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inflammation and repair Flashcards

1
Q

what is injury?

A

an alteration in the environment that causes tissue damage. eg chemical, physical, microorganisms, nutritional deficiencies

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2
Q

natural (innate) defenses against injury

A

i. ) intact skin/mucosa is a physical barrier.
ii.) enzymes in saliva have an antibacterial activity.
iii.) flushing action of tears, saliva, urine and diarrhea removes foreign substances.

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3
Q

inflammation

A

a nonspecific response to injury; occurs in the same manner regardless of the nature of the injury

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4
Q

localized signs of inflammation

A

redness, swelling, pain, loss of normal tissue function.

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5
Q

systemic signs of inflammation

A

fever, leukocytosis, elevated C-reactive protein, lymphadenopathy

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6
Q

sequence of microscopic events

A
  1. injury to tissue
  2. constriction of microcirculation
  3. dilation of microcirculation
  4. increase in permeability
  5. exudate leaves microcirculation
  6. increased blood viscosity
  7. decreased blood flow
  8. margination and pavement in of WBCs
  9. WBCs (leukocytes) enter tissue
  10. WBCs (leukocytes) ingest foreign material.
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7
Q

hyperemia

A

increased blood flow in capillary of injured tissue;
will produce redness and heat

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8
Q

exudate

A

increase blood plasma and proteins in injured tissue;
helps dilute injurious agents but results in excess fluid in tissues - EDEMA

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9
Q

SEROUS exudate

A

mainly plasma fluids and proteins, few WBCs; thin, clear

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10
Q

purulent exudate (suppuration)

A

contains plasma fluids and proteins, tissue debris and many WBCs;
thick white-to-yellow pus

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11
Q

what can happen due to exudate?

A

swelling develops, drainage may occur through fistula; incision and drainage may be required; pressure from exudate and chemical mediators may cause pain;

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12
Q

how can blood viscosity increase?

A

it may increase due to loss of plasma fluids

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13
Q

what is margination?

A

white blood cells migrate to the periphery of the vessel.

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14
Q

what is emigration? (transendothelial migration)

A

the process by which WBCs escape from blood vessels through gaps in endothelial cells

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15
Q

what is chemotaxis?

A

directed movement of WBCs toward the site of injury

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16
Q

what is phagocytosis?

A

the process by which WBCs ingest and then digest foreign substances; may include pathogenic organisms and tissue debris

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17
Q

what are the six different types of WBCs?

A
  1. Neutrophils (PMNs)
  2. Monocytes (macrophages)
  3. Lymphocytes
  4. Plasma cells
  5. Eosinophils
  6. Mast cells
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18
Q

which WBC is first to arrive at site of injury?

A

Neutrophils (PMNs) are the primary cell in acute inflammation; most common

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19
Q

which WBC is second to arrive?

A

Monocytes (macrophages); monocyte(in blood) becomes a macrophage as it enters tissue inflammation

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20
Q

which WBCs are seen in CHRONIC inflammation and the immune response?

A

both lymphocytes (3) and plasma cells (4)

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21
Q

which WBCs are seen in both inflammation AND the immune response?

A

eosinophils (5) and mast cells (6)

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22
Q

which WBCs become predominant with chronic inflammation?

A

macrophages, lymphocytes and plasma cells

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23
Q

which WBc decrease in number?

A

circulating neutrophils

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24
Q

Which WBC is derived from stem cells in bone marrow and contains lysosomal enzymes?

A

Neutrophils (PMNs)

