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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
Q

How is Cellular exudate formed?

A

Neutrophil polymorph movement to extravascular space

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26
Q

How is capillary calibre controlled?

A

They have no smooth muscle but are single cell thick

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27
Q

How is arteriolar blood flow controlled?

A

They have smooth muscle and form precapillary sphincters to regulate flow through capillary bed

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28
Q

What happens to precapillary sphincters during acute inflammation?

A

The sphincters relax
Blood flow increases
Redness and Heat

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29
Q

What happens to osmotic pressure in normal capillaries?

A

There is a high osmotic pressure in the vessel due to plasma proteins
Fluid returns to the vascular compartment

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30
Q

What happens to hydrostatic pressure in normal capillaries?

A

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

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31
Q

What happens to pressure in acutely inflamed capillaries?

A

High hydrostatic pressure
Plasma proteins leak into extravascular space
High osmotic pressure
More fluid leaves the vessel than returns
Vascular Permeability Increases

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32
Q

What is fluid exudate?

A

The protein-rich fluid that leaves

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33
Q

What are the causes of immediate transient vascular permeability?

A

Chemical mediators (histamine, bradykinin, NO2, C5a, Leukotrine B4 and platelet activating factor)

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34
Q

What are the causes of immediate sustained vascular permeability?

A

Severe direct vascular injury

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35
Q

What are the causes of delayed prolonged vascular permeability?

A

Endothelial cell injury (x-ray, bacterial toxins….)

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36
Q

What is the diagnostic histological characteristic of acute inflammation?

A

Neutrophil polymorph accumulation in extracellular space

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37
Q

What are the stages of neutrophil polymorph emigration?

A

Margination
Adhesion
Emigration
Diapedesis

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38
Q

What is neutrophil margination?

A

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

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39
Q

What is neutrophil adhesion?

A

Pavementing occurs in venules

Increased leucocyte adhesion with endothelium

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40
Q

What is pavementing?

A

Adhesion of neutrophils with endothelium at the site of acute inflammation

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41
Q

What is neutrophil emigration?

A

NEUTROPHILS/ Eosinophil polymorphs/ macrophages insert pseudopodia between ENDO. CELLS
Move between the cells through to the BASAL LAMINA and then the VESSEL WALL

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42
Q

What is pseudopodia?

A

Cytoplasm filled temporary PROJECTION directed in the way of movement

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43
Q

How do leukocytes travel?

A

They migrate through venule walls and veins

They don’t normally exit capillaries

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44
Q

What is diapedesis?

A

The passive movement of RBC escape from vessels via hydrostatic pressure

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45
Q

What does the presence of a large number of red blood cell suggest in the extracellular space?

A

Implies severe vascular injury

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46
Q

Why does acute inflammation spread?

A

Injured tissue releases chemical substances which spread to uninjured tissue

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47
Q

What causes the up-regulation of adhesion molecules initially?

A

Histamine and Thrombosis production

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48
Q

What is the result of the initial increased Histamine and Thrombosis production?

A

Very firm neutrophil adhesion

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49
Q

What are the endogenous chemical mediators of acute inflammation?

A

Histamine and Thrombosis

50
Q

What do the endogenous chemical mediators cause (VNCII)?

A 
Vasodilation
Neutrophil Emigration
Chemotaxis
Increased vascular permeability
Itching and pain
51
Q

What is chemotaxis?

A

The attraction of neutrophil polymorphs toward certain chemicals

52
Q

What does histamine do?

A

It causes vascular dilation

Transient phase of Increased vascular permeability

53
Q

Why does Histamine have an immediate effect?

A

It is stored in preformed granules which release histamine quickly

54
Q

Where is Histamine found?

A

Mostly in MAST CELLS
Basophils
Eosinophils
Platelets

55
Q

What stimulates Histamine release?

A

C3a and C5a complement

Lysosomal proteins released from neutrophils

56
Q

What is mast cell degranulation?

A

The release of Histamine granules from mast cells

57
Q

What are the 6 types of chemical mediators?

A 
Histamine 
Thrombosis
Lysosomal compounds
Eicsanoids (prostoglandin)
Seretonin
Chemokine
58
Q

What are the 4 plasma enzymatic cascade systems (CKCF)?

