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Pathological Processes > PP 2 Acute Inflammation > Flashcards

PP 2 Acute Inflammation Flashcards

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1
Q

Inflammation definition

A

Response of living tissue to injury

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2
Q

Features of acute inflammation

A

Immediate
Short duration
Innate/normal
Stereotyped - same regardless
Limits damage

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3
Q

Causes of acute inflammation

A

Trauma/foreign body
Micro organisms/infections
Hypersensitivity - allergies
Other illnesses e.g. cancer, necrosis

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4
Q

Clinical signs of acute inflammation

A

Rubor: redness
Tumour: swelling
Calor: heat
Dolor: pain
Loss of function

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5
Q

How long does vasoconstriction last and what is it?

A

Decreased diameter for a few seconds

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6
Q

How does calor arise?

A

Vasodilation
Increased diameter
More blood

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7
Q

How does rubor arise?

A

Vasodilation
Increased diameter
More blood

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8
Q

What occurs in vasodilatation?

A

1- arterioles dilate
2- flow accelerates into capillaries
3- capillary pressure increases
4- increases delivery of fluids tend leukocytes to injury site

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9
Q

What does increased permeability of walls cause?

A
  • Fluid + cells to move out of vessel
  • causing oedema
  • increase the viscosity of blood > stasis
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10
Q

Stasis meaning

A

Reduced blood flow in vessels

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11
Q

Where does interstitial fluid drain to?

A

Lymph nodes
Stimulates adaptive immune response

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12
Q

Types of interstitial fluid

A

Exudate
Transudate

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13
Q

Difference between exudate and transudate

A

Exudate - protein rich that develops in inflammation
Transudate - lacks proteins + occurs in normal vessels

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14
Q

How does exudate form?

A
  • Tissue injury > release of vasoactive mediators
  • arteriolar dilation > ^ capillary hydrostatic pressure
  • inflammatory mediators cause ^ permeability of walls
  • fluid + plasma proteins diffuse into interstitial space
  • osmotic pressure increase = holds fluid in the interesitial spae
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15
Q

Examples of proteins in exudate

A

Fibrin- mesh limits spread of toxin
Immunoglobulin- from adaptive immune response

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16
Q

What does exudate formation occur in?

A

Inflammation

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17
Q

Vascular permeability in exudate formation

A

Increased permeability

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18
Q

Vascular permeability in transudate formation

A

Unchanged

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19
Q

How does transudate form?

A

Fluid moves out due to:
Increased hydrostatic pressure
Decreased oncotic pressure

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20
Q

What does transudate formation occur in?

A

Hepatic failure
Heart failure
Renal failure

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21
Q

Causes of increased wall permeability

A
  • Retraction of endothelial cells
  • Direct injury e.g. burns, toxins, trauma
  • Leukocyte dependent injury
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22
Q

What are the primary WBC in acute inflammation?

A

Neutrophil

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23
Q

How do neutrophils escape vessels

A

1- migration: cells pushed to vessel wall
2- rolling
3- adhesion
4- emigration/diapedesis: cells move out of vessel

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24
Q

What are responsible for rolling in the cellular phase?

