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Basic PT Skills F10
Skin conditions
| Question | Answer |
|---|---|
| Functions of the Skin | -thermoregulation -sensation -synthesis of Vitamin D |
| Name the layers of the skin | epidermis and dermis |
| Epidermis | -outer layer -thin (.006 to .6 mm) -lines hair follicles, sweat and sebaceous glands -fingernails and toenails -cellular, avascular- depends on dermis for blood supply -constantly being renewed (26-42 days) |
| What type of cells is the epidermis made of? | -Keratinocytes= 80-90% of cells in epidermis, produce nails and hair -Melanocytes= produce melanin (pigment) |
| Functions of the Epidermis | -protection from water loss -regulates fluid -protection from shear, friction and toxic irritants -synthesis of Vitamin D -pigmentation -assists with thermoregulation -outward appearance |
| Dermis | -thickest layer (2-4mm) -responsible for giving skin its bulk -is vascularized and innervated -major proteins are collagen and elastin |
| Two sub layers of the dermis | -Papillary Dermis -Reticular Dermis |
| Papillary Dermis | -outer most layer of dermis -forms dermal papillae that contain capillary loops that supply epidermis |
| Reticular Dermis | -forms base of dermis -contains complex of cutaneous blood vessels -has thick dense collagenous fibers which give structural support |
| Cells in the Dermis | -Macrophages -Lymphocytes -Mast cells -Fibroblasts |
| Macrophages | phagocytosis of bacteria and damaged tissue |
| Lymphocytes | produce antibodies which helps mediate the immune response in the skin |
| Mast cells | secretory cells that produce chemical mediators of inflammation (histamine) |
| Fibroblasts | secrete collagen and elastin |
| Dermal Proteins | -collagen: major structural protein -elastin: provides skin with elastic recoil |
| Basement Membrane Zone | -separates dermis from epidermis -anchors epidermis to dermis -layer where blisters form |
| Rete Ridges | -basement membrane -epidermal protrusions into dermis -height of ridges decrease with age, making you more at risk for skin tears |
| Hypodermis | -subcutaneous tissue forms a layer below dermis -attaches skin to underlying structures -composed of loose connective tissue and fat cells -well supplied (nn & blood) -subcutaneous fat insulates and protects underlying structures |
| skin changes with age | decreased: -dermal thickness -fatty layers, therefore protection loss -collagen and elastin fibers -decreased Rete Ridges (easier separation of two layers) -sensation and metabolism -sweat glands (dry skin) -circulation -epidermal regulation |
| Phases of Wound Healing | 1. Inflammatory 2. Proliferative 3. Remodeling |
| Inflammatory Phase | -lasts 3 to 7 days -provides hemostasis through platelet aggregation, formation of fibrin clot and vasocinstriction -provides removal of cellular debris through phagocytosis -growth factors are released (proteins that regulate and mediate cell activity |
| Signs of Inflammatory Phase | -color change in skin -increased skin temperature -increased swelling -increased pain -loss of function |
| Proliferative Phase | -3 to 5 days post injury -overlaps and succeeds inflamm phase -fills in wound defect through new tissue formation -processes used are andiogenesis, collagen synthesis and wound contraction -growth factors help mediate process |
| Important Cells in the Proliferative Phase | -fibroblasts -myofibroblasts -endothelial cells |
| Epithelialization | reconstruction of injured epithelium by kerotinocytes -occurs in the proliferative phase |
| Remodeling Phase | -begins after granulation tissue forms and continues 1-2 years post injury -increases tensile strength in the scar -final max strength of scar will be 80% of pre-injury tissue |
| Chronic Wound Characteristics | -failure or delay of healing -cells unresponsive or senescent -often caused by disease or condition -medications such as steroids or immunosuppressive drugs can affect healing |
| What to Include in a Wound Assessment | -Medical History -Current and past wound history -medications -social and psychological history -Musculoskeletal assessment -Pain -Sensation |
| Data About the Wound | -wound location (position on a clock; 12:00=head) -wound size (measure and tell directions of measurements- also depth) -tissue type and colors -include % of each -amount, color and odor of drainage -condition of skin surrounding -include a photograp |
