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Semester 2 - Mechanism of Disease > MoD S2 - Acute inflammation > Flashcards

MoD S2 - Acute inflammation Flashcards

1
Q

Define acute inflammation and its purpose

A

Response of living tissue to injury and is initiated to limit tissue damage

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2
Q

List the features of acute inflammation

A

Short duration, innate, stereotyped and immediate

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3
Q

List the possible causes of acute inflammation

A
  • Microbial infection
  • Chemical
  • Physical agents
  • Tissue necrosis
  • Hypersensitivity reactions
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4
Q

What are the macroscopic consequences of acute inflammation?

A

Rubor, dolor, calor, tumor and loss of function

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5
Q

What are the two phases of acute inflammation?

A

Vascular phase and cellular phase

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6
Q

What changes in blood flow occur during the vascular stage of acute inflammation?

A
  • Transient vasoconstriction of arterioles
  • Vasodilation of capillaries and arterioles
  • Increase in blood flow creates calor and rubor
  • Increased permeability of vessels means that there is more extrusion of protein rich fluid into tissues creating stasis in blood vessels
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7
Q

What is oedema?

A

Excess fluid in the interstitial

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8
Q

What is the difference between transudate and exudate?

A

Transudate has a low protein content whereas exudate is protein rich

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9
Q

How does the body respond to oedema?

A

Increased lymphatic drainage

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10
Q

What are the different mechanisms of vascular leakage?

A
  • Endothelial contraction
  • Cytoskeletal reorganisation
  • Direct injury
  • Leucocytic dependent injury
  • Increased transcytosis
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11
Q

What causes each of these mechanisms to occur?

A
  • Endothelial contraction‐ histamines, leukotrienes
  • Cytoskeletal reorganisation‐ cytokines, IL‐1 and TNF alpha
  • Direct injury
  • Leucocytic dependent injury‐ ROS and enzymes from leucocytes
  • Increased transcytosis‐ VEGF
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12
Q

Outline the process of neutrophil infiltration of cells

A

Margination‐ stasis causes neutrophils to line up along endothelium

Rolling‐ neutrophils roll along endothelium, stick intermittently

Adhesion‐ neutrophils stick avidly

Emigration‐ neutrophils move through blood vessel walls

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13
Q

How do neutrophils move through blood vessel walls?

A

Relaxation of inter‐endothelial cell junctions

Digestion of vascular basement membrane

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14
Q

Define chemotaxis

A

Movement of cells along the concentration gradient of chemoattractents

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15
Q

List the chemotoxin molecules

A

C5a, LT4B and bacterial peptides

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16
Q

How do neutrophils carry out phagocytosis?

A
  • Contact, recognition and internalisation facilitated by opsins
  • Cytoskeletal changes occur enabling the neutrophil to internalise the pathogen
  • Forms a phagosome which can fuse with the lysosome for digestion
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17
Q

What are the two mechanisms by which neutrophils kill cells

A

Oxygen dependent:

  • Superoxide radicals and hydrogen peroxide
  • H2O2‐ myeloperoxide‐halide system produces HOCl radicals

Oxygen independent:

  • Lysozyme and hydrolases
  • BPI
  • Cationic proteins (defensins)
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18
Q

What are the potential local complications of acute inflammation?

A

Swelling, compression, loss of fluid, pain and loss of function

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19
Q

What are the potential systemic complications of acute inflammation?

A

Fever, acute phase response, leucocytosis, shock

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20
Q

What are the causes of fever?

A

Endogenous pyrogens‐ IL‐1, TNF alpha

Prostaglandins

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21
Q

What are the causes of leucocytosis?

A

IL‐1 and TNF‐alpha accelerate release of WBC from bone marrow

T‐lymphocytes produce colony stimulating factors

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22
Q

What is the difference between leucocytosis in bacterial and viral infections?

A

Viral‐ elevated lymphocytes

Bacterial‐ elevated polymorphs

23
Q

What are the symptoms of the acute phase response?

A

Decreased appetite, disrupted sleep pattern and raised pulse rate

24
Q

Which proteins change in plasma concentration during the acute phase response?

A
  • C‐reactive protein
  • Alpha‐1 anti‐trypsin
  • Fibrinogen
  • Serum A amyloid protein
  • Haptoglobin
25
Q

Define shock

A

Clinical syndrome of circulatory failure

26
Q

Which inflammatory mediators cause increased vascular permeability?

A

Histmaines, leukotrienes

27
Q

Which inflammatory mediators cause vasodilation?

A

Histamines, prostaglandins

28
Q

Which inflammatory mediators cause neutrophil chemotaxis?

A

C5a, LTB4

29
Q

Which inflammatory mediators cause phagocytosis?

A

C3b

30
Q

How does exudation of fluid combat injury?

A
  • Delivers plasma proteins such as immunoglobulins, fibrinogen and inflammatory mediators
  • Dilute toxins
  • Increases lymphatic drainage
31
Q

How does infiltration of cells combat injury?

A

Removes pathogenic organisms and necrotic debris

32
Q

How does vasodilation combat injury?

A

Increases delivery to tissue and increases temperature

33
Q

How does an increase in temperature help to combat cell injury?

A

Most bacteria cannot survive at high temperatures

34
Q

How does pain and loss of function combat cell injury?

A

Enforces rest and prevents further damage to tissue

35
Q

What are the possible outcomes of acute inflammation?

A
  • Complete resolution
  • Continuous acute inflammation with chronic inflammation‐ abscess
  • Chronic inflammation with fibrous tissue repair and possible regeneration
  • Death
36
Q

What morphological changes occur in resolution of acute inflammation?

A
  • Neutrophils stop migrating
  • Vessel calibre returns to normal
  • Vessel permeability returns to normal
37
Q

Describe the process of resolution

A
  • Exudate drains to lymphocytes
  • Fibrin is broken down by plasmin and other proteases
  • Neutrophils die and are carried away or phagocytosed
  • Damaged tissue may regenerate
38
Q

List the mechanisms of resolution

A

Inactivation of inflammatory mediators by degredation

Binding of inhibitors to inflammatory mediators e.g. anti‐protease

Unstable inflammatory mediators

Inflammatory mediators are diluted in exudate

Specific inhibitors of acute inflammation changes e.g. endothelin, lipoxins

39
Q

Give two consequences of acute inflammation in serous cavities

A

Ascites, pleural or pericardial effusion

40
Q

What is bacterial menigtis?

A

Acute inflammation of the meninges

41
Q

What are the two consequences of bacterial meningitis?

A

Vascular thrombosis, reduced cerebral perfusion

42
Q

How does lobar pneumonia present?

A

Worsening fever, postration, hypoxaemia, dry cough and breathlessness

43
Q

What is the cause of hypoxaemia in lobar pneumonia?

A

Exudate fills the alveoli opposed to oxygen

44
Q

What colour does the exudate in skin blisters appear and why?

A

Clear as there is few inflammatory cells unless bacterial infection occurs

45
Q

List the potential causes of skin blisters

A

Heat, sunlight, chemicals

46
Q

What is an abscess?

A

Build up of inflammatory exudate in solid tissues that forces the tissue apart

47
Q

What type of necrosis is commonly seen in abcesses?

A

Liquifactive

48
Q

What are the two concequences of on absess?

A

High pressure causing pain

Tissue damage and squashing of adjacent structures

49
Q

Give an example of a disorder of acute inflammation causing a defect in neutrophil function

A

Chronic granulomatous disease

50
Q

What is opsin Fc a component of?

A

Present in all antibodies, it is the fixed non‐specific component of antibody structure

51
Q

Where are proteases produced?

A

Liver

52
Q

What is the purpose of fibrin in acute inflammation?

A

Localises the inflammation

53
Q

Why is lymphatic drainage of exudate so important for the body’s immune response?

A

Lymph nodes contain large quantities of T and B lymphocytes which can amount an adaptive immune response to pathogens carried to the lymph nodes in fluid exudate from inflamed tissues

54
Q

What is serositis?

A

Inflammation of a serous membrane

Semester 2 - Mechanism of Disease (10 decks)

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