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General Pathology > Chapter 2 > Flashcards

Chapter 2 Flashcards

1
Q

Inflammation is a ______ response to injury

A

vascular

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2
Q

Actions of inflammation

A
  1. kills and eliminates infective microbes
  2. removes cellular debris: injured cells/tissues
  3. initiates tissue repair
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3
Q

Leukocytes last ______ in circulation

A

4 days

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4
Q

Lymphocytes are granular or agranular?

A

Agranular

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5
Q

Monocytes are granular or agranular

A

Agranular

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6
Q

Neutrophils

A

granular WBCs associated with acute inflammation and allergies

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7
Q

Eosinophils

A

Granular WBCs associated with allergies

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8
Q

Basophils

A

Granular WBCs
Associated with Parasites
least numerous
produce heparin

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9
Q

2* tissue damage caused by inflammation can occur in what 3 situations discussed in class?

A
  1. highly virulent mic robes (HIV, TB)
  2. Prolonged/chronic infections
  3. inappropriate immune response
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10
Q

injury or infection is detected by what 3 cell types?

A

macrophages, dendritic cells, mast cells

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11
Q

5 steps of inflammation

A
  1. Recognize the injury/microbe
  2. Recruit leukocytes
  3. Remove agent (via phagocytosis)
  4. Regulate (control) response
  5. Resolution and repair
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12
Q

5 cardinal signs of inflammation

A

Rubor (redness), Calor (heat), Tumor (swelling), Dolor (Pain), Functio laesa (loss of function)

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13
Q

Self-limiting inflammation is described as…

A

pro-inflammatory mediators are inactivated

anti-inflammatory mediators are activated

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14
Q

Acute Inflammation

A

rapid onset, local and systemic signs (edema, rubor, ect.), neutrophils present, no fibrosis

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15
Q

Chronic Inflammation

A

insidious onset, few systemic signs, angiogenesis and fibrosis present
Macrophages, lymphocytes and plasma cells

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16
Q

How does Graston and similar therapies help with chronic inflammation?

A

Reintroduces controlled trauma which moves trauma from chronic state into acute state

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17
Q

2 major components of acute inflammation

A

vascular changes

leukocyte recruitment and activation

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18
Q

how do cells recognize harmful agents?

A

pattern recognition receptors
macrophages, dendritic cells, mast cells
recognize molecular patterns that are “non-self”

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19
Q

Toll-like receptors (TLRs)

A

recognize all types of infectious pathogens

located on the plasma membrane

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20
Q

Inflammasome

A

recognizes products of dead cells (uric acid, ATP) and crystals
located in cytoplasm

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21
Q

How can vessels alter themselves?

A

caliber, blood flow, permiability

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22
Q

3 vascular changes associated with inflammation

A
  1. Vasoconstriction (few seconds only)
  2. Vasodilation (rubor)
  3. Increases permeability
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23
Q

Margination

A

collection of WBCs along the vascular walls

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24
Q

migration of WBC

A

Diapedesis
movement of cell from point A to point B (inside vessel –> outside vessel)
AKA: transmigration, extravasation, emigration

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25
Q

Increased permeability causes this by reversing the osmotic gradient, allowing fluid to collect in the interstitial spaces?

A

Edema

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26
Q

Mechanisms for increased permeability in vessels (3)

A
  1. endothelial contraction
  2. endothelial necrosis
  3. leakage from angiogenesis
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27
Q

Endothelial contraction

A

Most common
Histamine binds leaving gaps in postcapillary venules
lasts for 15-30 min after acute inflammation

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28
Q

Endothelial necrosis

A

causes leakage in postcapillary venules until the vessel is repaired
caused by burns, severe infections, irradiation

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29
Q

Leakage from angiogenesis

A

new vessels have immature (leaky) endothelial cells

occurs during tissue repair and tumor growth

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30
Q

Exudate

A

Protein-rich

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31
Q

Transudate

A

Protein-poor

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32
Q

Edema occurs because…

A

lymphatic drainage cannot keep up

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33
Q

Lymphadenopathy

A

general disorder of the lymphatic system

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34
Q

lymphadenitis

A

Inflamed lymph nodes

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35
Q

Lymphangitis

A

Inflamed lymphatic channel

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36
Q

4 steps in leukocyte recruitment

A
  1. margination and rolling
  2. firm adhesion to endothelium (pavementing)
  3. transmigration between endothelial cells
  4. chemotaxis toward target tissue
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37
Q

Leukocytes migrate via….