| Tunneling | -a small tight area of depth extending out from the wound base -also referred to as sinus tract or just tract |
| Undermining | -eroded area extending under the skin beyond the visible wound edges -wider than tunneling |
| Granulation Tissue | temporary scaffolding of vascularized connective tissue |
| Hypergranulation | granulation tissue that has grown above the level of the surrounding skin |
| Necrotic tissue | -slough -usually yellow or tan -stringy or soft -leathery appearance if dry -Eschar -black -can be soft or hard -usually dry and thick -indication that underlying damage is most likely severe |
| Attached Wound Edges | -not very deep -wound heals faster |
| Unattached Wound Edges | usually deeper damage or undermining |
| Defined Wound Edges | associated with deeper wounds |
| Undefined Wound Edges | associated with superficial wounds where epithelialization is occuring |
| Rolled Wound Edges | -indicate chronic wound -healing can be stalled |
| Turgor | -decreased turgor is a sign of decreased hydration -Lightly pinch skin. if it does not quickly return to normal shape, sign of decreased turgor |
| Induration | -abnormal firmness surrounding wound bed -can indicate infection |
| nonblanchable erythema | can indicate ischemic damage due to pressure (important in staging pressure ulcers) |
| Periwound Skin color- Pale | can indicate decreased blood supply |
| Periwound Skin color- blue or ourole | can indicate severe or prolonged ischemia |
| Wound Drainage- Serous | clear or pale yellow, watery consistency |
| Wound Drainage- Sanguinous | red or dark brown, consistency more like blood |
| Wound Drainage- Serosanguinous | red or brown tinted, more watery that sanguinous |
| Wound Drainage- Purulent | -usually yellow, thicker consistency -can indicate infection or could be liquifying necrotic tissue |
| Wound Drainage- blue or green color | -indicates Pseudomonas infection- notify physician |
| Wound Drainage | -amt documented as minimal, mod, ma, or strike through; based on dressings -type of dressing and frequency of dressing change can affect amt -some dressings can alter appearance |
| Wound odor | -documented as present or absent -can indicate infection -so occlusive dressing will cause odor (not infection) -assess for odor throughout treatment as odor may be present on dressings but disappear after wound bed is cleaned |
| Pressure Ulcers | -area of tissue necrosis caused when soft tissue is compressed between a bony prominence and a firm surface over a long period of time |
| Prevalence of Pressure Ulcers | over 1.3-3 million Americans |
| Highest pressure areas (regarding pressure ulcers) | -supine= occiput, sacrum, coccyx, heels -sitting= ischial tuberosities -sidelying= trochanters |
| Risk Factors for PUs | -shear -friction -moisture -impaired mobility -malnutrition -impaired sensation -advanced age -previous pressure ulcer |
| Shear | -force parallel to soft tissue -common cause is hospital bed with head elevated causing pt to slide down in bed -stretch on the tissues causes ischemia -undermining is commonly seen |
| Friction | -caused when two surfaces move across each other -as in sliding a pt from a bed to a cart -does not directly cause PUs but can weaken skin and put pt more at risk |
| moisture | -wet skin is more easily abraded, more permeable and more readily colonized by bacteria -caused by wound drainage, perspiration or incontinence |
| Prevention of Pressure ulcers | -Identify those at risk -education -positioning -mobility -nutrition -management of incontinence |
| Scales for assessing PU risk | -Braden Scale for Predicting Pressure Sore Risk -Norton Risk Assessment Scale |
| Pressure Ulcer: Stage I | -nonblanchable erythema of intact skin -in those with highly pigmented skin, it may appear purple, blue or violet |
| Pressure Ulcer: Stage II | -partial thickness loss of dermis -presents as shallow, open ulcer with red/pink bed -no slough -may be an intact or rupture blister |
| Pressure Ulcer: Stage III | -full thickness tissue loss -subcutaneous fat may be visible but no bone, tendon or muscle exposed -may include undermining or tunneling |
