exam 1 Flashcards

(133 cards)

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
Hypoxia in CNS will produce what necrosis
liquefactive
26
Influx of intracellular calcium will stimulate _____ by activationg caspases
apoptosis
27
T/F ROS are produced during normal aerobic respiration
t
28
Which membrane is not considered among most damaging target of ROS: mitochon, plasma, mucous, lysosomal
mucous
29
What is steatosis
accumulation of triglycerides within tissue
30
What is dystrophic calcification
deposition of calcium into necrotic tissue; | cellular injusry and aging with abnormal accumulation of Ca salts
31
What is metastic calcification
accumulation of ca in normal tissue; pathological hypercalcemia
32
what is replicative senescence
telomere shortening, limiting the capacity to replicate
33
Inflammation most associated with macrophages is....
acute
34
Which inflammation gives scarring (fibrosis)
chronic
35
Which multi protein cytoplasmic complex recognizes products of dead cells and stimulates acute inflam.
inflammasome
36
What receptor recognize infections, pathogens, within plasma membrane in acute inflam
toll-like receptors
37
What initiates margination and rolling when stasis develops at site fo acute inflamm rxn
leukocytes
38
protein rich fluid accumulation from vascular permeability...
exudate
39
protein poor fluid accumlation due to vascular permeability...
transudate
40
inflammation associated with presence of monocytes
chronic (replacement)
41
when is the inflamm rxn over?
enzymatic degradation of various chemical mediators and normalization of vascular permeability
42
pattern of inflam w/ acne vulgaris
ulcerative
43
pattern of inflammation with propionibacterium acne
purulent
44
pattern of inflam of "blisters"
serous
45
focal collections of pus are called
abscesses
46
- carb binding lectins | - surface receptors that aggregate
collectins
47
what are the outcomes of acute inflam
1. resolution 2. chronic 3. fibrosis (scarring)
48
TNF, IL1, IL 6 are....
cytokines
49
activation of which system generates a pore-like membrane attack complex (MAC)
complement system
50
activation of kinin system leads to vascular permeability increase
bradykinin
51
Kinin system leads to ....
vasodilation, activates thrombin: clotting (thrombosis)
52
pyrogens stimulate _____ synthesis, which promote production of_____to change temperature set point
prostoglanding
53
WBC 16,000 cells per microliter is considered a_____
leukocytosis
54
leukocytosis #'s
15-20k
55
what are leukemoid rxns
extremely high blood leukocyte count that mimics leukemia | 40-100k
56
what causes leukemoid rxn
chronic inflam
57
when inflam process stops what does the body do
heal
58
normal size of cell population is balance of- proliferating, newly differentiated, and ______
apotosis
59
marginization is
lining up in a wall, 1st step in leukocyte recruitement
60
which cell is capable of proliferating in response to injury
labile
61
terminal differentiation limited replication (after injury)
stable
62
what are examples of stable
solid organs
63
examples of labile
epithelia
64
terminally differentiated, unable to proliferate following injury
permanent
65
hematopoietic (blood cell that gives rise to others) cells are examples of what cell type
labile
66
Where are hematopoietic cells found?
bone marrow and peripheral blood
67
What are the two properties of stem cells
self-renewal capacity and assymetric replication (some differentiate while others do not)
68
Embryonic or Adult stem cells more differentiated
adult
69
what would be increased if the result was more entry into the cell cycle and less apoptosis
increased GF
70
what component of ECM allows for tissue recoil following physical deformation?
elastin?
71
What fibrous structural protein in ECM provides structural integrity to vessel walls and ligmanents
elastin
72
What are the two fibrous proteins of ECM?
collagen, elastin
73
What are the two water hydrated gels of ECM
proteoglycans and hyluronan
74
What are 3 components of ECM
fibrous proteins, water-hydrated gels, adhesive glycoproteins
75
What water hydrated gel has the characteristics of compressability and GF storage
proteoglycans
76
What water-hydrated gels create gel like matrix
hyaluronan
77
What part of ECM connect elements of ECM to other cells
Adhesive glycoproteins: fibronectin, laminin, integrins
78
What % is the liver able to regenerate of surgically removed hepatocytes
60%
79
Granulated tissue is highly or poorly vascularized?
