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MoD > Lesson 2 > Flashcards

Lesson 2 Flashcards

1
Q

Give a brief description on acute inflammation

A 
Protective rapid response of living tissue to injury 
Immediate
Short duration 
Innate 
Stereotyped = always same result 
Initiated to limit tissue damage
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2
Q

State some causes of acute inflammation

A 
Microbial infections 
Hypersensitivity reactions 
Physical agents 
Chemicals
Tissue necrosis
Anything can injure tissue!
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3
Q

What are some key features of acute inflammation?

A

Vascular and cellular reactions = fluid exudate/neutrophils in tissue
Controlled by a variety of chemical mediators -> from plasma or cells
Protective but can cause complications

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4
Q

What are the five key clinical features of acute inflammation (Latin/english terms)?

A 
RUBOR = redness
TUMOR = swelling = oedema 
CALOR = heat 
DOLOR = pain 
FUNCTIO LAESA = loss of function
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5
Q

Describe the changes in tissue during acute inflammation

A

1 Red & hot = Increased blood flow
2 Exudation of fluid into tissue
3 Infiltration of inflammatory cells

1 & 2 = Vascular phase
3 = Cellular phase

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6
Q

Describe the vascular phase in relation to changes in blood flow

A

Transient vasoconstriction of arterioles
Followed by vasodilatation of arterioles and then capillaries -> Increased blood flow
Increased vascular permeability -> exudation of protein-rich fluid into tissues and slowing od circulation
Vascular stasis

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7
Q

Describe the vascular phase when related to increased vascular permeability

A

(1) Hydrostatic pressure
Arteriolar dilatation = hydrostatic pressure increase capillaries relative to pressure interstitial fluid

(2) Osmotic pressure = Increased venular permeability
(1) + (2) = Net flow of protein rich fluid into tissue spaces = oedema

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8
Q

Define Arteriolar dilatation

A

hydrostatic pressure increase capillaries relative to pressure interstitial fluid

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9
Q

What is Starling’s Law?

A

movement of fluid across vessel wall governed by balance of forces of hydrostatic + colloid osmotic pressure between intravascular and extravascular space.

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10
Q

Describe the vascular phase in terms of mechanisms on vascular leakage

A

Endothelial cell contraction = chemical mediators e.g. C5a , NO
Endothelial cell injury
Direct (Trauma, chemicals, microbial toxins)
Indirect (toxic oxygen species/proteolytic enzyme from neutrophils )
Structural re-organization of cytoskeleton
Transcytosis

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11
Q

What is the protein content of transudate?

A

LOW protein content

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12
Q

What is the protein content of exudate?

A

HIGH protein content

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13
Q

List the types of exudate?

A

Purulent ( meningitis )
Haemorrhagic (Malignancies )
Serous (Blister)
Fibrinous (Fibrinous pericarditis)

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14
Q

Describe the cellular phases of acute inflammation

A

Primary leucocyte = Neutrophil aka. Neutrophil leukocyte, neutrophil polymorph, PMN
WBC involved in acute inflammation
Type of granulocyte
Short-lived , 6-24hrs

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15
Q

Describe neutrophil extravasation

A

Vascular stasis -> neutrophils to line up along endothelium = MARGINATION
Roll along endothelium = ROLLING
Stick avidly to endothelium = ADHESION
Emigrate through the endothelium = MIGRATION / DIAPEDESIS

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16
Q

Describe the emigration of neutrophils during neutrophil extravasation

A

ROLLING : Selectins expressed by endothelial cells bind to carbohydrate ligands on neutrophils. Increased by several cytokines secreted by macrophages, mast cells and endothelial cells

ADHESION : Integrins expressed by neutrophils bind to integrin ligands on endothelium

17
Q

Explain diapedesis

A

Chemotaxis = movement along concentration gradients of chemoattractant/Chemotaxins
Chemotaxins : C5a, LTB4, cytokines bacterial products, clotted blood
Receptor ligand binding – selectins, integrins
Rearrangement of cytoskeleton

18
Q

What is the role of neutrophils in acute inflammation

A

Neutrophils migrate to site of injury by chemotaxis
Phagocytose and kill microorganisms
Eliminate foreign material and necrotic tissue
Produce growth factors for repair
But Activated neutrophils may release toxic metabolites and enzymes causing damage to normal host tissue

19
Q

What are some chemical mediators?

A

Modulate the inflammatory response
Short-lived
Endogenous
Every mediator has an inhibitor

20
Q

What are some chemical mediator groups?

A

Endogenous (Cell- derived )
Vasoactive amines ( Histamine , serotonin)
Vasoactive peptides ( Bradykinin)
Chemokines and Cytokines (Messengers )
Arachidonic acid metabolites from plasma membrane phospholipids
Nitric oxide

21
Q

Provide a list of vascular phase chemical mediators

A

Histamine – Mast cells
Serotonin – platelets

Vasoactive amines

Immediate early response
Response to many injurious stimuli
Cause vascular dilation , INCREASE venular permeability + pain

22
Q

Provide a examples of some anti-inflammatories

A 
Aspirin / NSAIN e.g naproxen , ibuprofen 
Antihistamine
Corticosteroids
Leukotriene antagonists e.g montelukast 
TNF alpha antagonists e.g .infliximab
23
Q

What are hallmarks of acute inflammation?

A

Exudate of fluid

Infiltrate of cells

24
Q

How do these responses aid to combat injury?

A
  1. Exudation of fluid
    Delivers plasma proteins, immunoglobulins/inflammatory mediators to area pf injury
    Serves to dilute toxins m reducing impact
    Oedema elicits increased lymphatic drainage; delivers antigens to immune system as well as microorganisms to phagocytes
  2. Vasodilatation
  3. Infiltration of inflammatory cells
  4. Pain and loss of function
25
Q

What are four main systemic effects of acute inflammation?

A
  1. Pyrexia
    Bacterial endotoxins
    Pyrogenic cytokines
  2. Leukocytosis (Increase WCC)
    Macrophages + endothelial cells release colony-stimuklating factord so BM produces more leucocytes
  3. Acute phase response in liver = constitutional symptoms
  4. Shock = circulatory failure
26
Q

What are examples of local complications?

A 
Swelling 
Inappropriate inflammation 
Exudation of fluid 
Loss of fluid 
Prolonged pain and loss of function 
Digestion of host tissues by harmful enzymes releases by neutrophils
27
Q

What disorders are a result of acute inflammation?

A 
Hereditary angio-oedema
Alpha-1 antitrypsin deficiency 
Inherited complement deficiencies 
Defected in neutrophil function 
Defects in neutrophil number
28
Q

Give a summary regarding hereditary angiodema

A

Rare
Autosomal dominant
Deficiency of C1 esterase inhibitor (a component of complement system)
Non-itchy cutaneous angio-oedema + intestinal oedema
FHx sudden death

29
Q

Give a description on Alpha 1 antitrypsin (A1AT) deficiency

A 
Autosomal recessive 
Low levels of A1AT 
A1AT = protease inhibitor which deactivates enzymes released from neutrophils during
Inflammation goes unchecked 
Emphysema + cirrhosis
30
Q

Give a description on chronic granulomatous disease

A

Genetic condition
Neutrophil is unable to generate free radical
Superoxide and so it cannot kill the bacteria
Chronic infections from the first year of life
Numerous granulomas and abscesses

MoD (11 decks)

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