4- Injury, Inflammation, & Healing Flashcards
1
Q
Define Ischemia
A
lack of blood supply to organ or tissue
2
Q
most vulnerable tissue to ischemia
A
Brian (stroke)
3
Q
brain uses about ____% of blood O2
A
20
4
Q
Myocardium (heart muscle) ischemia leads to
A
Myocardial infarction
5
Q
least vulnerable tissue to ischemia is
A
liver
6
Q
what type of tissues is very vulnerable to ionizing radiation
A
Tissue with high mitotic rates (liable tissue)
7
Q
liable tissue includes
A
Blood cells, gonads, hair follicles, & epithelial cells
8
Q
Radiation effect on blood cells
A
can lead to leukemia
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
10
Q
Most vulnerable tissue to radiation is
A
GI tract
11
Q
attraction of cells to a particular virus is called
A
Tropism
12
Q
Viruses are (Extracellular/intracellular)
A
intracellular
13
Q
HIV attacks which cells?
A
CD4 receptor cells
14
Q
CD4 receptor cells includes
A
T-helper, Macrophages
15
Q
Polio virus aka
A
Poliomyelitis
16
Q
Polio virus (Poliomyelitis) – resides in
A
Anterior horn of the spinal cord
17
Q
Polio virus (Poliomyelitis) effect on the area it hits
A
interrupting motor and trophic functions
18
Q
Rabies is Transferred via
A
Animal bite
19
Q
Rabies only cure is
A
vaccination
20
Q
Rabies is associated with
A
Fear of water (Hydrophobia)
21
Q
Acute Inflammation signs and symptoms:
A
• Rubor (redness) • Calor (heat) • Dolor (pain) • Tumor (swelling)
22
Q
what did Galen add later to the inflammation symptoms
A
Functio Laesa – loss of function
23
Q
describe the pathway of Micro-circulation
A
Arterioles -> Capillaries -> Post-capillary venules
24
Q
Between Arteriole and Capillaries, there is a
A
pre-capillary sphincter
25
the only region of the body where there is an exchange between the interstitial fluid and blood is
Capillaries
26
the ONLY location where gas exchange happens is
Capillaries
27
Capillary anatomy includes (2 layers)
Basement membrane, and Endothelial cells with gaps between them
28
Locations of Inflammation:
| which vessels
* Capillaries
| * Post capillary venules
29
3 Types of Blood Protein are
- Albumin 55%
- Globulin-antibodies 40-45%
- Fibrinogen 5%
30
Albumin function
maintains oncotic pressure within capillaries
31
Fibrinogen function
prevent blood loss - clotting
32
Def: response to mild injury in which only fluid is allowed to escape to interstitial fluid
Serous (mild) inflammation
33
Def: presence of fibrin (clotting factor), creating thick strands within exudate; increasing the seriousness of the inflammation
Fibrinous inflammation
34
example of Fibrinous inflammation
Rheumatic pericarditis
35
Describe Rheumatic pericarditis
occurs between the visceral and parietal pericardium, increasing friction
36
Def: pus exudate with dead bacteria and low in blood cells; bacterial death promotes tissue destroying enzymes
Supprative (purulent) inflammation
37
examples of Supprative (purulent) inflammation
Abscess, Cellulitis & Empyema
38
Abscess is localized accumulation of
Pus
39
Abscess develops at a focus when
an agent of injury is not quickly removed
40
Abscess can destroy
blood vessels leading to Perfuse Hemorrhage
41
Empyema is a collection of pus within
an existing cavity (plural, subdural)
42
Components of Inflammation can be divided into
Vascular & cellular
43
Vascular includes
Hyperemia, and Increased permeability of blood vessels
44
Describe the cellular component of inflammation
Escape of blood cells into the tissue
45
leakage of fluid portion of blood into the tissues at the site of injury is called
Exudate
46
Exudate Specific gravity
1.020 +
47
Exudate contains
Protein, WBC and tissue debris
48
Exudate provide space for
healing the damaged tissue
49
perfusion of fluid, little to no cells or protein, into the tissue is called
Transudate
50
Transudate Specific gravity
1.012
51
Exudate is benefits
➢ 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
52
WBC’s flows in ______ of the vessel
center
53
RBC’s flows in ______
peripheral
54
Platelets flow is _________
most peripheral
55
plasma portion of blood decrease _____ (plasma function)
friction
56
When injury occurs there is an interruption/impairment of
axial blood flow
57
Steps of Inflammation:
- Vascular-
1) Hyperemia
2) Increased permeability of vessels
- Cellular-
3) Margination
4) Pavementing
5) Leukocyte emigration
58
Hyperemia is the First reaction to injury of blood vessels to
