Unit 2 Flashcards

(137 cards)

0
Q

During acute inflammation when white blood cells move closer to the vascular wall it is termed?

A

Margination

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1
Q

lymph flow —— when acute inflammation occurs?

A

increase

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2
Q

Acute inflammation is associated with a(n) ________ in vascular permeability?

A

increase

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3
Q

In acute inflammation what vessel alterations occur?

A

caliber, blood flow and permeability

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4
Q

what does vessel alteration allow during acute inflammation?

A

allows cells and proteins to move into the target tissue.

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5
Q

how long does vasoconstriction last in acute inflammation?

A

a few seconds

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6
Q

what does vasodilation do in acute inflammation?

A

increase blood flow, redness and warm

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7
Q

what does increased permeability in acute inflammation allow?

A

fluid to leave tissue, increase viscosity (wbc’s collect along vascular wall called margination) then move into tissue

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8
Q

what names could migrationg of a white cell be called?

A

migration diapedesis, transmigration emigration

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9
Q

what is endothelial contraction?

A

histamine binding creates gaps in postcapillary venules (most commmon) 15-30 mins after acute inflammation

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10
Q

what is endothelial necrosis?

A

leakage until repaired. From severe burns, severe infections or even extreme radiation

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11
Q

What is leakage from angiogenesis?

A

new vessels have immature (leaky) endothelial cells.

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12
Q

what is exudate?

A

a protein rich fluid that comes with acute inflammation may contain wbc’s and rbc’s

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13
Q

what is edema?

A

lymphatic drainage can’t keep up with flow and backs up

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14
Q

what is a lymphadenopathy?

A

general disorder of lymph nodes

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15
Q

What is lymphadentis

A

inflammed nodes, they increase in size and pain. can be palpated

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16
Q

what is lymphangitis?

A

inflamed lymphatic channel.

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17
Q

what are the 4 steps of leukocyte recruitment?

A
  1. margination and rolling
  2. firm adhesion to endothelium
  3. transmigration between endothelial cells
  4. chemotaxis toward target tissue
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18
Q

what causes leukocytes to roll?

A

selectins along the vessel wall

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19
Q

what protein firmly bind leukocytes?

A

integrins

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20
Q

how to leukocyte migrate?

A

via pseudopodia

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21
Q

Neutrophils predominate where?

A

in acute inflammation

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22
Q

How do neutrophils die?

