Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

5- Path I > 4- Injury, Inflammation, & Healing > Flashcards

4- Injury, Inflammation, & Healing Flashcards

1
Q

Define Ischemia

A

lack of blood supply to organ or tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

most vulnerable tissue to ischemia

A

Brian (stroke)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

brain uses about ____% of blood O2

A

20

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Myocardium (heart muscle) ischemia leads to

A

Myocardial infarction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

least vulnerable tissue to ischemia is

A

liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what type of tissues is very vulnerable to ionizing radiation

A

Tissue with high mitotic rates (liable tissue)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

liable tissue includes

A

Blood cells, gonads, hair follicles, & epithelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Radiation effect on blood cells

A

can lead to leukemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

define leukemia

A

cancer that produces immature WBC’s or abnormal mature WBC’s which, stop the bone marrow from producing normal blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Most vulnerable tissue to radiation is

A

GI tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

attraction of cells to a particular virus is called

A

Tropism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Viruses are (Extracellular/intracellular)

A

intracellular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

HIV attacks which cells?

A

CD4 receptor cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

CD4 receptor cells includes

A

T-helper, Macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Polio virus aka

A

Poliomyelitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Polio virus (Poliomyelitis) – resides in

A

Anterior horn of the spinal cord

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Polio virus (Poliomyelitis) effect on the area it hits

A

interrupting motor and trophic functions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Rabies is Transferred via

A

Animal bite

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Rabies only cure is

A

vaccination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Rabies is associated with

A

Fear of water (Hydrophobia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Acute Inflammation signs and symptoms:

A

• Rubor (redness) • Calor (heat) • Dolor (pain) • Tumor (swelling)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what did Galen add later to the inflammation symptoms

A

Functio Laesa – loss of function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

describe the pathway of Micro-circulation

A

Arterioles -> Capillaries -> Post-capillary venules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Between Arteriole and Capillaries, there is a

A

pre-capillary sphincter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

the only region of the body where there is an exchange between the interstitial fluid and blood is

A

Capillaries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

the ONLY location where gas exchange happens is

A

Capillaries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Capillary anatomy includes (2 layers)

A

Basement membrane, and Endothelial cells with gaps between them

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Locations of Inflammation:

which vessels

A
  • Capillaries

* Post capillary venules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

3 Types of Blood Protein are

A
  • Albumin 55%
  • Globulin-antibodies 40-45%
  • Fibrinogen 5%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Albumin function

A

maintains oncotic pressure within capillaries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Fibrinogen function

A

prevent blood loss - clotting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Def: response to mild injury in which only fluid is allowed to escape to interstitial fluid

A

Serous (mild) inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Def: presence of fibrin (clotting factor), creating thick strands within exudate; increasing the seriousness of the inflammation

A

Fibrinous inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

example of Fibrinous inflammation

A

Rheumatic pericarditis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Describe Rheumatic pericarditis

A

occurs between the visceral and parietal pericardium, increasing friction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Def: pus exudate with dead bacteria and low in blood cells; bacterial death promotes tissue destroying enzymes

A

Supprative (purulent) inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

examples of Supprative (purulent) inflammation

A

Abscess, Cellulitis & Empyema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Abscess is localized accumulation of

A

Pus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Abscess develops at a focus when

A

an agent of injury is not quickly removed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Abscess can destroy

A

blood vessels leading to Perfuse Hemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Empyema is a collection of pus within

A

an existing cavity (plural, subdural)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Components of Inflammation can be divided into

A

Vascular & cellular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Vascular includes

A

Hyperemia, and Increased permeability of blood vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Describe the cellular component of inflammation

A

Escape of blood cells into the tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

leakage of fluid portion of blood into the tissues at the site of injury is called

A

Exudate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Exudate Specific gravity

A

1.020 +

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Exudate contains

A

Protein, WBC and tissue debris

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Exudate provide space for

A

healing the damaged tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

perfusion of fluid, little to no cells or protein, into the tissue is called

A

Transudate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Transudate Specific gravity

A

1.012

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Exudate is benefits

A

➢ Dissolution of toxins
➢ Promotion/accumulation of antibodies (if premade)
➢ Stimulation of nociceptors (pain sensation), due to swelling
➢ Promotion of phagocytosis
➢ Prevent infection and heal body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

