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ESA2 > MoD 2 (Acute Inflammation) > Flashcards

MoD 2 (Acute Inflammation) Flashcards

1
Q

Define acute inflammation:

A

Accumulation of fluid exudate and neutrophils in tissues, controlled by chemical mediators from plasma/cells for protection

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2
Q

Name the 5 major causes of acute inflammation:

A

1) Microbial infections
2) Physical agents
3) Chemical agents
4) Tissue necrosis
5) Immune hypersensitivity reactions

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3
Q

Name the 5 characteristic signs of acute inflammation:

A

1) Redness ‘rubor’
2) Swelling ‘tumor’
3) Heat ‘calor’
4) Pain ‘dolor’
5) Loss-of-function

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4
Q

What are the 3 main tissue changes that occur in acute inflammation?

A

1) Vascular changes
2) Fluid exudation into tissues
3) Neutrophil immigration into tissues

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5
Q

How do vascular changes during acute inflammation lead to production of heat, swelling and redness?

A

Vasodilation of arterioles and capillaries = heat + redness

Increased membrane permeability and slowing of circulation = Swelling

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6
Q

What is a transudate?

A

A fluid with a low-protein content, which has passed through a membrane from a tissue/blood vessel etc.

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7
Q

What is an exudate?

A

A fluid with a high-protein content, which has escaped from a blood vessel into tissue

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8
Q

What is the main difference between a transudate and an exudate?

A 
Transudate = low protein content
Exudate = high protein content
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9
Q

What causes fluid to move from a blood vessel into tissue space (transudate)?

A

Increased hydrostatic pressure, usually due to decreased protein levels within blood

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10
Q

What causes exudate to move from a blood vessel into tissue space?

A

Usually inflammation

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11
Q

Name 2 mediators which cause endothelial cell contraction, leading to exudation of fluid into tissues:

A

1) Histamine

2) Leukotriene

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12
Q

Name 2 cytokines which cause cytoskeletal reorganisation, leading to exudation of fluid into tissues:

A

1) TNF

2) IL-1

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13
Q

What is the primary type of WBC in acute inflammation?

A

Neutrophil (Polymorphonuclear leucocyte)

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14
Q

What is the approx. life span of a neutrophil?

A

~ 12-20 hrs

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15
Q

A neutrophil nucleus is lobular. How many lobes is it made up of?

A

~ 2-5 lobes

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16
Q

Approx. how many granules does a neutrophil contain?

A

~ 2000 granules

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17
Q

Where are neutrophils usually found?

A

Bone marrow and blood

Inflamed tissue

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18
Q

How quickly do neutrophils travel?

A

~ 30 um/min

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19
Q

Name the 6 stages a neutrophil goes through to capture and kill bacteria:

A

1) Chemotaxis
2) Activation
3) Margination, Rolling, Adhesion
4) Diapedesis
5) Recognition-Attachment
6) Phagocytosis + Killing

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20
Q

Define chemotaxis:

A

Directional movement towards a chemical attractant

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21
Q

Name the powerful chemotaxin released by leucocytes:

A

Leukotriene B4

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22
Q

What must happen to a neutrophil before it can marginate and roll along the endothelium of a blood vessel?

A

Activation (becomes ‘sticky’)

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23
Q

How do neutrophils move across blood vessel walls?

A

Diapedesis: they produce collagenase which degrades the basement membrane, allowing cellular movement

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24
Q

When neutrophils ‘roll’ along the endothelium, what are they transiently binding to?

A

Selectins

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25
Q

Neutrophils roll along the endothelium by binding to Selectins. What is the name of the receptor which traps neutrophils?

A

Integrins

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26
Q

What enzyme do neutrophils secrete to break down the basement membrane surrounding a blood vessel wall?

A

Collagenase

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27
Q

Define opsonin:

A

Any molecule which enhances phagocytosis

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28
Q

Name the complement element which is a potent opsonin:

A

C3b

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29
Q

What are the 2 ways a neutrophil can kill a bacterium after phagocytosis?

