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D2 Fall > Gen Path Exam 1 - Cell Injury/Death, Inflammation, Wound Healing, and Hemostasis > Flashcards

Gen Path Exam 1 - Cell Injury/Death, Inflammation, Wound Healing, and Hemostasis Flashcards

1
Q

Give examples of continuously dividing tissue

A

Skin, mouth, vagina, cervix, GI, exocrine ducts

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2
Q

Give examples of stable tissue that divide only in response to injury

A

Endothelial cells, fibroblasts, SM, solid organs (kidney, liver, pancreas)

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3
Q

Give examples of permanent tissue that never proliferate after birth

A

Neurons, heart muscle, skeletal muscle

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4
Q

Name endogenous causes of stress/injury

A

Hypoxia (most common)
Immunologic rxns
Genetic abnormalities
Aging

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5
Q

Name exogenous causes of stress/injury

A

Toxins (pollutants, asbestos, cig smoke)
Infectious pathogens
Nutritional imbalance
Physical agents (trauma)

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6
Q

Increase in size of cell and organ

A

Hypertrophy

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7
Q

Occurs in cells with limited capacity to divide (ex: skeletal muscle)

A

Hypertrophy

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8
Q

Give an example of physiologic hypertrophy

A

Uterus during pregnancy

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9
Q

Give an example of pathologic hypertrophy

A

Heart during hypertension

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10
Q

Increase in # of cells (controlled)

A

Hyperplasia

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11
Q

Occurs in tissue capable of division

A

Hyperplasia

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12
Q

Give an example of physiologic hyperplasia

A

Breast development (hormonal)
Liver regeneration (compensatory)

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13
Q

Give an example of pathologic hyperplasia (caused by excessive hormonal or growth factor stimulation)

A

Endometrial hyperplasia
Benign prostatic hyperplasia

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14
Q

Decrease in size of cells

A

Atrophy

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15
Q

Loss of cell substance by decreased protein synthesis or increased protein degradation

A

Atrophy

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16
Q

What are the causes of atrophy?

A

Decreased workload, blood supply, and endocrine stimulation
Inadequate nutrition
Aging

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17
Q

One cell type replaced by another cell type

A

Metaplasia

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18
Q

New type may better withstand stress, but can predispose to malignant transformation

A

Metaplasia

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19
Q

Give an example of metaplasia

A

Ciliated columnar cells become stratified squamous in bronchi of smokers

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20
Q

Disordered growth

A

Dysplasia

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21
Q

Division of precancerous cells, may be reversible, but may progress to cancer

A

Dysplasia

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22
Q

Failure of cell production in embryogenesis

A

Aplasia

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23
Q

Decrease in cell production in embyrogenesis

A

Hypoplasia

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24
Q

Describe the tolerance for ischemia without irreversible injury for:

Neurons
Heart cells
Skeletal muscle

A

Neurons = 3-5 mins
Heart cells = 1-2 hrs
Skeletal muscle = hrs

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25
Q

When stress exceeds cell’s adaptive ability

A

Cell injury

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26
Q

What are the 4 types of cell injury in this course?

A

Hypoxia
Oxidative stress
Reversible
Irreversible

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27
Q

Oxygen deficiency

A

Hypoxia

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28
Q

Examples of hypoxia

A

Lung disease
Anemia

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29
Q

Specific type of hypoxia

A

Ischemia

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30
Q

Reduced blood supply leads to oxygen deficiency (ex: blocked artery)

A

Ischemia

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31
Q

ATP needs _______ and cell metabolism needs ________

A

oxygen; ATP

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32
Q

Induced by reactive oxygen species

A

Oxidative stress

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33
Q

Oxygen derived free radicals

A

Reactive oxygen species

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34
Q

Chemically unstable, attack nucleic acids, proteins, and lipids

A

Free radicals

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35
Q

What do small amounts of reactive oxygen species normally result from?

A

Respiration and energy production

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36
Q

What do reactive oxygen species do normally? Where are they produced?