WBC’s flows in ______ of the vessel

A

center

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

RBC’s flows in ______

A

peripheral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Platelets flow is _________

A

most peripheral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

plasma portion of blood decrease _____ (plasma function)

A

friction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

When injury occurs there is an interruption/impairment of

A

axial blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Steps of Inflammation:

A
  • Vascular-
    1) Hyperemia
    2) Increased permeability of vessels
  • Cellular-
    3) Margination
    4) Pavementing
    5) Leukocyte emigration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Hyperemia is the First reaction to injury of blood vessels to

A

interruption of axial blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Hyperemia causes _____ of arteriole sphincters

A

vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

in Hyperemia , vasoconstriction is Immediately followed by

A

vasodilation of capillaries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

vasodilation causes fluid to pushed out of the cell forming

A

exudate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

in Hyperemia , Blood viscosity increases, slowing flow causing

A

stasis ( halting movement of blood in capillaries and post capillary venules)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

2) Increased permeability of vessels

Contraction of endothelial cells, which create:

A

large gaps

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

2) Increased permeability of vessels

Protein can increase outside blood vessels increasing

A

tissue osmotic pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

2) Increased permeability of vessels

The increase in osmotic pressure pulls fluid into

A

the tissue from the blood vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

3) Margination:

WBC’s are pushed to

A

the peripheral endothelial walls of the vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Margination occurs during

A

vasoconstriction when RBC’s adhere to each other

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

3) Margination

RBC’s adhere to each other to

A

increasing there size to move to the center of the vessel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

4) Pavementing: WBC’s adhere to

A

endothelial surfaces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

5) Leukocyte emigration

outpouring WBC’s from the blood, most commonly (which cells)

A

Neutrophils, Monocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Leukocyte emigration ONLY occurs in

A

post capillary venules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

passive escape of red blood cells is called

A

diapedesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Neutrophils characteristics

A

– 55-60%
– multi lobed (2-5)
– multinucleated – granules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Neutrophilia increase when there’s _______ infection

A

Bacterial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Eosinophils characteristics

A

– 2-4%
– bi-lobed
– multinucleated
– pink granules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Eosinophils increase when there’s _______

A

Allergic reaction,

Parasitic infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Basophils characteristics

A

– 0.5-1%
– bi-lobed
– multinucleated
– purple granules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Lymphocytes characteristics

A

– 20-25%
– B & T cells
– monogranular
– mononucleated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Lymphocytes increase when there’s _______

A

Viral infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Monocytes characteristics

A 
– 4-8% 
– largest 
– monogranular 
– mononucleated 
– 30+ year life
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Monocytes increase when there’s _______

A

Chronic Bacterial infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

when Monocytes leaves the blood stream and enter a tissue, it’s called:

A

Macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Macrophages characteristics

A

– directly kill/destroy intruders
– Antigen presenting cells
– determinant to immune specific cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Phagocytosis 2 main steps

A

Recognition and Attachment:

Ingestion (Kill/Degradation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Recognition and Attachment includes

A

chemotaxis

Pseudopod projections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

define chemotaxis

A

Finding locating intruder cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Ingestion includes

A

Engulfing
Lysosomes
Exocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Phagocytic Cells are

name the cells

A

➢ Neutrophils
➢ Monocyte/Macrophage
➢ Eosinophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Lysosomal Mechanisms: can be either

A

Oxygen IN-dependent

Oxygen Dependen

90
Q

Oxygen IN-dependent includes which enzymes?

A
  • Lysozyme
  • Elastase
  • Collagenase
  • Defensin (neutrophils)
91
Q

Lysosomes contain lysozyme, elastase, and collagenas are _____ enzymes

A

digestive

92
Q

define Defensin

A

antibody like substance in neutrophils (primary line of defense)