A

Complement
Kinins
Coagulation Factors
Fibronylitic system

59
Q

What is Rubor?

A

Redness

60
Q

What is Calor?

A

Heat

61
Q

What is Tumor?

A

Swelling

62
Q

What is Dolor?

A

Pain

63
Q

What is the purpose of the plasma enzymatic cascade systems?

A

To produce inflammatory mediators

64
Q

How can the cascade system remove/destroy antigens?

A

Lysis

Opsonisation

65
Q

What is Opsonisation?

A

Phagocytosis enhancement by Plasma Opsonins (factors)

66
Q

What activates the cascade system during acute inflammation?

A

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
Q

What is the Classical pathway?

A

Infection - complement activating antigen-antibody complexes formed

68
Q

What is the Alternative Pathway?

A

Infection - complement activating endotoxins released by gram-negative bacteria

69
Q

How does the Hageman factor (Coagulation factor XII) activate the Kinin complement?

A

Factor XII and Plasmin convert Prekallikien to Kallikrein

Kininogens are then converted to Kinins

70
Q

What can cause the conversion of Prekallikrien?

A

Activated factor XII and Plasmin

Leucocyte Proteases

71
Q

What 2 systems does Hageman factor (Coagulation factor XII) activate to produce fibrin?

A

Fibrinolytic System

Coagulation System

72
Q

How is Fibrin produced by the Fibrinolytic pathway?

A

Hageman factor activates the Fibrinolytic system

Plasmin degrades into Fibrin

73
Q

How is Fibrin produced by the Coagulation pathway?

A

Hageman factor activates the coagulation system

Fibrin is produced

74
Q

What are the chemical mediators of Vascular Dilation?

A

Histamine
Prostoglandins
NO2
PAF

75
Q

What are the chemical mediators of increased vascular permeability?

A

Transient- Histamine

Prolonged - Bradykinin, NO2, C5a, leucotriene B4, PAF

76
Q

What are the chemical mediators Leucocyte adhesion?

A

Adhesion Upregulation - IL-8, C5a, Leucotriene B4, Il-1 and TNF-Alpha

77
Q

What are the chemical mediators of Neutrophil Polymorph Chemotaxis?

A

IL-8 and Leucotriene B4

78
Q

What is the Cytokine IL-4?

A

Interleukin 4

79
Q

What is the Cytokine TNF- alpha?

A

Tumour necrosis factor- a

80
Q

What do tissue macrophages do in acute inflammation?

A

They secrete chemical mediators in response to injury/infection

81
Q

Which chemical mediators have an effect after Histamine and Thrombin?

A

IL-1

TNF-alpha

82
Q

What does IL-1 and TNF do to endothelial/epithelial cells and fibroblasts?

A

Secrete MCP-1 which attracts neutrophil polymorphs (Chemotaxis)

83
Q

How do blood monocytes become macrophages?

A

Blood monocytes enter inflammation site
Become macrophages when leaving blood vessel
Becmome more metabolically active, motile and phagocytic

84
Q

How is Phagocytosis enhanced?

A

Opsonisation by antibodies / complement

85
Q

In acute Inflammation, are macrophages or neutrophil polymorphs most dominant?

A

Neutrophil Polymorphs

Macrophages do not dominate until NP number decrease and M number increase by proliferation

86
Q

What is the role of macrophages in acute inflammation?

A

Clear away tissue/damaged cells

87
Q

What aids digestion of Inflammatory Exudate?

A

Lysosomal enzyme discharge from macrophages and neutrophils

88
Q

What is the lymphatic ?system

A

Collection of vessels, tissues and organs

89
Q

What does the lymphatic system carry?

A

It carries excess fluid and particulate from tissues to the bloodstream AKA lymph

90
Q

what are afferent lymphatic vessels?

A

These vessels enter into the lymph nodes, flowing into the sinus space below the capsule of the node.

91
Q

What is lymph?

A

A colourless, watery bodily fluid carried by the lymphatic system, consisting mainly of white blood cells

92
Q

What are germinal centres?

