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2 Principles of Disease > Lecture 2 > Flashcards

Lecture 2 Flashcards

1
Q

Causes of cell injury and disease

A

aging
ischemia
infectious agents
immune reactions
genetic factors
nutritional factors
physical factors
chemical factors

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2
Q

Response of cells when injured

A

Cell injury
inflammation
healing
atrophy/hypertrophy/hyperplasia/dysplasia

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3
Q

Free Radical theory

A

increase in free radical production or exposure causes a decline in cell function

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4
Q

Cellular senescence

A

viable nondividing state

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5
Q

What promotes free radical formation?

A

high levels of oxygen
UV exposure
cigarette smoke
pesticides
being given O2 too quickly after injury
intense or prolonged exercise

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6
Q

What antioxidants neutralize extra free radicals?

A

Endogenous (inside our body) = superoxide dismutase, produced by exercise
Exogenous

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7
Q

Free Radicals

A

has less than 8 electrons
naturally unstable so tries taking electrons from other atoms
formed in ATP formation

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8
Q

Telomere aging clock theory

A

every time a cell replicates, the telomere breaks down

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9
Q

Epigenetic clock theory

A

methylation changes as we age

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10
Q

Age-related cellular markers

A

telomere shortening
lipofuscin: intracellular pigment

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11
Q

Cellular aging

A

age-related cellular changes impair healing
certain lifestyle choices influence aging related markers

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12
Q

Ischemia

A

lack of blood supply below the minimum necessary to maintain cellular function

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13
Q

Hypoxia

A

decrease in oxygen delivery to cells or tissue

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14
Q

Anoxia

A

absence of oxygen delivery to cells or tissue

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15
Q

Influences on cell injury

A

infectious agents
immune reactions
genetic, nutritional, physical, chemical, psychosocial factors

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16
Q

Cell injury potential outcomes

A

Reversible = sublethal
Irreversible = cell death

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17
Q

Reversible cell injury

A

Can be acute or chronic
determined if the cell nucleus and membrane are INTACT

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18
Q

Chronic cell injury

A

Continued stress
results in cellular adaptations (atrophy, hypertrophy, hyperplasia, dysplasia) and intracellular accumulations of fats, proteins, carbs, pigments

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19
Q

Dysplasia

A

increase in number abnormal cells

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20
Q

HYperplasia

A

increase in number of cells within an area

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21
Q

Irreversible cell injury

A

changes in cell nuclei, mitochondria, lysosomes, breakdown of membrane
active cellular breakdown occurs

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22
Q

Enzymes and injured cells

A

dissolve dead cells

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23
Q

Phagocytes and injured cells

A

must remove dead tissue before healing can occur

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24
Q

Types of necrosis

A

Coagulative
Caseous
Liquefactive

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25
Q

Coagulative necrosis

A

Internal organs. Cells are dead, but architecture of tissue is intact and recognizable under microscope.
Frostbite, ischemia, dry gangrene

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26
Q

Caseous Necrosis

A

Usually associated with mycobacterium infection
tuberculosis

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27
Q

Liquefactive necrosis

A

overwhelming cell destruction with enzymatic breakdown of tissue structure. Can occur in brain, skin, wound, joints
wet gangrene, stroke

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28
Q

What happens when a single cell becomes hypoxic?

A

Mitochrondria: decreased ATP production, swelling of inner mitochondrial membrane
Plasma Membrane: loss of selective permeability, enzymes leak out of the cell
Gap junctions: loss of coupling

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29
Q

organelles that breakdown without oxygen

A

mitochondria
cell membrane
gap junctions

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30
Q

Key clinical pathology findings with hypoxia

A

leakage of soluble enzymes from damaged dying cells, leads to elevation of enzymes and other proteins into plasma

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31
Q

Heart attack leakage

A

CK leaks within 1 day
Troponin leaks within 1-2 days
Lactate dehydrogenase leaks within 3 days

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32
Q

Plasma

A

water
albumin
globulins/antibodies
fibrinogen/clotting factors
solutes

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33
Q

Albumin

A

major contributor to osmotic oressure of plasma. Its presence pulls water toward it.