interruption of axial blood flow
59
Hyperemia causes _____ of arteriole sphincters
vasoconstriction
60
in Hyperemia , vasoconstriction is Immediately followed by
vasodilation of capillaries
61
vasodilation causes fluid to pushed out of the cell forming
exudate
62
in Hyperemia , Blood viscosity increases, slowing flow causing
stasis ( halting movement of blood in capillaries and post capillary venules)
63
2) Increased permeability of vessels
| Contraction of endothelial cells, which create:
large gaps
64
2) Increased permeability of vessels
| Protein can increase outside blood vessels increasing
tissue osmotic pressure
65
2) Increased permeability of vessels
| The increase in osmotic pressure pulls fluid into
the tissue from the blood vessels
66
3) Margination:
| WBC’s are pushed to
the peripheral endothelial walls of the vessels
67
Margination occurs during
vasoconstriction when RBC’s adhere to each other
68
3) Margination
| RBC’s adhere to each other to
increasing there size to move to the center of the vessel
69
4) Pavementing: WBC’s adhere to
endothelial surfaces
70
5) Leukocyte emigration
| outpouring WBC’s from the blood, most commonly (which cells)
Neutrophils, Monocytes
71
Leukocyte emigration ONLY occurs in
post capillary venules
72
passive escape of red blood cells is called
diapedesis
73
Neutrophils characteristics
– 55-60%
– multi lobed (2-5)
– multinucleated – granules
74
Neutrophilia increase when there's _______ infection
Bacterial
75
Eosinophils characteristics
– 2-4%
– bi-lobed
– multinucleated
– pink granules
76
Eosinophils increase when there's _______
Allergic reaction,
| Parasitic infection
77
Basophils characteristics
– 0.5-1%
– bi-lobed
– multinucleated
– purple granules
78
Lymphocytes characteristics
– 20-25%
– B & T cells
– monogranular
– mononucleated
79
Lymphocytes increase when there's _______
Viral infection
80
Monocytes characteristics
```
– 4-8%
– largest
– monogranular
– mononucleated
– 30+ year life
```
81
Monocytes increase when there's _______
Chronic Bacterial infection
82
when Monocytes leaves the blood stream and enter a tissue, it's called:
Macrophages
83
Macrophages characteristics
– directly kill/destroy intruders
– Antigen presenting cells
– determinant to immune specific cells
84
Phagocytosis 2 main steps
Recognition and Attachment:
| Ingestion (Kill/Degradation)
85
Recognition and Attachment includes
chemotaxis
| Pseudopod projections
86
define chemotaxis
Finding locating intruder cell
87
Ingestion includes
Engulfing
Lysosomes
Exocytosis
88
Phagocytic Cells are
| name the cells
➢ Neutrophils
➢ Monocyte/Macrophage
➢ Eosinophils
89
Lysosomal Mechanisms: can be either
Oxygen IN-dependent
| Oxygen Dependen
90
Oxygen IN-dependent includes which enzymes?
* Lysozyme
* Elastase
* Collagenase
* Defensin (neutrophils)
91
Lysosomes contain lysozyme, elastase, and collagenas are _____ enzymes
digestive
92
define Defensin
antibody like substance in neutrophils (primary line of defense)
93
In Oxygen Dependent, what substance are produced
free radicals
94
free radicals affect
lipid of cell membrane
95
free radicals includes
* Superoxide anion
* Hypochlorite anion
* Hydrogen peroxide
96
Hydrogen peroxide is used to
Clean wounds – painless
97
Leukocyte Defects includes
| what diseases
➢ Chronic Granulomatous disease of Children
| ➢ Chediak – Higashi Syndrome
98
Chronic Granulomatous disease of Children etiology
Genetic
| inability to produce free-radicals
99
Chronic Granulomatous disease of Children prognosis
No prevention of infection, death within 2 years
100
Chediak – Higashi Syndrome etiology
Genetic
| absence of normal cell motility of phagocytes
101
WBC's in Chediak Lack
degranulation
| inability to release active enzymes
102
Ischemia & Leukemia can be associated with
phagocytic cells defects
103
what initiate inflammation
* 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
Mediators of Inflammation are
Histamine
Serotonin
Substance P
Nitric Oxide
105
2 Cell releasing Histamine
basophils in blood circulation
| mast cells in tissues
106
Histamine 4 Major Components
Vasodilation
Increased permeability of blood vessels
Bronchospasm
Increased mucous
107
Histamine is produced in response to
Response to physical injury
108
Histamine is due to what type of allergix rxn
Type I hypersensitive allergic reaction
109
Serotonin is associated with
platelet aggregation
110
