MoD 2 (Acute Inflammation) Flashcards
(113 cards)
1
Q
Define acute inflammation:
A
Accumulation of fluid exudate and neutrophils in tissues, controlled by chemical mediators from plasma/cells for protection
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
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
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
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
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.
7
Q
What is an exudate?
A
A fluid with a high-protein content, which has escaped from a blood vessel into tissue
8
Q
What is the main difference between a transudate and an exudate?
A
Transudate = low protein content Exudate = high protein content
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
10
Q
What causes exudate to move from a blood vessel into tissue space?
A
Usually inflammation
11
Q
Name 2 mediators which cause endothelial cell contraction, leading to exudation of fluid into tissues:
A
1) Histamine
2) Leukotriene
12
Q
Name 2 cytokines which cause cytoskeletal reorganisation, leading to exudation of fluid into tissues:
A
1) TNF
2) IL-1
13
Q
What is the primary type of WBC in acute inflammation?
A
Neutrophil (Polymorphonuclear leucocyte)
14
Q
What is the approx. life span of a neutrophil?
A
~ 12-20 hrs
15
Q
A neutrophil nucleus is lobular. How many lobes is it made up of?
A
~ 2-5 lobes
16
Q
Approx. how many granules does a neutrophil contain?
A
~ 2000 granules
17
Q
Where are neutrophils usually found?
A
Bone marrow and blood
Inflamed tissue
18
Q
How quickly do neutrophils travel?
A
~ 30 um/min
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
20
Q
Define chemotaxis:
A
Directional movement towards a chemical attractant
21
Q
Name the powerful chemotaxin released by leucocytes:
A
Leukotriene B4
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’)
23
Q
How do neutrophils move across blood vessel walls?
A
Diapedesis: they produce collagenase which degrades the basement membrane, allowing cellular movement
24
Q
When neutrophils ‘roll’ along the endothelium, what are they transiently binding to?
A
Selectins
25
Neutrophils roll along the endothelium by binding to Selectins. What is the name of the receptor which traps neutrophils?
Integrins
26
What enzyme do neutrophils secrete to break down the basement membrane surrounding a blood vessel wall?
Collagenase
27
Define opsonin:
Any molecule which enhances phagocytosis
28
Name the complement element which is a potent opsonin:
C3b
29
What are the 2 ways a neutrophil can kill a bacterium after phagocytosis?
1) O2 dependent (via free radicals)
| 2) O2 independent (via enzymes)
30
Name the enzyme contained within neutrophils which produces superoxide to kill bacteria:
NADPH oxidase
31
How can a neutrophil kill a bacteria using its O2 dependent pathway?
NADPH oxidase forms superoxide from O2,
Superoxide/Hydrogen peroxide/OH- releases via respiratory burst
Damages DNA/proteins/lipids
32
Which enzymes do neutrophils contain for O2-independent killing of bacteria?
Proteases
Phospholipases
Nucleases
Lysozymes
33
Which chemotaxin is expressed on the membrane of gram -ve bacteria?
Endotoxin
34
How does exudation and vasodilation help a tissue after injury?
- Dilutes toxins
- Maintains temperature
- Delivers nutrients/oxygen/cells/plasma proteins
35
How does pain and loss-of-function help a tissue after injury?
Enforces rest, allowing repair and preventing further damage
36
What is a vasoactive amine?
A substance which contains amino groups, and acts on blood vessels
37
Name 2 vasoactive amines:
1) Histamine
| 2) Serotonin
38
Which cells contain and release histamine?
Basophils
Mast cells
Platelets
39
Which cells contain and release serotonin?
Platelets
40
How does Histamine and Serotonin increase vascular permeability?
Stimulate contraction of endothelial cells, causing them to pull apart from each other
41
Both histamine and serotonin produce pain, arteriolar dilation and increased vascular permeability. What else does ONLY serotonin cause?
Stimulates fibroblasts
42
Name a vasoactive peptide which causes vasodilation:
- Bradykinin
- Morphine
- Parathyroid Hormone
- Substance P
- Vasoactive Intestinal Peptide
43
Name a vasoactive peptide which causes vasoconstriction:
- Vasopressin
- Thyrotropin-Releasing-Hormone
- Angiotensin II
- Prolactin
44
How is Bradykinin produced?