A

via apoptosis within 48 hours in acute inflammation

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23
Q

what happens in phagocytosis

A

removes dead tissue. engulfment and degradation (oxidative burst), Opsonins

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24
what are opsonins?
``` immunoglobulin G (igG), a label for cell destruction ```
25
What is leukocyte-induced tissue injury?
inadvertent cell dmg. WBC's don't distinguish and damage via ROS & enzymes
26
examples of persistent infections
Tb, varicella zoster virus (VZV, chicken pox)
27
What happens in acute phase reaction?
lethargy, somnolence, malaise, increase HR, anorexia, anhidrosis
28
Spondylodiscitis
infection in the back, have a fever, localized pain with spinal percussion.
29
how do you scan for spondylodiscitis?
MRI
30
with what is leukocytosis common with?
bacterial infections
31
What does a "shift to the left" mean?
increase in immature cells
32
in leukocytosis what are elevated when bacteria is the cause?
neturophils
33
When a viral type of Leukocytosis occurs what is elevated?
lymphocytes
34
What is a leukemoid reaction?
extremely high blood leukocyte count (some sort of chronic inflammation)
35
What can cause a leukemoid reaction?
Clostridum difficile or tb | that cause chronic inflammation
36
What is Leukopenia?
decrease in blood leukocyte count
37
what conditions cause leukopenia
HIV/AIDS, chemotherapy or radiation therapy
38
What is Regeneration?
replacing damaged cells with a return to pre-injury status.
39
In regeneration, how does the healing occur?
by uninjured tissues or stem cells proliferating (cells must be able to replicate)
40
What kind of cells go through a scaring mechanism when healing?
cells unable to replicate.
41
What is the process of fibrosis?
adding Abnormal/extensive collagen deposition (scar tissue)
42
Places where you don't want fibrosis
Lungs, liver, kidney, myocardium (heart)
43
Where is fibrosis common?
Frequent in tissues with: 1) chronic inflammation 2) damage to terminally differentiated cell
44
How does cardiac fibrosis occur?
ischemia in the heart (an infarct) causes fibrosis
45
What is regeneration stimulated by?
1. production of GFs | 2. Cellular response to GFs: entry into the cell
46
What kind of healing is a coordinated effort?
Regeneration
47
What is tissue hemoesasis
1. Cellular proliferation 2. apoptosis 3. Stem cell differentiation
48
What is physiologic proliferation?
a well-regulated repair or injured tissues with adaptions to stress which preserves normal cellular function.
49
What is pathologic proliferation?
An unregulated proliferation which results from genetic alteration. Neoplasia (tumors) are this kind of proliferation
50
What is the earliest phase of growth?
g1
51
Where do we check for genetic damage which is ignored by cancer cell?
at g1.
52
What is the G0 stage?
the dormancy stage of cells
53
What takes a cell from G0 to G1?
Growth factors
54
The checkpoints in the cell cycle check for what?
Quality, DNA repair, apoptosis, senescence, genetic errors
55
What are cyclins?
the regulators of the cell cycle
56
What do CDKIs cells do?
slow down the cell cycle?
57
Whats an example of a cyclin?
Cyclin dependent kinase (CDK) enzymes
58
Labile cells proliferate how often?
continuously dividing such as the epithelia (GI, skin) or hematopoietic cells
59
What are some labile cells?
GI, skin, hematopoietic cells
60
How often are Stable cells proliferating?
These cells are typically in a quiescent state (G0) and thus have a limited replication. Only proliferate in a response to injury.
61
What are some example of stable cells?
kidney, pancres , liver cells
62
What are some Pemanent cells?
1. CNS neurons 2. skeletal or cardiac muscle tissue. 3. older cells: near hayflick limit
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How often do Permanent cells proliferate?
These are unable to regenerate tissue following injury thus are terminally differentiated cells
64
Examples of permanent cells?
CNS Skeletal or cardiac muscle tissue Older cells: near hayflick limit
65
What are the properties of stem cells?
1. self-renewal capacity (undifferentiated) | 2. Asymmetric replication -- some cells differentiate, others remain undifferentiated
66
What is a pluripotent stem cells?
a stem cell that may form various cell types
67
What are some examples of regenerative medicine repopulation of damaged tissue?
strokes or M.I.
68
What factors do GFs play in proliferation?
1. stimulate growth control genes 2. ignore cell cycle checkpoints 3. prevent apoptosis
69
What steroid hormone helps with regeneration and healing (proliferation)?
growth factors
70
Do macrophages and lymphocytes secrete GFs?
yes
71
What kind of tissues will produce GFs when injured?
stromal or parenchymal tissues
72
What are the function of Gfs?
1. cellular proliferation/repair 2. cellular migration 3. cellular differentiation
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What are some examples of cellular proliferation for GFs?
angiogenesis and fibrinogenesis
74
What are some examples of cellular migration in GFs?
permeability, chemotaxis
75
What is an autocrine signaling mechanism for GFs?
acts on secreting cell
76
What GF signaling mechanism acts on adjacent cells?
paracrine
77
What GF signaling mechanism is systemic via the circulatory system?
endocrine
78
What is a mitogen?
a hormone that increases cellular proliferation
79
What supports cells structurally and supple scaffolding for tissue repair?
Extracellular matrix
80
what does the ecm store?
H2O, minerals, GFs
81
