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Path Processes > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

Define Inflammation

A

A rapid response to injury of VASCULARISED, LIVING tissue

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2
Q

What 5 characteristics define acute inflammation?

A
  • Immediate
  • Short duration
  • Innate
  • Stereotyped
  • Limits damage
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3
Q

What is the purpose of acute inflammation?

A

To deliver defensive materials to the site of injury to protect the body from infection, clear damaged tissue and initiate repair

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4
Q

Name some of the causes of acute inflammation

A
  • Foreign bodies (splinters, dirt, sutres)
  • Immune reactions
  • infections (bacterial, viral, parasitic)
  • Trauma
  • Tissue necrosis
  • Physical and chemical agents (burns, frostbite, irradiation, environmental chemicals)
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5
Q

What are the 5 clinical signs of acute inflammation?

A
  1. Rubor (readness)
  2. Calor (heat)
  3. Tumor (swelling)
  4. Dolor (pain)
  5. Loss of function
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6
Q

What is the sequence of changes in vascular tissue in acute inflammation?

A
  1. Initial vasoconstriction of arterioles (seconds)
  2. Followed by vasodilation of arterioles (minutes) promotes blood flow to injured area
  3. Permeability increases, venules become leaky
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7
Q

According to Starling’s Law, fluid movement is controlled by a balance between what 2 things?

A
  • Hydrostatic pressure
  • Oncotic pressure (pressure exerted by plasma proteins, draws fluid towards it)
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8
Q

How does oedema form in acute inflammation?

A
  • Venules become leaky causing proteins to leak into interstitium, increasing interstitial oncotic pressure
  • Net flow of fluid out of the vessel into intersitium causes oedema
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9
Q

What is the effect on the blood when oedema forms?

A

As fluid moves out of the vessel:

  • increased viscosity of blood
  • reduced flow through vessel = stasis
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10
Q

What is the difference between exudate and transudate?

A

Exudate = protein rich fluid caused by an increase in vascular permeability. Occurs in acute inflammation

Transudate= fluid loss into interstitium due to increased capillary hydrostatic pressure OR reduced capillary oncotic pressure - There is NO change in vascular permeability - occurs in heart failure/ hepatic failure/ renal failure

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11
Q

What 4 mechanisms causes increased vascular permeability in acute inflammation?

A
  1. Endothelial contraction by Release of histamine and leukotrienes
  2. Endothelial cytoskeleton reorganisation (cytokines IL-1, TNF)
  3. Direct injury chemical/ toxic burns
  4. Leucocyte dependent injury- free radical release can damage cells
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12
Q

What is the 1st cell to infiltrate into tissues in the inflammatory phase

A

Neutrophil

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13
Q

Describe how neutrophils escape from vessels into the interstitium during acute inflammation

A
  1. Neutrophils are ACTIVATED- switched to a higher metabolic level
  2. Stasis of blood causes neutrophils to line up at the edge of the blood vessels (MARGINATION)
  3. Neutrophils roll and intermittently stick along the endothelium (ROLLING)
  4. Neutrophils then stick more avidly (ADHESION)
  5. Neutrophils EMIGRATE through the blood vessel wall (Diapedesis)
  6. Summoned to place of injury- CHEMOTAXIS
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14
Q

Using Starling’s Law, explain how fluid moves into the interstitium in acute inflammation

A
  • Leaky semi-permeable membrane
  • Arterioles dilate increasing capillary pressure/ increased hydrostatic pressure
  • As plasma proteins escape, oncotic pressure drawing fluid back into vessels is reduced
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15
Q

What happens to the excess fluid produced in acute inflammation?

A

It is drained in the lymphatics, taking antigens with it presenting them to the innate immune system in the lymph nodes

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16
Q

What are the 3 main types of defensive proteins in exudate, and what is their function?

A

1) Opsonins- coat foreign materials making them easier to phagocytose
2) Complement- produce a bacteria perforating structure
3) Antibodies- bind to surface of micro-organisms and act as opsonins

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17
Q

What are the 2 main types of adhesion molecules involved in neutrophils invasion

A

Selectins - on the ENDOTHELIAL surface

Integrins- on the neutrophil surface, bind to recents on endothelial surface e.g ICAM-1

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18
Q

What is chemotaxis?

A

The directional movement toward a chemical attractant (chemotaxins)

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19
Q

What type of blood acts as a chemotaxin?

A

Clotted blood only

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20
Q

Name some complement proteins

A

C3a, C4a and C5a

21
Q

Name some opsonin proteins

A
  • IgG antibody (not present until bacterium encountered got the 1st time)
  • C3a- released when complement activated Fc
22
Q

Explain how chemotaxins activate neutrophils to move towards the injury

A
  • Chemotaxins bind to neutrophil receptors
  • Ca2+ and Na+ ions rush into the cell causing it to swell
  • The cytoskeleton is reorganised for form a pseudopod (extension in the direction of stimulus)
23
Q

What are the 2 ways in which neutrophils kill microorganisms?

