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Pathology > Week 1 Inflammation > Flashcards

Week 1 Inflammation Flashcards

1
Q

What is infection?

A

Inflammation due to Biological agents

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2
Q

What is Inflammation?

A

• reaction of living tissue to NONLETHAL injury
• is a dynamic process that starts with the injury and culminates with healing or repair.
• the intensity, duration and outcome is modified by a variety of host factors and factors related to the
etiological agent.

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3
Q

Defense mechanisms: Tears have________

A

Lysozyme

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4
Q

Defense mechanisms: Ears have_________

A

Cerumen

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5
Q

Defense mechanisms: Respiratory system has_________

A

1) Air flow
2) mucus
3) ciliated cells
4) alveolar macrophages

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6
Q

Defense mechanisms: Stomach________

A

Low pH

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7
Q

Defense mechanisms: Intestines have______

A

Intestinal Flora and proteolytic enzymes

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8
Q

Defense mechanisms: Urine has________

A

lysozyme and low pH

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9
Q

What is Exudate?

A

Extravascular fluid rich in proteins and cells with a specific gravity of > 1.020

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10
Q

Define exudation

A

Outpouring of fluids, proteins and cells from vessels into interstitium or body cavities.

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11
Q

What does presence of exudate indicate?

A

Alteration in the normal permeability of small blood vessels in the area of injury

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12
Q

What is Transudate?

A

ultrafiltrate of plasma

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13
Q

Define Transudation

A

Outpouring of fluid with little protein (albumin) with a specific gravity of

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14
Q

What does presence of transudate indicate?

A

Hydrostatic imbalance. Permeability is normal.

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15
Q

What is Edema?

A

excess interstitial fluid. It can be an exudate or a transudate.

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16
Q

What is Pus?

A

A cell rich exudate with mainly PMN’s and cell debris. It also contains powerful lysosomal enzymes

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17
Q

Pus aka

A

purulent exudate

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18
Q

What are the 5 cardinal signs of inflammation?

A
  1. Rubor → redness
  2. Tumour → swelling
  3. Calor → heat
  4. Dolor → pain
  5. Functio → impaired function
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19
Q

Acute inflammation features

A

1) short duration
2) exudation ( migration of leukocytes)
3) PMN (granulocytes)

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20
Q

Chronic inflammation features

A

1) Longer duration
2) Lymphocytes
3) Macrophages
4) Tissue repair

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21
Q

Changes in Vascular flow and Calibre in ACUTE inflammation

A
  1. Transient vasoconstriction of arterioles. Brief. Neurogenic. Inconstant.
  2. Vasodilatation: first of arterioles, then the remaining microcirculation. Chemically mediated. ↑ blood
    flow = heat and redness.
  3. Permeability changes with exudation (edema and swelling), (also by chemical mediators) with slowing
    of the circulation. It could culminate in stasis. (Increased blood viscosity and RBC packing).
  4. As blood flows more slowly and becomes more viscous, cellular events begin to take place.
  5. Time period from 1 to 4 varies with degree of injury (↑ injury, ↓ time).
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22
Q

What is the Triple response of Lewis?

A

Changes in Vascular Flow and Calibre in acute inflammation described by Sir Thomas Lewis (1927:

  1. Pale line along area of stroke
  2. Flare
  3. Swelling with blanching
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23
Q

What forces direct movement of fluid out of vessels?

A

o osmotic pressure of interstitial fluid

o intravascular hydrostatic pressure

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24
Q

What forces direct movement of fluid into vessels?

A

o osmotic pressure plasma proteins

o tissue hydrostatic pressure

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25
Q

How do you get transudate?

A

Increased intravascular hydrostatic pressure (vasodilation) or decrease intravascular osmotic pressure (decreased albumin) but NO changes in Permeability

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26
Q

How do you get exudate?

A

leaky endothelium (by permeability factors or direct endothelial damage) cause loss of high protein fluid

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27
Q

How does leaky endothelium in inflammation cause edema?

A

loss of high protein fluid (exudate) with reduction of intravascular osmotic pressure and increased interstitial
osmotic pressure causing further impairment of return of fluid to blood vessels (venules) producing marked inflammatory edema

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28
Q

name 4 substances excreted by normal endothelium.

