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Pathological Processes * > S2 Acute Inflammation > Flashcards

S2 Acute Inflammation Flashcards

1
Q

What is inflammation?

A

The response of living tissue to injury

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2
Q

What are the key features of acute inflammation?

A
  • immediate
  • short duration
  • innate (natural)
  • stereotyped (in-built mechanism)
  • limits damage
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3
Q

What are the two phases in inflammation?

A
  1. Vascular phase

2. Cellular phase

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4
Q

What is the vascular phase?

A

Changes in blood flow, accumulation of exudate

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5
Q

What is the cellular phase?

A

Delivery of neutrophils

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6
Q

What is inflammation controlled by?

A

Chemical mediators

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7
Q

What causes inflammation?

A
  • trauma/foreign body
  • microorganisms
  • hypersensitivity
  • other illness, including necrosis
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8
Q

What are clinical signs of acute inflammation?

A
  • rubor - redness
  • calor - heat
  • tumor - swelling
  • dolor - pain
  • loss of function
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9
Q

What changes in blood flow occur in the vascular phase?

A
  1. Vasoconstriction (seconds)
  2. Vasodilation (minutes) - causes heat and redness
  3. Increased permeability - fluid and cells can escape
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10
Q

What is Starling’s Law?

A

Movement of fluid is controlled by the balance of hydrostatics pressure and oncotic pressure

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11
Q

What is hydrostatic pressure?

A

The pressure exerted on a vessel wall by fluid (pushes fluid away)

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12
Q

What is oncotic pressure?

A

The pressure exerted by proteins e.g. albumin (draws fluid towards)

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13
Q

In a normal capillary, is there any net movement in and outer the vessel?

A

No, fluid movement out due to capillary hydrostatic pressure matches fluid movement in due to capillar oncotic pressure

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14
Q

What does vasodilation mean for hydrostatic/oncotic pressure?

A

It increases capillary hydrostatic pressure, has no effect on oncotic pressure

Due to more blood flow through the capillary

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15
Q

What does increased vessel permeability mean for hydrostatic and oncotic pressure?

A

Increased interstitial oncotic pressure

Due to plasma proteins moving into the interstitium

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16
Q

What does fluid movement/accumulation out of the vessel and into the interstitum cause?

A

Oedema (tumor)

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17
Q

What does movement of fluid out of the vessel mean for the blood viscosity? And on blood flow?

A

Blood viscosity is increased meaning reduced flow through the vessel (stasis)

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18
Q

What are the two types of interstitial fluid?

A
  1. Exudate

2. Transudate

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19
Q

What are the differences between exudate and transudate?

A
  • exudate results from increased vascular permeability, transudate has no change in permeability
  • exudate is protein rich fluid, transudate doesn’t
  • transudate fluid movement is due to increased capillary hydrostatic pressure and reduced capillary oncotic pressure
  • exudate occurs in inflammation, transudate occurs in heart failure, hepatic failure and renal failure
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20
Q

Why does transudate occur in heart, hepatic and renal failure?

A

Heart - can’t effectively pump blood around the body so blood remains in vasculature increasing the capillary hydrostatic pressure

Hepatic - a damaged liver means reduced plasma proteins (less production) so lower capillary oncotic pressure

Renal - loss of proteins urine, lower capillary oncotic pressure

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21
Q

How does a vessel wall become permeable?

A
  • endothelial cells retract (due to histamine, nitric oxide and leukotrienes)
  • direct injury (due to burns, toxins, direct trauma)
  • leucocyte dependent injury (due to enzymes/toxic oxygen species being released by activated inflammatory cells)
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22
Q

How is the vascular phase effective as a response to injury?

A

The interstitial dilutes toxin

The exudate delivers proteins e.g. fibrin (mesh limits the spread of toxin) and immunoglobulins (targeted destruction of pathogens - adaptive immune response)

Fluid drains into the lymph nodes and delivers antigens which stimulate the adaptive immune response

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23
Q

What is a neutrophil?

A

The primary white blood cell involved in acute inflammation

Is a granulocyte with a multi-/tri-lobed nucleus

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24
Q

How doe neutrophils get out of vessels?

