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PATHOPHYSIOLLOGY > Ch.2-4: Inflammation > Flashcards

Ch.2-4: Inflammation Flashcards

1
Q

ongoing, balanced

A

cell injury

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2
Q

allows recovery

A

reversible

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3
Q

apoptosis/necrosis

A

irreversible

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4
Q

Etiology of cell injury include

A

Physical (mechanical, thermal, electric)
Radioactive
Chemical (substances, drugs, lead, mercury)
Biologic (viruses, bacteria, parasites)
Nutritional imbalance (deficits & excesses)

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5
Q

Cell injury mechanisms/ direct&indirect: MAIN

A

free radicals formation
hypoxia and atp depletion
intra-cellular calcium accumulation

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6
Q

Cell injury mechanisms/ direct&indirect: OUTCOMES:

A

Reversible (cell injury recovery)
Swelling & Fatty changes
Irreversible (death)
Apoptosis & Necrosis

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7
Q

What are the Stresses that endanger norm structure & function cause adaptive cell change for function & survival?

A

overwhelming stress
ineffective adaptation
maladaptive change
death

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8
Q

Adaptive cell response is necessary for

A

normal cell function

determine cell differentiation charactheristics

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9
Q

cell are able to adapt to increase work demands or threats to survival by changing their size, number and form

A

adaptation

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10
Q

decrease in cell size

A

atrophy

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11
Q

increase in cell size

A

hypertrophy

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12
Q

increase in the number of cells

A

hyperplasia

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13
Q

reversible change in which an adult cell is replaced with another adult cell (chronic smoker)

A

metaplasia

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14
Q

deranged cell growth, changes vary, change is size, shape, and how they are organized (pap smear)

A

dysplasia

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15
Q

Refers to cell death in an organ or tissue that is still part of a living person. Differs from apoptosis.

A

necrosis

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16
Q

Path of cell dissolution include

A

liquefaction
coagulation
infarction

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17
Q

discharge of content

A

liquefaction

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18
Q

form of coagulation, soft cheese

A

caseous necrosis

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19
Q

denature of enzymes

A

coagulation

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20
Q

artery and body becomes occluded

A

infarction

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21
Q

mass of tissue - necroses, results from infection . clostridium

A

gas gangrene

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22
Q

A form of necrosis or programmed cell death.
A highly selective process that eliminates injured and aged cells, controlling tissue regeneration.Thought to be responsible for several normal physiologic processes, including programmed destruction of cells during embryonic development, hormone dependent involution of tissues, death of immune cells, cell death by T cells, and cell death in proliferating cell populations.

A

apoptosis

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23
Q

death receptor dependent

A

extrinsic pathway

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24
Q

death receptor independent

A

intrinsic pathway

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25
Q

execution phase of extrinsic and intrinsic pathways begins by prolitic enzymes called

A

caseaspaces

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26
Q

the reaction of vascularized tissues to cell injury or death. It is characterized by the elaboration of inflammatory mediators and the movement of fluid an d leukocytes from the vascular system into the extravascular tissues.

A

inflammation

27
Q

Common causes of inflammation

A

burns, chemical irritants, frostbite, toxins, infection by pathogens, physical injury, hypersensitive immune reactions, ionizing radiation, foreign bodies, stress, and trauma.

28
Q

Acute inflammation:

Vascular response

A

increased blood flow
vascular permeability
leakage of protein-rich fluid into the extravascular tissues

29
Q

Acute inflammation:

Cellular Response

A

changes in endothelial cell lining

movement of phagocytes to injury

30
Q

Cellular Response:

Delivery and activation of leukocytes STEPS:

A

Adhesion and margination
Transmigration
Chemotaxis
Activation and phagocytosis

31
Q

CARDINAL SIGNS OF INFLAMMATION:

A 
rubor (redness)
swelling
heat
pain
loss of function/ alteration in function
32
Q

persistent (weeks to years) condition, recurrent
Etiologies: persistent infection, viruses, bacteria, fungi, parasites, injured tissue, chronic/ autoimmune disease, obesity
Manifestations: mononucleosis, angiogenesis, fibrosis, DNA damage (cancer risk)

A

chronic inflammation

33
Q

Acute inflammation

A

vascular change, edema, neutrophils
cardinal signs/ systemic manifestation
exudate production
tissue repair

34
Q

Chronic inflammation

A

monocytes predominant, angiogenesis/ fibrosis
follow acute inflammation
insidious onset, asymptomatic to tissue damage
aimed at treating persistence

35
Q

vasoactive/ first mediators to be released

A

histamine and seretonin

36
Q

broad inflammatory effects, enhance serotonin releases, enhanced leukocyte adhesion, and stimulate the production of prostaglandin

A

platelet-activating factor

37
Q

regulate/ amplify inflammatory process

A

nitric oxide, and oxygen derived free radicals

38
Q

anti-inflammatory effect on cell membrane- fish

A

omega 3 polyunsaturated fatty acids

39
Q

mediate inflammation

A

cytokines/ chemokines

40
Q

clear, watery fluid

A

serous

41
Q

bloody meshwork

A

fibrinous

42
Q

necrotic cells enmeshed in fibroprulent exudate

A

membranes

43
Q

yellow/greenish, contains pus which is composed of degraded WBCs, proteins, and tissue debris

A

purulent

44
Q

red leakage of red blood cells from capillaries

A

sanguineous

45
Q

pink (combo of serous and sanguineous)

A

sero- sanguineous

46
Q

Systemic manifestation of inflammation include:

A

fever
leukocytosis
lethargy/fatigue

47
Q

Increases set point of hypothalamic thermoregulation center

To promote pathogen-hostile environment

A

fever

48
Q

Increased leukocyte count to 15K-20K
To efficiently fight inflammation/infection
Release pyrogenic (fever-making) mediators

A

leukocytosis

49
Q

Metabolism change from energy-making to heat-making

To maintain fever-induced pathogen-hostile environ

A

lethargy/fatigue

50
Q

Types of fever:

return to normal after 24 hours

A

intermittent fever

51
Q

Types of fever:

temp above normal, very little variation

A

sustained fever

52
Q

Types of fever:

does not return to the normal level

A

remittent fever

53
Q

Types of fever:

recurrent, last for days between each episode

A

relapsing fever

54
Q

LAB TEST:

ESR

A

erythrocyte sedenmation
measures the rate RBC settle
normal: M-15 F-20
increase in ESR (rise in fibrinogen/ RBC stack)

55
Q

LAB TEST:

CRP

A

C-reactive protein
normal: less than 1.0
rise acute infection

56
Q

Acetaminophen

A

antipyretic, analgesic

NOT INFLAMMATORY

57
Q

Acetylsalicylic acid (ASA)

A

antipyretic, analgesis, anti-inflammatory (NSAID)

58
Q

Tissue type:
(continuously-dividing)
Readily regenerate if stem cell pool preserved (skin)

A

labile

59
Q

Tissue type:
(restricted dividing)
Capable of regeneration if proper stimuli (kidney)

A

stable

60
Q

Tissue type:
(non-dividing)
Incapable of regeneration, fibrous scar switch (nerves)

A

fixed

61
Q

Local and systemic factors of wound healing:

A 
blood flow, and O2 delivery
Infection, wound separation, forcing bodies
nutrition
inflammation
aging
62
Q

sutured surgical incision

A

primary intention

63
Q

larger wounds (greater loss of tissue & contamination

A

secondary intenion

64
Q

Healing phases include:

A

inflammatory (prepares for healing)
proliferative
maturation/remodeling

PATHOPHYSIOLLOGY (9 decks)

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