A

Destroy microbes
Produced in phagocytic leukocytes

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37
Q

Accumulation of reactive oxygen species is BAD. When does this happen?

A

Radiation
Exogenous chemicals
Inflammation

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38
Q

What mechanisms are there to minimize injury by reactive oxygen species?

A

Free radical scavengers
Anti-oxidants

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39
Q

Name the 3 free radical scavengers

A

Superoxide dismutase
Glutathionine peroxidases
Catalase

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40
Q

Block formation of free radicals and scavenge after they have been formed

A

Anti-oxidants

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41
Q

Can be exogenous or endogenous

A

Anti-oxidants

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42
Q

Name 4 anti-oxidants

A

Vitamins E, A, C
Beta carotene

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43
Q

What are the mechanisms of injury by reactive oxygen species?

A

Membrane damage
DNA damage
Protein cross-linking

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44
Q

Normal function/morphology returns when stimulus leaves

A

Reversible cell injury

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45
Q

What is the most common change in reversible cell injury?

A

Cellular swelling

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46
Q

Cells can’t recover and will die

A

Irreversible cell injury

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47
Q

What are the main causes of irreversible cell injury?

A

Loss of mitochondrial function
Loss of structure/function of membranes
Loss of DNA/chromatin structural integrity

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48
Q

What can happen to the nucleus during cell death?

A

Condensation (pyknosis)
Fragmentation (karyorrhexis)
Dissolution (karyolysis)

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49
Q

What are the 2 different mechanisms of cell death?

A

Necrosis
Apoptosis

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50
Q

Describe necrosis

A

Cell membranes fall apart
Enzymes leak out and digest cell
Inflammation
Messy
Damages surrounding cells

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51
Q

Describe apoptosis

A

Programmed cell death
Cell shrinks
Nucleus condenses and fragments
Apoptotic bodies fall from cell and removed by macrophages
NO inflammation

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52
Q

Which necrosis?

Caused by infarct in solid organs; does NOT occur in brain

A

Coagulative necrosis

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53
Q

Which necrosis?

Tissue looks firm

A

Coagulative necrosis

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54
Q

Which necrosis?

Cell outlines preserved, NO NUCLEUS, eosinophilic (pink)

A

Coagulative necrosis

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55
Q

Which necrosis?

Caused by bacterial/fungal infections and hypoxia in CNS

A

Liquefactive necrosis

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56
Q

Which necrosis?

Dissolution of tissue into viscous liquid

A

Liquefactive necrosis

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57
Q

Which necrosis?

Ischemia of limb

A

Gangrenous necrosis

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58
Q

Which necrosis?

Coagulative necrosis -> looks like mummified tissue
Can have superimposed liquefactive necrosis

A

Gangrenous necrosis

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59
Q

Which necrosis?

Caused by TB infections because body tries to wall off infection

A

Caseous necrosis

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60
Q

Which necrosis?

Cheese-like, friable yellow/white necrotic tissue

A

Caseous necrosis

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61
Q

Which necrosis?

Caseating granulomas

A

Caseous necrosis

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62
Q

Granuloma with central necrosis

A

Caseating granuloma

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63
Q

Group of macrophages that form in response to infection, inflammation, foreign material

A

Granuloma

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64
Q

Which necrosis?

Caused by lipase breaking down fat cells, Ca2+ accumulates, seen in pancreatitis

A

Fat necrosis

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65
Q

Which necrosis?

Chalky, white deposits in fat

A

Fat necrosis

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66
Q

Which necrosis?

Outlines of dead fat cells, NO NUCLEUS

A

Fat necrosis

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67
Q

Which necrosis?

Caused by immune-mediated conditions, hypertension, occurs in vessels

A

Fibrinoid necrosis

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68
Q

Which necrosis?