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34
Q

Oncotic pressure

A

osmotic pressure of proteins

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35
Q

Blood makeup

A

Plasma
Formed Elements

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36
Q

Formed elements

A

RBC
WBC
platelets

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37
Q

Erythrocytes

A

lack nuclei, transport O2 + CO2, short lived, 120 days

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38
Q

Platelets

A

also known as thrombocytes
involved in clotting, plug the area

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39
Q

Leukocytes

A

WBC
include granular and nongranular

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40
Q

Granular leukocytes

A

neutrophils = 1st on scene w/bacteria
eosinophils = allergies
basophils = heparine, histamine

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41
Q

Nongranular leukocytes

A

monocytes = circulate short time, become macrophages in tissue
lymphocytes = B-cells and T-cells

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42
Q

Inflammation

A

coordinated reaction of tissues to cellular injury and death caused by microbes or physical insult

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43
Q

Acute inflammation

A

immediate and early response to injury
characterized by exudative response and PMNs (neutrophils)
defensive reaction and vital

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44
Q

Chronic inflammation

A

ongoing response to an injurious agent
characterized by mononuclear cells (monocytes, lymphocytes) and fibroblasts

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45
Q

What does acute inflammation help with?

A

tissues are protected against microorganisms
any tissue damage that does occur is swiftly repaired
the process of healing can begin

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46
Q

Inflammation can be problematic…

A

can lead to chronic inflammation and disease
can spiral out of control

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47
Q

Major events in acute inflammation

A

Vascular changes
cellular events
hemostasis

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48
Q

Intracellular compartment

A

inside cell plasma membranes, 2/3 of total body water

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49
Q

Extracellular compartment

A

1/3 total body water
interstitium tissue = 80%
intravascular/plasma makes rest

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50
Q

Net filtration pressure

A

pushes fluid out of the capillary and into interstitial tissue

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51
Q

Oncotic pressure

A

plasma proteins exert a pressure that pulls fluid back into capillary from the interstitial tissue

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52
Q

Lymph vessels and nodes

A

widely distributed throughout body
drain excess interstitial tissue fluid, returns to venous system
infectious agents can spread via lymph nodes

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53
Q

Vascular changes

A

1st step of inflammation

Transient vasoconstriction
vasodilation of arterioles
increased vascular permeability

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54
Q

Transient vasoconstriction

A

helps prevent blood loss

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55
Q

Vasodilation

A

of arterioles, capillaries, venules
due to relaxation of smooth muscle lining vessels
slows blood velocity which allows WBC to move to edge of capillaries

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56
Q

Increased vascular permeability

A

endothelial cells contract, leading to increased space between cells
leakage of fluid and plasma proteins out of capillaries and into the interstitial

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57
Q

Edema

A

accumulation of plasma in interstitial tissue
“inflammatory leakage”

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58
Q

Transudate edema

A

protein-poor fluid

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59
Q

Exudate edema

A

protein-rich fluid that may also contain phagocytic cells

60
Q

Effusion

A

“inflammatory leakage”
leakage material that fills an anatomic space

61
Q

Hemorrhagic Exudate

A

sanguinous
bright red or bloody
expected after surgery/trauma
concerning when its sudden, large amounts may indicate hematoma

62
Q

Serosanguinous exudate

A

blood-tinged yellow or pink
expected 48-72 hours after injury/trauma
concerning when there is a sudden increase may indicate wound dehiscence

63
Q

Wound dehiscence

A

wound opening up

64
Q

Exudate

A

a mass of cells and fluid that has seeped out of blood vessels or an organ, especially in inflammation

65
Q

Types of exudates

A

serous
purulent
hemorrhagic
serosanguinous

66
Q

Serous exudate

A

watery, clear yellow, or straw-colored, contains albumin and antibodies
expected in early stages of most inflammations. Common with blisters, joint effusions, viral infections
concerning when there is sudden increase may indicate draining seroma

67
Q

Purulent exudate

A

viscous cloudy pus, contains cellular debris from necrotic cells and during PMNs
usually caused by pus forming bacteria and indicates infection

68
Q

Cellular events in acute inflammation

A

Step 2 includes:
movement and accumulation of WBC
recognition and adherence
Phagocytosis and intracellular degradation

69
Q

Movement and accumulation of WBCs

A

comes from the blood to the tissues
Neutrophils, first line of defense
Monocytes; next cells to emigrate

70
Q

Recognition and adherence

A

Opsonization: coating of foreign particles with proteins that accelerates phagocytosis

71
Q

Phagocytosis and intracellular degradation

A

neutrophils and macrophages ingest particles and degranulate. granules within phagocytes contain bactericidal enzymes that digest invading bacteria

72
Q

Margination

A

blood stasis allows WBCs to accumulate and stick to lining of blood vessels at injury site

73
Q

Diapedesis

A

WBCs actively move out of blood vessels into interstitial space
neutrophils and monocytes squeeze through tiny gaps between endothelial cells

74
Q

Chemotaxis

A

WBCs actively move toward injured/infected area by attraction to cytokines released from tissue or cells

75
Q

Oposonization/phagocytosis/degranulation

A

neutrophils and monocytes/macrophages engulf and destroy foreign substances and debris

76
Q

Neutrophilia

A

neutrophils are the primary cell type in tissue/fluid during acute inflammation

77
Q

How do WBCs move toward an area of tissue damage or infection?

