Tissue Repair Flashcards
1
Q
hypoxia
A
- decreased ability to obtain or use oxygen
- most common cause of cell injury
2
Q
hypoxemia
A
reduced transfer of oxygen from lungs to blood
3
Q
ischemia
A
decreased blood flow to tissues
4
Q
physical agents include
A
mechanical trauma (hit, cut, punctured), temperature extremes 9hot or cold), radiation (external or medical), and electric shock
5
Q
potential causes of a hypoxic event
A
- lack of air to breath in
- no hemoglobin available to carry oxygen
- hemoglobin lack the ability to carry oxygen
- lack of blood flow to tissue
- hypothermia (vasoconstriction of vessel)
6
Q
free radicals
A
- missing an electron
- electrically uncharged atom or group of atoms with an unpaired electron
- will attack a healthy atom to get an extra electron
7
Q
Endogenous antioxidant system
A
- come from within our own body
- production decreases with age
- contributes to premature aging and degenerative diseases
8
Q
Exogenous antioxidents
A
- come for outside our body
9
Q
are endo/exo antioxidants more potent
A
endogenous antioxidants are far more potent
10
Q
what foods should you avoid
A
- nutrient poor foods and deficient in antioxidants
11
Q
oxidative stress
A
- over production of free radicals
- plays a major part in the development of chronic and degenerative ailments such as cancer, arthritis, aging, autoimmmune disorders, cardiovascular and neurodegenerative diseases
12
Q
free radical have a _____ role
A
dual (toxic and beneficial compounds)
13
Q
how does the body counteract oxidative stress
A
antioxidants
- naturally (much more potent) or consuming foods and supplements
14
Q
what are antioxidants
A
healthy atoms that will share an electron with the free radical atom preventing it from attacking another health atom, preventing cell damage
15
Q
what is the best sources of antioxidants
A
vitamin C
- fruits and vegtables
16
Q
foods to avoid
A
- processed food
- high glycemic food, limit processed meats (bacon, sausage, salami), limit red meat, dont reuse cooking fats and oils, limit alcohol
17
Q
Asphyxiation
A
failure of cells to recieve or use oxygen
18
Q
Suffocation
A
- systemic hypoxia
- no air is exchanged in the lungs
19
Q
strangulation
A
- causes of cerebral hypoxia
- compression and closure of airway
- external pressure on neck
20
Q
types of strangualtion
A
- hanging
- ligature
- manual
21
Q
hanging
A
“V” inverted on neck
22
Q
ligature
A
- horizontal mark
- petechia more common, internal injury rare
23
Q
manual strangulation
A
- severe internal damage, bruising and fractures of hyoid
24
Q
drowning
A
- no oxygen exchange in the lungs due to being filled with fluid
- prevents the delivery of oxygen to tissues
25
carbon monoxide
- binds to hemoglobin
- unable to transport oxygen in the blood
26
carbon monoxide build up symptoms
- headache, nausea, weakness, tinnitus, vomiting
27
treatment of carbon monoxide build up
- fresh air
- hyperbaric chamber (high pressure oxygen; forces the carbon monoxide off the hemoglobin)
28
Chemical asphyxiation
- cyanide blocks the intercellular use of oxygen
29
Chemical asphyxiation symptoms
weakness, nausea, confusion, difficulty breathing, seizure, cardiac arrest
30
Chemical asphyxiation treatment
- identify source
- activated charcoal orally if ingestion has occurred
- oxygen
31
Chemical asphyxiation occurs
in building fires
32
types of asphyxiation
- suffocation
- strangulation
- drowning
- chemical
33
Contusion
bruise
- bleeding into the skin or underlying tissues
34
Laceration
- tear or rip resulting when tensile strength of skin or tissue is exceeded
- ragged and irregular
35
Abrasion
- superficial laceration
- EXAMPLE: scrape on the knee
36
Avulsion
- wide area of tissue is pulled away
- only skin (either loose or torn)
37
Fracture
- blunt force blows or impacts can cause bone to break or shatter
- multiple types
38
Incised wound
- wound that is longer than it is deep
- can be straight or jagged
- not always surgical
39
stab wound
- deeper than it is long
- can be surgical
- EXAMPLE; stabbed with a knife
40
puncture wound
- weapon has a sharp point but not sharp edges
- EXAMPLE: punctured with a needle
41
reverse injury
- cell recovery
42
cell death
necrosis
43
programmed cell removal
cell apoptosis
- controlled cell death
44
Autophagy
- controlled process
- cell recycles part of itself (eliminates nonfunctioning parts of the cell)
- consumption of cells own contents as metabolic process occcurs in starvation and certain diseases (use nutrients to feed itself)
- can prevent apoptosis
45
Apoptosis
- dealth of cells which occurs as a normal and controlled part of an organisms growth or development
- orderly process