A

1) prostaglandins
2) coagulant factor VIII,
3) collagens
4) anticoagulant (plasminogen activator)

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29
Q

Name 5 mechanisms of increased vascular permeability

A
  1. Immediate Transient response- Endothelial cell contraction leading to wide intercellular gaps.
  2. Junctional retraction is cytokine mediated.
  3. Direct endothelial injury with endothelial cell necrosis and detachment. In more severe injuries such
    as burns, infections, cuts, abrasions, etc causes “immediate sustained” response. Direct injury of endothelial cells may also induce a “delayed prolonged leakage”
  4. “Leukocyte dependent endothelial injury”
  5. “Increased transcytosis” : occurs in the presence of vascular endothelial growth factor and other
    mediators. They increase the venular permeability via a vesiculovacuolar intracellular pathway.
30
Q

What causes endothelial CELL contraction?

A
  • Mediated by histamine and other chemical mediators.

- It is reversible, short lived (15–30’) This is called “immediate transient” response.

31
Q

What is junctional contraction?

A

It involves structural reorganization of the cell’s cytoskeleton and disruption of endothelial cells junctions of venules.
This has been demonstrated experimentally using TNF and interleukin 1.

32
Q

When does Junctional contraction occur?

A

Occurs 4-6 hrs after injury and lasts for 24 hrs or more.

33
Q

Where does endothelial cell contraction occur?

A

Occurs only in small venules (20um 60 um), not in capillaries or arterioles.
It is not known why venules are the only affected, however, they are known to have more histamine receptors.

34
Q

What is the Immediate Sustained response?

A

In direct endothelial injury, The endothelial detachment is secondary to platelet adhesion and thrombosis. It begins immediately after the injury and persists for hours or days. This reaction is known as “immediate sustained“ response.

35
Q

When is delayed prolonged leakage?

A

Occurs In direct endothelial damage after a delay of 2-12 hours, lasts for hours/days and involves capillaries and venules. The best examples are sunburn and bacterial toxins

36
Q

When is Leukocyte dependent endothelial injury seen?

A

occur when during inflammation, activated inflammatory cells release toxic Oxygen species and proteolytic enzymes causing endothelial cell detachment. This
occurs mostly in venules, pulmonary capillaries. It is usually late in the inflammatory process.

37
Q

Where does Leukocyte dependent endothelial injury occur?

A

This occurs mostly in venules, pulmonary capillaries. It is usually late in the inflammatory process.

38
Q

Most clinically significant injuries are immediate-________.

A

sustained

39
Q

What is the role of leukocytes in Inflammation?

A
  • engulf, degrade bacteria, immune complexes and cell debris
  • release lysosomal enzymes
  • release chemical mediators
  • release toxic radicals.
40
Q

What are the 4 steps in migration of leukocytes (exudation)?

A

1) Margination- pushed to periphery of vessel
2) Pavementing and Rolling - CAMs
3) Adhesion and Emigration - endothelial adhesion molecules binding to integrins on leukocytes
4) Chemotaxis and activation

41
Q

Why are leukocytes marginated in inflammation?

A

When blood is viscous there is sludging of RBCs (rouleaux). WBCs are pushed to periphery of vessels because they are smaller particles (law of physics).

42
Q

What % of leukocytes are normally marginated ?

A

~50%

43
Q

What are CAMs?

A
  • Cell adhesion Molecules
  • 2 categories : Ca2+ dependant and Ca+ independant
    -Involved in Inflammation (Rolling)
  • are either expressed, induced or enhanced by chemical
    mediation
  • involved in the process of cell recognition and adhesion that takes place during the organization of embryonic tissues and organs in the cellular interactions of post natal life
44
Q

What are the group of CAMs involved in inflammation?

A

Selectins:

1) L- Selectins
2) E-Selectins aka ELAM-1 (endothelial cell - leukocyte adhesion molecules)
3) P- Selectins

45
Q

What cells are L- Selectins found on ?

A 
present on the phagocytes surface [inflammatory cell capable of phagocytosis such
as PMNs (polymorphonucleated neutrophils), macrophages, basophils, etc.].
46
Q

Which selectins are found on Endothelial cell surface?

A
  • P-Selectin and E-Selectin.
  • Their number increases (upregulation) with cytokines.
  • They interact with the phagocyte adhesion molecules.
47
Q

What are the receptors on leukocytes that cause adhesion?

A

Integrins:

1) LFA-1 (CD11a/CD18)
2) Mac1 (CD11b/ CD18)
3) VLA-4

48
Q

What are the receptors on endothelial cells that cause adhesion?

A

ICAM-1 and VCAM-1

Both are upregulated by various cytokines

49
Q

Describe process of Adhesion

A

The integrin receptors for ICAM-1 are LFA-1 (CD11a/CD18) & Mac1 (CD11b/ CD18), while VCAM-1 binds to the integrin VLA-4. These integrins only adhere to their ligands when the leukocytes are activated by inflammatory chemotactic factors.