| Pressure Ulcer: Stage IV | -full thickness tissue loss with exposed bone, tendon or muscle -slough or eschar may be present -often will have undermining or tunneling |
| Pressure Ulcer: Unstageable | -full thickness tissue loss in which actual depth of the ulcer is completely obscured by slough and/or eschar |
| Pressure Ulcer: Suspected Deep Tissue Injury | -Purple or maroon area of discolored intact skin or blood filled blister -tissue may be painful, firm, mushy, boggy, warmer or cooler as compared to adjacent skin -likely to evolve into deeper damage |
| Lower Extremity Arterial Ulcers | -caused by a decrease in arterial blood supply, or arterial insufficiency (PVD or PAD) -most common etiology is arteriosclerosis -most common problem seen by vascular surgeons |
| Signs of PAD | -thin atrophic skin -dependent rubor -pallor with elevation -absence of pedal pulses -non-healing wounds -muscle wasting -hair loss -hypertrophic nails |
| Pathophysiology of PAD/Arterial Ulcers | -decreased delivery of oxygen -tissue ischemia -tissue loss -decreased ability to fight infection -decreased healing |
| Risk Factors of PAD | -hyperlipidemia -smoking -one cigarette decreases wound & tissue O2 saturation by 30% in one hour in healthy indiv. -Diabetes -increased prevalence of calcific arterial insufficiency, increased prevalence of microvascular disease -adva |
| Assessing Arterial ulcers | -palpate pedal pulses -capillary refill (normal < 3 secs) -rubor of dependency -Ankle Brachial Index |
| Ankle Brachial Index | (ABI)= non-invasive measure of peripheral tissue perfusion -ratio of systolic blood pressure of LE to that of UE -easily done in clinic -just need hand held doppler and blood pressure cuff |
| Interpreting the ABI | 1.1-1.3= Vessel Calicification 0.9-1.1= Normal 0.7-0.9= Mild to mod arterial insuff. 0.5-0.7= Mod arterial insuff, intermitt claudication >0.5= Severe areterial insuff, rest pain >0.3= Rest pain and gangrene |
| Arterial Ulcer characteristics | -usually below the knee -common on tips & between toes, corners of nail beds, bony prominences -round, regular appearance w/ well marked edges -pale, dry base -skin can't feel cool -high pain levels -min to no wound drainage |
| Chronic Venous Insufficiency | -1-2% of pop is diagnosed -venous insufficiency ulcers are most common type of leg ulcer (70-90% of all ulcers) -up to 91% pf venous ulcers can be resolved through conservative measures -recurrence rate ranges from 13 to 81% (often due to noncompliance |
| Signs and Symptoms of Chronic Venous Insufficiency | -pain -spider veins -varicose veins -leg heaviness and fatigue -swollen limbs -skin changes and skin ulcers -hemosiderin staining |
| Hemosiderin staining | caused by RBCs leaked into interstitial fluid |
| Superficial Veins | -just beneath skin -drain into deep veins through perforator veins -can form varicose veins |
| Perforator Veins | -connect superficial and deep veins -perforate deep fascia ans they connect |
| Deep Veins | return blood to the heart |
| Vein Facts | -have thinner walls and increased diameter compared to arteries -90% of venous blood moves due to the calf muscle pump -venous insufficiency caused by incompetent valves due to thrombus or venous wall distension causing venous hypertension |
| Fibrin Cuff Theory | -vessel hypertension & distension cause incr in vasc perm -fluids leak from vessels into interst tissues causing edema -protein fibrinogen converts to fibrin & adheres to capillary walls -forming a cuff thats a barrier to xchange of nutr & causes necro |
| White Blood Cell Trapping Theory | -venous hypertension & distension=> congestion -decr BF => WBC to marginate on vessel walls impeding circulation -WBCs become activated & begin inflamm process -WBCs move into interstitium & release inflamm substances, further contribute to cell damage |
| Theories on Etiology of Venous Ulcers | Fibrin Cuff Theory White Blood Cell Trapping Theory |
| Risk Factors for Venous Ulcers | -vein dysfunction -calf muscle pump failure -trauma -previous venous ulcer -advanced age -diabetes -multiple pregnancies -obesity -standing profession -previous DVT -family history |
| Lipodematosclerosis | -progressive replacement of skin and subcutaneous tissue by fibrous tissue -skin will be thick, hard, contracted and tight -ankle is narrower- "inverted champagne bottle" -conversion to scar tissue -sign of long standing venous insufficiency |