- controlled cellular fragmentation (phagocytosis occurs as phagocyte envelopes the cell and fragments)
46
necrosis
- swelling and bursting of the cell membrane
- death of most or all of the cells in an organ or tissue due to disease, injury, or failure of blood supply
- rupture of the cell and damage to the area
47
Coagulative necrosis
- Kidney, heart, and adrenal glands
- loss of nucleus with cellular outline preserved
- caused by ischemia or infraction
- cellular degeneration is delayed
- architecture is maintained
48
ischemia
inadequate blood supply to an organ
49
infraction
obstruction of the blood supply to an organ or region of tissue
50
Liquefactive necrosis
- Neurons, brain
- transforms tissue into liquid (brain has high content of lipid and water
- caused by infraction or abcess
51
Caseous necrosis
- lungs
- caused by tuberculous
- dead tissue appears as a soft and white proteinaceous dead cell mass
52
Fatty necrosis
- breast, pancrease, and other abdominal organs
- usually harmless
- can be surgically removed in bothersome, but can go away on its own
53
gangrenous necrosis
- severe hypoxic injury
- interrupted blood supply
- medium for bacteria growth and it is impending health wound healing
54
dry gangreen
- result of coagulative necrosis
- bllod supply is slowly reduced
- skin becomes dry, wrinkled, skin changes to dark brown or black
55
wet gangreen
- blood supply is suddenly reduced
- pus is release, very painful
56
Gas gangreen
- infection of the injured tissue by Clostridium (bacteria)
- blood supply is reduced
- produce hydrolytic enzymes and toxins that destroy connective tissues and cause gas bubbles
57
Innate immunity
- what we are born with
- includes physical, chemical and cellular defenses against pathogens
58
what is the most common cause of cellular death
hypoxia
59
what happens in inflammation to cause hypoxia
- increase in the metabolic demands of cells and reduction in metabolic substrates (energy producers) caused by thrombosis, trauma, compression, or atelectasis
60
What happens in hypoxia to cause inflammation
- mainly oxidative stress, acidosis, and apoptosis
61
What leads to the visible inflammation
- rapid leakage of K+
62
who are the first responders
- inflammatory cells and cytokines
- begin inflammatory response and trap bacteria and other offending agents or start healing of injured tissue
63
Major events in local inflammatory response
macrophages are activated, capillaries dialate and become more permeable, fluid clooting agents move into tissues, clotting begins, chemokines release phagocytic cells, attracts netrophils/macrophages to engulf pathogens/debris, healing begins
64
what are sings of infection
- redness
- swelling
- pus
65
Hallmark signs
heat, pain, redness, swelling, and loss of function
66
pain is caused by
- systemic response
- fever and proliferation of leukocytes
- increased fluid at site triggers nerves
67
redness and swelling is caused by
- increased permeability
- fluid released into tissues
68
heat is caused by
- capillary widening which increases blood flow
69
tenderness is caused by
- attraction of leukocytes
- extravasation of leukocytes to the site of injury
70
Adaptive immune response (acquired immune system)
- has memory
- can develop due to an antigen or vaccination
71
inflammation is the ___ line of defense
2nd `
72
release of cytokines in Acute phase causes:
- fever caused by affect on hypothalmus
- increased neutrophil production cause by effect on bone marrow
- lethargy caused by effect on the CNS
- increased erythrocyte sedimentation rate (ESR) and increased C-reactive protein caused by affect on liver
73
Fever
- local activity
- caused by direct activity of cytokines or through local activity of prostaglandins
74
Lethargy
- stress induced
- cytokines increase energy within the cells
- taxing on the body
75
ESR
rate at which red blood cells settle in saline solution
76
ESR in someone with inflammation
- protein in plasma is increased in inflammation
- RBC's stack and become heavier
- settle out of solution faster
77
C - reactive protein
- made in the liver
- increases in response to inflammation
78
increased Sed rate and C reactive protein
inflammation
79
acute inflammation is caused by
- chemical irritants
- frostbite
- cuts, laceration, stabbing
- trauma
- allergic reactions
- burns
- infection
80
chronic inflammation is caused by
- cardiovascular disease
- autism
- rheumatoid arthritis
- autoimmune disease
- depression
- neurological disease
- alzheimers
- cancer
81
Acute inflammation
- less than 2 weeks, short term
- visible (easy to see, localized, quick to diagnose, responds to treatment)
- in response to physical and chemical damages, pathogen invasion, tissue necrosis..
