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5 semestre > Inflammation - Pathology > Flashcards

Inflammation - Pathology Flashcards

0
Q

Pathology of inflammation (4)

A

circulatory changes
vessel wall changes
mediators of inflammation (M of I)
cellular events of inflammation

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1
Q

What are the sings & symptoms of inflammation? (5)

A 
heat
redness
swelling
pain
impaired function
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2
Q

What are the circulatory changes?

A

injury stimulation–>vasoconstriction–>vasodilation—>:

1) hyperemia (redness, swelling, warmth): increased intracapillary pressure
2) edema: (in capillaries and venules) filtration of plasma through vessel wall
3) congestion: blood flow in dilated capillaries and venules is slow
- -> WBCs attach to endothelium (wall of blood vessel)–> release of mediators of inflammation (derived from WBC and platelets)–> platelets initiate clotting

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3
Q

Vessel wall changes

A

changes in permeability of capillary walls in response to inflammation

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4
Q

Reasons for vessel wall changes during inflammation

A

1) increased intravascular pressure (congestion)
2) slowing of the circulation => less oxygen and nutrients to endothelial cells
3) adhesion of WBC and platelets to endothelial cells
4) release of mediator of inflammation (from WBC, platelets, endothelial cells, plasma)

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5
Q

What are the mediators of inflammation? (2)

A

plasma derived

cell derived

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6
Q

Plasma derived inflammatory mediator

A

circulate in inactive form -> transformed into active form by ACTIVATOR

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7
Q

Cell derived inflammatory mediator

A

1) preformed and stored in WBC, platelets … or synthesized on demand.
2) preformed mediators - quick release (histamine)
3) synthesized mediators - released later

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8
Q

Sample of preformed cell derived inflammatory mediator

A

histamine

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9
Q

Chemistry of mediators of inflammation

A
  • biogenic amines (histamine)
  • peptides (bradykinin)
  • arachidonic acid derivatives (prostaglandins)
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10
Q

Effects of meditoary of inflammation

A
  • vasodilation or vasoconstriction
  • alternation of vascular permeability
  • activation of inflammation cells
  • chemotaxis
  • cytotoxicity
  • degradation of tissues
  • fever
  • pain
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11
Q

Which cells release histamine during inflammation? (3)

A

platelets
mast cells
basophils

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12
Q

Effects of histamine

A
  • increased blood vessel permeability => fluids and cells can exit into intersititial spaces
  • vasodilation
  • effects are quick but last less than 30 min. (histamine inactivated by enzyme histaminase)
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13
Q

bradykinin

A

plasma protein

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14
Q

Effects of bradykinin

A
  • similar to histamine but slower
  • amplifies and sustains response to injury
  • PAIN
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15
Q

Which chemical causes pain during inflammation?

A

bradykinin

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16
Q

What can activate the complement system of inflammation?

A

antigen-antibody complexes, bacterial toxins, fungi, snake venom, etc.

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17
Q

All components of complement system promote ____.

A

inflammation

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18
Q

Where does arachidonic acid derived from?

A

phospholipids of cell membrane

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19
Q

Arachidonic acid synthesis blocks by _______.

A

corticosterioids

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20
Q

Prostaglandin synthesis blocks by _______.

A

ASPRIN

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21
Q

emigration of leukocytes (WBC)

A

diapedesis = active movement of WBCs through capillary wall into tissues

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22
Q

transudation

A

leakage of fluid rich in proteins

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23
Q

transudate from capillaries (more permeable) into interstitial space

A

edema

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24
Q

exudation

A

emigration (diapedesis) of cells and fluid through capillary wall

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25
Q

What’s the difference between transudation and exudation?

A

exudation contains inflammatory cells (WBCs) and much more protein than transudation

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26
Q

What’s chemotaxis?

A

active movement of WBCs towrads certain chemicals;

movement along concentration gradient of those chemicals.

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27
Q

What’s chemoattractant?

A

It’s chemotactic agent.

It derived from bacteria damaged tissues, activated complement, etc.

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28
Q

What cells arrive first in acute I inflammation?