A
  1. Marigination
  2. Rolling
  3. Adhesion
  4. Emigration (diapedesis)
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25
Q

How does rolling occur? What adhesion molecule is involved?

A

Occurs due to weak intermittent bonds between the neutrophil and endothelial cells

Selectins - expressed on the activated endothelial cells, they’re activated by chemical mediators

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26
Q

How does adhesion occur? What adhesion molecule is involved?

A

The neutrophil binds more strongly to the endothelial cells

Integrins - on the neutrophil surface, able to change from a low affinity state to high affinity state

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27
Q

What is diapedesis?

A

Passage of a blood cells through an intact capillary wall

28
Q

How do neutrophils move through the interstitium?

A

Move by chemotaxis - movement along an increasing chemical gradient of chemoattractants e.g. bacterial peptides or inflammatory mediators

And the rearrangement of the neutrophil cytoskeleton aids this movement

29
Q

What do neutrophils do?

A

Phagocytosis - phagosomes fuse with lysosomes (containing lysozymes) and produce phagolysosomes

Release inflammatory mediators

30
Q

How do neutrophils recognise what to phagocytose?

A

Due to opsonisation

Toxin covered in C3b and Fc opsonins, the neutrophil surface contains receptors for these opsonins

31
Q

What are the two pathways for how neutrophils destroy pathogens?

A
  1. Oxygen dependent

2. Oxygen independent

32
Q

What is the oxygen dependent pathway for neutrophils killing pathogens?

A
  • uses reactive oxygen intermediates (e.g. superoxide, hydroxyl radical, hydrogen peroxide)
  • used reactive nitrogen intermediates (e.g. nitric oxide, nitric dioxide)
33
Q

What is the oxygen independent pathway for neutrophils killing pathogens?

A

Use lysozymes, hydrolysing enzymes and defensins

34
Q

How is the cellular phase (neutrophils) effective?

A
  • it removes pathogens and necrotic tissue
  • it releases inflammatory mediators

Reduces the possibility of further inflammation

35
Q

What are inflammatory mediators?

A

Chemical messengers that control and coordinate the inflammatory response.

They have varying chemical structures and overlapping functions.

36
Q

What do inflammatory mediators originate from?

A
  • activated inflammatory cells
  • platelets
  • endothelial cells
  • toxins e.g. chemoattractants
37
Q

What are two common responses to chemical mediators?

A

Motion (contraction/relaxation, chemotaxis, phagocytosis) and secretion

38
Q

How are chemical mediators regulated?

A

Inhibitors and the fact that mediators have short-lives (seconds to minutes for a minutes to hours response)

39
Q

What are the 7 groups of chemical mediators?

A
  1. Vasoactive amines e.g. histamine and serotonin
  2. Vasoactive peptides e.g. bradykinin
  3. Complement components e.g. C3a and C5a
  4. Clotting and fibrinolytic cascades
  5. Mediators derived from phospholipids e.g. prostaglandins, thromboxanes and leukotrienes
  6. Cytokines and chemokines e.g. interleukins, tumour necrosis factor (TNF) and interferons
  7. Exogenous mediators of inflammation e.g. endotoxins produced by gram -ve bacteria
40
Q

What inflammatory mediators cause vasodilation?

A

Histamine, serotonin, prostaglandins, nitric oxide

41
Q

What inflammatory mediators cause increased permeability?

A

Histamine, bradykinin, leukotrienes, C3a and C5a

42
Q

What inflammatory mediators cause chemotaxis?

A

C5a, TNF-a, IL-1 and bacterial peptides

43
Q

What inflammatory mediators cause fever?

A

Prostaglandins, IL-1, IL-6 and TNF-a

44
Q

What inflammatory mediators cause pain?

A

Bradykinin, substance P, prostaglandins

45
Q

Why do you want to induce pain as part of the inflammatory response?

A

To induce rest

46
Q

What are the local complications of acute inflammation?

A
  • swelling
  • exudate
  • loss of fluid
  • pain
47
Q

What is the complication with swelling and exudate?