| Venous Ulcers | -dull pain or heaviness incr standing -most common on med aspect of LE or med malleolus -rarely on knee, never on plantar surface -superf & irreg w/ mod to high amts of drain -ruddy gran tissue or slough -edema -periwound w/ dermatitis & dry scaling |
| treatment of venous ulcers | *compression -check ABI before using compression -underlying arterial disease= contraindication -lifetime compression (no cure for venous insuff) -maintenance of edema |
| Incidence of Diabetic/Neuropathic Ulcers | -caused by neuropathy (which is most often caused by diabetes) -incidence= as high as 25% |
| Incidence of Neuropathy in Diabetes | -30-40% of people with type II -even higher percentage of people with type I |
| Sensory neuropathy | -loss of sensation (starts in ft & can progress to hands) -gradual and painless (pt often unaware) -pt will not detect injury to ft & ulcer can develop |
| Motor Neuropathy | -affects intrinsic mm of ft -results in weakness & structural changes that cause increased plantar pressures & shear forces, making skin break down more easily |
| Autonomic Neuropathy | -loss of sweat & oil production -skin integrity is decreased and skin can be dry and cracked, making it vulnerable to breakdown |
| Signs of Neuropathic feet | -clawed toes -prominent metatarsal heads -small muscle wasting -dry, flaky skin |
| Charcot Foot | -Neuropathic fracture and dislocation -results in structural change in foot; arch reverses ("rocker bottom" foot) -causes increased plantar pressures |
| Risk Factors for Diabetic Ulceration | -vascular disease -DM leading risk factor in PVD -neuropathy -structural deformity -trauma and improperly fitted shoes -history of previous ulcer or amputation -limited joint mobility -uncontrolled hyperglycemia -poor vision (can't see ft to ch |
| Assessment for Diabetic Ulcers | -assess for signs of decreased circulation -joint ROM & strength -sensory assessment -inability to perceive 10g of monofilament indicates loss of protective sensation -assess for dry skin, foot deformities, callus formation |
| Treatment if Diabetic Ulcers | -refer to vascular surgeon if ABI warrants -dressing management -eliminate pressure over wound bed -change footwear if necessary *plantar ulcers must be offloaded (different boots/casts available- total contact casting=gold standard) |
| Types of burns | -scalds: liquid, grease, steam -contact burns -fire: flash & flame burns -chemical -electrical -radiation |
| Superficial Burns | -compare to 1st degree -epidermal damage only -redness, dry skin -painful to touch -peeling skin -blanch with pressure -complete healing, no scarring -sunburn/flash injuries |
| Superficial partial Thickness Burns | -compare to 2nd degree -entire epidermis and upper part of dermis is affected -blisters -wet, pink wound beds -good blood supply -low risk of infection -heals in 10-12 days w/o scarring |
| Deep Partial Thickness Burn | -compare to 2nd degree -epidermis and almost all of dermis affected -re-epithelialization is very slow -grafting usually done -lack of blister formation -dry, white or charred skin -minimal pain -high risk for infection -healing=2-3 months -sever |
| Full Thickness Burn | -compare to 3rd and 4th degree -desruction of entire epidermis and dermis -absence of pain -high risk for infetion -4th degree involves underlying fascia, muscle, bone or other structures -require extensive debridement and complex reconstruction |
| Debridement | -removal of necrotic tissue, foreign material & debris from wound bed -reduces bacterial load -stimulates production/release of growth factors -facilitates angiogenesis -eliminates physical barrier to wound healing -shorten inflamm phase -decr wound |
| Indications for Debridement | -necrotic tissue is impeding wound healing -epibole at wound edges -callus formation periwound -blisters |
| Contraindications for debridement | -viable tissue -stable heel ulcers: dry eschar need not be removed if they do not have edema, erythema, fluctuance or drainage -muscle, tendon, ligament, capsule, fascia, bone, nerves, tendons & blood vessels (surgery) -gangrenous tissue -ischemic wou |
| Autolytic debridement | -uses body's own enzymes to digest necrotic tissue through use of moisture-retentive dressing; left in place for several days -non-invasive -doesn't destroy healthy tissue (selective) -may be used along w/ other types of debridement -painless & simple |