A

neutrophils

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29
Q

What cells have longest life among cells of inflammation?

A

macrophages

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30
Q

Among cells of inflammation, which cells have similar function?

A

neutrophils and macrophages

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31
Q

Which cells create fever in acute I inflammation?

A

neutrophils

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32
Q

Among cells of inflammation, which cells are response to allergy?

A

eosinophils, basophils

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33
Q

What cells contain histamine among cells of inflammation?

A

basophils

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34
Q

List the cells of inflammation

A

neutrophils, eosinphils, basophils, macrophages, other cells (lymphocytes, plasma cells, platelets)

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35
Q

Among cells of inflammation, which can release histamine?

A

basophils, and platelets

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36
Q

What is the main function of platelets?

A

hemostasis (vascular spasm, platelet plug formation, blood coagulation)

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37
Q

What does histamine do during inflammation?

A

promoting formation of connective tissue

38
Q

What are the 4 ways to classify inflammation?

A

duration
etiology
location
morphology

39
Q

How long does Acute I inflammation last?

A

few hours to few days (or kill you)

40
Q

examples of Chronic I inflammation

A

tuberculosis

autoimmune diseases

41
Q

What are the infectious agents for inflammation?

A

bacterial, viral, protozoal, fungal, helmintic

42
Q

What are the chemical causes of inflammation?

A

acids, alkaline substances

43
Q

What are the physical causes of inflammation?

A

heat, radiation, etc.

44
Q

What are the immune causes of inflammation?

A

eczema, autoimmunity

45
Q

Which of the following is localized inflammation?

a) furuncle
b) furunculosis
c) measels

A

a) furuncle

46
Q

Which of the following is widespread inflammation?

a) furuncle
b) furunculosis
c) measels

A

b) furunculosis

47
Q

Which of the following is systemic inflammation?

a) furuncle
b) furunculosis
c) measels

A

c) measels

48
Q

What is the mildest form of inflammation?

A

serous inflammation

49
Q

Serous inflammation is the ___ stages of most inflammation?

A

early

50
Q

Examples of serous inflammation

A

1) viral infection
2) autoimmune diseases (pericarditis, pleuritis, peritonitis, rheumatoid arthritis)
3) blisters caused by 2nd-3rd burn

51
Q

Feature of fibrinous inflammation

A

transudate rich in fibrin (large protein molecules)

52
Q

What’s the major difference between transudation and exudation?

A

Transudation leaks clear fluid without cells.

Exudation leaks cells.

53
Q

Example of fibrinous inflammation

A

bacterial infections: strep throat, bacterial pneumonia, fibrinous pericarditis

54
Q

What causes purulent inflammation?

A

pus-forming bacteria (streptococci, staphylococci)

55
Q

What is absecess?

A

localized collection of pus within an organ or tissue

56
Q

What is empyema?

A

accumulation of pus in preformed cavity (gallbladder, thoracic cavity)

57
Q

What are the locations for ulcerative inflammation?

A

body surface or mucosa of hollow organs

58
Q

What is ulcer?

A

Defect involving epithelium, may extend into deeper connective tissue.

59
Q

Examples of ulcerative inflammation

A

decubitus ulcer

gastric ulcer

60
Q

What is pseudo-membranous inflammation?

A

fibrino and purulent exudation.

It has fibrin, pus, cellular debris, mucus form pseudo-membrane on the surface of ulcers.

61
Q

Example of pseudo-membranous inflammation

A

pseudomembranous colitis

diphtheria

62
Q

What’s the feature of chronic inflammation?

A

prolonged duration

more extensive tissue destruction

63
Q

What does chronic inflammation’s exudate contain?

A

lymphocytes, macrophages, plasma cells

64
Q

Chronic inflammation of kidney will cause kidney to ___.

A

shrink

65
Q

Examples of chronic inflammation

A

obliteration of fallopian tubes

66
Q

Healing of chronic inflammation

A

scars, fibrosis, adnesions

67
Q

What is granulomatous inflammation?

