Unit 1 Flashcards
How thick is the epidermis?
0.06 - 0.6 mm
How thick is the dermis?
2 - 4 mm
What are the 5 layers of the epidermis?
CLGSB
Stratum Corneum
Stratum Lucidum
Stratum Granulosum
Stratum Spinosum
Stratum Basale
Which layer of the epidermis is the thickest?
Stratum Corneum
Which layer of the epidermis is only found in the palms and soles of the feet?
Stratum Lucidum
Which layer of the epidermis is the water resistant barrier?
Stratum Granulosum
Which layer of the epidermis is also known as the prickly layer?
Stratum Spinosum
Which layer of the epidermis is the deepest layer and contains stem cells?
Stratum Basale
Which cell of the epidermis is responsible for light touch sensation?
Merkel cells
Which cell of the epidermis fights infection?
Langerhans
What is the function of mast cells?
Chemical mediators for inflammation - when you get a scratch and the area becomes raised, that is due to histamine released by mast cells
T/F: The dermis can regenerate.
False - the dermis is replaced with scar tissue
How do blisters occur?
Friction between the epidermis and dermis
What tissues are involved in superficial wounds?
Epidermis only
What tissues are involved in partial-thickness wounds?
Epidermis and Dermis
What tissues are involved in full thickness wounds?
Epidermis, dermis, subcutaneous tissue, may extend to sub-dermal layers
What is the purpose of the inflammatory stage of healing?
Control bleeding, fight germs and bacteria
What is the purpose of the proliferation stage of healing?
Growth and production of cells, produce tissues required to close the wound
What are the 4 crucial events that occur in the proliferation stage?
AGCE - A girl can eat
Angiogenesis
Granulation Tissue Formation
Wound Contraction
Epithelialization
What wound shape contracts the slowest?
Circular wounds
What is the function of fibroblasts?
Build granulation tissue
What is the function of myofibroblasts?
Cause wound contraction
What is the function of keratinocytes?
Re-epithelialize the surface of the wound
What is primary closure?
Simplest and quickest form of closure; the wound is clean, edges are approximated by sutures/staples/wound glue
What is secondary closure?
Wound is too large for edges to approximate and must heal by going through phases of healing
What is delayed primary closure?
Combination of primary and secondary closure; dirty wound left open for healing
T/F: Inflammation is necessary for healing.
True - it is the first stage of healing
Which wounds are considered at risk for hypertrophic scarring/keloids?
Wounds that cross joints, prolonged proliferation stage, burns
What is the difference between a keloid scar and hypertrophic scar?
Keloids extend outside the margin of the original wound
Why are scabs poor for wound healing?
Scabs are collections of dead cells and proteins that retard epithelial cell migration
What are arterial wounds?
Wounds that result from a lack of blood flow which deprives the area of oxygen
Etiology of arterial insufficiency
Trauma - damage to an artery
Acute embolism
DM
RA
Thomboangitis (Buerger’s disease)
Arteriosclerosis - thickening/hardening of vessels
What conditions can AI typically present with?
Intermittent claudication or Ischemic rest pain
What is intermittent claudication?
Activity-specific discomfort due to local ischemia
Pain stops within 1-5 mins of ceasing the activity
Pain characterized as cramping, burning, fatigue
What is ischemic rest pain?
More significant arterial disease
Burning pain is exacerbated with elevation and relieved by dependency
What is the progression of AI to an ulcer?
AI > Intermittent claudication > Ischemic rest pain > Ulcer
Dry vs wet gangrene
Dry = stable; circulation proximal to wound; body would be able to close it off and start to heal underneath and toe would fall off
Wet = requires surgery; shows signs of infection
What are some contributing factors to arterial disease?
Smoking
Trauma
HTN
DM
Generally, what shape and where do arterial insufficiency wounds present?
Circular shape
Primarily LE, distal toes, dorsal foot
Where is the common site for occlusion?