A

1) O2 dependent (via free radicals)

2) O2 independent (via enzymes)

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30
Q

Name the enzyme contained within neutrophils which produces superoxide to kill bacteria:

A

NADPH oxidase

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31
Q

How can a neutrophil kill a bacteria using its O2 dependent pathway?

A

NADPH oxidase forms superoxide from O2,
Superoxide/Hydrogen peroxide/OH- releases via respiratory burst
Damages DNA/proteins/lipids

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32
Q

Which enzymes do neutrophils contain for O2-independent killing of bacteria?

A

Proteases
Phospholipases
Nucleases
Lysozymes

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33
Q

Which chemotaxin is expressed on the membrane of gram -ve bacteria?

A

Endotoxin

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34
Q

How does exudation and vasodilation help a tissue after injury?

A
  • Dilutes toxins
  • Maintains temperature
  • Delivers nutrients/oxygen/cells/plasma proteins
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35
Q

How does pain and loss-of-function help a tissue after injury?

A

Enforces rest, allowing repair and preventing further damage

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36
Q

What is a vasoactive amine?

A

A substance which contains amino groups, and acts on blood vessels

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37
Q

Name 2 vasoactive amines:

A

1) Histamine

2) Serotonin

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38
Q

Which cells contain and release histamine?

A

Basophils
Mast cells
Platelets

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39
Q

Which cells contain and release serotonin?

A

Platelets

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40
Q

How does Histamine and Serotonin increase vascular permeability?

A

Stimulate contraction of endothelial cells, causing them to pull apart from each other

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41
Q

Both histamine and serotonin produce pain, arteriolar dilation and increased vascular permeability. What else does ONLY serotonin cause?

A

Stimulates fibroblasts

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42
Q

Name a vasoactive peptide which causes vasodilation:

A
  • Bradykinin
  • Morphine
  • Parathyroid Hormone
  • Substance P
  • Vasoactive Intestinal Peptide
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43
Q

Name a vasoactive peptide which causes vasoconstriction:

A
  • Vasopressin
  • Thyrotropin-Releasing-Hormone
  • Angiotensin II
  • Prolactin
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44
Q

How is Bradykinin produced?

A

Kallikrein cleaves Kininogen into Bradykinin

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45
Q

What effect does Bradykinin have on the body?

A
  • Pain
  • Increases vascular permeability
  • Vasodilation
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46
Q

Name a mediator derived from phospholipids:

A
  • Prostaglandins
  • Leukotrienes
  • Thromboxane
47
Q

What substance is metabolised into Prostaglandins and Thromboxane, and which enzyme is required for this?

A

Arachidonic Acid

Cyclo-oxygenase

48
Q

What enzyme catalyses the conversion of Arachidonic acid into Prostaglandins?

A

Cyclo-oxygenase

49
Q

Which Leukotriene is the main leukocyte chemotaxin?

A

Leukotriene B4

50
Q

Which 3 types of metabolites can be produced from Arachidonic Acid?

A

1) Leukotrienes
2) Prostaglandins
3) Thromboxane

51
Q

What effect do Prostaglandins have on the vasculature?

A

Vasodilation

52
Q

Which complement proteins mediate inflammation and phagocyte recruitment?

53
Q

What is the function of the ‘Membrane-Attack-Complex’ produced by the complement system?

A

Can punch holes in bacteria, killing them

or can phagocytose bacteria

54
Q

What type of bacteria releases endotoxins?

A

Gram negative bacteria

55
Q

How can phagocytosis during acute inflammatory reaction cause damage to healthy surrounding tissue?

A

During phagocytosis, the phagosome starts releasing hydrolytic enzymes before it has completely fused around the bacteria, causing enzymes to leak out, damaging surrounding tissue

56
Q

Name 4 complications of acute inflammation:

A
  • Damage to normal tissue
  • Loss of fluid
  • Pain/ Loss-of-function
  • Obstruction of tubes (due to exudate)
57
Q

Define pyrogen:

A

Substance which produces a fever when released into the blood

58
Q

What is the role of Prostaglandin E2 in fever?

