Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
56 Cards in this Set
- Front
- Back
|
When might a PT provide intervention for a wound?
|
they will help promote chronic wounds by secondary intention
|
|
|
How might a chronic wound be described?
|
- wound whose progression through the phases of healing is prolonged or arrested because of underlying conditions
|
|
|
What does it mean if a chronic wound has an absent phase? Which phase might be absent?
|
absent: absent proliferation, moved through the inflammatory phase but never progressed
|
|
|
What are 7 things that can go wrong with a normal healing wound?
|
1. infection
2. perfusion (inadequate blood supply) 3. hydration (too wet or dry) 4. nutrition (how many calories are they taking in?) 5. excessive/prolonged inflammation (chemical or mechanical trama) 6. trauma (in a tissue) 7. wound senescence (absent phase don't look bad, but just aren't going anywhere) |
|
|
What are factors involved with perfusion?
|
- it is NECESSARY for full inflammatory process
- brings in WBCs to remove necrotic tissue - need O2 to support the healing process - carry away metabolic byproducts and tissue breakdown components |
|
|
What are factors involved with hydration during wound healing?
|
- moist wounds heal the best
- too wet or dry is problematic (can impair O2 diffusion, wet skin is weaker, dry wounds are more prone to inflammation, crusting, and impaired epithelialization) dry skin: loses its electrical signaling, epithelialization doesn't happen effectively |
|
|
What are factors involved with nutrition during wound healing?
|
- necessary to provide wound healing substrates
- not only reduced intake (also GI conditions and medications) - loss of subcutanous tissue (fat soluable vitamins A, D, E, and K) |
|
|
Which vitamins are fat soluable?
|
A, D, E, and K
|
|
|
What are factors involved with inflammation during wound healing?
|
- can be from repetative trauma or unrelieved trauma
- tissue damage - delayed revascularization |
|
|
What are factors involved with trauma during wound healing?
|
- mechanical (mobility, sensation, treatment related)
- chemical (inflammatory, antiseptics) |
|
|
What mechanical trauma for chronic wounds, what might this include?
|
turning schedule, not getting up, excessive trauma on skin, ill-fitting WC, poor sensation
|
|
|
What are factors involved with senescence during wound healing?
|
- associated with aging
- reduced growth factors in exudate from chronic vs. acute wounds (will inhibit proliferation of normal, healthy cells) **controlled trauma may jump start system into healing up - |
|
|
With senescence, all cell types exhibit reduced or impaired .... (3)
What modalities could be used and why? |
- rate of replication
- protein synthesis (fragmented fibronectin) - motility Estim or US might reset normal response signals |
|
|
What is fibronectin and how is it involved in the wound healing process?
|
it promotes proliferation and epithelialization
fetal wounds are high in fibronectin and they heal completely without a scar |
|
|
What are hallmarks of a wound with a chronic inflammatory phase? (3)
|
1. signs of inflammation (out of proportion, too long of a time)
2. prominent necrotic tissue (d/t the prolonged inflammation) 3. some drainage with a variable appearance |
|
|
What are the hallmarks of a wound in a chronic proliferation state? (3)
|
1. pale (d/t decreased granulation tissue)
2. hypo or hypergranulation 3. tissue integrity not re-established |
|
|
What are the hallmarks of a wound in a chronic epithelialization state? (3)
Define epiboley. |
1. rolled wound edges
2. edges may be disconnected from wound bed 3. hypertrophic scarring Epiboley: rolled in on itself, won't come across to close the wound |
|
|
What percentage of wounds are d/t arterial insufficiency? what is the cause?
|
10-15%
impaired oxygenation - associated with LDLand blood lipids, DM, smoking, NV disorders (Raynaud's Syndrome, Buerger's Disease) |
|
|
What sort of an insult does it take to get an arterial insufficiency ulcer?
|
minor insults can set off chronic wounds
- metabolic supply can't meet the demand (when combined with PVD, creates an ulcer that just won't heal) **these are difficult to treat conservatively |
|
|
Address the 7 factors of wound healing for arterial insufficiency ulcers.
|
1. infection -- decreased immune cells to area
2. perfusion -- decreased 3. hydration -- fairly dry 4. nutrition -- goes with perfusion, problematic at local level 5. excessive/prolonged inflammation -- decreased, but stay in phase for a long time 6. trauma -- minor trauma 7. senescence -- don't get perfusion/hydration so don't progress to the next phase |
|
|
What type of bacteria might present in an arterial insufficiency ulcer?