What are the two types of ECM?
interstitial matrix and basement membrance
82
where is interstitial matrix found?
between cells in connective tissues
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what produces interstitial metrix?
fibroblast
84
where is basement membrane found?
surrounds cavities and organ surfaces
85
what produces basement membrane?
epithelium
86
What are the 3 functional components of ECM?
fibrous proteins water-hydrated gels adhesive glycoproteins
87
what are fibrous proteins for?
tensile strength
88
What are the fibrous proteins found in ECM?
Collaagen: tensile strength; triple helix, scars Elastin: recoil; arteries, uterus, skin, ligaments
89
where can elastin be found?
arteries, uterus, skin, ligaments
90
What are the water-hydrated gels in ECM?
hyaluronan | proteoglycans
91
What does hyaluonan do?
binds H2O in a gel-like matrix
92
what do proteoglycans do i the ECM?
compressibility, GF storage
93
What do the adhesive glycoproteins of the ECM do?
connect elements of ECM to other cells (cellular adhesion)
94
What are the ECM adhesive glycoproteins?
fibronectin, laminin, integrins, selectins
95
why are GFs stored in ECM?
for quick deployment
96
what cells are rapidly replaced?
labile cells
97
what cells have limited repair?
stable cells
98
what organ has possible compensatory growth?
kidney
99
what cells have a unique capacity to heal (40-60% resection?)
Hepatocytes (liver)
100
Why is the ability to replace injured tissues variable?
1. cells inherent capacity to proliferate | 2 severity/nature of injury (extend of ECM damage and stem cell damage)
101
When does scarring occur?
when repair cannot be achieved by regeneration
102
What kind of damage will cause scar to form? (fibrosis)
1. severe damage (ECM, parenchyma, epithelia 2. Chronic/prolonged injury (liver abscess) 3. Terminally differentiated cells
103
What an example of chronic or prolonged injury that can cause fibrosis (scar formation)
Liver abscess
104
During fibrosis what replaces the original cells?
connective tissue replaces original cells
105
What are the four steps in scar formation?
1. angiogenesis 2. Fibroblast migration & proliferation 3. Collagen deposit (scar) 4. Remodeling (lifetime)
106
how long does it take for granulation tissue appear?
within 3-5 days
107
What makes up the soft pink tissue in granulation tissue?
Fibrolasts, capillaries, connective tissue, WBCs
108
what are the other names of angiogenesis?
neovascularization or vasculogenesis (embryonic)
109
Why is angiogenesis critical for healing injured tissues?
nutrient delivery collateral circulation to ischemic tissue involved with tumor growth
110
What are the two methods of sprouting new vessels in angiogenesis?
A. capillary sprout from existing vessels (MC) | B. Endothelial precursor cells (EPC) from marrow
111
What are the steps in angiogenesis? (5 steps)
1. vasodilation 2. pericyte seperation 3. endothelial migration & proliferation 4. Capillary remodeling 5. Development & maturation of: pericytes, smooth muscle, & basement membrane
112
What are the 2 steps in scar tissue deposition?
1. fibroblast migration to site of injury | 2. deposition of ECM: irregular collagen
113
Why do scars go from a pinkish to pale color?
originally, highly vascular granulation tissue but progressively decreases in vascularity
114
What are MMPs regulated by?
regulated and inhibited by TIMPs
115
What do Matrix Metalloproteins require as a cofactor?
Zinc
116
What are MMPs produced by?
fibroblasts, macrophages, neutrophils, & epithelial cells
117
What do MMPs breakdown?
breakdown collagen
118
What are the factors influencing repair?
``` Infection Nutritional deficiency Glucocorticoids poor perfusion Etc. (age, pressure, anemia, foreign) ```
119
What is an example of nutritional deficiency affecting healing?
Deficiency in Vitamin C can lead to decreased basement membrane which leads to vessel fragility
120
What is an example if poor perfusion for wound healing?
atherosclerosis, diabetes
121
What are the effects of poor perfusion?
decreased arterial supply (blood) | decreased venous drainage
122
What can glucocorticoids do to wound healing?
the anti-inflammatory effects can cause decreased fibroblast activity (decreased healing)
123
What is a keloid?
Scar tissue beyond boundaries of wound
124
How is a Keloid formed?
Excessive collagen deposition and exuberant granulation tissue
125
Will Keloids regress?
NO
126
what are the characteristics of keloids?
flesh-colored: pink, red, dark brown and will not regress
127
Where do keloids form?
any cutaneous tissue that is injured (associated more with dermal injuries)
128
Keloids can cause pain and what else?
pruritus (itching)
129
What are the phases of the healing of skin wounds?
1. inflammation 2. formation of granulation tissue 3. ECM deposition & remodeling (they all overlap)
130
when can we expect maximal strength of scar tissue?
after 3 months
131
After being removed, how long until the wound is up to 70% strength?
1 month
132
What happens on the 1t day of healing by 1st intention?
clotting
133
what happens in day 3 of healing by first intention?
granulation tissue
134
What happens on the 5th day of healing by first intention?
peak angiogenesis, collagen bridges the wound
135
what happens in 1 month of healing by first intention?
inflammation is absent, epidermis is essentially normal
136
What are the steps i healing by first intention?
1 day = clotting day 3 = granulation tissue day 5 = peak angiogenesis, collagen bridges the wound 1 month = inflammation is absent, epidermis is essentially normal