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25
what is the function of neutrophils?
is phagocytosis and then enzymatic destruction of foreign substances; neutrophils then perish; enzymes can leak causing further tissue damage
26
which WBC makes up 3-8% of WBC population and is derived from stem cells in bone marrow?
macrophages
27
which WBC responds to chemotactic factors, is mobile, can phagocytize - also plays a role in the immune system?
macrophages
28
biochemical mediators
- cause many of the events in the inflammatory response - basic mediators can recruit other mediators and immune mechanism - may be derived from blood, endothelial cells, WBCs and platelets - pathogenic organisms as they injure the tissue
29
what are the three interrelated systems?
interaction takes place during activation, among their products, and within their various actions A. Kinin system B. Clotting mechanism C. Complement system
30
kinin system
active in early phases of inflammation - activated by substances in plasma and injured tissue - causes increased; dilation of BV at site of injury permeability of local BV INDUCES pain
31
clotting mechanisms
clots blood and mediates inflammation. - some products that are activated during tissue injury cause local vascular dilation and permeability by activating kinin
32
complement system
involves the production of sequential cascade plasma proteins; - present in blood in an inactive form - a trigger initiates sequence of steps. - these plasma proteins function in inflammation and immunity.
33
some components cause which WBCs to release what?
Mast cells to release histamine which causes an increase in vascular permeability and vasodilation
34
what do other components cause?
cell death, form chemotactic factors for WBCs, and enhance phagocytosis.
35
prostaglandins (other biochemical mediators released by body)
cause increased vascular dilation and permeability, tissue pain and redness and changes in connective tissue.
36
Lysosomal enzymes (other biochemical mediators released by body)
act as chemotactic factors; may cause damage to connective tissues and to the clot.
37
endotoxin (released by pathogenic microorganisms)
produced by cell walls of gram- negative bacteria; serves as chemotactic factor, can activate complement, function as an antigen and damage bone and tissue
38
lysosomal enzymes (pathogenic MO)
have a similar chemical composition and action as those released by WBCs
39
anti-inflammatory drugs
blocks/suppress the inflammatory response; prevent or reduce clinical signs of inflammation and adverse reactions to the injury. eg. aspirin, ibuprofen NSAID, prednisone (steroidal)
40
fever
controlled by the hypothalamus; associated with systemic inflammatory response
41
pyrogens
fever producing substances produced by WBCs and pathogens. act on the hypothalamus; hypothalamus increases body temp by way of prostaglandins
42
leukocytosis
increase the number of WBCs in a response; primary cell PMN; rate of formation is increased and immature forms are released from bone marrow into the blood; body is attempting to produce more for phagocytosis
43
elevated C-reactive protein
is produced in liver; plays important role in interacting with complement system; elevated levels are present during acute or infection; may continue with chronic
44
what can levels of elevated C-reactive protein help assess?
rheumatoid arthritis and systemic lupus erythematosus; a chronic increased level is associated with an increased risk for cardiovascular disease
45
lymphadenopathy
enlarged and palpable superficial lymph nodes; follow route of lymphatic drainage; occur due to changes in lymphocytes (primary cells of immune response)
46
hyperplasia
an increase in the number of cells often in response to chronic irritation or abrasion
47
hypertrophy
enlargement of individual cells; may be seen in cardiac muscle as a result of hypertension
48
Granuloma (chronic inflammation)
microscopic groupings of macrophages surrounded by lymphocytes and plasma cells; usually contain multinucleated giant cells; large macrophages with multiple nuclei associated with foreign body reactions and some infections such as tuberculosis
49
atrophy
a decrease in size or function of a cell, tissue, organ or entire body
50
regeneration
if inflamed area returns to normal structure and function
51
repair
occurs when the damage is too great for the tissue to return to normal; functioning cells and tissue often are replaces with non functioning scar tissue
52
how long does the microscopic events that occur during repair?
about 2 weeks; occurs simultaneously in both epithelium and connective tissue
53
day of injury
blood flows into injured tissue to produce a clot - the clot contains fibrin, clumped RBCs and platelets
54
one day after injury
NEUTOPHILS migrate from the micro circulation into injured tissue in an ACUTE inflammatory response; they phagocytize foreign material and necrotic tissue
55
two days after injury
monocytes migrate from micro circulation and become macrophages in tissue. (also phagocytize). fibroblasts increase in number and produce new collagen fibers. granulation tissue is formed in connective tissue portion of injury. - new surface epithelium formed; use fibrin mesh work to migrate; this protects newly formed tissue from additional injury. - lymphocytes and plasma cells migrate to the area as chronic inflammation and the immune response begins.
56
seven days after injury
fibrin is digested by tissue enzymes - sloughs off and the initial repair is complete - new tissue is red, new epithelium is thin, new CT is highly vascularized
57
two weeks after injury
initial granulation tissue and its fivers are remodeled; new tissue is scar tissue; whiter paler due to increased collagen and decreased vascularity
58
primary intention
healing of an injury where there is little loss of tissue - margins are close together and very little granulation tissue forms
59
secondary intention
edges of the injury cannot be joined during healing; a large clot forms, resulting in increased granulation tissue; may result in excess scar tissue - a keloid
60
tertiary intention
delaying surgical tissue repair until infection is resolved; an injured area may become infected - especially with puncture wounds. - in some situations an infected injury is left open until infection is controlled.
61
what are local factors that impair healing?
bacterial infection, tissue destruction and necrosis, hematoma, excessive movement of injured tissue, poor blood supply
62
what are systemic factors that impair healing?
malnutrition, immunosuppression, genetic connective tissue disorders, metabolic disorders
63
bone tissue repair
osteoblasts create new bone tissue. may be delayed by: -increased movement of bone -edema -infection in the tissue -excessive or inadequate movement of bone tissue

Oral Pathology (2 decks)

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