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Phase 2A Mehdi > Intro and Acute Inflammation > Flashcards

Intro and Acute Inflammation Flashcards

1
Q

What is Inflammation?

A

Local physiological response to tissue injury

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2
Q

What is acute inflammation?

A

Initial and transient series of tissue reactions

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3
Q

The benefit of inflammation

A

Prevents spread of infection by destroying microorganisms and wailing off abscess cavities

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4
Q

What is Evisceration?

A

examination of all organs in situ by a y-shaped incision

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5
Q

Describe the steps of Acute Inflammation (TVVN)

A

Tissue injury reaction
Vessel dilation
Vascular protein leakage
Neutrophil polymorph recruitment

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6
Q

What are the outcomes of Acute Inflammation (RSOC)?

A

Resolution
Suppuration
Organisation
Chronic Inflammation

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7
Q

What is Suppuration?

A

Pus (neutrophils and bacteria in all states) formation
Caused by pyogenic bacteria (S.aureus, S.pyrogenies, Neisseria and coliform)
Healing of the pus forms a pyogenic membrane and leads to granulation tissue and scarring

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8
Q

How is a scar formed in Organisation?

A
  • Tissue loses ability to regenerate specialised cells
  • Dead tissue and exudate removed by macrophages
  • Fibroblasts proliferate via TGF-beta = fibrosis
  • Tissue replaced with granulation tissue
  • Collagen is produced by granulation to form a scar
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9
Q

What are the causes of Acute Inflammation (MHPCT)?

A 
Microbial Infection
Hypersensitivity Reaction
Physical Agent
Chemicals
Tissue Necrosis
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10
Q

How do viruses kill cells?

A

Intracellular Multiplication

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11
Q

How does bacteria kill cells?

A

Release inflammation initiating exotoxins

Release endotoxins

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12
Q

In what instances are hypersensitivity reactions important?

A

Parasitic Infection

Tuberculous Inflammation

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13
Q

How does a hypersensitivity reaction damage tissue?

A

An altered state of an immunological response causes a wrong reaction

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14
Q

How do physical agents damage tissue?

A

Physical trauma
Radiation
Burning
Cooling

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15
Q

How do chemicals cause inflammation?

A

Gross tissue damage

Direct irritation to Inflammation

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16
Q

How does tissue necrosis cause inflammation?

A

Hypoxic tissue dies

Peptide released from dead tissue

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17
Q

What are the physical characteristics of acute inflammation (RHSPF)?

A 
Redness
Heat
Swelling
Pain
Function Loss
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18
Q

Why is there redness in Acute inflammation?

A

Caused by dilation of small blood vessels

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19
Q

Why is there heat in Acute inflammation?

A

Increased blood flow (hyperaemia)
Vascular dilation
Systemic Fever from chemicals

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20
Q

Why is there swelling in Acute inflammation?

A

Oedema - fluid in extravascular space
Movement of inflammatory cells
Formation of Connective Tissue

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21
Q

Why is there pain in Acute inflammation?

A

Distortion from oedema
Pressure from Pus
Bradykinin, Prostaglandins and Serotonin

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22
Q

Why is there loss of function in Acute inflammation?

A

Movement is consciously/reflex inhibited

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23
Q

What accumulates in the early stages of acute inflammation in Extracellular space?

A

Oedema Fluid
Fibrin
NEUTROPHIL POLYMORPHS

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24
Q

Describe the acute inflammatory process?

A

Vessel gets wider and increases blood flow
Increases vascular permeability
Formation of fluid exudate
Cellular exudate formation