highly
80
Major source of GF that stimulate and activate fibroblasts are derived from ....
endothelial cells
81
ECM is degraded by MMP...
zinc ions
82
ECM produced by
fibroblasts, macrophages, neutrophils, and epithelial cells
83
Peak neovascularization from surgical incision is on day
5
84
Wounds will regain ~____% of original tissue strength within 3 months of healing
80
85
Wounds will regain ~____% of original tissue strength within 1 month of healing
70% due to collagen deposition
86
Wounds will regain ~____% of original tissue strength within 1 week of healing
10%
87
What cells sense injury/microbe
macrophages, dendritic, mast
88
cardinal sign of inflam
rubor, calor, tumor, dolor, functio laesa
89
what cell is typically associated with acute inflammation
neutrophil
90
cells associated with chronic
lymphocytes, macrophages, and neovascularization
91
neutrophil time frame
24-48 hrs
92
name the two receptors for acute inflammation
toll like receptor and inflammasome
93
what is a toll like receptor (TLR)
on lipid bilayer recognize pathogen stimulate membrane proteins
94
what are inflammasomes
in cytoplasm | dead cell recognition
95
1st vascular change with inflam
vasoconstriction: only a few seconds
96
After dilation with inflam, blood becomes more or less viscous....why
more... so leukocytes can attach to wall
97
what is margination
lining up of leukocytes
98
what is diapedesis
leaving of leukocytes into the tissue
99
MC way to change vessel permeability
endothelial contraction
100
endothelial contraction is associated with
histamine
101
5 steps delivering leukocytes
margination and rolling adheasion transmigration: diapedesis chemotaxis
102
Opsonization is.... (IgG antibodies)
marked for death
103
what is secondary tissue injury
damage to host from leukocyte from ROS or enzymes
104
Examples that cause secondary tissue injury
reperfusion and hypersensitivity (allergies, autoimmune)
105
3 outcomes of acute inflam
resolution, chronicity, scarring (fibrosis)
106
Morphology of inflammation 4 major types
serous: virus or burn fibrinous: severe increase in permeability (vessel wall) purulent: pus formation ulcerative
107
cell derived mediators of inflamm (7)
``` vasoactive amines ara metabolites cytokines ROS nitric oxide lysosomal enzymes neuropeptides ```
108
what are vasoactive amines
histamine: inc. permeability of vasodilation serotonin: vasoconstriction during clotting
109
what do cytokines to in inflam
recruit leukocyte, promote adheasion and migration
110
ROS
associated w/ killing off micros
111
Nitric Oxide
vasodilation and microbial killing
112
lysosomal enzymes
microbial killing
113
Plasma protein drived
complement proteins coagulation proteins kinins
114
What protein goes w/ MAC
complement
115
Kinins lead to....
bradykinin formation, inc vessel perm and production of fibrin clots
116
chronic inflam cells...
macrophages and lymphocytes (b&t)
117
granuloma is
accumulation of macrophages
118
Pyrogen cytokines stimulate _____ synthesis
prostaglandin
119
2 mechanism of tissue repair
regeneration | scarring: irregular CT
120
Fibrosis is
abnormal collagen deposition, loosing original functionality
121
checkpoint control in cell cycle
cyclin dependent kinase
122
stem cell unique properties
self-renewal capacity | asymmetric replication
123
what are pluripotent stem cells
can form various cell types
124
3 important facts of GF
stimulate growth control genes ignore cell cycle checkpoints prevent apoptosis
125
3 types signaling GF
autocrine: self: positive feedback paracrine: release to local surrounding endocrine
126
2 forms of ECM
``` interstitial matrix basement membrane (chicken wire) ```
127
what is soft pink tissue under scab
granulation type tissue
128
4 stages of scar formation
angiogenesis fibroblast migration ecm deposition eventual removdeling
129
MMPS do what
break down CT, critical zinc ions
130
What is keloid
abnormal healing: increase collagen accumulation
131
steps in cutanous wound healing
inflam granulation wound contraction
132
first intention healing to get no inflam
30 days
133
2nd intention healing takes
6+ weeks, considerable scar contraction