Substance P is produced in
CNS/PNS
111
Substance P is Involved in (what systems)
GI and Respiratory tracts
112
Substance P function
o Promote production of pain signals
o Regulate BP
o Increase vessel permeability
o Influence vessel tone
113
Nitric Oxide a.k.a
Endothelial Derived Relaxing Factor
114
Nitric Oxide is produced by
Endothelial cells
115
Nitric Oxide function
o Powerful vasodilator – hyperemia
| o Inhibit leukocyte recruitment – cell component
116
metabolites of Arachidonic Acid is called
Eicosanoids
117
what is made from the cell membrane phospholipids (via Phospholipase)
Arachidonic Acid
118
what enzyme takes free Archidonic acid and produces Prostaglandin G2 (PGG2)
Cyclooxygenase
119
what is produced by various blood cells; vascular component of inflammation
Prostaglandins
120
Prostaglandins General function
Regulation of Na+; H2O in kidneys
Protect GI tract from ulcerations
Regulate BP
121
what increases # of Mast cells; recruit eosinophil’s; important in allergic
PGD2
122
what causes fever; increase pain perception (hyperalgesia)
PGE2
123
not testable, unknown function
PGF2
124
released from endothelial cells; causes vasodilation and prevents platelet (thrombocyte) aggregation
Prostacyclin (PGI2)
125
produced by platelets; causes vasoconstriction and promotes platelet aggregation
Thromboxane A2 (TXA2)
126
Cox Inhibitors (inhibit
Cyclooxygenase
127
Cox-1 inhibitor inhibits
both the normal function and inflammatory function of prostaglandins
128
Cox-1 inhibitor will also inhibit
Cox-2
129
example of Cox-1 inhibitor
Aleve (Naproxen)
Ibuprofen (Advil)
Indomethacin
Aspirin
130
Cox-2 inhibitor – only block
Cox-2
131
what increase production of additional prostaglandins, above the normal
functioning level
Cox-2
132
Examples of cox 2
Vioxx (increased risk of thrombosis)
Celebrex
Meloxicam
133
cox 2 drugs are
Weak anti-inflammatory drugs
| Increased side effect, death
134
enzyme, which takes free Arachidonic acid and produces Leukotriene’s
5-Lipoxygenase
135
promotes vasoconstriction, increase permeability of blood vessels, bronchospasm
12-Lipoxygenase
136
promote vasodilation, inhibit neutrophil chemotaxis – cellular component
Lipoxins
137
what breakdowns tumor cells
Tumor Necrosis Factor
138
can be produced by many cells in the body, but mainly macrophages (T helper cell)
Interleukin 1&6
139
Interleukin 1&6 Induces
acute inflammatory response
140
Acute Phase of Inflammation Responses includes:
* Fever
* Decrease apetite
* Increase sleep
* Increase acute phase proteins (C-Reactive Protein)
* hemodynamic affects (shock)
* Neutrophilia
141
In Tissue Injury Response, which clotting factor is activated
Hageman (Clot) Factor (XII)
142
Activation of Hageman cascade
▪ Coagulation
▪ Fibrinolytic
▪ Complement
▪ Kinin
143
Fibrinolytic regulates
coagulation
144
Kinin is specifically designed for
inflammatory response
145
Coagulation, Fibrinolytic, and Complement are NOT
direct inflammatory responses
146
which Complement participate in the inflammatory response
C3a, C5a, C4a
147
Complement (C3a, C5a, C4a) Potentiates the function of
histamine with its role in anaphylactic allergic response (anaphylatoxins)
148
Kinin cascade
1) Hageman factor
2) Pre-kallikren
3) Kallikren
4) Kininogen
5) Bradykinin
149
what irritate chemoreceptors, creating the perception of pain (hyperalgia)
Bradykinin
150
Antibodies are derived by
Plasma
151
Inflammation is usually associated with
| what other symptoms
fever (systemic), pain, exudate
152
Lymphatic system collects
interstitial fluid into lymph capillaries
153
Interstitial fluid when it enters the capillaries is called
Lymph
154
where the fluid and possible infection move post lymph capillaries
Lymph nodes
155
infection of the lymph node is called
Lymphangitis
156
Lymphangitis; this can cause swelling of the lymph nodes called
Lymphangeitis
157
infection moving into the circulation causes
bacteremia
158
bacteremia is identified by leukocyte count of
> 9,000/ cubic mm
159
Acute Inflammation Duration
1 week to 10 days
160
in Acute Inflammation the amounts of exudate are
Large
161
Acute Inflammation is characterized with large amounts of what WBCs?
Neutrophils and Macrophages
162
Chronic inflammation Duration
> 6 weeks
163
In Chronic inflammation, exudate is
not produced, or only produced during “flaring” attacks
164
Chronic Inflammation is characterized with large amounts of what WBCs?