93
Q

In Oxygen Dependent, what substance are produced

A

free radicals

94
Q

free radicals affect

A

lipid of cell membrane

95
Q

free radicals includes

A
  • Superoxide anion
  • Hypochlorite anion
  • Hydrogen peroxide
96
Q

Hydrogen peroxide is used to

A

Clean wounds – painless

97
Q

Leukocyte Defects includes

what diseases

A

➢ Chronic Granulomatous disease of Children

➢ Chediak – Higashi Syndrome

98
Q

Chronic Granulomatous disease of Children etiology

A

Genetic

inability to produce free-radicals

99
Q

Chronic Granulomatous disease of Children prognosis

A

No prevention of infection, death within 2 years

100
Q

Chediak – Higashi Syndrome etiology

A

Genetic

absence of normal cell motility of phagocytes

101
Q

WBC’s in Chediak Lack

A

degranulation

inability to release active enzymes

102
Q

Ischemia & Leukemia can be associated with

A

phagocytic cells defects

103
Q

what initiate inflammation

A
  • Substances released from injured cells
  • Direct stimulus to Mast Cells (trauma, cold, etc.)
  • Microbial products
  • Exposure of basement membrane or CT components
  • Deposition of antigen/antibody complexes
  • Disruption of vascular integrity
  • Complement activation
104
Q

Mediators of Inflammation are

A

Histamine
Serotonin
Substance P
Nitric Oxide

105
Q

2 Cell releasing Histamine

A

basophils in blood circulation

mast cells in tissues

106
Q

Histamine 4 Major Components

A

Vasodilation
Increased permeability of blood vessels
Bronchospasm
Increased mucous

107
Q

Histamine is produced in response to

A

Response to physical injury

108
Q

Histamine is due to what type of allergix rxn

A

Type I hypersensitive allergic reaction

109
Q

Serotonin is associated with

A

platelet aggregation

110
Q

Substance P is produced in

A

CNS/PNS

111
Q

Substance P is Involved in (what systems)

A

GI and Respiratory tracts

112
Q

Substance P function

A

o Promote production of pain signals
o Regulate BP
o Increase vessel permeability
o Influence vessel tone

113
Q

Nitric Oxide a.k.a

A

Endothelial Derived Relaxing Factor

114
Q

Nitric Oxide is produced by

A

Endothelial cells

115
Q

Nitric Oxide function

A

o Powerful vasodilator – hyperemia

o Inhibit leukocyte recruitment – cell component

116
Q

metabolites of Arachidonic Acid is called

A

Eicosanoids

117
Q

what is made from the cell membrane phospholipids (via Phospholipase)

A

Arachidonic Acid

118
Q

what enzyme takes free Archidonic acid and produces Prostaglandin G2 (PGG2)

A

Cyclooxygenase

119
Q

what is produced by various blood cells; vascular component of inflammation

A

Prostaglandins

120
Q

Prostaglandins General function

A

Regulation of Na+; H2O in kidneys
Protect GI tract from ulcerations
Regulate BP

121
Q

what increases # of Mast cells; recruit eosinophil’s; important in allergic

A

PGD2

122
Q

what causes fever; increase pain perception (hyperalgesia)

A

PGE2

123
Q

not testable, unknown function

A

PGF2

124
Q

released from endothelial cells; causes vasodilation and prevents platelet (thrombocyte) aggregation

A

Prostacyclin (PGI2)

125
Q

produced by platelets; causes vasoconstriction and promotes platelet aggregation

A

Thromboxane A2 (TXA2)

126
Q

Cox Inhibitors (inhibit

A

Cyclooxygenase

127
Q

Cox-1 inhibitor inhibits

A

both the normal function and inflammatory function of prostaglandins

128
Q

Cox-1 inhibitor will also inhibit

A

Cox-2

129
Q

example of Cox-1 inhibitor

A

Aleve (Naproxen)
Ibuprofen (Advil)
Indomethacin
Aspirin

130
Q

Cox-2 inhibitor – only block

A

Cox-2

131
Q

what increase production of additional prostaglandins, above the normal
functioning level

A

Cox-2

132
Q

Examples of cox 2

A

Vioxx (increased risk of thrombosis)
Celebrex
Meloxicam

133
Q

cox 2 drugs are

A

Weak anti-inflammatory drugs

Increased side effect, death

134
Q

enzyme, which takes free Arachidonic acid and produces Leukotriene’s

A

5-Lipoxygenase

135
Q

promotes vasoconstriction, increase permeability of blood vessels, bronchospasm

A

12-Lipoxygenase

136
Q

promote vasodilation, inhibit neutrophil chemotaxis – cellular component

A

Lipoxins

137
Q

what breakdowns tumor cells

A

Tumor Necrosis Factor

138
Q

can be produced by many cells in the body, but mainly macrophages (T helper cell)

