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aPATH P COPY (SC) > Acute inflammation > Flashcards

Acute inflammation Flashcards

1
Q

acute inflammation overview

A
  • immediate response
  • short duration
  • innate
  • stereotype
  • limits damage
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2
Q

stereotyped meaning

A

always the same regardless of the stimulus

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3
Q

acute inflammation is tightly controlled by

A

chemical emdiators

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4
Q

although acute inflamamrtionc an be protective

A

can give rise to complications

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5
Q

phases of acute inflammation (2)

A

1) vascular phase

2) cellular phase

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6
Q

1) vascular phase

A
  • changes in blood flow
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7
Q

goal of vascular phase

A

accumulation of exudate

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8
Q

2)cellular phase

A

delivery of neutrophils

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9
Q

what causes inflammation

A
  • Trauma/foreign body
  • Microorganisms
  • Hypersensitivity (pollen and gluten)
  • Other illnesses e.g. necrosis
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10
Q

clinical signs of acute inflammation

A
  • Tumor- swelling
  • Rubor- redness
  • Calor- heat
  • Dolor- pain
  • Loss of function
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11
Q

outline the vascular phase

A
  1. stimulus causes vasoconstriction (only lasts a few seconds)
  2. Then vasodilation (minutes)
    - heat and redness
    - allows more blood to flow to area
  3. vessel becomes more permeable allowing fluid, cells and proteins to escape
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12
Q

vasoconstriction

A

increase capillary hydrostatic pressure

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13
Q

increased vessel permeability

A

Plasma proteins move into interstitial space. Increased interstitial oncotic pressure

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14
Q

fluid movement

A

Out of vessel into interstium – OEDEMA (swelling/tumor)

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15
Q

fluid movement out of vessel

A

Out of vessel into interitem – OEDEMA (swelling/tumor)

  • Increases viscosity of blood
  • Reducing flow through the vessel- STATSIS
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16
Q

starlings law

A

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

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17
Q

hydrostatic pressure

A

ressure exerted on vessel wall by fluid- pushes water out of vessels

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18
Q

oncotic pressure

A

the pressure exerted by proteins- draws fluid back into vessel (proteins)

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19
Q

types of interstitial fluid

A

exudate and trannsudatre

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20
Q

exudate

A
  • Arises due to change in vascular permeability
  • Protein rich interstitial fluid
  • Occurs due to inflammation
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21
Q

transudate

A

not released during inflammation
- Vessel permeability unchanged
- Not due to change in protein conc in the interstitial
- Fluid movement due to
- Increased capillary hydrostatic pressure
- Reduced capillary oncotic pressure
o E.g. heart failure/hepatic failure (reduced production of proteins) /renal failure (lose protein in the urine)
o Can cause pulmonary oedema- fluid escapes in blood

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22
Q

how do the vessels become leaky?

A

1) Endothelial cells retract meaning space between them is bigger- passive of cells, fluid etc
- Due to chemokines e.g. histamine

2) Endothelial cell damage  allow proteins and cells to escape
3) Leukocytes (WBC e.g. neutrophils) become activate which release enzymes which damage the endothelial cells

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23
Q

why is vascular phase important

A

• Interstitial fluid dilutes toxins
• Exudates- delivers proteins
- e.g. fibrin -mesh limits spread of toxins around the body
- e.g. immunoglobulins from adaptive immune response
• Fluid drains to lymph nodes - delivery of antigens —> stimulates immune response (proliferation of lymphocytes)

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24
Q

cellular phase (2) is centred around the

A

neutrophil

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25
Q

neutrophil

A
  • Primary white blood cell involved in acute inflammation
  • Trilobed nucleus
  • A granulocytes
  • Bigger than RBC
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26
Q

how do neutrophils escape the vessel

A

1) Neutrophil margination- helped by thickness of blood
2) Rolling- weak intermittent bonds form between neutrophil and endothelium
• Selectins- expressed on activated endothelial cells (activated by chemical mediators)
o Responsible for rolling
• Integrins- found on neutrophil surface
o Change from low affinity to high affinity state – responsible for adhesion
3) Adhesion
4) Emigration (diapedesis)

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27
Q

selecting

A

responsible for rolling

28
Q

integrins

A

found on neutrophil surface- responsible for adhesion

29
Q

diapedesis

A

the passage of blood cells through the intact walls of the capillaries, typically accompanying inflammation.