Monocytes and Lymphocytes
165
Specific substances are typically cause chronic inflammation are
o Viral infection
o Persistent Microbial Infection
o Prolonged potentially toxic agents
o Autoimmune Diseases
166
Persistent Microbial Infection includes
```
▪ Mycobacterium tuberculosis (TB)
▪ Mycobacterium laprae (Leprosy)
▪ Treponema pallidum (Syphilis)
▪ Brucella (Brucellosis)
▪ Listeria (Listeriosis)
```
167
toxic agents (non-biological) – foreign bodies includes
▪ Asbestos (Asbestosis)
▪ Silica (Silicosis)
▪ Beryllium (Berylliosis)
▪ Organic dust
168
Inhalation of large amounts of Silica causes
Silicosis
169
Silicosis Inflammatory response:
| Phagocytosis occurs, but the cell is unable to
digest silica and remains in the cell
170
digest silica and remains in the cell leads to
Cell is destroyed, lysozymes are expelled and damages the lungs
171
if Silicosis continues to occur causes
chronic tissue damage
cells unable to regenerate
CT replaces functional tissue
172
Silicosis aka
Pneumoconiosis
173
2 Types of Chronic Inflammation
Non-specific inflammation
| Granulomatous inflammation
174
which Type of Chronic Inflammation is more common
Non-specific inflammation
175
Granulomatous inflammation is associated with granulomas resulting from
TB or Leprosy
176
Infection is restricted to
specific site of inflammation
177
Granulomas are formed by
macrophages around the mycobacterium causing inflammation
178
Giant multinucleated cells – formed by
interferon gamma
179
interferon gamma causes many cells
| coalesce together leading to
chronic granulomatous reactions (Ghon’s focus)
180
Granuloma formation steps:
Infection
Giant cells
Lymphocytes
Fibroblasts
181
steps of granular formation in kidens
Kidney inflammation
Replaced by connective tissue
Shrinkage of CT
Granular appearance – chronic granulomatous nephritis
182
in Aseptic osteonecrosis, Compressed blood vessel leads to
infarction
183
in Aseptic osteonecrosis, Dissolution of bone without infection leads to
joint and bone loss
184
characteristic function cells that forms most organs
parenchyma
185
parenchyma are bound together with connective tissue and vessels forming
stroma
186
Four major components of healing are
Regeneration
Repair
Revascularization
Surface restoration
187
Regeneration is when tissue is
replaced from parenchyma by cell division
188
Volume of tissue formed is equal to
volume of tissue lost
189
in regeneration, there're 3 types of tissue
| (different patterns of regeneration)
Labile
Stable
Permanent
190
Labile tissue that divide continually to
replace cells that are constantly being depleted by normal processes
191
Examples of labile tissue
```
epithelia of skin
mucous membranes
lining of various ducts
red bone marrow
lymphoid tissues
```
192
Cells divide, but only slowly beyond adolescence when normal development is complete are called
Stable
193
Stable are Cells are able to function throughout life so it doesn't require:
high mitosis rates
194
Stable mitosis rate increases when
damaged tissue must be replaced
195
Examples of Stable cells
Glands
osteoblasts
smooth muscle fibers
vascular endothelium
196
Permanent are cells that lost
all mitotic ability after birth
197
Loss of Permanent cells leads to
functional loss
198
Permanent cells when lost are replaced with
scar tissue
199
during repair phase, fibrous scar tissue fills
the gaps left by the loss of damaged tissue
200
Fibrosis is the formation of
collagen fibers
201
Fibroblast are present in
stroma
202
Fibrosis formation starts with the secretion of
procollagen
203
procollagen Enzymatically altered to from
long filaments of collagen
204
filaments of collagen join together to form
collagen fiber bundle
205
production of new blood vessels to supply and drain the site of damage is called
Angiogenesis
206
Angiogenesis Occurs in
the loosely gelled, protein-rich exudates that forms at the damage site
207
Revascularization (Angiogenesis) ends up with
Granulation tissue
208
Surface restoration is restoring the
protective epithelium
209
Primary Healing: is healing of
incision, or severing wound of the skin
210
Secondary Healing: is healing of
wound edges are not closely apposed
211
Complication of healing includes
```
Adhesions
Contracture
Dehiscence
Keloids
Proud Flesh
Suture complications
Therapy
```
212
newly formed collagen demonstrates an exaggerated wound contraction response as it matures is called
Contracture
213
joining of serous membranes that leads to restriction of movement in structures is called
Adhesions
214
breaking open of a healing wound; possibly due to pressure on the wound is called
Dehiscence
215
irregular masses of scar tissue that protrude from the surface of skin is called
Keloids
216
Keloids results from over production of
dermal collagen during healing.
217
overproduction of granulation tissue is called
Proud Fles
218
interruption of epithelium is called
Suture complications
219
Therapy – inhibitory effects includes
anticancer drug
anti-inflammatory drugs
Corticosteroid
220
anticancer drugs suppress
mitosis
221
anti-inflammatory drugs suppress
protein synthesis
wound contraction
regeneration of new epithelium
222
Corticosteroid interfere with
fibroblast migration to injured site
| immune system suppression
