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ESA 2 > MoD Session 2: acute inflammation > Flashcards

MoD Session 2: acute inflammation Flashcards

1
Q

Causes of acute inflammation?

A 
Foreign bodies
Microbial infection
Hypersensitivity
Tissue necrosis
Trauma
Physical agents (thermal injury, irradiation)
Chemicals
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2
Q

Hallmarks of acute inflammation?

A 
Rubor (redness)     [vasodilation]
Tumor (swelling)  [fluid and leukocytes]
Calor (heat)   [vasodilation]
Dolor (pain)  [nerve endings stimulated by mediators]
Loss of function
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3
Q

Vascular phase of acute inflammation?

A
  1. Transient vasoconstriction of arterioles (A few seconds, least important)
  2. Vasodilation of arterioles then capillaries (rubor + calor)
  3. Increased permeability of blood vessels (exudation of protein-rich fluid into tissues, slowing of circulation, increased resistance)
  4. Stasis of blood flow
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4
Q

Role of histamine in vascular phase of acute inflammation?

A

Vasoactive amine released from mast cells, basophils and platelets due to trauma, immune reactions, complement proteins, IL-1…
Causes endothelial cells to contract and pull apart, gaps appear, plasma protein can pass through causing fluid leakage

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5
Q

How does a fluid exudate form?

A

Arteriole and capillary dilation causes increased hydrostatic pressure
Increased permeability of vessel walls causes loss of protein, so the interstitium has a higher colloid osmotic pressure
Both of these factors cause net flow out of the vessel (so more fluid in tissue spaces–> oedema). Fluid can be transudate or exudate

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6
Q

What is a transudate?

A

Due to increased hydrostatic pressure
Low protein
Occurs in cardiac failure or venous outflow

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7
Q

What is an exudate?

A

Occurs in acute inflammation
High protein content
Leads to increased lymphatic drainage, taking microbes and antigens to lymph nodes, can get lymphadenitis

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8
Q

Mechanisms of vascular leakage?

A

Endothelial contraction-gaps (histamine, leukotrienes)
Cytoskeletal reorganisation-gaps (cytokines IL-1 & TNF)
Direct injury: toxic burns, chemicals
Leukocyte-dependent injury: toxic oxidative species and enzymes from leukocytes
Increased transcytosis (VEGF)

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9
Q

Role of fibrin in fluid exudate?

A

Is rich in exudate
Activated in inflammation, mesh–>clot
Localised area around injured tissue

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10
Q

Defensive forces of the exudate?

A

Opsonins: coat foreign matrials and make them easy to phagocytose
Complement: produce a bacteria-perforating structure locally
Antibodies: also act as opsonins

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11
Q

The four stages in the infiltration of neutrophils?

A
  1. Margination (line up at edge of blood vessels along endothelium due to stasis: usually flow down middle when laminar flow)
  2. Rolling (roll along endothelium and loosely stick to it)
  3. Adhesion (stick more tightly)
  4. Emigration (through blood vessel wall)
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12
Q

How do neutrophils move?

A

Chemotaxis

Move along the concentration gradients of chemoattractants e.g. C5a, receptor-ligand binding

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13
Q

Neutrophil activation?

A

Switched to a higher metabolic level

Ca2+ and Na+ move in, cell swells and reorganises cytoskeleton, stickier cells

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14
Q

Neutrophil other names?

A

Neutrophil leucocyte
Main WBC of acute inflammation
A type of granulocyte
Also called polymorphs (old terminology)

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15
Q

Diapedesis of neutrophils?

A

Produce collagenase-digests basement membrane

Move by pulling themselves along collagen fibres towards target

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16
Q

What are opsonins?

A

Substances that make it easier for phagocytes to recognise targets. If there are no opsonins then the phagocyte can recognise surface antigens
They are plasma proteins
E.g. complement protein C3b, IgG antibody

17
Q

What is phagocytosis?

A

Phagocyte membrane forms crater shape around target particle
Plasma membrane fuses with phagocyte surrounding it making a phagosome
Granules move towards phagosome aand fuse
Inject their bactericidal substances causing degranulation and removal of necrotic cell debris

18
Q

How do neutrophils kill bacteria?

A
  1. Oxygen-dependent: use free radicals in respiratory burst

2. Oxygen-independent: use enzymes e.g. proteases, nucleases

19
Q

Name the main chemical mediators of acute inflammation

A

Proteases (e.g. complement)
Prostaglandins (cause vasodilation, increase flow, fever, pain. Blocked by aspirin and NSAIDs to reduce pain and fever)
Leukotrienes (increase permeability)
Histamine (increase blood flow and permeability)
Cytokines and chemokines (from WBCs. E.g. IL, TNFa)
Bradykinin (permeability, vasodilation, pain)
Complement components (form a hole in bacteria)
Exogenous mediators (e.g. endotoxin made by gram negative bacteria)

20
Q

List the main roles of inflammatory mediators

A

Vasodilation (histamine and serotonin)
Increased vascular permeability (hisamine, serotonin, bradykinin)
Chemotaxis (leukotrienes, complement proteins)
Phagocytosis (C3b)
Pain (bradykinin)

21
Q

How do inflammatory mediators constitute an effective response to injury?