A

It stimulates the hypothalamus and medulla, which increases SNS activity:

  • Vasoconstriction
  • Increased muscle tone
  • Shivering
59
Q

How do endotoxins cause fever?

A

Stimulate macrophages to produce pyrogenic cytokines (IL-1, TNF), causing increased secretion of Prostaglandin E2, which causes increased SNS activity (vasoconstriction, shivering, increased muscle tone) = increases body temp.

60
Q

How does Aspirin reduce fever?

A

Aspirin inhibits cyclo-oxygenase, preventing synthesis of Prostaglandin E2, which causes fever by increasing SNS response.

61
Q

An increase of what kind of leukocytes is associated with a bacterial infection?

A

Neutrophils

62
Q

An increase in what kind of leukocyte is associated with a viral infection?

A

Lymphocytes

63
Q

Name 5 acute phase proteins released by the liver during acute inflammation:

A

1) Fibrinogen
2) C-reactive protein
3) Ceruloplasmin
4) C3 (complement)
5) alpha-1-antitrypsin

64
Q

Where is albumin synthesised?

65
Q

Where is alpha-1-antitrypsin synthesised?

66
Q

What serum protein synthesised in the Liver is reduced during acute inflammation?

67
Q

What are the symptoms of acute phase response?

A

Decreased appetite
Increased pulse
Sleepiness

68
Q

What is the most useful acute phase protein released in acute inflammation?

A

C-reactive protein

69
Q

What are the 4 possible outcomes of acute inflammation?

A

1) Complete resolution
2) Continues into chronic inflammation
3) Chronic inflammation + Fibrous repair
4) Death

70
Q

What happens to the neutrophils after acute inflammation?

A

Undergo apoptosis and are phagocytosed with necrotic debris

71
Q

What are the 4 types of exudate?

A

1) Pus
2) Haemorrhagic
3) Serous
4) Fibrinous

72
Q

Why does pus have a creamy/white appearance?

A

Rich in dead neutrophils

73
Q

What type of exudate is common in chemotactic bacterial infections?

74
Q

What type of exudate is common in destructive infections or malignant tumours?

A

Haemorrhagic

75
Q

How is serous exudate different to plasma?

A

Serous exudate doesn’t contain fibrinogen

76
Q

What are the differences between a fibrinous and haemorrhagic exudate?

A 
Fibrinous
 - contains fibrin so causing blood clot formation, 
 - doesn't contain red blood cells
Haemorrhagic
 - doesn't contain fibrin 
 - contains red blood cells
77
Q

Name the type of bacteria which causes lobar pneumonia:

A

Streptococcus pneumoniae

78
Q

What is Lobar pneumonia?

A

Acute exudative inflammation of a lobe of a lung

79
Q

Name the 4 stages of lobar pneumonia:

A

1) Congestion
2) Red hepatisation
3) Grey hepatisation
4) Resolution

80
Q

What type of exudate is produced during the congestion stage of lobar pneumonia?

81
Q

What type of exudate is produced in the red hepatisation stage of lobar pneumonia?

82
Q

What type of exudate is produced in the grey hepatisation stage of lobar pneumonia?

83
Q

How is the exudate removed allowing resolution of lobar pneumonia?

A

Drained into lymphatic system and airways

84
Q

What are the symptoms of Lobar pneumonia?

A

Fever
Cough (may have bloody sputum)
Pleuritic pain = sharp stabbing pain to lateral chest and upper back, worsens with inhalation/cough

85
Q

List some complications of Lobar pneumonia:

A

Empyema
Scarring
Abscess formation
Bacteraemia

86
Q

Describe ‘pleuritic’ chest pain:

A

Sharp stabbing pain to lateral chest and/or upper back, worsens with inhalation/cough

87
Q

What causes Bacterial meningitis?

A

Streptococcus pneumonia
Neisseria meningitidis
Listeria monocytogenes
Escherichia coli in neonates

88
Q

What is bacterial meningitis?