Kallikrein cleaves Kininogen into Bradykinin
45
What effect does Bradykinin have on the body?
- Pain
- Increases vascular permeability
- Vasodilation
46
Name a mediator derived from phospholipids:
- Prostaglandins
- Leukotrienes
- Thromboxane
47
What substance is metabolised into Prostaglandins and Thromboxane, and which enzyme is required for this?
Arachidonic Acid
| Cyclo-oxygenase
48
What enzyme catalyses the conversion of Arachidonic acid into Prostaglandins?
Cyclo-oxygenase
49
Which Leukotriene is the main leukocyte chemotaxin?
Leukotriene B4
50
Which 3 types of metabolites can be produced from Arachidonic Acid?
1) Leukotrienes
2) Prostaglandins
3) Thromboxane
51
What effect do Prostaglandins have on the vasculature?
Vasodilation
52
Which complement proteins mediate inflammation and phagocyte recruitment?
C3a
| C5a
53
What is the function of the 'Membrane-Attack-Complex' produced by the complement system?
Can punch holes in bacteria, killing them
| or can phagocytose bacteria
54
What type of bacteria releases endotoxins?
Gram negative bacteria
55
How can phagocytosis during acute inflammatory reaction cause damage to healthy surrounding tissue?
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
Name 4 complications of acute inflammation:
- Damage to normal tissue
- Loss of fluid
- Pain/ Loss-of-function
- Obstruction of tubes (due to exudate)
57
Define pyrogen:
Substance which produces a fever when released into the blood
58
What is the role of Prostaglandin E2 in fever?
It stimulates the hypothalamus and medulla, which increases SNS activity:
- Vasoconstriction
- Increased muscle tone
- Shivering
59
How do endotoxins cause fever?
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
How does Aspirin reduce fever?
Aspirin inhibits cyclo-oxygenase, preventing synthesis of Prostaglandin E2, which causes fever by increasing SNS response.
61
An increase of what kind of leukocytes is associated with a bacterial infection?
Neutrophils
62
An increase in what kind of leukocyte is associated with a viral infection?
Lymphocytes
63
Name 5 acute phase proteins released by the liver during acute inflammation:
1) Fibrinogen
2) C-reactive protein
3) Ceruloplasmin
4) C3 (complement)
5) alpha-1-antitrypsin
64
Where is albumin synthesised?
Liver
65
Where is alpha-1-antitrypsin synthesised?
Liver
66
What serum protein synthesised in the Liver is reduced during acute inflammation?
Albumin
67
What are the symptoms of acute phase response?
Decreased appetite
Increased pulse
Sleepiness
68
What is the most useful acute phase protein released in acute inflammation?
C-reactive protein
69
What are the 4 possible outcomes of acute inflammation?
1) Complete resolution
2) Continues into chronic inflammation
3) Chronic inflammation + Fibrous repair
4) Death
70
What happens to the neutrophils after acute inflammation?
Undergo apoptosis and are phagocytosed with necrotic debris
71
What are the 4 types of exudate?
1) Pus
2) Haemorrhagic
3) Serous
4) Fibrinous
72
Why does pus have a creamy/white appearance?
Rich in dead neutrophils
73
What type of exudate is common in chemotactic bacterial infections?
Pus
74
What type of exudate is common in destructive infections or malignant tumours?
Haemorrhagic
75
How is serous exudate different to plasma?
Serous exudate doesn't contain fibrinogen
76
What are the differences between a fibrinous and haemorrhagic exudate?
```
Fibrinous
- contains fibrin so causing blood clot formation,
- doesn't contain red blood cells
Haemorrhagic
- doesn't contain fibrin
- contains red blood cells
```
77
Name the type of bacteria which causes lobar pneumonia:
Streptococcus pneumoniae
78
What is Lobar pneumonia?
Acute exudative inflammation of a lobe of a lung
79
Name the 4 stages of lobar pneumonia:
1) Congestion
2) Red hepatisation
3) Grey hepatisation
4) Resolution
80
What type of exudate is produced during the congestion stage of lobar pneumonia?