A

A special form of chronic inflammation.

macrophages and T-lymphocytes accumulate at the site of injury and form nodules = granulomas

68
Q

Features of granulomatous inflammation

A 
persist for a long time
destroy tissues
undergo central necrosis
fibrosis
microorganisms can survive in fibrotic lesions
69
Q

Tuberculosis is __________ inflammation.

a) pseudo-membranous I.
b) granulomatous I.
c) ulcerative I.
d) purulent I.

A

b) granulomatous I.

70
Q

Clinicopathologic correlations of inflammation

A
  • local findings (5 signs & symptoms of inflammation)
  • fever
  • leukocytosis
  • constitutional (nonspecific) symptoms: fatigue, weakness, depression, lack of appetite, generalized pain, exhaustion
71
Q

What are the constitutional symptoms for inflammation?

A

fatigue, weakness, depression, lack of appetite, generalized pain, exhaustion

72
Q

What are the consequences of healing of acute inflammation?

A

no consequences

or progression to chronic inflammation

73
Q

Example of mitotic cells

A

basal layer of skin or mucosa

bone marrow cells (precursors of blood cells)

74
Q

What are the mitotic cells?

A

never stop dividing (unstable cells)

=labile cells

75
Q

What are the facultative mitotic cells?

A

They are stable cells.

Do not divide regularly, can be stimulated to divide.

76
Q

Where can you find facultative mitotic cells?

A

liver, kidney

77
Q

What are the postmitotic cells?

A

permanent cells

nondividing

78
Q

Examples of postmitotic cells

A

neurons, myocardial cells

79
Q

Postmitotic cells can only be repaired by _____.

A

fibrous scarring

80
Q

List of all cells related to healing

A

neutrophils, macrophages, myofibroblasts, angioblasts, fibroblasts

81
Q

What does neutrophils do during inflammation?

A

scavenging the site of injury.

82
Q

What does macrophages do during wound healing?

A 
produce growth factors
produce chemicals (mediators) that act on other cells (fibroblasts, angioblasts, myofibroblasts)
83
Q

What does myofibroblasts do during wound healing?

A

secrete substances like fibroblasts (collagen)

contract like muscle cells => reduction of defect, holding margins in close approximation

84
Q

What does angioblasts do during wound healing?

A

(precusors of blood vessels)

sprout from small blood vessels around the wound

85
Q

What does fibroblasts do during wound healing?

A

produce extracellular matrix of connective tissue

collagen fibers need to mature, cross-link => full strength of scar tissue (several weeks after injury)

86
Q

What are the substances needed for collagen formation?

A

Vitamin C, zinc, protein

87
Q

Describe the healing by First intention

A

(sterile surgical wounds)

  1. blood clot -> scab
  2. invasion of neutrophils and macrophages
  3. ingrowth of myofibroblasts, angioblasts, fibroblasts
  4. granulation tissue formation (=vascularized CT) - temporary structure, undergoes changes
  5. collagenous scar (3-6 weeks)
  6. proliferation of epithelial cells from margins of the wound (3-7 days)
88
Q

Describe the healing by Second intention

A

(large, infected wounds)
wound contraction cannot be accomplished by myofibroblasts
granulation tissue remains exposed (more abundant)
epithelial cells take longer to cover the defect
more excessive scarring

89
Q

What are the factors for wound healing?

A
  1. site of the wound (skin, brain)
  2. mechanical factors: approximation of margins, tension, movement, foreign particles
  3. size of the wound
  4. infection (prevention, treatment）
  5. circulatory status: ischemic tissues heal poorly (diabetes mellitus, smoking)
  6. nutritional and metabolic factors: protein, zinc, vitamin C
  7. Age
  8. Sleep
90
Q

What are keloids?

A

hypertrophic scars composed of immature collagen.

91
Q

What can cause excess scar formation?

A

keloids

contractures due to large scars, esp. after burns -> immobilization or lower ROM

92
Q

What can cause deficient scar formation?

A

ischemia due to diabetic micro-angiopathy and metabolic disturbances
excess of corticosteroids
poor scar tissue development => dehiscence (separation of margins)

5 semestre (19 decks)

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