A

Infection and subsequent inflammation of meninges, causing swelling of the brain

89
Q

What are the symptoms of bacterial meningitis?

A 
Fever
Headache
Neck stiffness
Confusion
Seizures
Vomiting
90
Q

How can doctors test for bacterial meningitis?

A

Extract CSF via lumbar puncture, test for bacteria which commonly cause meningitis.

91
Q

What are the common causes of Ascending Cholangitis?

A

Gut bacteria: E coli, Klebsella spp, Enterobacter spp,

Obstruction of biliary tree via Gallstones

92
Q

What type of pain is caused by ascending cholangitis?

A

Biliary colic: ache in upper right quadrant

93
Q

What symptom can inform of ascending cholangitis affecting the liver?

94
Q

What is Ascending Cholangitis?

A

Acute inflammation spreading up the biliary tree

95
Q

What are the main causes of Acute Appendicitis?

A

Infection
Inflammatory Bowel Disease
Fecal stasis
Parasites

96
Q

What is Acute Appendicitis?

A

Acute inflammation of the Appendix

97
Q

What are the main symptoms of Acute Appendicitis?

A

Colic: may be specific to lower right quadrant if ruptured
Anorexia
Nausea/vomiting

98
Q

What are the main complications of Acute Appendicitis?

A
  • Fistula formation
  • Rupture = Peritonitis
  • Abscess formation
99
Q

Name 3 inherited disorders affecting acute inflammation:

A

1) Hereditary angioedema
2) Chronic Granulomatous Disease
3) alpha-1-antitrypsin deficiency

100
Q

What genetic inheritance pattern does hereditary angioedema follow?

A

Autosomal dominant

101
Q

What are the symptoms of hereditary angioedema?

A
  • Non-itchy cutaneous attacks
  • Abdominal attacks = abdominal pain, nausea, vomiting, diarrhoea
  • Laryngeal attacks = tight, sore, dyspnoea, voice changes
102
Q

What is hereditary angioedema?

A

Deficinecy of C1-esterase inhibitor, which is required for regulation of the inflammatory response

103
Q

How does a deficiency of C1-esterase inhibitor cause oedema?

A

Deficiency causes an increase in unwanted peptides, which increase the plasma oncotic pressure and the capillary permeability, causing fluid to move from the capillary into the tissue.

104
Q

Name the rare autosomal dominant disorder which causes a deficiency of C1-esterase inhibitor:

A

Hereditary angioedema

105
Q

What are the symptoms of alpha-1-antitrypsin deficiency?

A

Breathlessness, wheezing, cough, jaundice

106
Q

How can alpha-1-antitrypsin deficiency cause Liver disease?

A

Abnormal alpha-1-antitrypsin produced by liver and not exported, so accumulates and causes hepatocyte damage

107
Q

How can alpha-1-antitrypsin deficiency cause COPD or emphysema?

A

Alpha-1-antitrypsin is a protease inhibitor which is especially important in the lungs, therefore when deficient, proteases can damage lung tissue leading to fibrosis and scar formation

108
Q

What genetic inheritance pattern does alpha-1-antitrypsin deficiency follow?

A

Autosomal recessive

109
Q

Where is alpha-1-antitrysin produced?

110
Q

Name the rare autosomal recessive disorder which can cause emphysema and cirrhosis due to a deficiency of a protease inhibitor:

A

Alpha-1-antitrypsin deficiency

111
Q

What is Chronic Granulomatous disease?

A

Mutation in NADPH oxidase, which is required by phagocytes to produce superoxide radicals to kill bacteria.

112
Q

What are the symptoms of Chronic Granulomatous disease?

A

Chronic infections

113
Q

Why can a mutation in NADPH oxidase cause chronic infection?

A

NADPH oxidase is required by phagocytes to produce superoxide radicals, to kill bacteria
So if deficiency of functional protein, then phagocytes cannot fight infection.

ESA2 (27 decks)

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