Eosinophilic (pink) deposits in walls of blood vessels

A

Fibrinoid necrosis

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69
Q

Normal response to injury, cells travel where they’re needed to kill infectious agents and clean damage

A

Inflammation

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70
Q

Name the cardinal signs

A

Heat (calor)
Redness (rubor)
Swelling (tumor)
Pain (dolor)
Loss of function (functio lasea)

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71
Q

Main cell type in acute inflammation

A

Neutrophils

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72
Q

How long does acute inflammation develop?

A

Mins/hrs

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73
Q

How long does acute inflammation last?

A

Hrs/days

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74
Q

Describe the tissue injury in acute inflammation

A

Mild and self-limited

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75
Q

Main cell types in chronic inflammation

A

Lymphocytes and macrophages

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76
Q

How long does chronic inflammation develop?

A

Days

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77
Q

Describe the tissue injury in chronic inflammation

A

Severe/progressive

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78
Q

What are the 4 causes of inflammation?

A

Infection (bacteria, fungus, parasite)
Necrosis
Foreign bodies (exogenous, endogenous)
Immune reactions (allergies, autoimmune diseases)

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79
Q

What are the 5 “Rs” of the inflammatory response?

A

Recognition of injurous agent
Recruitment of leukocytes
Removal of agent
Regulation of response
Resolution

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80
Q

What are the 3 key features of “Recognition of injurous agent”

A

Toll-like receptors
Inflammasomes
Circulating proteins

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81
Q

Receptors for microbes

A

Toll-like receptors

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82
Q

Where are Toll-like receptors found?

A

Plasma membranes for extracellular microbe detection
Endosomes for ingested microbe detection

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83
Q

What are Toll-like receptors expressed by?

A

Macrophages and dendritic cells

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84
Q

What do Toll-like receptors recognize in microbes?

A

PAMPs

85
Q

What do Toll-like receptors produce to trigger immune response?

A

Cytokines

86
Q

Sensors of cell damage and initiate inflammation

A

Inflammasomes

87
Q

What do Inflammasomes recognize?

A

DAMPs

88
Q

Name 3 examples of DAMPs

A

Uric acid (product of DNA breakdown)
ATP (released from damaged mitochondria)
DNA (shouldn’t be in cytoplasm)

89
Q

Inflammasomes activate a cascade resulting in ___________ production, which is what induces ______________

A

cytokine; inflammation

90
Q

What do circulating proteins play a role in?

A

Complement system

91
Q

Name the steps of “Recruitment of leukocytes”

A

Margination
Rolling/loose attachment
Adhesion
Transmigration
Chemotaxis

92
Q

Cells go to periphery

A

Margination

93
Q

Mediated by selectins; “speed bumps”

A

Rolling/loose attachment

94
Q

Mediated by integrins

A

Adhesion

95
Q

Travel between endothelial cells to exit

A

Transmigration

96
Q

Chemical attractants direct to site of injury

A

Chemotaxis

97
Q

Blood vessels maximize movement of plasma proteins and leukocytes out of circulation to site of injury by which 2 mechanisms?

A

Vasodilation
Increased vascular permeability

98
Q

What occurs during “Removal of the agent”?

A

Phagocytosis

99
Q

Consumption of pathogens or necrotic tissue

A

Phagocytosis

100
Q

What happens to the agent during phagocytosis

A

Recognition by phagocyctic receptors
Engulfment
Destruction

101
Q

What occurs during “Regulation of response”?

A

Response declines after inflammatory stimulus is gone
Anti-inflammatory lipoxins made

102
Q

What is the half life of neutrophils in blood?

A

Hours to 2 days after leaving blood

103
Q

What occurs during “Resolution”

A

Apoptosis of neutrophils
Disappear within 24 hours after resolution

104
Q

What are the cell derived mediators of acute inflammation?

A

Arachidonic acid metabolites
Mast cell products
Cytokines

105
Q

Produced from cell membrane phospholipids

A

Arachidonic acid metabolites

106
Q

What are the key metabolites of Arachidonic acid metabolites?

