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Pathology 1 > exam 1 > Flashcards

exam 1 Flashcards

1
Q

what is etiology

A

origin of disease: why

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2
Q

what is pathogenesis

A

steps in development: how

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3
Q

What is hyperplasia

A

increase in # of cells

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4
Q

What is metaplasia

A

replacement of 1 differentiated cell type to another

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5
Q

What is hypertrophy

A

increase in size of cells

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6
Q

What is an example of hypertrophy: physio and patho

A

phys: lifting weights
path: hypertension

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7
Q

what is atrophy

A

decrease in # of cells

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8
Q

Wart formation is an example of

A

hyperplasia

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9
Q

diminished blood supply or loss of innervation will produce

A

atrophy

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10
Q

What happens in atrophy to protein synthesis

A

decrease synthesis and increase breakdown

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11
Q

Which cellular adaptation is there a likelihood of adaptation

A

metaplasia

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12
Q

T/F Injured cell will always die

A

f

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13
Q

Inflammation is associated with apoptosis or necrosis

A

necrosis

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14
Q

Which necrosis requires histologic exam

A

fibro necrosis

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15
Q

Name the 3 types of necrosis

A

karyolysis, pyknosis, karyorhexis

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16
Q

What is karyolysis

A

nuclear fading

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17
Q

What is pyknosis

A

nuclear shrinkage

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18
Q

Karyorhexis

A

nuclear fragmentation

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19
Q

Is mitochondria resistant to deleterious effects of hypoxia

A

f o2 is final

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20
Q

what is caseous necrosis

A

cheeselike appearance, walled off area

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21
Q

What time of necrosis goes with TB

A

caseous

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22
Q

what is the most common activation of apoptosis

A

Mitochondrial pathway: decrease GF or increase membrane permeability
Capsase 9

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23
Q

What is the death receptor (extrinsic) pathway of apoptosis

A
  • Antigens stimulate cellular surface molecules
  • Caspase 8
  • TNF
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24
Q

What is autophagy

A

“self eating”

lysosomal digestion of cellular components

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25
Q

Hypoxia in CNS will produce what necrosis

A

liquefactive

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26
Q

Influx of intracellular calcium will stimulate _____ by activationg caspases

A

apoptosis

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27
Q

T/F ROS are produced during normal aerobic respiration

A

t

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28
Q

Which membrane is not considered among most damaging target of ROS: mitochon, plasma, mucous, lysosomal

A

mucous

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29
Q

What is steatosis

A

accumulation of triglycerides within tissue

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30
Q

What is dystrophic calcification

A

deposition of calcium into necrotic tissue;

cellular injusry and aging with abnormal accumulation of Ca salts

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31
Q

What is metastic calcification

A

accumulation of ca in normal tissue; pathological hypercalcemia

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32
Q

what is replicative senescence

A

telomere shortening, limiting the capacity to replicate

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33
Q

Inflammation most associated with macrophages is….

A

acute

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34
Q

Which inflammation gives scarring (fibrosis)

A

chronic

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35
Q

Which multi protein cytoplasmic complex recognizes products of dead cells and stimulates acute inflam.

A

inflammasome

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36
Q

What receptor recognize infections, pathogens, within plasma membrane in acute inflam

A

toll-like receptors

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37
Q

What initiates margination and rolling when stasis develops at site fo acute inflamm rxn

A

leukocytes

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38
Q

protein rich fluid accumulation from vascular permeability…

A

exudate

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39
Q

protein poor fluid accumlation due to vascular permeability…

A

transudate

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40
Q

inflammation associated with presence of monocytes

A

chronic (replacement)

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41
Q

when is the inflamm rxn over?