50
Q

What is Diapedesis?

A

Movement of leukocytes across the basement membrane to the extravascular space ( active process)
RBC migration is passive

51
Q

What type of leukocytes are the first to appear at site of inflammation?Why?

A

PMNs except in VIRAL INFECTION ( lymphocytes)
This is partly due to the fact that they are faster and more numerous. It is short-lived, the monocyte migration is sustained longer and chemotactic factors for PMN and monocytes are activated at different periods

52
Q

Define Chemotaxis

A
  • Unidirectional migration of cells toward an attractant or, locomotion oriented along a chemical gradient.
  • Chemotactic factors can be exogenous and endogenous.
53
Q

Define chemokenesis

A

accelerated random locomotion cells , not directed as in chemotaxis

54
Q

What is Leukocyte adhesion disorder?

A

A familial disorder where leukocytes dont have L- selectin , so there are no phagocytes at the site of infection

55
Q

Most Important Chemotactic Factors for PMN:

A
  • bacterial products (E. coli and staph. aureus best studied
  • complement fractions (C5a)
  • arachidonic acid metabolites (leukotriene B4)
  • cytokines (chemokines)
56
Q

Describe chemotaxis

A

1) Specific receptors for chemotactic agents on cell surfaces
2) Receptor binding is rapid.
3) Once receptor-ligand interaction takes place, mobilization of membrane associated Ca++.

57
Q

Why is Ca2+ required for chemotaxis?

A

Ionic Ca is essential for contractile elements necessary for cell locomotion.
Locomotion: pseudopods have actin/myosin which is Ca++ dependent

58
Q

3 steps of phagocytosis

A
  1. recognition and attachment- need opsonins
  2. engulfment- can cause some H2O2 leakage
  3. killing and/or degradation
    (i) O2 dependant mechanisms
    (ii) O2 independent mechanism
59
Q

What is required for recognition of micro-organism?

A

Opsonins

60
Q

2 main opsonins and how are they recognized by PMNs and macrophages.

A

IgG and C3b are opsonins.
PMNs and Macrophages have the following receptors:
• a receptor for Fc fragment of IgG (to react with IgG opsonin)
• a receptor to C3b (to react with C3b opsonin)

61
Q

Describe engulfment process.

A

1) pseudopods enclose organism (requires Ca2+ and Mg2+)
2) fuses with lysosome to form a phagolysosome
3) some H2O2 is leaked into tissue in the process leading to tissue damage

62
Q

What is the role of Ca2+ in engulfment?

A

Ca++ acts as a second messenger to initiate the cell events in the microfilaments and microtubules, culminating with engulfment

63
Q

How do the oxygen dependant mechanism work?

A

Metabolites exert their bactericidal properties in one of two ways:
i) the H2O2-myeloperoxidase-halide system,
- in which the physiological halide is the Cl-.
-The final reactive radical being the HOCl, which is a
powerful oxidant and antimicrobial (chlorination).
- This mechanism is deficient in people with chronic
granulomatous disease of childhood. This is the most
efficient system.
ii) MPO independent killing: also requires O2.
H2O2 + O2- → OH + OH- + O2
the OH- being a potent free radical.

64
Q

How do the oxygen independent mechanism work?

A

H+ ion from increased lactate and from action of carbonic anhydrase produces marked reduction of intravacuolar pH, which is bactericidal.

65
Q

Describe degradation process

A

Following killing, acid hydrolases degrade bacteria within phagolysosomes

66
Q

Which bacteria can survive in a phagocyte

A

Tuberculosis

67
Q

How does phagocytosis process make inflammation worse?

A

Extracellular release of leukocyte products such as:
• Lysosomal enzymes.
• Oxygen derived metabolites
• Products of arachidonic acid metabolism (prostaglandins, leukotrienes)

68
Q

How does the extracellular release of leukocyte products occur in phagocytosis ?

A
  1. Regurgitation during feeding.
  2. Reverse endocytosis (frustrated phagocytosis)
  3. Cytotoxic release (following cell death).
69
Q

What are the two types of mediators of inflammation?

A

1) neurogenic mechanisms

2) chemical mediators

70
Q

Describe neurogenic mechanisms of inflammation

A

• only in very early phases of inflammatory reaction.
• fleeting phase of vasoconstriction.
• blocked by anesthesia.
• vasoconstriction is followed by antidromic reflex with inhibition of vasoconstrictive impulses
contributing to the vasodilatation.
• absence of innervation does not prevent inflammation.

Pathology (4 decks)

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