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25
How is Cellular exudate formed?
Neutrophil polymorph movement to extravascular space
26
How is capillary calibre controlled?
They have no smooth muscle but are single cell thick
27
How is arteriolar blood flow controlled?
They have smooth muscle and form precapillary sphincters to regulate flow through capillary bed
28
What happens to precapillary sphincters during acute inflammation?
The sphincters relax Blood flow increases Redness and Heat
29
What happens to osmotic pressure in normal capillaries?
There is a high osmotic pressure in the vessel due to plasma proteins Fluid returns to the vascular compartment
30
What happens to hydrostatic pressure in normal capillaries?
There is a high hydrostatic pressure at the arteriolar end Fluid is forced into extravascular space Fluid returns at the venous end at low hydrostatic pressure
31
What happens to pressure in acutely inflamed capillaries?
High hydrostatic pressure Plasma proteins leak into extravascular space High osmotic pressure More fluid leaves the vessel than returns Vascular Permeability Increases
32
What is fluid exudate?
The protein-rich fluid that leaves
33
What are the causes of immediate transient vascular permeability?
Chemical mediators (histamine, bradykinin, NO2, C5a, Leukotrine B4 and platelet activating factor)
34
What are the causes of immediate sustained vascular permeability?
Severe direct vascular injury
35
What are the causes of delayed prolonged vascular permeability?
Endothelial cell injury (x-ray, bacterial toxins....)
36
What is the diagnostic histological characteristic of acute inflammation?
Neutrophil polymorph accumulation in extracellular space
37
What are the stages of neutrophil polymorph emigration?
Margination Adhesion Emigration Diapedesis
38
What is neutrophil margination?
Cells travel in the plasmatic (peripheral) zone of blood vessels due to loss of IV fluid Increase in plasma viscosity so slow flow at the site of inflammation
39
What is neutrophil adhesion?
Pavementing occurs in venules | Increased leucocyte adhesion with endothelium
40
What is pavementing?
Adhesion of neutrophils with endothelium at the site of acute inflammation
41
What is neutrophil emigration?
NEUTROPHILS/ Eosinophil polymorphs/ macrophages insert pseudopodia between ENDO. CELLS Move between the cells through to the BASAL LAMINA and then the VESSEL WALL
42
What is pseudopodia?
Cytoplasm filled temporary PROJECTION directed in the way of movement
43
How do leukocytes travel?
They migrate through venule walls and veins | They don't normally exit capillaries
44
What is diapedesis?
The passive movement of RBC escape from vessels via hydrostatic pressure
45
What does the presence of a large number of red blood cell suggest in the extracellular space?
Implies severe vascular injury
46
Why does acute inflammation spread?
Injured tissue releases chemical substances which spread to uninjured tissue
47
What causes the up-regulation of adhesion molecules initially?
Histamine and Thrombosis production
48
What is the result of the initial increased Histamine and Thrombosis production?
Very firm neutrophil adhesion
49
What are the endogenous chemical mediators of acute inflammation?
Histamine and Thrombosis
50
What do the endogenous chemical mediators cause (VNCII)?
``` Vasodilation Neutrophil Emigration Chemotaxis Increased vascular permeability Itching and pain ```
51
What is chemotaxis?
The attraction of neutrophil polymorphs toward certain chemicals
52
What does histamine do?
It causes vascular dilation | Transient phase of Increased vascular permeability
53
Why does Histamine have an immediate effect?
It is stored in preformed granules which release histamine quickly
54
Where is Histamine found?
Mostly in MAST CELLS Basophils Eosinophils Platelets
55
What stimulates Histamine release?
C3a and C5a complement | Lysosomal proteins released from neutrophils
56
What is mast cell degranulation?
The release of Histamine granules from mast cells
57
What are the 6 types of chemical mediators?
``` Histamine Thrombosis Lysosomal compounds Eicsanoids (prostoglandin) Seretonin Chemokine ```
58
What are the 4 plasma enzymatic cascade systems (CKCF)?
Complement Kinins Coagulation Factors Fibronylitic system
59
What is Rubor?
Redness
60
What is Calor?
Heat
61
What is Tumor?
Swelling
62
What is Dolor?
Pain
63
What is the purpose of the plasma enzymatic cascade systems?
To produce inflammatory mediators
64
How can the cascade system remove/destroy antigens?
Lysis | Opsonisation
65
What is Opsonisation?
Phagocytosis enhancement by Plasma Opsonins (factors)