A
  1. Fluid exudation (so move lymph drainage and more proteins to site and dilutes toxin)
  2. Infiltration of cells
  3. Vasodilation
  4. Pain and loss of function (enforces rest)
22
Q

Local complications of acute inflammation?

A

Swelling
Exudate (can compress e.g. cardiac tamponade)
Damage of normal tissue
Fluid loss (e.g. in burns as fluid can leak continually from a surface wound)
Pain and loss of function

23
Q

Systemic effects of actue inflammation: can be seen within one day

A
  1. FEVER-endogenous pyrogens (IL-1, TNFa) increase prostaglandin synthesis. Can be useful at killing bacteria. Aspirin inhibits cyclooxygenase to reduce prostaglandin made so reduce fever
  2. LEUKOCYTOSIS-increased no. circulating leucocytes
  3. ACUTE PHASE RESPONSE-within hours change in pattern of protein synthesis so change in levels of plasma proteins (e.g. CRP-an opsonin). Causes symptoms of decreased appetite, fatigue and increased heart rate)
  4. SHOCK-dramatic fall in blood pressure due to vasodilation and increased permeability causing fluid exudation. Often fatal. As bacterial products or inflammatory mediators spread around body
24
Q

Sequeale of unresolved acute inflammation?

A

Abscess (AI + CI)
Chronic inflammation and fibrous repair
Death

25
Q

Morphological changes in AI resolution?

A

Neutrophils stop marginating
Vessel permeability to normal
Vessel calibre back to normal

26
Q

Effects of AI resolution?

A

Exudate drains to lymphatics
Fibrin degraded by proteases
Neutrophils apoptosise and are phagocytosed
Damaged tissue may be able to regenerate
If tissue architecture destroyed and complete resolution not possible, fibrous scar tissue will form

27
Q

Describe the four types of exudate

A

Pus/abscess: creamy/white, rich in neutrophils, often bacterial
Haemorrhagic: RBCs so appears red, indicates significant vascular damage, seen in destructive infections and malignancy
Serous: plasma proteins but few leucocytes, clear, e.g. in blisters. Not transdudate as has proteins
Fibrinous: a blood clot without the RBCs, in pericardial/pleural spaces

28
Q

Describe hereditary angio-oedema

A

Autosomal dominant, rare, potentially life threatening
Deficiency in a complement enzyme (C1-esterase inhibitor)
Symptoms: episodic swelling attacks in hands/face/airway etc, recurrent abdo pain (intestinal oedema)

29
Q

Describe alpha 1-antitrypsin deficiency?

A

Autosomal recessive condition
Low levels of this protease inhibitor which deactivates enzymes released by neutrophils
Develop emphysema as proteases act unchecked to destroy tissue, and cirrhosis as hepatocytes produce incorrectly-folded protein so damages them

30
Q

What is chronic granulomatous disease?

A

Phagocytes can’t generate superoxide radical
Bacteria are phagocytosed but not killed as can’t generate oxygen burst
Leads to chronic infections: numerous granulomas and abscesses

31
Q

Brief overview of lobar pneumonia?

A

Acute, exudative inflammation of a pulmonary lobe. Alveoli have exudate
Cause gram +ve diplococci -Streptococcus pneumoniae
Can be resolved completely if treated

32
Q

Brief overview of acute appendicitis?

A

Appendix lumen obstructed by faecolith or generalised AI
If not removed: gangrene +perforation = peritonitis
Presentation: vague abdo pain localised to R iliac fossa,nausea etc. ESR and CRP bloods
Complications: paralytic ileus, peritonitis-septicaemia-multi organ failure

33
Q

Brief overview of bacterial meningitis?

A

Sudden onset, many symptoms
AI of meninges: congested with neutrophils, pus forms, causes adhesions, cranial nerve palsies and hydrocephalus result, vascular thrombosis-reduced cerebral perfusion. Exudate in a small space-cerebral oedema
Viscous grey-green exudate

34
Q

Brief overview of ascending cholangitis?

A

Infection of bile duct
High morbidity and mortality. Need IV antibiotics and bile duct drainage
Jaundice, lethargy, abdo pain, hypotension
Severe cases result in liver abscess

ESA 2 (58 decks)

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