How might an infected ulcer present in an AI patient? |
1. wound has dec. oxygen, many microbes function anaerobically (staphylococcus aureus)
2. malaise: feel sick, lethargic, run down - they have an infection but fail to mount a proper immune response, systemic conditions take longer to treat |
|
|
What is an intervention for AI?
|
fem-pop bypass (vascular bypass)
walking program for conservative treatment which can induce collateral circulation |
|
|
What is the chief symptom of AI?
|
initially, asymptomatic
-intermittent claudication: pain when walking, ischemic discomfort (50%+ occlusion) |
|
|
What if an AI patient has pain at rest. What might this indicate?
|
they have increased pain when resting and elevating their feet
- more serious - conservative treatment less likely to be successful (walking) |
|
|
What affect does walking (conservative treatment) have on AI patients?
|
many were able to double the distance they could originally walk before developing pain after 6 months of slowing improving their walking distance
- induces collateral circulation |
|
|
What percentage of ulcers are due to venous insufficiency?
What is the cause of a venous insufficiency ulcer? |
70-90%
results from a cycle of venous HTN, backflow and distension |
|
|
What is venous stasis?
|
statis blood, sitting in one area instead of being returned to the heart
- vascular trauma (inflammation) - impaired flow (WBC trapping -- a lot of pressure, hard for them to diffuse through the walls) - unwanted activation of clotting pathways -- fibrin in the area causes an increased risk of an embolus |
|
|
Compare and contrast trauma needed to induce VI and AI ulcers.
|
either may result from minimal trauma, however, the venous insufficiency ulcer is much more likely to result from a spontaneous ulceration d/t the excessive edema present
|
|
|
How are the 7 factors of wound healing affected with a venous insufficiency ulcer?
|
1. infection -- inc. but not as musch movement of proteins (mainly once wound opens)
2. perfusion -- dec, pressure in the area closes down vessels) 3. hydration -- too much, inc. edema 4. nutrition 5. excessive/prolonged inflammation -- lots of inflammation/drainage (expect infection when there isn't one) 6. trauma -- can be minimal, but likely spontaneous d/t excessive edema 7. senescence -- not progressing |
|
|
What color is the limb of someone who has venous insufficiency?
|
see hemosidering staining -- break down from blood, brown/dark pigmentation
|
|
|
Which (AI/VI) ulcer has a better response to conservative treatment?
Which one is likely to reappear after healing? |
VI responds better to conservative treatment (AI can't meet metabolic demand, impaired oxygenation, usually requires surgical intervention)
VI more prone to reoccurence |
|
|
What is the mechanism for developing a pressure ulcer?
|
localized tissue necrosis resulting from mechanical compression
- perpendicular force per unit area - problem with perfusion (an ischemic injury, inflammatory response varies with vascular status) |
|
|
Where are places that could develop pressure ulcers?
|
bony prominences (sacrum, coccyx, trochanters, heels)
nostrils from nasal canula, scapl from immobilization while on vent places where body parts "kiss" (knees, butt, joint spaces where there are contractions) |
|
|
What is the main emphasis for treating a pressure ulcer?
|
PREVENTION moreso than any other type of ulcer, these can cost around $70K/ulcer
|
|
|
At what pressure do the capillaries close down?
What pressure is applied to butt when in supine? Ischial tuberosities in sitting? |
13-32 mmHg
Butt/supine: 70 mmHg Ischial tuberosities/sitting: 300 mmHg |
|
|
What relationship determine whether a patient is at risk for developing a pressure ulcer?
|
time--intensity relationship (how long have they not moved, how much pressure is applied to the area)
|
|
|
How do we begin to treat pressure ulcers?
|
must REMOVE pressure or it won't heal
|
|
|
Where do pressure ulcers begin?
|
- pressure ulcer begins from inside out d/t decreased blood flow = inc. ischemia (epidermis relies on the dermis for vascularization so the insides starts to break down)
|
|
|
What are intrinic risk factors for developing a pressure ulcer? (4)
|
1. age
2. smoker? 3. nutrition 4. comorbidies (mobility, sensation, previous ulcers) |
|
|
What are 4 things to consider for extrinsic risk factors for developing a pressure ulcer?
