

26
Q

What is serous inflammation of mucosa also called?

A

Catarrhal inflammation

27
Q

What is fibrinous acute inflammation? What areas of the body does this affect?

A

Outpouring of serum with fibrin and clotted exudate

Lungs and joints

28
Q

What is the difference between fibrinous acute inflammation and fibroplastic chronic inflammation?

A

Fibrin can be pulled apart in fibrinous acute inflammation (scrambled egg like)
Fibroplastic chronic inflammation - connective tissue so can’t be pulled off

29
Q

What is fibrinonecrotising acute inflammation? (AKA diptehroid)

A

Clotting of fibrinous exudate within layers of necrotic tissue

30
Q

What is suppurative chronic inflammation? What cell predominates in this?

A

Pus - contains neutrophils, fibrin and necrotic tissue

31
Q

Pyometra/pyothorax is pus in uterus/thorax. When is some puss classed as being sterile?

A

If not caused by an infectious agent

32
Q

Pus includes pustules, empyema, cellulitis and abscesses. What are these?

A

Pustules - pus within dermis/epidermis
Empyema - within pre-existing space (nasal cavity)
Cellulitis - connective tissue pus
Abscess - pus within cavity which developed due to tissue necrosis

33
Q

What is haemorrhagic acute inflammation? When might this occur?

A

RBCs included in serous/fibrinous/suppurative exudate

Severe blood vessel damage

34
Q

What is necrotising acute inflammation?

A

Inflammation with exudation and severe tissue necrosis leading to ulcer
(seen with specific bacteria)

Pathology (22 decks)

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