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Pathophysiology > Adaptation, Cellular Injury, Inflmmation, and Healing > Flashcards

Adaptation, Cellular Injury, Inflmmation, and Healing Flashcards

1
Q

Cellular Adaptation

A

Allows stressed tissue to survive or maintain function

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2
Q

Atrophy

A

decreased or shrinkage in cellular size due to decrease in work demand or adverse conditions

It can be physiological or pathological

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3
Q

Hyperplasia

A

increase in # of cells

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4
Q

Hypertrophy

A

Increase in cell size

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5
Q

Metaplasia

A

reversible change of one cell type for another in response to hostile environment

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6
Q

When does metaplasia occur?

A

in response to chronic irritation and inflammation

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7
Q

Dysplasia

A

Deranged cell growth

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8
Q

What is Dysplasia a precursor to?

A

cancer, does not guarantee but a strong implicator

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9
Q

Name the two Pathologic calcification

A

Dystrophic calcification

Metastatic Calcification

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10
Q

Dystrophic Calcification

A

occurs in dead or dying tissue

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11
Q

Metastatic Calcification

A

occurs in healthy tissue

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12
Q

two patterns of reversible cell injury

A

Cellular swelling

Fatty change

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13
Q

Hypoxic injury

A

deprives cell of oxygen and interrupts oxidative metabolism and the generation of ATP

Causes acute cellular swelling

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14
Q

Free radical cell injury

A

highly reactive chemical species

Immune cells called macrophages produce free radicals while fighting off invading germs. These free radicals can damage healthy cells, leading to inflammation

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15
Q

Impaired Calcium Homeostasis

A

Inappropriate release activates enzyme

regulates calcium flow to and from the bones

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16
Q

Programmed cell death

A

apoptosis ; pathological

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17
Q

Necrotic cell death

A

unregulated death caused by injuries to cell

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18
Q

Dry Gangrene

A

caused by lack of arterial blood supply but venous flow can carry fluid out of tissue

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19
Q

Wet Gangrene

A

lack of venous flow lets fluid accumulate in tissue

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20
Q

What is inflammation?

A

an innate , automatic response to cell injury that

  • neutralizes harmful agents
  • removes damaged and dead tissue
  • generates new tissue
  • promotes healing
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21
Q

3 types of imflammation

A

acute inflammation
chronic inflammation
systemic manifestations

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22
Q

5 cardinal signs of inflammation

A 
redness
swelling
warmth
pain
loss of function
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23
Q

Cellular Stage of inflammation

A

vasoconstriction - last only a few seconds

vasodilation - increases blood flow to injury

capillary permeability - allows exudate to escape into the tissue

pain
phagocytosis

systemic effects

coagulation

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24
Q

systemic effects

A

fever, TNF, prostaglandins

25
Q

Local signs of inflammation

A

Exudate ,ulceration

26
Q

Serous exudate

A

watery fluid

common with inflammation process

27
Q

hemorrhagic exudate

A

associated with severe tissue injury that causes damage blood vessels

or

when there is significant leakage of RBC from capillaries

28
Q

Fibrinous exudate

A

large amt of fibrinogen and forms from a thick and steak meshwork

29
Q

Membrandous or pseudomembranous exudate

A

necrotic cells enmeshed in a fibropurulent exudate

30
Q

Purulent / suppurative exudate

A

pus consists of WBC, proteins, and tissue debrie

31
Q

Chronic inflammation

A

longer duration (lasting for weeks to years)

body attempts to repair connective tissue involving proliferation of blood vessels , tissue necrosis, and fibrosis (scarring)

32
Q

Granuloma formation occurs in chronic inflammation

A

the immune system is treating the chronic inflammation as “out of sight, out of mind”

Long term management of irritant

33
Q

Systemic Manifestations of Inflammation 1st mechanism

A

Acute Phase (released by liver)