A

chemotaxis

78
Q

Circulating platelets produce…

A

serotonin, help with vasoconstriction

79
Q

Tissue mast cells

A

between internal and external boundaries
secrete histamine, increases vasodilation and permeability

80
Q

Basophils

A

secrete histamine

81
Q

Endothelial cells

A

line every capillary, contraction, increase space when needed

82
Q

Injured tissues release

A

arachidonic acid derivatives. helps to keep inflammation going

83
Q

Cytokines

A

chemical signals that help to guide cells
produced by WBCs
interleukin produces multiple effects on metabolic and endocrine systems
produces fever by making PGE in hypothalamus

84
Q

Enzymes derived from plasma

A

blood coagulation cascade
fibrinolytic system
complement system

85
Q

Vasoactive amines

A

Serotonin
Histamine

86
Q

Serotonin

A

Vasoactive amine
causes vasocontriction
primary source from platelets

87
Q

Histamine

A

vasoactive amine
vasodilation of arterioles
leads to endothelial cell contraction, increased permeability
short duration of action
primary source are mast cells, basophils, platelets

88
Q

Arachidonic acid metabolites

A

Released from injured tissue, specifically from phospholipid bilayer
prostaglandins/thromboxane
leukotrienes

89
Q

prostaglandins E2

A

type of AA metabolites
induce fever and mediates pain responses

90
Q

prostacyclin

A

AA metabolite
inhibits platelet aggregration and causes vasodilation

91
Q

Thromboxane

A

type of AA metabolite
facilitates platelet aggregation

92
Q

Leukotrienes

A

potent bronchoconstrictor
increased vascular permeability

93
Q

AA metabolites promote…

A

the 5 classic local signs/symptoms of acute inflammation
rubor, calor, tumor, dolor, functio laesa

94
Q

Chemical mediators of acute inflammation

A

Plasma proteases
complement system
cytokines
AA metabolites
Vasoactive amines

95
Q

Plasma proteases

A

kinins
same vascular action as histamine
induce pain by activating nocioceptors

96
Q

Complement system

A

group of plasma proteins that lie dormant until activated
cause opsonization, formation of membrane attack complex

97
Q

Hemostasis

A

all the processes that minimize blood loss when a blood vessel is opened
causes 4 events; vasoconstriction, formation of plug, formation of fibrin web/clot, clot retraction/dissolution

98
Q

Systemic response to inflammation

A

fever
leukocytosis
elevated erythrocyte sedimentation rate

99
Q

Fever

A

due to pyrogens released from WBCs

100
Q

Leukocytosis

A

increased # of WBCs in the blood

101
Q

Erythrocyte Sedimentation Rate

A

ESR or sed rate
rate at which RBCs in unclotted blood plasma sink to bottom of test tube
sed rate increases during inflammatory processes
Why? high proportion of fibrinogen causes RBCs to stick and sink faster
nonspecific measure of inflammation

102
Q

Potential outcomes of inflammation

A

Complete resolution
healing by scarring
abscess formation
progression to chronic inflammation

103
Q

Chronic Inflammation

A

healing of tissues, but not full return to function
can be caused by extensive injury, tissue necrosis, inability of parenchymal cells to regenerate, persistence of agent, repeated episodes of inflammation, low immune system

104
Q

Characteristics of chronic inflammation

A

chronic inflammatory cells
tissue destruction
fibroblast proliferation

105
Q

Chronic inflammatory cells

A

macrophages, lymphocytes, and plasma cells infiltrate involved areas
possible granuloma formation

106
Q

Tissue destruction

A

hallmark of chronic inflammation

107
Q

Fibroblast proliferation

A

common cause for compromise/failure of organ system (fibrosis)

108
Q

Type 1 collagen

A

predominant collagen in the body, prominent in mature scars, tendon, bonem joints, labrums. most abundant

109
Q

Type 2 collagen

A

predominant type in growth plate and hyaline cartilage

110
Q

Type 3 collagen

A

primarily in vascular and visceral tissue. first type of collage deposited in wound healing

111
Q

Type 4 collagen

A

found in basement membranes

112
Q

Regeneration

A

process by which destroyed or lost cells are replaced by vital cells. restores tissue to intactness. EXACT cells are replaced
only occurs if parenchymal cells undergo mitosis

113
Q

Repair

A

process by which damaged tissue is replaced by connective scar tissue
may result from tissue necorsis with removal of the connective tissue matrix

114
Q

Labile cells

A

can regenerate
cells with high turnover rate. Skin, GI, etc

115
Q

Stable cells

A

can regenerate
cells with low turnover rate
do not normally divide, can undergo mitosis with certain stimulus
skeletal cells, kidney cells

116
Q

Regeneration can only occur if….