A

enzymatic degradation of various chemical mediators and normalization of vascular permeability

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42
Q

pattern of inflam w/ acne vulgaris

A

ulcerative

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43
Q

pattern of inflammation with propionibacterium acne

A

purulent

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44
Q

pattern of inflam of “blisters”

A

serous

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45
Q

focal collections of pus are called

A

abscesses

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46
Q
  • carb binding lectins

- surface receptors that aggregate

A

collectins

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47
Q

what are the outcomes of acute inflam

A
  1. resolution
  2. chronic
  3. fibrosis (scarring)
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48
Q

TNF, IL1, IL 6 are….

A

cytokines

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49
Q

activation of which system generates a pore-like membrane attack complex (MAC)

A

complement system

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50
Q

activation of kinin system leads to vascular permeability increase

A

bradykinin

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51
Q

Kinin system leads to ….

A

vasodilation, activates thrombin: clotting (thrombosis)

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52
Q

pyrogens stimulate _____ synthesis, which promote production of_____to change temperature set point

A

prostoglanding

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53
Q

WBC 16,000 cells per microliter is considered a_____

A

leukocytosis

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54
Q

leukocytosis #’s

A

15-20k

55
Q

what are leukemoid rxns

A

extremely high blood leukocyte count that mimics leukemia

40-100k

56
Q

what causes leukemoid rxn

A

chronic inflam

57
Q

when inflam process stops what does the body do

A

heal

58
Q

normal size of cell population is balance of- proliferating, newly differentiated, and ______

A

apotosis

59
Q

marginization is

A

lining up in a wall, 1st step in leukocyte recruitement

60
Q

which cell is capable of proliferating in response to injury

A

labile

61
Q

terminal differentiation limited replication (after injury)

A

stable

62
Q

what are examples of stable

A

solid organs

63
Q

examples of labile

A

epithelia

64
Q

terminally differentiated, unable to proliferate following injury

A

permanent

65
Q

hematopoietic (blood cell that gives rise to others) cells are examples of what cell type

A

labile

66
Q

Where are hematopoietic cells found?

A

bone marrow and peripheral blood

67
Q

What are the two properties of stem cells

A

self-renewal capacity and assymetric replication (some differentiate while others do not)

68
Q

Embryonic or Adult stem cells more differentiated

A

adult

69
Q

what would be increased if the result was more entry into the cell cycle and less apoptosis

A

increased GF

70
Q

what component of ECM allows for tissue recoil following physical deformation?

A

elastin?

71
Q

What fibrous structural protein in ECM provides structural integrity to vessel walls and ligmanents

A

elastin

72
Q

What are the two fibrous proteins of ECM?

A

collagen, elastin

73
Q

What are the two water hydrated gels of ECM

A

proteoglycans and hyluronan

74
Q

What are 3 components of ECM

A

fibrous proteins, water-hydrated gels, adhesive glycoproteins

75
Q

What water hydrated gel has the characteristics of compressability and GF storage

A

proteoglycans

76
Q

What water-hydrated gels create gel like matrix

A

hyaluronan

77
Q

What part of ECM connect elements of ECM to other cells

A

Adhesive glycoproteins: fibronectin, laminin, integrins

78
Q

What % is the liver able to regenerate of surgically removed hepatocytes

A

60%

79
Q

Granulated tissue is highly or poorly vascularized?

A

highly

80
Q

Major source of GF that stimulate and activate fibroblasts are derived from ….

A

endothelial cells

81
Q

ECM is degraded by MMP…

A

zinc ions

82
Q

ECM produced by

A

fibroblasts, macrophages, neutrophils, and epithelial cells

83
Q

Peak neovascularization from surgical incision is on day

A

5

84
Q

Wounds will regain ~____% of original tissue strength within 3 months of healing

A

80

85
Q

Wounds will regain ~____% of original tissue strength within 1 month of healing

A

70% due to collagen deposition

86
Q

Wounds will regain ~____% of original tissue strength within 1 week of healing

A

10%

87
Q

What cells sense injury/microbe

A

macrophages, dendritic, mast

88
Q

cardinal sign of inflam

A

rubor, calor, tumor, dolor, functio laesa

89
Q

what cell is typically associated with acute inflammation

A

neutrophil

90
Q

cells associated with chronic

A

lymphocytes, macrophages, and neovascularization

91
Q

neutrophil time frame

A

24-48 hrs

92
Q

name the two receptors for acute inflammation

A

toll like receptor and inflammasome

93
Q

what is a toll like receptor (TLR)