| Enzymatic Debridement | -apply topical debriding agent to devitalized tissue on wound surface -Collegenase-Santyl: provides selective debr of collegen in necrotic tissue -selective -rarely painful -cross-hatch thick eschar to allow better penetration -prescription from phys |
| Mechanical Debridement | use of force to remove necrotic tissue, foreign material and debris |
| Wound Scrubbing | -type of mechanical debridement -use gauze or a sponge -non-selective so can damage and granulation tissue present |
| Wet to Dry dressings | -type of mechanical debridement -apply moistened gauze, allow to dry & adhere to wound tissue -when gauze is removed, tissue 'sticks' and is also removes -non-selective -painful |
| Whirlpool in wound debridement | -type of mechanical debridement -softens necrotic tissue -increases circulation -cleanses wound of exudate -loosens debris -removes residual topical agents -hydrates the wound bed -eases ROM for burn patients -can decrease pain -nonselective |
| Consequences of whirlpool in debridement | -may cause maceration -increase edema -can disrupt or damage healty granulation tissue -risk of cross contamination |
| Pulsed Lavage with Suction | -type of mechanical debridement -pulsed irrigation for cleansing combined w/ suction -good for large/multiple wound beds -return suction assists w/ debridement -can perform bedside -can be used on tunneling & undermining w/ use of diff application ti |
| Sharp Debridement | -involves use of forceps,scissors,scalpel to remove devitalized tissue -selective debridement -fastest methos after surgical interv. -can be painful (premidicate) -can be used with other methods -only certain people can perform |
| Electrical Stimulation on Wound Healing | -efficacy supported by research -High Volt most common -after 30 days of failed treatments, Estim is covered my medicare and medicaid -more appropriate for chronic,nonhealing wounds or patients at risk for wound healing |
| Ultrasound in wound healing | -research not very strong --indicated for chronic, nonhealing wounds that are clean or infected -wound bed is covered by protective barrier- transparent film dressing or sheet hydrogel -fill any depth with NS or hydrogel |
| Negative Pressure Wound Therapy (NPWT) | -sub-atmospheric pressure (suction) applied to wnd -dressing usually foam w/ semiocclusive film overlay -edema reduction -incr in profusion -tension-stress effect on cells; stim of gran formation w/ foam -removal of wnd exudate -promotes wnd contrac |
| Indications for NPWT | -chronic, acute and traumatic wounds -partial thickness burns -a wound that has burst open (gap) -pressure ulcers -neuropathic ulcers -muscle flaps -skin grafts -can be used over exposed bone, tendon, muscle or hardware |
| Contraindications to NPWT | -wounds with eschar -wounds with less than 70% gran tissue -untreated osteomyelitis |
| General Rules for Wound Dressings | -goal is moist wound healing -a moist wound heals 3-5 times faster than dry wound -let amt of drainage guide frequency of dressing change but keep to a min -can be limited by cost & availability -always cleanse wound bed perform applying dressing |
| primary dressing | -comes in contact with the wound bed -also known as contact layer |
| secondary dressing | -placed over primary dressing to provide protection, cushioning, absorption or occlusion |
| gauze | -can be used in wound scrubbing or cleansing -used to fill depth -removal can be traumatic |
| transparent films | -primary or secondary -partial thickness wounds -stage I or II PU's -low exudating wounds -see through -promotes autolytic debridement |
| hydrocolloids | -best for partial and superficial full thickness wounds -maintains moist environment -helps clean wounds and promotes autolytic debridement in necrotic wounds -not recommended for infections -sometimes causes hypergranulation -occlusive & can get wet |
| Effects of Estim of Wounds | -incr circulat & decr edema -inhib bacterial growth -incr epidermal cell prolif & migration -incr derminal fibroblastic activity- collagen secretion -incr phagocytosis bc attraction of macrophages & neutrophils -lysis of necrotic tissue -stim gran t |
Created by:
CWestrick
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