66
What activates the cascade system during acute inflammation?
Tissue Necrosis - complement activating enzyme released Infection - complement activating antigen-antibody complexes formed (Classical Pathway) complement activating endotoxins released by gram-negative bacteria (Alternative Pathway)
67
What is the Classical pathway?
Infection - complement activating antigen-antibody complexes formed
68
What is the Alternative Pathway?
Infection - complement activating endotoxins released by gram-negative bacteria
69
How does the Hageman factor (Coagulation factor XII) activate the Kinin complement?
Factor XII and Plasmin convert Prekallikien to Kallikrein | Kininogens are then converted to Kinins
70
What can cause the conversion of Prekallikrien?
Activated factor XII and Plasmin | Leucocyte Proteases
71
What 2 systems does Hageman factor (Coagulation factor XII) activate to produce fibrin?
Fibrinolytic System | Coagulation System
72
How is Fibrin produced by the Fibrinolytic pathway?
Hageman factor activates the Fibrinolytic system | Plasmin degrades into Fibrin
73
How is Fibrin produced by the Coagulation pathway?
Hageman factor activates the coagulation system | Fibrin is produced
74
What are the chemical mediators of Vascular Dilation?
Histamine Prostoglandins NO2 PAF
75
What are the chemical mediators of increased vascular permeability?
Transient- Histamine | Prolonged - Bradykinin, NO2, C5a, leucotriene B4, PAF
76
What are the chemical mediators Leucocyte adhesion?
Adhesion Upregulation - IL-8, C5a, Leucotriene B4, Il-1 and TNF-Alpha
77
What are the chemical mediators of Neutrophil Polymorph Chemotaxis?
IL-8 and Leucotriene B4
78
What is the Cytokine IL-4?
Interleukin 4
79
What is the Cytokine TNF- alpha?
Tumour necrosis factor- a
80
What do tissue macrophages do in acute inflammation?
They secrete chemical mediators in response to injury/infection
81
Which chemical mediators have an effect after Histamine and Thrombin?
IL-1 | TNF-alpha
82
What does IL-1 and TNF do to endothelial/epithelial cells and fibroblasts?
Secrete MCP-1 which attracts neutrophil polymorphs (Chemotaxis)
83
How do blood monocytes become macrophages?
Blood monocytes enter inflammation site Become macrophages when leaving blood vessel Becmome more metabolically active, motile and phagocytic
84
How is Phagocytosis enhanced?
Opsonisation by antibodies / complement
85
In acute Inflammation, are macrophages or neutrophil polymorphs most dominant?
Neutrophil Polymorphs | Macrophages do not dominate until NP number decrease and M number increase by proliferation
86
What is the role of macrophages in acute inflammation?
Clear away tissue/damaged cells
87
What aids digestion of Inflammatory Exudate?
Lysosomal enzyme discharge from macrophages and neutrophils
88
What is the lymphatic ?system
Collection of vessels, tissues and organs
89
What does the lymphatic system carry?
It carries excess fluid and particulate from tissues to the bloodstream AKA lymph
90
what are afferent lymphatic vessels?
These vessels enter into the lymph nodes, flowing into the sinus space below the capsule of the node.
91
What is lymph?
A colourless, watery bodily fluid carried by the lymphatic system, consisting mainly of white blood cells
92
What are germinal centres?
Places within secondary lymph nodes to which B cells migrate to proliferate and differentiate based on an antigen response
93
Describe the transport of of lymph in vessels
Interstitial Space has Lymph which filters into Capillaries feed into Collecting vessels into Afferent vessels into trunks/nodes
94
What valves are present in the lymph vessels?
Mini-valves - in capillary endothelium letting lymph in | Semilunar valves - promote forward travel (with muscular contraction) in collecting vessels and prevent backflow
95
As well as fluid, what else can enter the lymph nodes
Pathogens Proteins Tumour cells
96
How is lymph filtered of pathogens at the nodes?
The nodes contain lymphocytes such as B and T cells to produce immune response (B cells can produce antigen specific response)
97
How does the lymphatic system help target acute inflammation?
The Lymphatic channels dilate They drain away oedema fluid of inflammatory exudate This decreases the amount of tissue oedema fluid
98
How are neutrophil polymorphs charecterised?
Most abundant lymphocyte | Under H+E stain, blue nucleus and pink cytoplasm
99
List the roles of neutrophil polymorph in acute inflammation
Microorganism Adhesion Phagocytosis Intracellular death Lysosomal release
100
Describe microorganism adhesion