A

Selectins

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25
Where are selectins found?
On activated endothelial cells
26
What are activated endothelial cells?
Endothelial cells which are actively doing something
27
What are selectins activated by?
Chemical mediators
28
What is responsible for adhesion in the cellular phase?
Integrins
29
Where are integrins found?
On neutrophil surface
30
Chemotaxis meaning
Directional movements towards a chemical attractant
31
How do neutrophils move through the intersisitum?
Chemotaxis
32
Examples of chemoattractants
Bacterial peptides Inflammatory mediators - C5a, LTB4 Rearrangement of neutrophil cytoskeleton
33
Opsonisation meaning
Adding opsonin to pathogen to make it visible to neutrophil for phagocytosis
34
Examples of opsonin
C3b C4b IgG antibody IgM antibody CRP Collectins
35
List the order of events that neutrophil follow to capture and kill bacterium
Chemotaxis Activation Margination Diapedesis Recognition attachment Phagocytosis
36
List the stages of acute inflammation
1- stimulus 2- vascular phase 3- cellular phase 4- resolution or persistence
37
Steps in the vascular phase
1- vasoconstriction of arterioles 2- vasodilation of arterioles, then capillaries 3- increased permeability of blood vessels 4- increased viscosity > stasis
38
How does Tumor arise?
Increased permeability in vessel walls Increased fluid in interstitial space - exudate
39
Function of exudate
- to **deliver fibrin, inflammatory mediators and immunoglobulins** to site of damage - **dilutes toxins**: reduces damage to tissues - **^ lymphatic drainage** > delivers antigens + pathogens to lymph nodes > **initiates immune response**
40
Types of exudate
Pus/purulent Haemorrhagic Serous Fibrinous
41
What colour is pus and why?
White/creamy Rich in neutrophils
42
What is pus typical in?
Pyogenic bacterial infectoin
43
What colour is haemorrhagic exudate and why?
Red Lots of RBCs
44
What does haemorrhagic exudate indicate?
Significant vascular damage RBCs are normally too big to leave
45
What colour is serous exudate and what does this indicate?
Clear No micro organisms
46
What is serous exudate produced in?
Blisters and burns
47
What sound does fibrinous exudate make and why?
Rubbing sound Deposition of fibrin causes friction between serosal surfaces
48
Local complications of acute inflammation
- Swellling - compression of tubes - Compression of organs e.g cardiac tamponae - Loss of fluid - Pain - Loss of function
49
Systemic complications of acute inflammation
Fever Acute phase response Leucocytosis Acute phase proteins Septic shock
50
What is a pyrogen? Examples
A substance which produces a fever when in the blood *e.g. prostaglandins, IL-1, IL-6 and TNF-a*
51
How does leucocytosis occur in acute inflammation?
Inflammatory mediators act on bone marrow to produce more leucocytes
52
What WBCs are measure in FBC in bacterial infections?
Neutrophil
53
What WBCs are measure in FBC in viral infections?
Lymphocytes
54
Acute phase proteins present in acute inflammation
C-reactive protein - marker of severity Fibrinogen Alpha-1 antitrypsin
55
What is the acute phase response?
A change in the level of plasma proteins as liver changes its levels of protein synthesis
56
What does the acute phase response cause?
Decreased appetite Tachycardia Altered sleep Change in plasma proteins Malaise
57
Malaise meaning
Feeling of discomfort
58
What occurs in septic shock?
Huge release of chemical mediators Widespread vasodilatation Hypotension Tachycardia Multi-organ failure
59
What can happen after acute inflammation?
- Complete resolution - Repair with connective tissue - fibrosis - Progression to chronic inflammation
60
What occurs in complete resolution of acute inflammation?
- Neutrophils stop marginating - Vessel permeability returns to normal - Exudate drained via lymphatics - Neutrophils undergo apoptosis + get phagocytosed - regeneration - if tissue architecture is preserved - inflammatory mediators degrade
61
Clinical examples of acute inflammation
Bacterial meningitis Pneumonia Acute appendicitis Abscess Inflammation off serous cavities
62
What causes inflammation in serous cavities?
When exudate pours into cavity
63
What is an abscess?
Accumulation pf dead + dying neutrophils
64
What can an abscess cause?
Compression of surrounding structures Pain Blockage of ducts
65
What is diapedesis?
Movement of blood cells through intact blood vessel wall
66
What is an opsonin?
Substate which coats pathogen and makes them easier to phagocytose
67
What is a free radial?
Molecule with a single unpaired electron in outer orbit
68
Examples of protection against free radicals
Antioxidant scavengers *e.g. vitamin A,C + E* Enzymes *e.g. superoxide dismutase + catalase and glutathione peroxidase*
69
How do anti-oxidant scavengers protect against free radicals?
Donate an electron to the free radical and neutralise it
70
Examples of chemoattractants
Thrombin Endotoxin Fibrin degradation products C3a C4a C5a Leukotriene B4 Interleukin 8
71
What mechanisms do neutrophils use to destroy pathogens?
Oxygen independent Oxygen dependent
72
How do neutrophils kill pathogens (oxygen independent)?
Lysozyme Hydrologic enzymes Defensins
73
How do neutrophils kill pathogens (oxygen dependent)?
- ROS *e.g. hydrogen peroxide, OH radical, superoxide anion* - RNS *e.g nitric oxide, nitrogen dioxide*
74
Where do chemical messengers originate from?
Activated inflammatory cells Platelets Endothelial cells Toxins
75
What do chemical messengers do?
Control and coordinate the inflammatory response
76
Inflammatory mediators which bring about vasodilatation
Histamine Serotonin Prostaglandins Nitric oxide
77
Inflammatory mediators which increase permeability
Histamine Bradykinin Leukotrienes C3a C5a
78
Inflammatory mediators which bring about Chemotaxis
Interleukin 1 C5a TNF-a Bacterial peptides
79
Inflammatory mediators which bring about fevers
Prostaglandins Interleukin 1 Interleukin 6 TNF-a
80
What is TNF?
Tumour necrosis factor Inflammatory mediators
81
Inflammatory mediators which bring about pain
Bradykinin Substance P Prostaglandins
82
Outline the cellular phase
1- neutrophils leak out Margination, rolling, adhesion, diapedesis 2- release inflammatory mediators > chemotaxis 3- phagocytosis 4- opsonisation
83
What is alpha-1 antitrypsin deficiency?
Autosomal recessive disorder where there are low levels of alpha-1 antitrypsin
84
What is seen in alpha-1 antitrypsin deficiency?
Emphysema Hepatocyte damage >> cirrhosis
85
What is hereditary angio-oedema?
Autosomal dominant condition Inherited deficiency of C1-esterase inhibitor
86
What is seen in hereditary angio-oedema?
Non-itchy cutaneous angio-oedema Recurrent abdominal pain
87
What is chronic granulomatous disease?
Condition where phagocytes are unable to generate superoxide Phagocytes cannot kill bacteria as they cant generate an oxygen burst
88
What is seen in chronic granulomatous disease?
Recurrent infections Skin abscesses
89
What are prostaglandins and what do they cause?
Substances produced in inflammation from cell membrane phospholipids Cause vasodilation, fever + increased pain sensitivity
90
What is seroma?
A tissue space filled with clear, sterile fluid that occurs as a post-operative complications
91
What are the complications following lobar pneumonia? (5)
- bacteraemia - lung abscesses - empyema - pleural effusion - lung fibrosis
92
What distinguishes acute and chronic inflmmation at a cellular level?
Acute inflammation involves a rapid response with neutrophils Chronic inflammation features lymphocytes + macrophages
93
How can NSAIDs affect acute inflammation?
NSAIDs inhibit COX enzymes > reduces production of pro-inflammatory mediators like prostaglandins

Pathological Processes (14 decks)

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