A

pseudopodia

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38
Q

Neutrophils are replaced by macrophages and lymphocytes after being killed via apoptosis within __ hours.

A

48

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39
Q

opsonins

A 
immunoglobulin G (IgG), complement
enhance macrophages binding and breakdown
"marked for death"
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40
Q

Leukocyte-induced tissue injury

A

2* tissue injury
once activated, WBCs don’t distinguish
causes damage via ROS and enzymes
Secrete cytokines

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41
Q

3 common opportunities for leukocyte-induced tissue injury

A
  1. persistent infections (TB, VZV)
  2. complication of ischemia (ischemia-reprofusion injury)
  3. Hypersensitivity reactions (allergies, autoimmune conditions)
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42
Q

3 Outcomes of Acute Inflammation

A
  1. Resolution
  2. Chronic Inflammation
  3. Scarring
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43
Q

Resolution of Acute inflammation

A

Regeneration and repair

normalization of vessel permeability, WBC apoptosis, Lymph drainage, angiogenesis, restored structure

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44
Q

Chronic inflammation as an outcome of acute inflammation

A

caused by failure to remove offending agent
severity of damage and cellular regeneration capacity
either restored or scarred

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45
Q

Scarring after acute inflammation

A

FIbrosis
Severe tissue damage, unable to regenerate
Filled with connective tissues = decreased function

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46
Q

Serous inflammation

A

serum accumulation within or below the epidermis
watery effusion
produces a blister: burn, virus

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47
Q

Fibrinous inflammation

A 
severe injury, Increase vessel permeability, allows large molecules out of circulation, produce fibrin-rich exudate
Severe fibrosis (adhesions)
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48
Q

Suppurative inflammation

A

Purulent
local infection with a pus-forming organism (Staph. aureus)
produces abscesses

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49
Q

Abscess

A

focal collection of pus

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50
Q

Pus contains…

A

neutrophils, necrotic cells, edema

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51
Q

Ulcerative Inflammation

A

local tissue necrosis on tissue surface, defect follows sloughing of necrotic tissue
peptic ulcer, aphthous ulcer

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52
Q

pseudomembranous inflammation

A

caused by Corynebacterium diphtheria, Clostridium difficile

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53
Q

Granulomatous inflammation

A

produces a granuloma

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54
Q

Condition which causes caseating granuloma?

A

Tuberculosis (TB)

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55
Q

Mediator of inflammation that we talked about in class

A

Arachidonic acid metabolites from WBCs, Mast cells, endothelia, & platelets

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56
Q

Prostaglandins

A

Arachidonic acid metabolite that causes vasodilation, pain and fever

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57
Q

NSAIDs effect on prostaglandins

A

block prostaglandin synthesis (anti-inflammatory)

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58
Q

3 characteristics of chronic inflammation

A
  1. mononuclear leukocyte cells
  2. tissue destruction and fibrosis
  3. vessel production (angiogenesis) and repair
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59
Q

2 types of macrophage activation

A

Classic (M1) and Alternative (M2)

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60
Q

Classic (M1) Activation

A

Microbes, endotoxins, active T cells, cytokines, crystals, dead cell particles

ROS –> microbial actions: phagocytosis & killing of many bacteria
Cytokines –> inflammation

61
Q

Alternative (M2) Activation

A

cytokines, mast cells, eosinophils

non-microbial: tissue repair, fibrosis, anti-inflammatory effects

62
Q

4 systemic effects of inflammation

A

Acute-phase reaction, Leukocytosis, Leukemoid reactions, Leukopenia

63
Q

Acute-phase reaction

A

charactarized by lethargy, somnolence, malaise, increased HR, increased BP, anorexia, anhidrosis

produces fever & elevated plasma proteins

64
Q

Fever caused by:

A

pyrogens –> prostaglandin synthesis

tells the hypothalamus to increase the temperature set point

65
Q

Elevated plasma proteins

A

increased cytokines produces increase hepatic synthesis of proteins (C-reactive protein [biiomarker for inflammation], fibrinogen)

causes increased Erythrocyte Sedimentation Rate (ESR)

66
Q

Leukocytosis

A

increased blood leukocyte count
common with bacterial infections

15-20K/ul, increase immature cells “shift to left”

67
Q

Bacterial leukocytosis is characterized by an increase in ___.

A

neutrophils

68
Q

Viral leukocytosis is characterized by an increase in ___.

