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Pathophysiology > The Inflammatory Response > Flashcards

The Inflammatory Response Flashcards

1
Q

t/f: most diseases result from an inflammatory response

A

true-immune system responding to injury

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2
Q

inflammatory response purpose

A

-pathologic/physiologic response to inflammatory mediators: eliminate cause of cell injury, removed damaged tissue, generate new tissue
-destroy, enzymatically digest, neutralize harmful agents (ex: foreign agents, infectious organisms)

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3
Q

repair process

A

interwoven with inflammatory response, replaces damaged tissue, fills in wounds with scar tissue

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4
Q

inflammatory conditions are named by…

A

adding the suffix -itis (appendicitis, pericarditis)

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5
Q

5 cardinal signs of inflammation

A

-reaction of vascualized tissue to injury
-rubor (redness), tumor (swelling), calor (heat), dolor (pain), functio laesa (loss of function-results from all signs)

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6
Q

acute inflammation has:

A

vascular phase, cellular phase (leukocyte margination, adhesion and transmigration), leukocyte activation and phagocytosis

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7
Q

vascular phase of acute inflammation

A

-changes in small blood vessels at the site of injury marked by tissue edema
-vasodilation causes heat and redness
-loss of protein-rich fluid (exudate) into extravascular spaces from increased vascular permeability

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8
Q

edema

A

abnormal amount of fluid in interstitial tissue

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9
Q

(vascular phase) increased vascular permeability causes:

A

-decrease in capillary osmotic pressure
-increases interstitial osmotic pressure (edema)
-produces swelling, pain, impaired function

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10
Q

vascular response patterns

A

immediate transient, immediate sustained, delayed hemodynamic

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11
Q

immediate transient response happens with:

A

minor injuries, ex: paper cut, very small wounds

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12
Q

immediate sustained response happens with:

A

more serious injuries, ex: badly skinned knee
-continues for several days, damages vessels in area

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13
Q

delayed hemodynamic response happens with:

A

an increase in capillary permeability that occurs 4-24 hours after injury
-ex: sunburn

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14
Q

cellular phase of acute inflammation

A

-movement of phagocytic blood cells (leukocytes) into injury site (leukocytosis)
-neutrophils>primary early arrival (shift to the left), bacteria/fungal infection
-eosinophils>parasitic, allergic responses
-basophils>respond later
-macrophages (monocytes)>secrete cytokines

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15
Q

types of leukocytes

A

-all granulocytes: neutrophils, basophils, eosinophils
-all monocytes (largest WBC, secrete cytokines): macrophages

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16
Q

“shift to the left”

A

increase in immature neutrophil count (inflammation)

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17
Q

cytokines

A

-“chemical messengers of immune system”
-chemical growth signs (direct leukocytes)

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18
Q

direction of cellular response

A

margination, transmigration, chemotaxis
-cytokines tell leukocytes where to go
-accumulation of leukocytes
-adhesion molecules (selectins, integrins, immunoglobulin)

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19
Q

adhesion molecules during the cellular response (cellular phase of acute inflammation)

A

initiate adhesion, aggregate (cluster) inflammatory cells, move into underlying tissue

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20
Q

phagocytosis in cellular phase

A

-last stage of cellular phase
-engulfment
-intracellular killing of toxic oxygen and nitrogen products, lysozymes, proteases and defensins

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21
Q

inflammatory mediator classification

A

-those with vasoactive (dilate BV) and smooth-muscle constricting properties: histamine, arachidonic acid metabolites (prostaglandins, leukotrienes, platelet-activators)
-those with chemotactic factors (tell leukocytes where to go): cytokines, complement fragments
-plasma proteases that activate parts of the complement system, coagulation factors of clotting cascade, vasoactive peptides of kinin system
-reactive molecules/cytokines freed from leukocytes that can damage surrounding tissue/cells in the extracellular environment

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22
Q

plasma-derived mediators

A

from the liver, acute-phase proteins (fever, inflammation), complement system proteins, clotting and kinin system

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23
Q

cell-derived mediators

A

-preformed mediators (mast cells>histamine, platelets, neutrophils/macrophages)
-newly synthesized (leukocytes, macrophages, cytokines)

24
Q

how corticosteroid medications work

A

-in the cyclooxygenase pathway: (aspirin, NSAIDs) prostaglandins inhibit inflammatory cell functions, thromboxane causes vasoconstriction, promotes platelet functoin
-in the lipoxygenase pathway: induces smooth muscle contractions, increase microvascular permeability