- redness, increased blood flow and edema
- 5 cardinal signs: pain, heat, swelling, and limited movement
82
chronic inflammation
- not visible
- long term (years or months)
- related to unsuccessful acute inflammatory response
- no cardinal signs
- fibrosis and angiogenesis
83
fibrosis
permanent scar tissue
84
angiogensis
formation of new blood cells
85
in chronic inflammation, when macrophages are unable to protect the body, the body will form
granuloma cells
- attemt to wall of infected area
86
systemic signs of chronic inflammation
- fever
- lethargy
- increased ESR and C-reactive protein
- granuloma
- hyperplasia of spleen or lymph nodes
- fluid exudation and edema
- depression
- insomnia
- weight loss/weight gain
87
purulent (suppurative exudate
- consists of plasma with both active and dead neutrophils, fibrogen, and necrotic parenchymal cells
- commonly referred to as pus
88
necrotic parenchymal cells are commonly referred to as
pus
89
fibrinous exudate is composed mainly of
fibrogen and fibrin
90
what are the 3 stages of wound healing
1. inflammation stage
2. proliferation phase
3. remodelling phase
91
Inflammation stage
- platelets, neutrophils, and macrophages bring wound healing mediators, recruit fibroblasts which promote angiogenesis
92
proliferation stage
- fibroblast proliferation = collagen synthesis
- epithelization
93
remodelling and Maturation Phase
- cellular differentiation
- scar tissue formation
- scar remodelling (several weeks to 2 years)
- contraction (myofibroblasts)
94
primary intention
- clean incision, early suture, fine scar
95
Secondary Intention
- gaping wound
- granulation
- epithelium grows over scar
- loss of tissue
- wound is extensive and edges cant be brought together
- pressure ulcer
- good for contaminated/infected wounds
96
Tertiary intention
- open wound
- increased granulation
- late suturing
- allows for observation of wound
- delayed primary closure
97
complications of wound healing
- adhesions
- strictures and contractures
- infection
- dehiscence and evisceration
- excess scar formation
98
adhesions
abnormal union of membranous surfaces due to inflammation or injury
99
Strictures and Contractures
- excess of wound contraction
- burn victims
- luzo gloves
100
infection
- wound re-infects with initial pathogen or is contact with an external pathogen
101
dishescence and evisceration
- seperation of wound edges or intraabdominal contents come out of the surgical wound
102
excess scar formation
- hypertonic scare are confined with the original wound bed
- keloid scars extend beyond
- caused by excess tension/movement
103
dysfunctional wound healing can be caused by
- blood supply
- obesity
- excessive fibrin
- diabetes
- wound infection
- nutrition
- medications
104
ischemic tissue (dysfunctional wound healing)
- suceptiable to cellular death
- prolongs inflammation and delays healing
105
excessive bleeding (dysfunctional wound healing)
- large clots increase space granulation must fill
106
decreased blood volume (dysfunctional wound healing)
inhibits inflammatory process
107
obesity (dysfunctional wound healing)
- impaired leukocyte function
- predisposes to infection
108
excessive fibrin (dysfunctional wound healing)
- fibrin released needs to be reabsorbed to prevent formation of fibrous adhesions
109
Diabetes (dysfunctional wound healing)
- prolonged wound healing
- potential for small vessel disease
- hyperglycemia
- suppression of macrophages
- risk for infection
110
medications (dysfunctional wound healing)
- Antineoplastic (slow cell divsion and inhibit angiogenesis
- NSAIDS (delayed wound healing)
111
steriods (dysfunctional wound healing)
prevent macrophages form migrating to site
112
NSAIDS
- work against inflammatory process
- decreased permeability
- delays healing