30
Q

selectins

A

expressed on activated endothelial cells (activated by chemical mediators)
o Responsible for rolling

31
Q

chemotaxis

A

Movement along an increasing chemical gradient of chemoattractant

32
Q

chemoattractants

A

o Bacterial peptides, inflammatory mediators (CF5a, LTB4)

o Rearrangement of neutrophil cytoskeleton

33
Q

role of neutrophils

A

1) Phagocytosis

2) release inflammatory mediators

34
Q

phagocytosis

A

o Bacterial peptides, inflammatory mediators (CF5a, LTB4)

o Rearrangement of neutrophil cytoskeleton

35
Q

how do neutrophils recognise targets for phagocytosis

A
  • Opsonisation
36
Q

outline opsonisation

A

o Pathogen becomes coated in molecules such as complement (C3b and Fc)
o Neutrophil has corresponding receptors- receptor binds to ligand and neutrophil introduced to pathogen

37
Q

how do neutrophils kill (2)

A

1) Oxygen dependent

2) Oxygen independent

38
Q

1) Oxygen dependent

A

o Reactive oxygen intermediates (Free radicals e.g. ROS and RNI)
 O. (superoxide anion)
 OH. (hydroxyl radicals)
 H2O2 (hydrogen peroxide)

39
Q

2) oxygen independent

A

Enzymatic
 Lysozyme
 Hydrolytic enzymes e.g. defensins

40
Q

how is the cellular phase effective

A

1) Removal
• Pathogens
• Necrotic tissue

2) Release
• Inflammatory mediators

41
Q

chemical mediators

A
  • Control and co-ordinate the inflammatory response
  • Varying chemical structures
  • Overlapping functions
42
Q

chemical mediators originate from

A
  • Activated inflammatory cells
  • Platelets
  • Endothelial cells
  • Toxins themselves
43
Q

chemical mediators which cause vasodilation

A

o Histamine
o Serotonin
o Prostaglandins
o Nitric oxide

44
Q

chemical mediators which cause leaky vessels

A

o Histamine
o Bradykinin
o Leukotrienes
o C3a and C5a

45
Q

chemical mediators which cause chemoattraction

A

o C5a
o TNF-a
o IL-a
o Bacterial peptides

46
Q

chemical mediators which cause increased body temp

A

o Prostaglandins
o Il-1
o Il-6
o TNF-a

47
Q

chemical mediators which cause pain

A

o Bradykinin
o Substance P
o Prostaglandins

48
Q

complications of acute inflammation can be

A

local or systemic

49
Q

local complications

A
  • swelling
  • exudate
  • loss of fluid
  • pain
50
Q

Swelling

A

o Compression of tubes e.g. airway (epiglottitis)/bile duct/intestines

51
Q

exudate

A

compression of organs e.g. cardiac tamponase

52
Q

loss of fluid

A

e.g. burns (die of severe dehydration)

53
Q

pain

A

muscle atrophy, psycho-social consequences etc

54
Q

systemic complications

A
  • fever
  • leucocytosis
  • acute phase repsonse
  • septic shock
55
Q

fever

A

o Brought about by chemical mediators – pyrogens
 E.g. prostaglandins, IL-1,IL-6 etc
 Act on hypothalamus to alter temperature
• Use NSAIDs
o Block COX enzymes (involved in production of prostaglandins)

56
Q

leucoytosis

A

o Leucoytosis
 Increased production of white cells
 Inflammatory mediators act on bone marrow promoting production of WBC in bone marrow
• WBC conc can be measured in blood

57
Q

Bacterial

A
  • neutrophils
58
Q

Viral

A
  • lymphocytes
59
Q

acute phase response

A 
	Brought about by acute phase proteins e.g. CRP
•	Common blood test-marker of severity 
•	Useful in monitoring inflammation and infection (would expect CRP to come down with antibiotics)
•	Causes:
o	Malaise
o	Reduced appetite altered sleep
o	Tachycardia
	All induce rest
60
Q

septic shocj

A 
	Huge release of chemical mediators
•	Widespread vasodilation
•	Hypotensions, tachycardia
o	Cant pump blood to the heart
•	Multi-organ failure
•	Can be fatal
61
Q

what happens after acute inflammation

A

(1) Complete resolution
o Mediators have short half lives – diluted, inactivated/ derailed
o Vessel calibre and permeability returns to normal
o Neutrophil undergoes apoptosis and get phagocytised
o Exudate drained

(2) Repair with connective tissue (fibrosis)- if there has been substantial destruction

(3) Progression to chronic inflammations
o Prolonged inflammation with repair

62
Q

appendicitis

A

o Blocked lumen (fecalith- hard faeces)
o Accumulation of bacteria and exudate
 Increased pressure and perforation

63
Q

pneumonia

A 
o	Many causative organisms
	Streptococcus pneumoniae
	Haemophilus influenzae
o	Signs and symptoms:
	Shortness of breath
	Cough
	Sputum
	Fever
o	Risk factor:
	Pre-existing lung condition (COPD, asthma/ malignancy)
64
Q

bacterial meningitis

A 
o	Brain covered by meninges
	Becomes infected
	E.g. Group B streptococcus
	E.coli
	Neisseria meningitides 
o	Signs and symptoms
	Headache
	Neck stiffness- meninges also cover spinal cord
	Photophobia
	Altered mental state
	Need immediate antibiotics
65
Q

abscess

A

accumulation of dead and dying neutrophils

o Associated with liquefactive necrosis

66
Q

inflammation of serous cavities

A

o Exudate pours into serous cavities (variety of causes)
 Pleural space= pleural effusion
 Peritoneal space= ascites
 Pericardial space= pericardial effusion

67
Q

rare inflammatory disorders

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

aPATH P COPY (SC) (19 decks)

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