A

Interleukin 1&6

139
Q

Interleukin 1&6 Induces

A

acute inflammatory response

140
Q

Acute Phase of Inflammation Responses includes:

A
  • Fever
  • Decrease apetite
  • Increase sleep
  • Increase acute phase proteins (C-Reactive Protein)
  • hemodynamic affects (shock)
  • Neutrophilia
141
Q

In Tissue Injury Response, which clotting factor is activated

A

Hageman (Clot) Factor (XII)

142
Q

Activation of Hageman cascade

A

▪ Coagulation
▪ Fibrinolytic
▪ Complement
▪ Kinin

143
Q

Fibrinolytic regulates

A

coagulation

144
Q

Kinin is specifically designed for

A

inflammatory response

145
Q

Coagulation, Fibrinolytic, and Complement are NOT

A

direct inflammatory responses

146
Q

which Complement participate in the inflammatory response

A

C3a, C5a, C4a

147
Q

Complement (C3a, C5a, C4a) Potentiates the function of

A

histamine with its role in anaphylactic allergic response (anaphylatoxins)

148
Q

Kinin cascade

A

1) Hageman factor
2) Pre-kallikren
3) Kallikren
4) Kininogen
5) Bradykinin

149
Q

what irritate chemoreceptors, creating the perception of pain (hyperalgia)

A

Bradykinin

150
Q

Antibodies are derived by

A

Plasma

151
Q

Inflammation is usually associated with

what other symptoms

A

fever (systemic), pain, exudate

152
Q

Lymphatic system collects

A

interstitial fluid into lymph capillaries

153
Q

Interstitial fluid when it enters the capillaries is called

A

Lymph

154
Q

where the fluid and possible infection move post lymph capillaries

A

Lymph nodes

155
Q

infection of the lymph node is called

A

Lymphangitis

156
Q

Lymphangitis; this can cause swelling of the lymph nodes called

A

Lymphangeitis

157
Q

infection moving into the circulation causes

A

bacteremia

158
Q

bacteremia is identified by leukocyte count of

A

> 9,000/ cubic mm

159
Q

Acute Inflammation Duration

A

1 week to 10 days

160
Q

in Acute Inflammation the amounts of exudate are

A

Large

161
Q

Acute Inflammation is characterized with large amounts of what WBCs?

A

Neutrophils and Macrophages

162
Q

Chronic inflammation Duration

A

> 6 weeks

163
Q

In Chronic inflammation, exudate is

A

not produced, or only produced during “flaring” attacks

164
Q

Chronic Inflammation is characterized with large amounts of what WBCs?

A

Monocytes and Lymphocytes

165
Q

Specific substances are typically cause chronic inflammation are

A

o Viral infection
o Persistent Microbial Infection
o Prolonged potentially toxic agents
o Autoimmune Diseases

166
Q

Persistent Microbial Infection includes

A 
▪ Mycobacterium tuberculosis (TB)
▪ Mycobacterium laprae (Leprosy)
▪ Treponema pallidum (Syphilis)
▪ Brucella (Brucellosis)
▪ Listeria (Listeriosis)
167
Q

toxic agents (non-biological) – foreign bodies includes

A

▪ Asbestos (Asbestosis)
▪ Silica (Silicosis)
▪ Beryllium (Berylliosis)
▪ Organic dust

168
Q

Inhalation of large amounts of Silica causes

A

Silicosis

169
Q

Silicosis Inflammatory response:

Phagocytosis occurs, but the cell is unable to

A

digest silica and remains in the cell

170
Q

digest silica and remains in the cell leads to

A

Cell is destroyed, lysozymes are expelled and damages the lungs

171
Q

if Silicosis continues to occur causes

A

chronic tissue damage
cells unable to regenerate
CT replaces functional tissue

172
Q

Silicosis aka

A

Pneumoconiosis

173
Q

2 Types of Chronic Inflammation

A

Non-specific inflammation

Granulomatous inflammation

174
Q

which Type of Chronic Inflammation is more common

A

Non-specific inflammation

175
Q

Granulomatous inflammation is associated with granulomas resulting from

A

TB or Leprosy

176
Q

Infection is restricted to

A

specific site of inflammation

177
Q

Granulomas are formed by

A

macrophages around the mycobacterium causing inflammation

178
Q

Giant multinucleated cells – formed by

A

interferon gamma

179
Q

interferon gamma causes many cells

coalesce together leading to

A

chronic granulomatous reactions (Ghon’s focus)

