Session 2 - Acute Inflammation Flashcards

1
Q

What are 6 causes of acute inflammation?

A
Foreign bodies 
Immune reactions 
Infections
Tissue necrosis
Trauma
Physical and chemical agents
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2
Q

What are the 5 signs of acute inflammation?

A
Redness 
Heat
Swelling
Pain
Loss of function
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3
Q

What is rubor?

A

Redness

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4
Q

What is calor?

A

Heat

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5
Q

What is tumor?

A

Swelling

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6
Q

What is dolor?

A

Pain

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7
Q

What is inflammation?

A

Response of living tissue to injury

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8
Q

What are 2 phases of inflammation?

A

Vascular

Cellular

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9
Q

What happens during vascular phase with regard to blood flow?

A

Brief vasoconstriction for seconds
Longer lasting vasodilation, causing heat and redness
Increased permeability so fluid and cells can escape

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10
Q

What is Starling’s Law?

A

Movement of fluid is controlled by the balance of hydrostatic pressure and oncotic pressure

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11
Q

What is hydrostatic pressure?

A

Pressure exerted on a vessel wall by a fluid, pushing fluid away from blood vessels

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12
Q

What is oncotic pressure?

A

Pressure exerted by proteins, drawing fluid towards blood vessels

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13
Q

Why does heat and redness present during acute inflammation?

A

Vasodilation

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14
Q

Why does oedema present during acute inflammation?

A

Vasodilation increases capillary hydrostatic pressure, increased vessel permeability allows plasma proteins to move into interstitial, causing increased interstitial oncotic pressure, hence fluid moves out of vessel into interstitial fluid

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15
Q

What is stasis?

A

Reduced flow through vessel

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16
Q

Why does acute inflammation cause stasis?

A

Fluid moves out of vessel, increasing viscosity of blood

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17
Q

What is exudate?

A

Protein rich fluid occurring in inflammation when vascular permeability increases

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18
Q

What is transudate?

A

Ultrafiltrate of plasma occurring during organ failure as fluid moves due to increased capillary hydrostatic pressure and decreased capillary oncotic pressure, and vascular permeability is unchanged

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19
Q

What are 3 ways of increasing permeability of vessel walls?

A

Retraction of endothelial cells
Direct injury
Leukocyte dependent injury

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20
Q

What are 3 main components that makes vascular phase effective?

A

Interstitial fluid
Exudate
Lymph nodes

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21
Q

What is the role of interstitial fluid during acute inflammation?

A

Dilutes toxins

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22
Q

What are the 2 roles of exudate in acute inflammation?

A

Delivers proteins

  • fibrin to limit spread of toxin
  • immunoglobulins from adaptive immune response
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23
Q

What is the role of lymph nodes in acute inflammation?

A

Fluid drains to lymph nodes, stimulating adaptive immune response

24
Q

What is the primary white blood cell involved in cellular phase of acute inflammation?

A

Neutrophils

25
Q

What are the 4 steps of neutrophils escaping vessels?

A
  1. Margination
  2. Rolling
  3. Adhesion
  4. Emigration / diapedesis
26
Q

What are the 2 main adhesion molecules used by neutrophils to escape from vessels?

A

Selections

Integrins

27
Q

What do selectins do?

A

Responsible for rolling, expressed on activated endothelial cells and are activated by chemical mediators

28
Q

What do integrins do?

A

Found on neutrophil surface, changes from low affinity to high affinity, responsible for adhesion

29
Q

How do neutrophils move through the interstitium?

A

Chemotaxis, along an increasing chemical gradient of chemoattractants

30
Q

How do neutrophils recognize what to phagocytose?

A

Opsonisation - toxin covered in C3b and Fc and neutrophils have the respective receptors on its surface

31
Q

What are the 2 types of opsonins?

A

C3b and Fc

32
Q

What are 2 ways neutrophils destroy pathogens?

A

Oxygen dependent

Oxygen independent

33
Q

What are the 2 molecules that oxygen dependent killing mechanisms use?

A

Reactive oxygen intermediates and nitrogen intermediates

34
Q

What are the 3 types of molecules used in oxygen independent killing mechanisms?

A

Lysosome
Hydrolytic enzymes
Defensins

35
Q

What are 2 ways that cellular phase is effective in acute inflammation?

A

Removal of pathogens and necrotic tissue

Release of inflammatory mediators

36
Q

What are inflammatory mediators?

A

Chemical messengers that control and coordinate inflammatory response

37
Q

What are 3 examples of mediators that controls vasodilation?

A

Histamine
Serotonin
Prostaglandins

38
Q

What are 3 mediators that increases vascular permeability?

A

Histamine
Bradykinin
Leukotrienes

39
Q

What are 3 mediators that controls chemotaxis?

A

C5a
TNF-a
IL-1

40
Q

What are 3 mediators that causes systemic responses?

A

Prostaglandins
IL-6
IL-1

41
Q

What are 3 mediators that control pain?

A

Bradykinin
Substance P
Prostaglandin

42
Q

What are 4 types of local complications of acute inflammation?

A

Swelling can cause compression of tubes, exudate compresses organs, loss of fluid, pain can lead to psychosocial consequences

43
Q

What are 4 forms of systemic effects of acute inflammation?

A

Fever - pyrogens act on hypothalamus to increase temperature
Leucocytosis - mediators act on bone marrow to increased production of white cells
Acute phase response - reduced appetite, altered sleep to induce rest
Septic shock - dramatic drop in BP due to widespread vasodilation

44
Q

What are 3 possible outcomes after acute inflammation?

A
  1. Complete resolution
  2. Repair with connective tissue (fibrosis)
  3. Progression to chronic inflammation (prolonged inflammation with repair)
45
Q

What is hereditary angio-oedema?

A

Inherited deficiency of C1-esterase inhibitor

46
Q

What is alpha-1 antitrypsin deficiency?

A

Low levels of alpha-1 antitrypsin, a protease inhibitor which deactivates enzymes released from neutrophils at the site of inflammation, so proteases act unchecked and destroy normal parenchyma tissue

47
Q

What are the symptoms of alpha-1 antitrypsin deficiency?

48
Q

What is chronic granulomatous disease?

A

Phagocytes cannot generate free radical superoxide, bacteria phagocytosed but phagocytes cannot kill them as they cannot do oxygen burst, results in many chronic infections

49
Q

How does appendicitis occur?

A

Lumen is blocked by faecolith, accumulation of bacteria and exudate leads to increased pressure and eventually perforation

50
Q

What are 2 organisms that cause pneumonia?

A

Streptococcus Pneumoniae

Haemophilus influenzae

51
Q

What are 4 symptoms of pneumonia?

A

Shortness of breath
Cough
Sputum
Fever

52
Q

What are 2 risk factors of pneumonia?

A

Smoking

Pre existing lung infection

53
Q

What is bacterial meningitis?

A

Inflammation of meningitis

54
Q

What are 3 causative organisms of bacterial meningitis?

A

Group B streptococcus
E. Coli
Neisseria meningitides

55
Q

What are 4 symptoms of bacterial meningitis?

A

Headache
Neck stiffness
Photophobia
Altered mental state

56
Q

What are abscesses?

A

Accumulation of dead and dying neutrophils with associated liquefaction necrosis