|
1. moisture (breakdown of skin, incontinence)
2. shear (force parallel to tissue, compromise/injury vasculature, tear drop wound) 3. friction (weakens epidermis) 4. inappropriate care (antiseptics/donuts which increase pressure around ulcer and worsen the condition) |
|
|
What is another term for neuropathic ulcers and why might this not be the best alternate name?
|
diabetic ulcers, someone without DM can have an neuropathic ulcer
|
|
|
What is a neuropathic ulcer? How big of a problem is this type of ulcer?
|
a problem in the DM population
- 80% result in amputations - 50% have a contralateral amputation within 1.5 years - 3 year survival rate post-amputation -- 35-50% |
|
|
What are the 3 types of neuropathies? How do they contribute to chronic wound development?
|
1. sensory -- don't feel the noxious stimulus
2. motor -- can't move well, loss of intrinsic musclulature, changes the pattern of walking 3. autonomic -- CV, moisture management |
|
|
What other factors (other than neuropathies) are at work for the patient with DM with a chronic ulcer? (4)
|
1. vascular problems leading to neuropathies
2. poor nutrition/metabolism 3. effect specific to insulin deficiency? 4. trophic changes in denervated skin |
|
|
What sorts of trophic changes are seen in the DM patient with a chronic ulcer?
|
- defective collagen synthesis (decreased type I, increased type III)
- reduced adrenergic receprors - loss of GAGs to urinary excretion (usually hold onto these) - shiny skin, lack of hair on toes |
|
|
What type of neuropathy is at greatest risk for developing a neuropathic ulcer?
What size microfilament is the threshold for protective sensation? |
sensory neuropathy (repetative trauma that isn't felt)
5.07 filament (at greater risk for pressure ulcer if they can't feel this) |
|
|
What is the best strategy for treating a neuropathic ulcer?
|
similar to the pressure ulcer, PREVENTION is the best medication
- education (DM education and foot/ulcer care) **multiple pathologies make for a poor prognosis |
|
|
Why does having a sensory neuropathy put someone at a greater risk for developing an ulcer than the other 2 types of neuropathies?
|
motor is a problem as well as autonomic, but if you have sensation you can correct for these
|
|
|
What are the treatment strategies for the different types of ulcers?
|
Arterial Insufficiency: fem-pop bypass, walking/conservative program
Venous insufficiency: compression to help return the blood to the heart Pressure: removal all external forces |
|
|
How is perfusion impared with the different types of ulcers?
|
AI: arterial, problem with the supply line getting blood to the areas
VI: edema, pressure builds up so nothing can get in Pressure: prolonged pressure decreases/cuts off all circulation to the area |
|
|
What are the underlying causes of impairments for the different types of ulcers?
|
AI: arterial dysfunction causing impaired tissue oxygenation
VI: venous HTN, backflow, distension, vascular trauma, WBC trapping, unwanted activation of clotting pathways Pressure: prolonged shear/friction/moisture causing skin breakdown |
|
|
What type of neuropathy is at greatest risk for developing a neuropathic ulcer?
What size microfilament is the threshold for protective sensation? |
sensory neuropathy (repetative trauma that isn't felt)
5.07 filament (at greater risk for pressure ulcer if they can't feel this) |
|
|
What is the best strategy for treating a neuropathic ulcer?
|
similar to the pressure ulcer, PREVENTION is the best medication
- education (DM education and foot/ulcer care) **multiple pathologies make for a poor prognosis |
|
|
Why does having a sensory neuropathy put someone at a greater risk for developing an ulcer than the other 2 types of neuropathies?
|
motor is a problem as well as autonomic, but if you have sensation you can correct for these
|
|
|
What are the treatment strategies for the different types of ulcers?
|
Arterial Insufficiency: fem-pop bypass, walking/conservative program
Venous insufficiency: compression to help return the blood to the heart Pressure: removal all external forces |
|
|
How is perfusion impared with the different types of ulcers?
|
AI: arterial, problem with the supply line getting blood to the areas
VI: edema, pressure builds up so nothing can get in Pressure: prolonged pressure decreases/cuts off all circulation to the area |