180
Q

Granuloma formation steps:

A

Infection
Giant cells
Lymphocytes
Fibroblasts

181
Q

steps of granular formation in kidens

A

Kidney inflammation
Replaced by connective tissue
Shrinkage of CT
Granular appearance – chronic granulomatous nephritis

182
Q

in Aseptic osteonecrosis, Compressed blood vessel leads to

A

infarction

183
Q

in Aseptic osteonecrosis, Dissolution of bone without infection leads to

A

joint and bone loss

184
Q

characteristic function cells that forms most organs

A

parenchyma

185
Q

parenchyma are bound together with connective tissue and vessels forming

A

stroma

186
Q

Four major components of healing are

A

Regeneration
Repair
Revascularization
Surface restoration

187
Q

Regeneration is whentissue is

A

replaced from parenchyma by cell division

188
Q

Volume of tissue formed is equal to

A

volume of tissue lost

189
Q

in regeneration, there’re 3 types of tissue

(different patterns of regeneration)

A

Labile
Stable
Permanent

190
Q

Labile tissue that divide continually to

A

replace cells that are constantly being depleted by normal processes

191
Q

Examples of labile tissue

A 
epithelia of skin
mucous membranes
lining of various ducts
red bone marrow 
lymphoid tissues
192
Q

Cells divide, but only slowly beyond adolescence when normal development is complete are called

A

Stable

193
Q

Stable are Cells are able to function throughout life so it doesn’t require:

A

high mitosis rates

194
Q

Stable mitosis rate increases when

A

damaged tissue must be replaced

195
Q

Examples of Stable cells

A

Glands
osteoblasts
smooth muscle fibers
vascular endothelium

196
Q

Permanent are cells that lost

A

all mitotic ability after birth

197
Q

Loss of Permanent cells leads to

A

functional loss

198
Q

Permanent cells when lost are replaced with

A

scar tissue

199
Q

during repair phase, fibrous scar tissue fills

A

the gaps left by the loss of damaged tissue

200
Q

Fibrosis is the formation of

A

collagen fibers

201
Q

Fibroblast are present in

A

stroma

202
Q

Fibrosis formation starts with the secretion of

A

procollagen

203
Q

procollagen Enzymatically altered to from

A

long filaments of collagen

204
Q

filaments of collagen join together to form

A

collagen fiber bundle

205
Q

production of new blood vessels to supply and drain the site of damage is called

A

Angiogenesis

206
Q

Angiogenesis Occurs in

A

the loosely gelled, protein-rich exudates that forms at the damage site

207
Q

Revascularization (Angiogenesis) ends up with

A

Granulation tissue

208
Q

Surface restoration is restoring the

A

protective epithelium

209
Q

Primary Healing: is healing of

A

incision, or severing wound of the skin

210
Q

Secondary Healing: is healing of

A

wound edges are not closely apposed

211
Q

Complication of healing includes

A 
Adhesions 
Contracture 
Dehiscence 
Keloids 
Proud Flesh
Suture complications
Therapy
212
Q

newly formed collagen demonstrates an exaggerated wound contraction response as it matures is called

A

Contracture

213
Q

joining of serous membranes that leads to restriction of movement in structures is called

A

Adhesions

214
Q

breaking open of a healing wound; possibly due to pressure on the wound is called

A

Dehiscence

215
Q

irregular masses of scar tissue that protrude from the surface of skin is called

A

Keloids

216
Q

Keloids results from over production of

A

dermal collagen during healing.

217
Q

overproduction of granulation tissue is called

A

Proud Fles

218
Q

interruption of epithelium is called

A

Suture complications

219
Q

Therapy – inhibitory effects includes

A

anticancer drug
anti-inflammatory drugs
Corticosteroid

220
Q

anticancerdrugssuppress

A

mitosis

221
Q

anti-inflammatorydrugs suppress

A

protein synthesis
wound contraction
regeneration of new epithelium

222
Q

Corticosteroidinterfere with

A

fibroblast migration to injured site

immune system suppression

5- Path I (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions