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

Adaptation, Cellular Injury, Inflmmation, and Healing Flashcards

(58 cards)

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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

Study These Flashcards
A

fever, TNF, prostaglandins

25
Local signs of inflammation
Exudate ,ulceration
26
Serous exudate
watery fluid | common with inflammation process
27
hemorrhagic exudate
associated with severe tissue injury that causes damage blood vessels or when there is significant leakage of RBC from capillaries
28
Fibrinous exudate
large amt of fibrinogen and forms from a thick and steak meshwork
29
Membrandous or pseudomembranous exudate
necrotic cells enmeshed in a fibropurulent exudate
30
Purulent / suppurative exudate
pus consists of WBC, proteins, and tissue debrie
31
Chronic inflammation
longer duration (lasting for weeks to years) body attempts to repair connective tissue involving proliferation of blood vessels , tissue necrosis, and fibrosis (scarring)
32
Granuloma formation occurs in chronic inflammation
the immune system is treating the chronic inflammation as "out of sight, out of mind" Long term management of irritant
33
Systemic Manifestations of Inflammation 1st mechanism
Acute Phase (released by liver) - fever, lethargy - increased ESR and hsCRP
34
Systemic Manifestations of Inflammation 2st mechanism
White Blood Cell Response - Leukocytosis : increased in WBCs - Immature neutrophils released into blood
35
Systemic Manifestations of Inflammation 3rd mechanism
Enlarged lymph nodes
36
Bacterial infections
= increase in neutrophils
37
parasitic and allergic responses
= increase in eosinophilis
38
viral infections
= decrease in neutrophils and increase
39
Fever mechanism
Controlled by hypothalamus | increases metabolism
40
Fever types:
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
Heat Loss
- 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
Proliferative Capacity: Continuously dividing cells
readily regenerate uterus, GI tract, bone marrow, skin
43
Proliferative Capacity: Stable tissue cells
normal quiet cells, but when given correct stimulus, they will reconstitute smooth muscle, fibroblasts,
44
Proliferative Capacity: Permanent tissue
Do not proliferate and terminally differentiated nerve cells, skeletal muscle cells
45
Connective tissue healing : Phase 1
acute inflammation : platelet activation and immune mobilization Clot formation phagoytosis neutrophils - stimulate release of growth hormone
46
Connective tissue healing : Phase 2
proliferation : cells multiplication and matrix deposition filling in the gap / rebuilding epithelization
47
Connective tissue healing : Phase 3
Remodeling : scar formation and tissue restoration remodeled due to fibroblast / collagenase
48
Wound healing
Primary intention : no skin tissue lost, will not have granulation, can turn into secondary Secondary : will have granulation
49
Dysfunctional Wound Healing
- 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
gas gangrene
clostridium infection hydrogen sulfide bubbles in muscle
51
Acute inflammation
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
Factors involved in wound healing
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
Liquenfaction
necrotic cell death release of enzymes following cell death
54
coagulation necrotic cell death
acidosis develops and denatures proteins characteristics of hypoxic injury
55
Caseous necrotic cell death
soft- cheese life debris commonly found in the center of TB granulomas
56
Leukotrienes
Key cell-derived Mediator slow reacting substances of anaphylaxis's, (SRS-A) causes slow and sustained constriction of the bronchioles
57
Prostaglandins
Key cell-derived Mediator induces vasodilation and bronchoconstriction inhibits inflammatory cell function PGI2 / PGF2a
58
Thromboxane
Key cell-derived Mediator Causes : Vasoconstriction Bronchoconstriction Promotes platelet function TxA2

Pathophysiology (4 decks)

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