A
  • Oxygen dependent (ROS and RNS)
  • Oxygen independent (lysozyme producing hydrolytic enzymes)
24
Q

How do neutrophils undergo diapedesis?

A

They produce collegenase which digests the basement membrane

25
Q

How does oedema limit damage?

A
  • Dilutes toxins
  • Delivers plasma proteins to area of injury
  • fibrin mesh limits spread of toxin
  • increased lymphatic draining from area (inducing adaptive immune response)
26
Q

How do inflammatory cells limit damage?

A
  • remove toxins and pathogenic organisms
  • remove necrotic tissue
  • release of chemical mediators stimulates and regulates further inflammation
  • stimulated pain (bradykinin) encourages rest
27
Q

Name some vasodilators

A
  • Histamine
  • Serotonin
  • Prostaglandin
  • NO
28
Q

Name some chemical mediators that increase vascular permeability

A
  • Histamine
  • Bradykinins
  • Leukotrienes
  • C3a and C5a
29
Q

Name some chemical mediators that cause fever

A
  • Prostaglandins
  • IL-1
  • TNF-alpha
  • IL-6
30
Q

Name some chemical mediators that cause pain

A
  • Bradykinin
  • Substance P
  • Prostaglandin
31
Q

Name some local complications of acute inflammation

A

1) Swelling - can block nearby tubes/ ducts
2) Exudate- can compress organ e.g cardiac tamponade
3) Evaporation of exudate causes loss of fluid e.g in burns
4) Pain and loss of function - may cause muscular atrophy and have psych-social consequences

32
Q

How does fever arise as a systemic complication of acute inflammation?

A
  • Endogenous pyrogens (TNFa, prostaglandins, IL-1) act on the hypothalamus altering baseline temp control
  • Patient feels hotter than normal, sweats more
  • And colder than they actually are causing muscle spasm
33
Q

How are NSAIDs used to treat fever?

A

Block cyclo-oxygenase enzymes (involved in production of prostaglandins)

34
Q

What is 1 side effect of NSAIDs?

A

GI bleeding

35
Q

How can leucocytosis (increased WBC production) arise from acute inflammation?

A
  • IL-1 and TNFa stimulate bone marrow to increase production
  • bacterial infection = more neutrophils
  • viral infection= more lymphocytes
36
Q

How can septic shock arise as a consequence of acute inflammation?

A
  • In overwhelming infection a huge amount of chemical mediators are released
  • causes widespread vasodilation
  • tachycardia and hypotensions
  • leads to multi organ failure as not perfused
  • ultimately death
37
Q

How would you treat suspected septic shock?

A

Broad IV spectrum antibiotics given within 1hr

38
Q

What are the 4 possible outcomes that follow acute inflammation?

A
  1. Complete resolution
  2. Continued acute inflammation and chronic inflammation (abscess)
  3. Chronic inflammation and fibrous repair
  4. Death
39
Q

What happens in complete resolution?

A

All changes gradually reverse

  • vascular permeability returns to normal
  • exudate drains via lymphatics
  • neutrophils die and get phagocytosed
  • fibrin degraded
  • damaged tissue regenerates if architecture preserved
  • mediators inactivated/diluted/degraded
40
Q

Explain how acute inflammation can lead to appendicitis?

A
  • Lumen of appendix blocked, commonly by faecolith (poo rock)
  • causes bacteria accumulation, increased pressure and reduced blood flow leading to ISCHEMIA
  • if perforated can spread to peritoneal cavity -> peritonitis
41
Q

What is an abscess?

A
  • An accumulation of dead/dying neutrophils
  • associated with liquefactive necrosis
  • can compress surrounding structures/nerves causing pain or duct blockage
42
Q

What is a haemorrhage exudate?

A

Exudate containing RBC, looks bloody to naked eye

-indicates significant vascular damage has occurred

43
Q

What is pus made of?

A

Dead neutrophils

44
Q

What does a serous exudate contain?

A

Plasma proteins but few leucocytes commonly seen in blisters

45
Q

What is a fibrous exudate and what does it cause?

A

Exudate with significant fibrin

means serousal surfaces don’t slide smoothly over each other causing a friction/ rubbing sound

46
Q

What is hereditary angio-oedema?

A
  • rare autosomal dominant deficiency in C1-esterase inhibitor (compliment)
  • Causes non-itching cutaneous angio-oedema
  • recurrent abdominal pain from intestinal oedema
47
Q

What is alpha-1-antitryspin ?

A

Protease inhibitor that inactives enzymes released from neutrophils at the site of inflammation

48
Q

What happens in alpha-1-antitrypsin deficiency?

A
  • Unable to deactivate proteases released by neutrophils
  • develop emphysema
  • liver disease as liver produces abnormal version protein that cannot be exported from the ER
49
Q

What is chronic granulomatous disease?

A
  • Phagocytes unable to generate free radial superoxide (genetic), therefore cannot kill bacteria
  • causes chronic infections in 1st year of life
  • numerous abscesses in skin, lymph node, lung, liver and bone

Path Processes (12 decks)

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