Microorganisms are opsonised by immunoglobulins/complement components Alternative Pathway- bacterial lipopolysaccharide activate complement to make C3b(Opsoniser) Classical Pathway - antibody-bacterial antigen complex activates complement to make C3b(Opsoniser)
101
How can neutrophils bind to micro-organisms?
Imunnoglobulins bind to the FAB region of micro-organisms Fc component is exposed Neutrophils bind to the Fc region then ingest
102
Describe neutrophil phagocytosis
Opsonisation of the particle Phagocyte ingests by surrounding particle with pseudopodia Arms of pseudopodia fuse and form phagosome around particle Lysosomes bind with phagosome to initiate intracellular killing
103
Describe intracellular killing
Neutrophil polymorphs contain noxious agents.... - H202 reacts with myeloperoxidase in the presence of a halide = potent agent - lysozyme and lactoferrin
104
What happens when lysosomal products are released?
Local tissue is damaged by proteolysis from elastase and collagenase Coagulation factor XII activated Leukocytes attracted -Some compounds increase Vas. Permeability -Some compounds are pyrogens
105
What are pyrogens?
They are compounds that induce systemic fever by acting on the hypothalamus
106
What is the role of mast cells in Acute inflammation?
mast cell degradation - releases histamine and metabolises arachidonic acid into leukotrienes, prostaglandins and thromboxane
107
Types of Inflammation (descriptive)
``` Serous - fluid release Supparative - pus filled Membranous Pseudomembranous Necrotising - gangrenous ```
108
Beneficial effects of Fluid Exudate
Toxin dilution - carried away in lymphatics Antibody entry (via inc. vas. permeability) - neutralise toxins, lysis via complement system or phagocytosis via opsonisation Drug transport Fibrin formation - from fibrinogen which can trap microorganisms and allow the formation of granulation tissue O2 and nutrient delivery - Increased fluid flow delivery for highly metabollic neutrophils Immune response - Lymphatic system
109
Harmful effects of lysosomal enzymes
Tissue Digestion - by collagenases and proteases Swelling - harmful in children such as acute epiglottis swelling from influenza (airway obstruction) - acute meningitis = increased cranial pressure = ischaemic damage Inappropriate Inflammatory Response - Type 1 Hypersensitivity reactions (environmental allergies)
110
Describe resolution
Complete restoration - minimal cell death - occurrence in regenerative systems - Rapid response to cause - Good vascular drainage
111
What is an abscess?
A collection of pus where the bacteria is inaccessible to antibiotic drugs and antibodies
112
What happens if an abscess burst?
The abscess cavity collapses and is taken over by organisation and scarring
113
What is the result of an abscess in a hollow organ?
Mucosal layers of the outflow tract can fuse by fibrin causing an empyema(pus filled pocket)
114
What is organisation?
Tissue replacement by granulation tissue because.... -Large amounts of fibrin formed -Necrotic tissue Exudate/debris cannot be removed
115
How can acute inflammation progress to chronic
- If stimulus is not removed - The nature of the exudate changes - Neutrophil polymorphs replaced by lymphocytes, macrophages, giant cells and fibroblasts
116
What are the systemic effects of Inflammation
- Pyrexia (fever) - Reticuloendothelial reactive hyperplasia - Haematological changes - Amyloidosis
117
What causes pyrexia
Neutrophil polymorphs/Macrophages produce endogenous pyrogens (IL-2) which set thermoregulation at a higher temperature -Pyrogen release is stimulated by phagocytosis, endotoxins and immune complexes
118
What are the constitutional symptoms of inflammation
Malaise (weakness) Anorexia Nausea Weight loss- negative nitrogen balance due to increased energy use with inflammatory mediators
119
What is reactive hyperplasia of the reticuloendothelial system
Lymph node enlargement | Splenomegaly (Increased spleen size)
120
What are the haematological changes of inflammation
Increased levels of.... - white blood cells - neutrophils (pyogenic infection and tissue destruction) - eosinophils (allergic disorders and parasitic infection) - lymphocytes (Chronic/ viral infections and whooping cough) - monocytes (Bacterial infections)
121
Why may anaemia be a result of inflammation
Blood loss into the inflammatory exudate (ulcerative colitis) or due to haemolysis by bacterial toxins
122
What is Amyloidosis
Long standing chronic inflammation caused by elevating serum amyloid A protein which can deposit into various tissues

Phase 2A Mehdi (6 decks)

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