A

Prostaglandins
Thromboxane A2
Leukotrienes

107
Q

Promote vasodilation and vascular permeability; lead to redness/swelling

A

Prostaglandins
Histamine

108
Q

Promotes platelet aggregation, vasoconstriction, clot formation

A

Thromboxane A2

109
Q

Increase vascular permeability, act as chemotactic agents for leukocytes, contribute to bronchospasm

A

Leukotrienes

110
Q

Role is to amplify and sustain inflammatory response

A

Arachidonic acid metabolites

111
Q

What is the key product of mast cells?

A

Histamine

112
Q

Role is to initiate and sustain inflammatory response, especially in allergic reactions

A

Mast cells

113
Q

What is the key cytokine?

A

Interleukins

114
Q

Promotes endothelial activation, fever, and activates leukocytes

A

Interleukins

115
Q

Role is to regulate intensity and duration of inflammatory response

A

Cytokines

116
Q

What is the plasma protein derived mediator of acute inflammation?

A

Complement system

117
Q

Group of proteins that circulate blood in inactive form

A

Complement system

118
Q

What are the key actions of the complement system?

A

Inflammation (release histamine)
Phagocytosis (coat pathogens)
Lysis of microbe (form MAC to puncture cell membranes for destruction)

119
Q

Role is to bridge innate and adaptive immunity, enhancing ability to clear microbes and damaged cells

A

Complement system

120
Q

What are the 3 activation pathways in the complement system?

A

Classical
Alternative
Lectin

121
Q

Which activation pathways in the complement system?

ABs bind to pathogens

A

Classical

122
Q

Which activation pathways in the complement system?

Activated directly by pathogen surfaces

A

Alternative

123
Q

Which activation pathways in the complement system?

Mannose-binding lectin attaches to pathogen surface

A

Lectin

124
Q

What are the 4 patterns of acute inflammation?

A

Serous
Purulent
Fibrinous
Ulcer

125
Q

Exudation of cell-poor fluid into spaces; result from burn or viral infection

A

Serous

126
Q

Produces pus, which is exudate of neutrophils, liquified debris of necrotic cells, and fluid (cell-rich); result from bacterial infection

A

Purulent

127
Q

Localized collection of pus

A

Abscess

128
Q

Fibrinous exudate; vascular leaks are large or a local procoagulant stimulus is present

A

Fibrinous

129
Q

Local defect of surface epithelium produced by sloughing of inflamed necrotic tissue; common in oral cavity

A

Ulcer

130
Q

What are the 3 possible outcomes of acute inflammation?

A

Complete resolution
Healing by CT replacement
Progression to chronic inflammation

131
Q

Which outcome of acute inflammation?

Damaged parenchymal cells regenerate
Macrophages remove cellular debris and microbes
Edema resorbed by lymphatics

A

Complete resolution

132
Q

Which outcome of acute inflammation?

Scarring or fibrosis
Substantial destruction, tissue can’t regenerate, or abundant fibrin exudate can’t be cleared
CT grows into area, creating mass of fibrous tissue

A

Healing by CT replacement

133
Q

Which outcome of acute inflammation?

Injurous agent persists or something interferes with normal healing process

A

Progression to chronic inflammation

134
Q

What type of inflammation?

Caused by persistent infections, hypersensitivity diseases, or prolonged exposure to toxins

A

Chronic inflammation

135
Q

What are the 3 morphologic features of chronic inflammation?

A

Mononuclear cells (lymphocytes, macrophages, plasma cells)
Tissue destruction
Attempts at repair (angiogenesis, fibrosis)

136
Q

Name the 4 main cell types involved in chronic inflammation

A

Macrophages
Lymphocytes
Plasma cells
Eosinophils

137
Q

What cell?

Monocytes in blood, but become this cell in tissue

A

Macrophages

138
Q

What cell?

Functions include phagocytosis, antigen presentation to T cells, cytokine production, tissue repair (secrete growth factors)

A

Macrophages

139
Q

What cell?

Amplify and propagate chronic inflammation

A

Lymphocytes

140
Q

What cell?