A

lynphocytes

69
Q

Leukemoid Reactions

A

extremely high blood leukocytes count (40-100k/ul)
mimics leukemia
caused by chronic inflammation (TB, Clostridium difficile)

70
Q

Leukopenia

A

Decreased blood leukocyte count (>4000)

71
Q

What are the 2 causes of cardiac fibrosis?

A
  1. Ischemic Necrosis (myocardial infarction)

2. Possible ischemia-reprofusion injury

72
Q

A mild/transient injury can be regenerated to a “pre-injury status”. True or false?

A

True

73
Q

Prolonged injury:

A

cells are unable to divide, cannot be restored to “pre-injury status”
leukocytes, angiogenesis, granulation tissue
scar formation

74
Q

Two types of cellular proliferation

A

physiologic and pathologic

75
Q

physiologic cellular proliferation

A

well-regulated, repairs injury tissues, adaptations to stress, preserves normal cellular functions

76
Q

Pathologic cellular proliferation

A

unregulated proliferation, result of genetic alterations, neoplasia

77
Q

GFs promote cell shift from G1 phase to G2. True or false?

A

False. G0 –>G1

promote entry into the cell cycle

78
Q

Cyclins

A

regulators of the cell cycle

79
Q

2 types of cyclins

A

Cyclin-dependent kinase (CDK) enzymes

Cyclin-dependent kinase inhibitors (CDKIs)

80
Q

CDKIs effect on the cell cycle

A

slows it down

81
Q

GFs effect on CDKIs

A

suppression

pushes cell through the cycle

82
Q

3 types of proliferative capacity

A

labile, stable, permanent

83
Q

Labile cells

A

continuously dividing, continuously lost and quickly regenerated

i.e., epithelia & hematopoietic cells

84
Q

Stable cells

A

in quiescent state
limited replication (usually only in response to injury)
i.e., solid organs (kidney, liver, pancreas)

85
Q

Permanent cells

A

terminally differentiated cells

injury is irreversible & highly disabling
CNS neurons, skeletal & cardiac muscle, old cells (near Hayflick limit)

86
Q

Hayflick Limit

A

limited number of times the cell can divide before its done… really old cells

they die when they reach it

87
Q

most tissues have what proliferative capacity??

A

combination of all 3!

88
Q

properties of stem cells

A

self-renewal capacity (undifferentiated)

asymmetric replication

89
Q

asymmetric replication

A

some cells differentiate, other remain undifferentiated

keeps producing more stem cells during division

90
Q

GFs function during regeneration & healing

A
  1. stimulate growth control genes
  2. ignore cell cycle checkpoints
  3. prevent apoptosis
91
Q

GFs are produced by what 2 cells at the site of inflammation?

A

Macrophages & lymphocytes

92
Q

Autocrine GF signaling

A

GFs act on the secreting cell (rare)

93
Q

Paracrine GF signaling

A

GFs act on the cells adjacent to the secreting cell

94
Q

Endocrine GF signaling

A

systemic, via circulatory system

95
Q

GFs are normally produced where?

A

Anterior pituitary gland

96
Q

Mitogen

A

increases cell proliferation

Pituitary growth hormone is an example of this

97
Q

Extracellular matrix is characterized by:

A

network of proteins
structural support - “scaffolding” for tissue repair
constantly remodeling

98
Q

Other functions of Extracellular matrix

A

storage of water, minerals, GFs

regulation of cell proliferation and movement

99
Q

2 types of ECM

A

Interstitial matrix

basement membrane

100
Q

interstitial matrix

A

between cells in connective tissues
3D gel with no specific shape
produced by fibroblasts

101
Q

basement membrane

A

Surrounds cavities & organ surfaces
“chicken-wire” mesh
produced by epithelium

102
Q

3 components to ECM

A

fibrous proteins
water hydrated gels
adhesive glycoproteins

103
Q

fibrous proteins in ECM

A

collagen: tensile strength, triple helix, scars

elastin, recoil, arteries, skin, ligaments, etc

104
Q

water-hydrated gels in ECM

A

resilience, lubrication
Hyaluronan: binds water, gel-like
Proteoglycans: compressibility, GF storage

105
Q

Adhesive glycoproteins in ECM

A

connect elements of ECM to other cells (cellular adhesion)

fibronectin, laminin, integrins, selectins

106
Q

ECM functions

A 
Mechanical support (scaffolding) for repair
Regulation of cellular proliferation
107
Q

Scaffolding for repair

A

increased disruption in ECM increases fibrosis

108
Q

Regulation of Cellular proliferation

A

storage & quick deployment of GFs
regulates cellular differentiation
integrins create firm adhesion, endothelial transmigration

109
Q

Ability to replace injured tissues is dependent on what 2 factors?