A

Compression of tubes e.g. airways, bile duct, intestines

Compression of organs e.g. cardiac tamponade

48
Q

What is the complication with loss of fluid?

A

The exudate can evaporate leading to dehydration

49
Q

What is the complication with pain?

A

Can lead to muscle atrophy and has psycho-social consequences

50
Q

What are the systemic complications of acute inflammation?

A
  • fever
  • leucocytosis
  • acute phase response
  • septic shock
51
Q

What are the complications with fever? How can it be controlled?

A

If temp is too high, can die.

Controlled using non-steroidal anti-inflammatory drugs (NSAIDs) which stop the production of prostaglandins so reduced temp. and pain

52
Q

What is the problem with leucocytosis?

A

Increased production of white cells (bone marrow is targeted by inflammatory mediators)

53
Q

What is the problem with acute phase response?

A

Malaise, reduced appetite, altered sleep, tachycardia which induces rest (could lead to too much rest?)

Can determine the severity by measuring blood levels of CRP

54
Q

What is the complication with septic shock?

A

There’s a huge release of chemical mediators causing widespread vasodilation (hypotension and tachycardia).

Multi-organ failure occurs

Can be fatal

55
Q

What are the 3 outcomes of acute inflammation?

A
  1. Complete resolution
  2. Repair with connective tissue (fibrosis) - if theres been substantial tissue destruction
  3. Progression to chronic inflammation
56
Q

What happens in complete resolution?

A
  • as mediators have short half lives, they are diluted/inactivated/degraded
  • vessel diameter and permeability becomes normal again
  • neutrophils undergo apoptosis and are phagocytosed
  • exudate drains via lymphatics
57
Q

What are some clinical examples of acute inflammation?

A
  • appendicitis
  • pneumonia
  • bacterial meningitis
  • abscess
  • inflammation of serous cavities
58
Q

What happens in appendicitis?

A

The lumen is blocked, leads to an accumulation of bacteria and exudate.

The increased pressure causes perforation.

59
Q

What are some examples of what causes pneumonia? What are signs and symptoms? What are risk factors?

A

Caused by streptococcus pneumoniae or haemophilus influenzae

Shortness of breath, cough, sputum and fever

Smoking and pre-existing lung condition

60
Q

What are some causes of bacterial meningitis? What are the signs and symptoms?

A

Caused by group B Streptococcus, E.Coli or Neisseria meningitides

Headache, neck stiffness, photophobia and altered mental state

61
Q

What causes an abscess? What are it’s complications?

A

Accumulation of dead and dying neutrophils with associated liquefactive necrosis

If it is large enough, it can cause compression of surrounding structures leading to pain and blockage of ducts

62
Q

What happens in inflammation of serous cavities?

A

Exudate pours into the pleural space/peritoneal space/pericardial space

63
Q

What are 3 disorders of acute inflammation?

A
  1. Hereditary anti-oedema
  2. Alpha-1 antitrypsin deficiency
  3. Chronic granulomatous disease
64
Q

What is hereditary angio-oedema?

A

Rare autosomal dominant condition.

Deficiency of C1-esterase inhibitor (component of compliment system)

Attacks of non-itchy cutaneous angio-oedema, recurrent abdominal pain due to intestinal oedema

65
Q

What is alpha-1 antitrypsin deficiency?

A

Autosomal recessive disorder

Low levels of alpha-1 antitrypsin (protease inhibitors - deactivated enzymes released from neutrophils at site off inflammation)

Develop emphysema as proteases act on lungs unchecked and destroy normal parenchyma tissue. Liver disease occurs as hepatocytes produce an abnormal version of the protein (incorrectly folded) so it can’t be polymerised and removed from the ER so leads to hepatocytes damage and cirrhosis

66
Q

What is chronic granulomatous?

A

Genetic condition in which phagocytes can’t generate free radical superoxide.

The phagocytes engulf the bacteria but can’t kill them (as can’t generate oxygen burst).

Results in many chronic infections in 1st year of life.

Numerous granulomas, abscesses affecting the skin, lymph nodes and sometimes lung, liver and bones occur

Pathological Processes * (10 decks)

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