Common femoral artery bifurcation
What test is the first you should do when suspecting arterial insufficiency?
ABI
What is a normal ABI range?
0.9-1.1
What is TCOM?
Transcutaneous oxygen monitoring - used for slow healing wounds, measures healing potential (notebook for values)
What are some PT management techniques for AI?
General considerations and education
Address etiology and modifiable risk factors
Limb protection education - protect from trauma, chemicals (including caffeine), excessive heat/cold, open wounds
Healthy living - diet, exercise, meds, smoking, proper footwear
When to contact MD
Protect surrounding skin - moisturize, avoid adhesives, reduce friction between toes
What types of therapeutic exercise can pts with AI participate in?
Gait training and mobility
Aerobic conditioning - usually have CAD
Resistive exercise
Stretching
Positioning - avoid excess knee and hip flexion
What is venous insufficiency?
Condition where the veins, particularly in the LE have difficulties sending blood back to the heart
Which type of vein carries 80-90% of blood back to the heart?
a) Deep
b) Superficial
c) Perforating
Deep
Which type of vein is subject to trauma?
a) Deep
b) Superficial
c) Perforating
Superficial
Which method is the main way we get blood back to heart?
a) calf muscle pump
b) respiratory pump
c) valves
Calf muscle pump
What is the etiology of VI?
Sustained venous HTN
T/F: Most VI appears to be caused by reflux.
True
What is the WBC trapping theory?
Congestion and distention is caused by VI. Distention encourages WBC to come to the area which further increases congestion. WBCs adhere vessels walls and become trapped. They then trigger the inflammatory response which encourages more cells to an already congested area as well as WBC releasing substances that further damage endothelial lining of veins. Ulcer ultimately will develop from local hypoxia caused by trapped WBC and congestion. This is why VI was once called venous stasis ulcers.
What is fibrin cuff theory?
Suggests that the distention by venous HTN will make the veins leaky. These leaky veins allow proteins to escape into interstitial tissue causing swelling or edema. One of the proteins = fibrinogen which converts to fibrin which adheres to capillary walls and prevents oxygen and nutrient exchange which leads to death of skin and ulcer develops.
What are the risk factors for VI ulcer development?
Vein dysfunction
Valve damage
Calf muscle pump failure
Trauma
Previous VI
Advanced Age
Obesity
DM
What is the gold standard for clinical assessment for DVT?
Venogram
Wha’s the average healing time for venous ulcers?
8 weeks
What are contraindications to using compression on VI pts?
ABI < 0.5
Acute infection
Pulmonary edema
Uncontrolled or severe CHF
Active DVT
Claustrophobia (relative)
T/F: Short stretch compression wrap has a high working pressure and a low resting pressure.
True
T/F: Pressure ulcers may not develop for days after pressure application.
True
Risk factors for PI
Shear
Anhydrous skin and moist skin
Incontinence
Prevention of PI
Education - daily skin checks, position changes, transfer techniques, incontinence mgmt
Positioning
Mobility
Nutrition
Mgmt of incontinence
Prognosis of PI
Heal very slowly
Stage 1 = 1-3 wks
Stage 2 = 23 days
Stage 3-4 = 8-13 wks
At what time frame should PIs be reassessed for alternative/adjunctive interventions when they are not decreasing in size?
2 weeks
What is Charcot foot?
Tarso-metatarsal joints are most affected, and the bones start to fracture. They end up looking like they have rocker bottom sole so the mid foot collapses and there’s a pressure point on the bottom of the foot
Which location of ulcer heals faster: forefoot or heel?
Forefoot
What gait pattern is used to decrease plantar pressure?
Step-to pattern
T/F: MLD can be used on any kind of edema.
True
Zone of coagulation
Central portion, irreparable damage
Characterized by coagulation, ischemia, necrosis
Zone of Stasis
Area of cellular injury and compromised perfusion
Conversion - widening and deepening of necrosis
Zone of Hyperemia
Outer edges, minimal cellular injury