A
  1. cell’s inherent capacity to proliferate

2. severity/nature of injury (extent of ECM & stem cell damage)

110
Q

Compensatory growth

A

Stable cells

R kidney can grow bigger if L kidney is damaged or removed

111
Q

hepatocytes

A

have a unique capacity to heal

good in case you need a liver transplant, living donor can give a lobe and survive

112
Q

Steps of Scar formation

A
  1. angiogenesis
  2. fibroblast migration & proliferation
  3. collagen deposition –> scar
  4. remodeling (lifetime)
113
Q

Within 24 hours of injury…

A

fibroblasts accumulate, endothelia begins repair

114
Q

Within 3-5 days…

A

granulation tissue appears

contain fibroblasts, capillaries, connective tissue, WBCs

115
Q

Formation of new vessels

A

capillaries spout from existing vessels

endothelial precursor cells (EPCs) from marrow

116
Q

angiogenesis vie pre-existing vessels

A

limited to site of injury

117
Q

Vasculogenesis

A

EPCs = endothelial precursor cells (angioblasts)

118
Q

Scar tissue deposition in relation to granulation tissue

A

scar tissue is built upon granulation tissue

119
Q

2 steps of scar tissue deposition

A
  1. fibroblast migration to site of injury

2. deposition of ECM irregular collagen

120
Q

originally, scar tissue is ___ in vascularity

A

high

121
Q

progressively, scar tissue ___ in vascularity

A

decreases

122
Q

Remodeling of connective tissue

A

ECM continues to be remodeled causing a balance between ECM synthesis and breakdown

123
Q

Matrix Metalloproteinase (MMPs) are produced by:

A

fibroblasts, macrophages, neutrophils, and endothelial cells

124
Q

MMPs breakdown ___

A

collagen

125
Q

MMPs require

A

zinc as a cofactor

126
Q

MMPs are regulated by

A

TIMPs (tissue inhibitor of metalloproteiinases)

127
Q

Factors influencing repair

A

infection, nutritional deficiency, glucocorticoids (steroids), poor profusion, etc.

128
Q

Infection influence on repair

A

prolongs inflammation, leukocyte-induced tissue injury

129
Q

Nutritional deficiency influence on repair

A

Vitamin C

decrease basement membrane = vessel fragility

130
Q

Glucocorticoids (steroids) influence on repair

A

anti-inflammatory, decrease fibroblast activity

131
Q

Poor profusion influence on repair

A

decrease arterial supply, decrease venous damage

132
Q

Keloid

A

scar tissue beyond boundaries of wound caused by excessive collagen deposition and exuberant granulation tissue

133
Q

keloids are characterized by:

A

raised flesh colored scars that do not regress and get worse following excision

134
Q

Deeper injuries to dermis increase or decrease risk of keloids?

A

increase

135
Q

healing of skin wounds is a combination of:

A

epithelial regeneration and fibrosis

136
Q

Phases of healing which overlap

A
  1. inflammation
  2. formation of granulation tissue
  3. ECM deposition & remodeling with possible wound contraction
137
Q

Healing by first intention (primary union)

A

incision, sutured
small wound, few cells die
minimal fibrosis, minimal wound contraction

138
Q

Day 1 primary union

A

clot formation

139
Q

Day 3 primary union

A

granulation tissue

140
Q

Day 5 primary union

A

peak angiogenesis, collagen bridges the wound

141
Q

1 month primary union

A

inflammation is absent, epidermis is essentially normal

142
Q

Healing by second intention (secondary union)

A

large wound, intense inflammation with possible 2* tissue injury
large clot/scab and abundant granulation tissue
prominent wound contraction via myofibroblasts

143
Q

timeline for secondary union

A

more than 6 weeks

144
Q

sutures are removed after…

A

1 week

145
Q

at 1 week post suture, wound is __% of normal strength

A

10%

146
Q

increased wound strength over 1st month to around…

A

70%

147
Q

Strength of wound is at max around 3 months: up to __%

A

80%

148
Q

Scar remodeling is a process of making the wound less prominent and can take….

A

several years, basically forever…

149
Q

triggering of the inflammasome results in activation of what enzyme?

A

Caspase-1

General Pathology (6 decks)

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