Serous
81
What type of exudate is produced in the red hepatisation stage of lobar pneumonia?
Fibrinous
82
What type of exudate is produced in the grey hepatisation stage of lobar pneumonia?
Pus
83
How is the exudate removed allowing resolution of lobar pneumonia?
Drained into lymphatic system and airways
84
What are the symptoms of Lobar pneumonia?
Fever
Cough (may have bloody sputum)
Pleuritic pain = sharp stabbing pain to lateral chest and upper back, worsens with inhalation/cough
85
List some complications of Lobar pneumonia:
Empyema
Scarring
Abscess formation
Bacteraemia
86
Describe 'pleuritic' chest pain:
Sharp stabbing pain to lateral chest and/or upper back, worsens with inhalation/cough
87
What causes Bacterial meningitis?
Streptococcus pneumonia
Neisseria meningitidis
Listeria monocytogenes
Escherichia coli in neonates
88
What is bacterial meningitis?
Infection and subsequent inflammation of meninges, causing swelling of the brain
89
What are the symptoms of bacterial meningitis?
```
Fever
Headache
Neck stiffness
Confusion
Seizures
Vomiting
```
90
How can doctors test for bacterial meningitis?
Extract CSF via lumbar puncture, test for bacteria which commonly cause meningitis.
91
What are the common causes of Ascending Cholangitis?
Gut bacteria: E coli, Klebsella spp, Enterobacter spp,
| Obstruction of biliary tree via Gallstones
92
What type of pain is caused by ascending cholangitis?
Biliary colic: ache in upper right quadrant
93
What symptom can inform of ascending cholangitis affecting the liver?
Jaundice
94
What is Ascending Cholangitis?
Acute inflammation spreading up the biliary tree
95
What are the main causes of Acute Appendicitis?
Infection
Inflammatory Bowel Disease
Fecal stasis
Parasites
96
What is Acute Appendicitis?
Acute inflammation of the Appendix
97
What are the main symptoms of Acute Appendicitis?
Colic: may be specific to lower right quadrant if ruptured
Anorexia
Nausea/vomiting
98
What are the main complications of Acute Appendicitis?
- Fistula formation
- Rupture = Peritonitis
- Abscess formation
99
Name 3 inherited disorders affecting acute inflammation:
1) Hereditary angioedema
2) Chronic Granulomatous Disease
3) alpha-1-antitrypsin deficiency
100
What genetic inheritance pattern does hereditary angioedema follow?
Autosomal dominant
101
What are the symptoms of hereditary angioedema?
- Non-itchy cutaneous attacks
- Abdominal attacks = abdominal pain, nausea, vomiting, diarrhoea
- Laryngeal attacks = tight, sore, dyspnoea, voice changes
102
What is hereditary angioedema?
Deficinecy of C1-esterase inhibitor, which is required for regulation of the inflammatory response
103
How does a deficiency of C1-esterase inhibitor cause oedema?
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
Name the rare autosomal dominant disorder which causes a deficiency of C1-esterase inhibitor:
Hereditary angioedema
105
What are the symptoms of alpha-1-antitrypsin deficiency?
Breathlessness, wheezing, cough, jaundice
106
How can alpha-1-antitrypsin deficiency cause Liver disease?
Abnormal alpha-1-antitrypsin produced by liver and not exported, so accumulates and causes hepatocyte damage
107
How can alpha-1-antitrypsin deficiency cause COPD or emphysema?
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
What genetic inheritance pattern does alpha-1-antitrypsin deficiency follow?
Autosomal recessive
109
Where is alpha-1-antitrysin produced?
Liver
110
Name the rare autosomal recessive disorder which can cause emphysema and cirrhosis due to a deficiency of a protease inhibitor:
Alpha-1-antitrypsin deficiency
111
What is Chronic Granulomatous disease?
Mutation in NADPH oxidase, which is required by phagocytes to produce superoxide radicals to kill bacteria.
112
What are the symptoms of Chronic Granulomatous disease?
Chronic infections
113
Why can a mutation in NADPH oxidase cause chronic infection?
NADPH oxidase is required by phagocytes to produce superoxide radicals, to kill bacteria
So if deficiency of functional protein, then phagocytes cannot fight infection.