A

Places within secondary lymph nodes to which B cells migrate to proliferate and differentiate based on an antigen response

93
Q

Describe the transport of of lymph in vessels

A

Interstitial Space has Lymph
which filters into
Capillaries feed into
Collecting vessels into Afferent vessels into trunks/nodes

94
Q

What valves are present in the lymph vessels?

A

Mini-valves - in capillary endothelium letting lymph in

Semilunar valves - promote forward travel (with muscular contraction) in collecting vessels and prevent backflow

95
Q

As well as fluid, what else can enter the lymph nodes

A

Pathogens
Proteins
Tumour cells

96
Q

How is lymph filtered of pathogens at the nodes?

A

The nodes contain lymphocytes such as B and T cells to produce immune response (B cells can produce antigen specific response)

97
Q

How does the lymphatic system help target acute inflammation?

A

The Lymphatic channels dilate
They drain away oedema fluid of inflammatory exudate
This decreases the amount of tissue oedema fluid

98
Q

How are neutrophil polymorphs charecterised?

A

Most abundant lymphocyte

Under H+E stain, blue nucleus and pink cytoplasm

99
Q

List the roles of neutrophil polymorph in acute inflammation

A

Microorganism Adhesion
Phagocytosis
Intracellular death
Lysosomal release

100
Q

Describe microorganism adhesion

A

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
Q

How can neutrophils bind to micro-organisms?

A

Imunnoglobulins bind to the FAB region of micro-organisms
Fc component is exposed
Neutrophils bind to the Fc region then ingest

102
Q

Describe neutrophil phagocytosis

A

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
Q

Describe intracellular killing

A

Neutrophil polymorphs contain noxious agents….

  • H202 reacts with myeloperoxidase in the presence of a halide = potent agent
  • lysozyme and lactoferrin
104
Q

What happens when lysosomal products are released?

A

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
Q

What are pyrogens?

A

They are compounds that induce systemic fever by acting on the hypothalamus

106
Q

What is the role of mast cells in Acute inflammation?

A

mast cell degradation - releases histamine and metabolises arachidonic acid into leukotrienes, prostaglandins and thromboxane

107
Q

Types of Inflammation (descriptive)

A 
Serous - fluid release
Supparative - pus filled
Membranous 
Pseudomembranous
Necrotising - gangrenous
108
Q

Beneficial effects of Fluid Exudate

A

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
Q

Harmful effects of lysosomal enzymes

A

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
Q

Describe resolution

A

Complete restoration

  • minimal cell death
  • occurrence in regenerative systems
  • Rapid response to cause
  • Good vascular drainage
111
Q

What is an abscess?

A

A collection of pus where the bacteria is inaccessible to antibiotic drugs and antibodies

112
Q

What happens if an abscess burst?

A

The abscess cavity collapses and is taken over by organisation and scarring

113
Q

What is the result of an abscess in a hollow organ?

A

Mucosal layers of the outflow tract can fuse by fibrin causing an empyema(pus filled pocket)

114
Q

What is organisation?

A

Tissue replacement by granulation tissue because….
-Large amounts of fibrin formed
-Necrotic tissue
Exudate/debris cannot be removed

115
Q

How can acute inflammation progress to chronic

A
  • If stimulus is not removed
  • The nature of the exudate changes
  • Neutrophil polymorphs replaced by lymphocytes, macrophages, giant cells and fibroblasts
116
Q

What are the systemic effects of Inflammation

A
  • Pyrexia (fever)
  • Reticuloendothelial reactive hyperplasia
  • Haematological changes
  • Amyloidosis
117
Q

What causes pyrexia

A

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
Q

What are the constitutional symptoms of inflammation

A

Malaise (weakness)
Anorexia
Nausea
Weight loss- negative nitrogen balance due to increased energy use with inflammatory mediators

119
Q

What is reactive hyperplasia of the reticuloendothelial system

A

Lymph node enlargement

Splenomegaly (Increased spleen size)

120
Q

What are the haematological changes of inflammation

A

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
Q

Why may anaemia be a result of inflammation

A

Blood loss into the inflammatory exudate (ulcerative colitis) or due to haemolysis by bacterial toxins

122
Q

What is Amyloidosis

A

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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