  • fever, lethargy
  • increased ESR and hsCRP
34
Q

Systemic Manifestations of Inflammation 2st mechanism

A

White Blood Cell Response

  • Leukocytosis : increased in WBCs
  • Immature neutrophils released into blood
35
Q

Systemic Manifestations of Inflammation 3rd mechanism

A

Enlarged lymph nodes

36
Q

Bacterial infections

A

= increase in neutrophils

37
Q

parasitic and allergic responses

A

= increase in eosinophilis

38
Q

viral infections

A

= decrease in neutrophils and increase

39
Q

Fever mechanism

A

Controlled by hypothalamus

increases metabolism

40
Q

Fever types:

A

Neurological fever - hypothalamus is damaged/ thermostat is broken. Results from damage/trauma to CNS

Drug Fever - a drug inadvertently leads to a hypermetabolic fever inducing state

41
Q

Heat Loss

A
  • Conduction - lying on cold surfaces
  • Radiation - loss of head from a distant cold objects like windows or walls
  • Evaporation - sweating
  • Convection - use of fans or effect of cold drafts
42
Q

Proliferative Capacity:

Continuously dividing cells

A

readily regenerate

uterus, GI tract, bone marrow, skin

43
Q

Proliferative Capacity:

Stable tissue cells

A

normal quiet cells, but when given correct stimulus, they will reconstitute

smooth muscle, fibroblasts,

44
Q

Proliferative Capacity:

Permanent tissue

A

Do not proliferate and terminally differentiated

nerve cells, skeletal muscle cells

45
Q

Connective tissue healing : Phase 1

A

acute inflammation : platelet activation and immune mobilization

Clot formation
phagoytosis
neutrophils - stimulate release of growth hormone

46
Q

Connective tissue healing : Phase 2

A

proliferation : cells multiplication and matrix deposition
filling in the gap / rebuilding

epithelization

47
Q

Connective tissue healing : Phase 3

A

Remodeling : scar formation and tissue restoration

remodeled due to fibroblast / collagenase

48
Q

Wound healing

A

Primary intention : no skin tissue lost, will not have granulation, can turn into secondary

Secondary : will have granulation

49
Q

Dysfunctional Wound Healing

A
  • Keloids
  • Contractures - shrinkage of wound tissue that pulls wound edges
  • Strictures - narrowing of tubular structures from the formation of scar tissue
  • Fistula
  • Adhesions - abnormal bands of internal scar tissue that can form , they can develop an obstruction from tihs
50
Q

gas gangrene

A

clostridium infection

hydrogen sulfide bubbles in muscle

51
Q

Acute inflammation

A

the early (appearing within minutes to hrs) host protective response of local tissues and their blood vessels to injury and is critical for restoration of tissue homeostasis

occurs before adaptive immunity and is aimed at removing the injurious agent and limiting the extend of tissue damage

52
Q

Factors involved in wound healing

A

Nutrition - Individuals most be in a state of positive nitrogen balance (protein best source in diet)

Immune Strength-conditions that contribute to immunocompromised states delay wound healing

Blood Flow and Oxygen delivery - adequate blood flow to bring O2 and remove waste

53
Q

Liquenfaction

A

necrotic cell death

release of enzymes following cell death

54
Q

coagulation necrotic cell death

A

acidosis develops and denatures proteins

characteristics of hypoxic injury

55
Q

Caseous necrotic cell death

A

soft- cheese life debris

commonly found in the center of TB granulomas

56
Q

Leukotrienes

A

Key cell-derived Mediator

slow reacting substances of anaphylaxis’s, (SRS-A)

causes slow and sustained constriction of the bronchioles

57
Q

Prostaglandins

A

Key cell-derived Mediator

induces vasodilation and bronchoconstriction

inhibits inflammatory cell function

PGI2 / PGF2a

58
Q

Thromboxane

A

Key cell-derived Mediator

Causes :
Vasoconstriction
Bronchoconstriction
Promotes platelet function

TxA2

Pathophysiology (4 decks)

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