A

normal connective tissue matrix and basement membrane are intact

117
Q

Basement membrane

A

provide mechanical support for resident cells as well as a scaffold for accurate regeneration of pre-existing structures

118
Q

Regeneration does not occur in

A

permanent cells

119
Q

Permanent cells

A

cells that do not have the ability to divide and there are no apparent stem cells. most neurons, myocardial cells

120
Q

How does the body repair damaged tissue?

A

synthesis of extracellular matrix
proliferation and migration of parenchymal cells and endothelial cells
tissue contraction
tissue regernation or repair

121
Q

Synthesis of extracellular matrix

A

Fibroblasts migrate into the damaged area and proliferate, synthesize, and secrete several proteins that make up extracellular matrix: fibronectin, collagen, proteogylcans/elastin

122
Q

Fibronectin

A

the glue
made from certain plasma proteins that leaked out of blood vessels
stabilizes fibrin
provides tensile strength and attracts more fibroblasts

123
Q

Collagen

A

structural integrity
most important protein to provide structural support and tensile strength for almost all tissues and organs

124
Q

Proteoglycans and elastin

A

hydration and strechability
proteogylcans bind to fibronectin and collagen, retain water, provide stability of collagen

125
Q

Tissue contraction

A

ECM shrinks due to the work of myofibroblasts. these help to approximate the wound margins

126
Q

Pathological repair

A

Deficient scar formation
Excessive scar formation
Contracture

127
Q

Deficient scar formation

A

can result in wound dehiscence, which is rupture or splitting open

128
Q

Excessive scar formation

A

hypertrophic scar
keloid

129
Q

Keloid

A

exaggerated growth of scar tissue

130
Q

Hypertrophic scar

A

widened scar, characterized by being red, raised, and rigid

131
Q

Contracture

A

remember that wound contraction is shrinkage, and is normal
a contracture is EXCESSIVE shrinkage, decreases ROM. it is pathological

132
Q

Local influences on tissue healing

A

adequacy of local blood supply
presence of infection or foreign body at injured site
type of cell
chance for immobilization/protection during healing

133
Q

General factors affecting healing

A

general health
age
vascular sufficiency and oxygen perfusion
substance use/abuse
nutritional status
systemic diseases

134
Q

Lung cell healing

A

can occur after injury if basement membranes are intact (pneumonia)
repair happens when theres damage to basement membrane (pulm fibrosis)

some agents can cause formation of scar tissue when not needed

135
Q

Peripheral nerve healing

A

axons can regenerate if nerve cell body is intact

myelin degeneration –> new axon, proliferation of schwann cells –> maintenance of neurotubules is necessary

136
Q

skeletal muscle cell healing after infection

A

cells can regenrate within sheaths and get return of function
if severe, fibers will be destroyed

137
Q

skeletal muscle cell healing after contusion/strain

A

incomplete healing with loss of strength and high rate of reinjury

138
Q

skeletal muscle cell healing after transection

A

regeneration can occur from undamaged stumps or satellite cells

139
Q

skeletal muscle cell healing after severe trauma

A

results in scar

140
Q

Phases of fracture healing

A

inflammatory
reparative phase
remodeling

141
Q

Inflammatory phase of fracture healing

A

pain, swelling, heat
local internal bleeding
initial fibrosis occurs at end of 1st week

142
Q

Reparative phase

A

6-12 wks
osteoclasts remove debris
soft callous formation
hard callous starts
many bone growth factors help

143
Q

Remodeling phase of fracture healing

A

months to years
clincal union to radiological union
healing depends on lots of different factors

144
Q

Tendon/ligaments cell healing

A

REPAIR not regeneration, replaced with weaker types of collagen
may take >40-50 weeks to regain normal strength
max contraction should be avoided for 2 months
ligaments follow the same pattern. Intra-ligaments heal poorly

145
Q

Articular cartilage healing

A

does not regenerate after adolescence
wihtout intervention, healing of cartilage occurs by scar tissue or doesn’t heal

146
Q

Fibrocartilage healing

A

tears heal by migration of cells from the synovial membrane
lacerations need surgery

2 Principles of Disease (7 decks)

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