A

on lipid bilayer
recognize pathogen
stimulate membrane proteins

94
Q

what are inflammasomes

A

in cytoplasm

dead cell recognition

95
Q

1st vascular change with inflam

A

vasoconstriction: only a few seconds

96
Q

After dilation with inflam, blood becomes more or less viscous….why

A

more… so leukocytes can attach to wall

97
Q

what is margination

A

lining up of leukocytes

98
Q

what is diapedesis

A

leaving of leukocytes into the tissue

99
Q

MC way to change vessel permeability

A

endothelial contraction

100
Q

endothelial contraction is associated with

A

histamine

101
Q

5 steps delivering leukocytes

A

margination and rolling
adheasion
transmigration: diapedesis
chemotaxis

102
Q

Opsonization is…. (IgG antibodies)

A

marked for death

103
Q

what is secondary tissue injury

A

damage to host from leukocyte from ROS or enzymes

104
Q

Examples that cause secondary tissue injury

A

reperfusion and hypersensitivity (allergies, autoimmune)

105
Q

3 outcomes of acute inflam

A

resolution, chronicity, scarring (fibrosis)

106
Q

Morphology of inflammation 4 major types

A

serous: virus or burn
fibrinous: severe increase in permeability (vessel wall)
purulent: pus formation
ulcerative

107
Q

cell derived mediators of inflamm (7)

A 
vasoactive amines
ara metabolites
cytokines
ROS
nitric oxide
lysosomal enzymes
neuropeptides
108
Q

what are vasoactive amines

A

histamine: inc. permeability of vasodilation
serotonin: vasoconstriction during clotting

109
Q

what do cytokines to in inflam

A

recruit leukocyte, promote adheasion and migration

110
Q

ROS

A

associated w/ killing off micros

111
Q

Nitric Oxide

A

vasodilation and microbial killing

112
Q

lysosomal enzymes

A

microbial killing

113
Q

Plasma protein drived

A

complement proteins
coagulation proteins
kinins

114
Q

What protein goes w/ MAC

A

complement

115
Q

Kinins lead to….

A

bradykinin formation, inc vessel perm and production of fibrin clots

116
Q

chronic inflam cells…

A

macrophages and lymphocytes (b&t)

117
Q

granuloma is

A

accumulation of macrophages

118
Q

Pyrogen cytokines stimulate _____ synthesis

A

prostaglandin

119
Q

2 mechanism of tissue repair

A

regeneration

scarring: irregular CT

120
Q

Fibrosis is

A

abnormal collagen deposition, loosing original functionality

121
Q

checkpoint control in cell cycle

A

cyclin dependent kinase

122
Q

stem cell unique properties

A

self-renewal capacity

asymmetric replication

123
Q

what are pluripotent stem cells

A

can form various cell types

124
Q

3 important facts of GF

A

stimulate growth control genes
ignore cell cycle checkpoints
prevent apoptosis

125
Q

3 types signaling GF

A

autocrine: self: positive feedback
paracrine: release to local surrounding
endocrine

126
Q

2 forms of ECM

A 
interstitial matrix
basement membrane (chicken wire)
127
Q

what is soft pink tissue under scab

A

granulation type tissue

128
Q

4 stages of scar formation

A

angiogenesis
fibroblast migration
ecm deposition
eventual removdeling

129
Q

MMPS do what

A

break down CT, critical zinc ions

130
Q

What is keloid

A

abnormal healing: increase collagen accumulation

131
Q

steps in cutanous wound healing

A

inflam
granulation
wound contraction

132
Q

first intention healing to get no inflam

A

30 days

133
Q

2nd intention healing takes

A

6+ weeks, considerable scar contraction

Pathology 1 (1 decks)

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