Include helper T cells (CD4), cytotoxic T cells (CD8), and B cells

A

Lymphocytes

141
Q

What cell?

Release cytokines to activate other immune cells like macrophages

A

Helper T cells (CD4)

142
Q

What cell?

Directly kill infected/damaged cells

A

Cytotoxic T cells (CD8)

143
Q

What cell?

Differentiate into plasma cells

A

B cells

144
Q

What cell?

Source is differentiated B cells

A

Plasma cells

145
Q

What cell?

Functions include AB production and formation of immune complexes

A

Plasma cells

146
Q

What cell?

Associated with allergic reactions and parasitic infections

A

Eosinophils

147
Q

What cell?

Functions include release of cytotoxic granules, produce cytokines and chemokines, release mediators that contribute to tissue damage and remodeling

A

Eosinophils

148
Q

Chronic inflammation that occurs when a material is difficult to digest or remove

A

Granulomatous inflammation

149
Q

In what settings is granulomatous inflammation usually present?

A

Persistent T cell response to microbes
Immune-mediated inflammatory disease
Foreign body

150
Q

Granulomas wall off the agent, but if the body can’t remove it, what does this lead to?

A

Fibrosis
Organ dysfunction

151
Q

Healing of granulomatous inflammation may cause what?

A

Extensive fibrosis

152
Q

Describe the histopathology of granulomatous inflammation

A

Large epithelioid macrophages
Surrounding lymphocytes
Multinucleated giant cells
Central necrosis

153
Q

What are the systemic effects of acute and chronic inflammation?

A

Fever
Lymphadenopathy
Leukocytosis
Acute-phase proteins
Increased HR/BP
Chills
Malaise

154
Q

Caused by pyrogens (prostaglandins, cytokines)

A

Fever

155
Q

Enlarged, tender lymph nodes due to immune cell proliferation

A

Lymphadenopathy

156
Q

Increased circulating leukocytes; cytokines stimulate production from precursors in bone marrow

A

Leukocytosis

157
Q

Made in liver, stimulated by cytokines, measured clinically to track progression of inflammation

A

Acute-phase proteins

158
Q

Examples are C reactive protein, fibrinogen, serum amyloid A

A

Acute-phase proteins

159
Q

What are the 2 main processes in repair?

A

Regeneration
Scar formation

160
Q

Proliferation of cells that survived injury (or stem cells)

A

Regeneration

161
Q

Deposition of CT, mostly collagen

A

Scar formation

162
Q

What cells play a central role in repair?

A

Macrophages

163
Q

What type of tissue ALWAYS results in scarring?

A

Permanent tissue (neurons, heart muscle, skeletal muscle)

164
Q

Name the 3 cells/tissues that proliferate during regeneration?

A

Injured tissue (attempt to restore normal structure)
Vascular endothelial cells (nutrients for repair process)
Fibroblasts (fibrous tissue for scar)

165
Q

Describe the repair sequence (days 1-14)

A

Clot forms immediately after injury
Day 1: Neutrophils phagocytose foreign substances/necrotic tissue
Day 2: Macrophages enter, granulation tissue forms, protected by fibrin clot
Day 3-6: Lymphocytes + plasma cells enter
Day 7: Clot digested, initial repair complete
Day 14: Fibroblasts mature, collagen remodeled forming scar tissue

166
Q

When should you take sutures out?

A

Between 1 and 2 weeks

167
Q

What scenarios will a scar form?

A

Permanent tissue
Extensive ECM damage

168
Q

Excessive scar tissue often seen in chronic inflammation

A

Fibrosis

169
Q

What is granulation tissue made of?

A

New blood vessels + immature fibroblasts

170
Q

What is the formation of new blood vessels in granulation tissue mediated by?

A

VEGF

(vascular endothelial growth factor)

171
Q

What is the migration and proliferation of fibroblasts in granulation tissue mediated by?

A

FGF

(fibroblast growth factor)

172
Q

What is FGF (fibroblast growth factor) made by?

A

Macrophages

173
Q

What does granulation tissue look like?