25
Q

which of the following molecules induce endothelial cell retraction?
a) omega-3 fatty acids
b) leukotrienes
c) histamine
d) vascular cell adhesion molecules

A

c) histamine

26
Q

inflammatory exudates

A

serous, hemorrhagic, membranous or pseudomembranous, purulent or suppurative, fibrinous

27
Q

serous exudates

A

watery fluids from plasma entering inflammatory site (ex: skin blisters)

28
Q

hemorrhagic exudates

A

blood-results from severe tissue injury that damages blood vessels or red cells from capillaries

29
Q

membranous or pseudomembranous exudates

A

develop on mucous membrane surfaces, made of necrotic cells in a fibropurulent exudate

30
Q

purulent or suppurative exudates

A

infections-contain pus, composed of degraded WBCs, proteins and tissue debris (ex: boils, abscess formation)

31
Q

fibrinous exudates

A

lots of fibrinogen, form thick and sticky meshwork (ex: adhesion following surgery)

32
Q

abscess formation example: splinter

A

1-bacterial invasion (the splinter) develops inflammation
2-suppuration (puss)-bacterial growth, neutrophil migration, tissue necrosis, purulent exudate
3-abscess formation-covers inflamed area and puss

33
Q

acute inflammatory response characteristics

A

rapid response (minutes or hours), localized site, short duration (self-limiting), removes injurious agent, limits and repairs tissue damage from the injury/response, granulocytes and monocytes present

34
Q

chronic inflammatory response characteristics

A

(ex: lupus) persistent and recurrent (and/or subtle), no acute response, lasts days/weeks or even years, tissue destruction from inflammatory cells, autoimmune disorders or precursors to diseases, lymphocytes and macrophages present in large numbers

35
Q

granulomatous inflammation

A

from foreign substances (splinters, sutures, silica) or microorganisms (causes tuberculosis, syphilis, fungal infections, brucellosis)

36
Q

systemic manifestations of inflammation

A

-acute-phase response: alterations in WBC count (leukocytosis, immunosupression, neutrophilia/shift to left if infection is severe)
-fever (tachycardia), lymph node reactions (non-specific to get immune response), anorexia (loss of weight/appetite), sepsis and septic shock (circulatory chock, systemic inflammatory response syndrome: deadly)

37
Q

t/f: in inflammation, blood vessels constrict

A

false-they dilate

38
Q

t/f: chronic inflammation is self perpetuating while acute inflammation is self limiting

A

true

39
Q

t/f: inflammatory mediators attract and guide leukocytes/plasma proteins to the injury site (chemotaxis)

A

true

40
Q

t/f: bleeding is a localized cardinal sign of infection

A

false

41
Q

t/f: inflammatory mediators cause vasodilation

A

true

42
Q

acute inflammation involves which 2 stages?

A

vascular and cellular phase

43
Q

t/f: inflammatory mediators increase leukocyte/WBC count

A

true

44
Q

t/f: infection and injury causes inflammation but signs and symptoms are caused by chemical mediators

A

true

45
Q

what is the term for recognition, engulfment and intracellular killing

A

phagocytosis

46
Q

what causes the local warm during the inflammatory response

A

the increased blood flow

47
Q

a client’s WBC count includes a “shift to the left”. what happened?

A

count of immature neutrophils increases as a result of bacterial infection

48
Q

what term refers to a vesicle (blister) that bursts releasing clear fluid

A

serous

49
Q

what is the role of mast cells during inflammation?

A

release histamine-a strong vasodilator

50
Q

a client has an acute-onset fever and malaise revealing an elevated neutrophil count. what kind of infection do they have?

A

bacterial-neutrophils fight off bacteria

51
Q

teresa reports pain with urination and has a temperature of 100.8. Her urine is positive for nitrates with elevated leukocyte counts. is this acute or systemic inflammation?

A

systemic

52
Q

Kyle has a dislocated knee. it is swollen and he cannot bend it. he feels nauseous and fatigued from the pain. is this acute or systemic inflammation?

A

acute

53
Q

David had corrective bowel surgery and has hypothermia, tachycardia, high plasma lactate, increased WBC and coagulation abnormalities. is this acute or systemic inflammation?

A

systemic

54
Q

a client undergoing chemotherapy is lethargic, their temperature is 101.3. blood tests show leukopenia and hyperglycemia. is this acute or systemic inflammation?

A

systemic

55
Q

a child has blisters from touching a hot pan in both hands. is this acute or systemic inflammation

A

acute

Pathophysiology (15 decks)

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