A

Red/pink and granular

174
Q

How many days after injury does granulation tissue appear?

A

3-5 days after injury

175
Q

Fibroblasts deposit ________, which is mediated by ________

A

collagen; TGF-beta

176
Q

Stimulates production of and inhibits breakdown of ECM proteins; anti-inflammatory

A

TGF-beta

177
Q

Migration and proliferation of fibroblasts and smooth muscle cells

A

PDGF

178
Q

Stimulates collagen synthesis and fibroblast migration

A

IL-13 (cytokine)

179
Q

What factors prevent healing and repair?

A

Infection
Nutrition
Steroid use
Poor perfusion
Foreign bodies
Type/extent/location of injury
Aberration of cell growth

180
Q

Excessive formation of collagen during repair process

A

Keloid

181
Q

What cell?

Released as inactive precursors, but activated by proteases at site of injury in remodeling process

A

Matrix metalloproteinases (MMPs)

182
Q

What cell inhibits Matrix metalloproteinases (MMPs)?

A

Tissue inhibitors of metalloproteinases (TIMPs)

183
Q

What do Matrix metalloproteinases (MMPs) degrade?

A

ECM proteins

184
Q

What process are Matrix metalloproteinases (MMPs) involved in?

A

Remodeling

185
Q

What are the 4 steps of hemostasis?

A

Arteriolar vasoconstriction
Primary hemostasis (platelet plug)
Secondary hemostasis (deposition of fibrin)
Clot stabilization & resorption

186
Q

What occurs immediately after injury to reduce blood flow to the area?

A

Arteriolar vasoconstriction

187
Q

What is arteriolar vasoconstriction mediated by?

A

Endothelin

188
Q

Endothelium-derived vasoconstrictor

A

Endothelin

189
Q

Which step of hemostasis is transient, meaning bleeding would resume if the next steps following it didn’t occur?

A

Arteriolar vasoconstriction

190
Q

What is exposed when endothelium is disrupted and promotes platelet adherence/activation?

A

vWF + collagen

191
Q

Activated platelets change _______ to increase their __________ _________

A

shape; surface area

192
Q

Which secretory granules do activated platelets release?

A

Adenosine diphosphate (ADP)
Thromboxane A2

193
Q

How do platelets adhere to ECM?

A

Through binding of vWF + glycoprotein Ib

194
Q

Activated platelets have high affinity for what?

A

Fibrinogen

195
Q

What does fibrinogen bind to?

A

Glycoprotein IIb/IIIa

196
Q

When platelets aggregate, what are they linked together by?

A

Fibrinogen

197
Q

What is exposed at site of injury to activate secondary hemostasis?

A

Tissue factor

198
Q

Membrane bound procoagulant glycoprotein

A

Tissue factor

199
Q

What does tissue factor bind and activate?

A

Factor VII

200
Q

Made by endothelial cells and limits clotting at site of injury

A

Tissue plasminogen activator (tPA)

201
Q

What cells are the regulators of hemostasis?

A

Endothelial cells

202
Q

Evaluates extrinsic pathway

A

Prothrombin Time

203
Q

TF, phospholipids, and Ca2+ are added to plasma; time to form fibrin clot is recorded

A

Prothrombin Time

204
Q

“Corrected Prothrombin Time,” since results may vary depending on brand/manufacturer of reagents used

A

International Normalized Ratio

205
Q

Evaluates intrinsic pathway

A

Partial Thromboplastin Time

206
Q

Negatively charged particles (ground glass) are added; time to form fibrin clot is recorded

A

Partial Thromboplastin Time

207
Q

Identifies problem with fibrinogen or thrombin inhibitor tissue

A

Thrombin Time

208
Q

Amplifies coagulation cascade by activating factor XIII, but becomes anti-coagulant when in contact with normal endothelium to help control clotting

A

Thrombin

209
Q

What 2 factors limit coagulation?

A

Dilution
Fibrinolytic cascade

D2 Fall (45 decks)

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