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Cardiopulm Patho > Pressure Ulcers > Flashcards

Pressure Ulcers Flashcards

1
Q

what is the pathophys behind pressure ulcers caused by presssure

A

unrelieved external pressure results in localized ischemia and/or necrosis of the underlying tissue

  • tissue damage w/ high pressures for short time or low pressures for long time
    note: “excess” pressure changes per tissue tolerance in each patient
  • average of capillary closing pressure in arterioles = 32 mmHg
  • average of capillary closing pressure in venules = 12 mmHg
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2
Q

what is the pathophys behind pressure ulcers caused by shear forces

A
  • acts parallel to skin’s surface, so skin is in fixed position but tissue underneath shifts, tearing the capillaries
  • may contribute to undermining and/or sinus tracts
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3
Q

what is the pathophys behind pressure ulcers caused by heat and moisture

A
  • moisture: causes maceration, which makes skin 5x more likely to breakdown than intact skin
  • heat: 1 deg C in skin temp=10% INC in tissue metabolism, but cutaneous capillaries can’t dilate to dissipate heat since pressure causes occlusion (create tissue hypoxia and necrosis)
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4
Q

what are the general risk factors to develop PU’s

A
  • decreased mobility
  • diminished mental capacity
  • incontinence (maceration)
  • PMH of PU’s
  • bed surfaces or tight clothing
  • medical devices
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5
Q

what are intrinsic risk factors to develop PU’s

A
  • malnutrition/dehydration since nutrients (calcium, vit C/A, zinc) are needed for collagen synthesis
  • prealbumin
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6
Q

stage 1

A

intact skin w/ non-blanchable redness of a localized area

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7
Q

stage 2

A

partial thickness loss of dermis, shallow ulcer w/ red/pink wound bed and NO slough or serum-filled blister
painful

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8
Q

stage 3

A

full-thickness loss, with possible slough and may be able to see subcutaneous fat

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9
Q

stage 4

A

full-thickness tissue loss and exposed bone, tendon or muscle, slough and eschar present

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10
Q

deep tissue

A

purple or maroon localized area of discolored intact skin or blood-filled blister
-usually progress to stage 3 and 4

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11
Q

unstageable

A

full-thickness tissue loss in which the base of the ulcer is covered by slough and/or eschar in the wound bed, so you can’t see what’s at the base

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12
Q

what is the pathophys behind neuropathic ulcers

A

numerous alterations occur in the structure/fxn of the foot, which leads to changes in weight bearing, posture, and gait to elevate focal pressure

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13
Q

what is the pathophys behind Charcot neuropathic ulcers

A
  • elevated BG from DM over long period of time cause this foot deformity
  • leads to: ankle equinus causing mechanical stress, increased peripheral blood flow due to sympathetic denervation, osteolysis or osteopenia, loss of protective sensation
  • cycle from fracture, healing and remodeling through a series of fractures due to perceived/unperceived trauma
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14
Q

what are the risk factors of neuropathic ulcers

A
  • DM >10 years
  • male
  • uncontrolled BG
  • peripheral neuropathy w/ loss of protective sensation
  • altered biomechanics
  • CV, retinal, or renal complications
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15
Q

what is a hallmark clinical sign of neuropathic ulcer

A

hyperkeratosis or callous formations

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16
Q

what is unique medical management of DFUs

A
  • total contact casting

- confirm vascular supple

17
Q

what is the pathophys of venous ulcers and where are they located

A
  • above malleoli
  • ambulation causes foot/calf muscle pumps to push venous blood up, which reduces venous pressure
  • if calf pump fails to activate conduit veins, pressure increases in the veins and ulcers develop from inc. internal pressure
  • venous thrombosis, obstruction, and hemorrhage all contribute as well
18
Q

describe how venous thrombosis increases likelihood of venous ulcers

A

as platelets adhere to endothelial walls and lumen become occluded, valves become damaged which can INC internal pressure

19
Q

describe how venous obstruction INC likelihood of venous ulcers

A
  • when obstruction is in superficial veins, rarely form ulcer b/c collateral vessels compensate
  • when obstruction is in deep veins, increase swelling and ulcer formation
20
Q

what is key component of med management

A
  • compression and calf muscle pump

- should heal w/l 1 mon

21
Q

what is clinical presentation of venous ulcer

A
  • distal medial third of leg
  • swelling, aching, heavy
  • pain worse in standing and better with elevation
  • hemosiderin staining from blood leeking
22
Q

what are med diagnostic tests for venous ulcers or arterial wounds

A
  • ABI
  • doppler US
  • venography or arteriogram
23
Q

what is the pathophys behind arterial insufficiency causing wounds

A

structure of arterial wall changes due to:
-lumen narrowed by lipid plaque (DM, smoking, HTN, older than 50)
-vasomotor diagnoses: Raynaud’s
structural changes cause lack of adequate perfusion, leading to ischemic skin changes and necrosis

24
Q

how can progression of arterial wounds be slowed down

A

exercise promotes growth of collateral vessels in patients w/ intermittent claudication
-Contraindicated in patient’s w/ critical limb ischemia (ABI

25
Q

what is the typical clinical presentation of arterial wounds

A
  • pain w/ elevation
  • diminished pulses
  • pale, dry wound base w/ little drainage
  • thin, shiny, and hairless skin
  • hypertrophic nails
  • ABI
26
Q

what is the med management of arterial wounds

A
  • angioplasty or stents
  • limb protection techniques
  • exercise if indicated
  • thrombolytics
27
Q

what is the pathophys of surgical wounds

A

risk factors for dehiscence (surgical wound re-opening):

  • infected wound
  • DM
  • high dose steroids
  • bacterial lvls
  • mechanical stress from malnutrition, compromised perfusion, and ab incision w/ coughing or sternal incision w large breasts
28
Q

what are the 2 different skin flap location in LE amputations? what are the 2 types of skin flaps?

A
  • equal ant. and post. flaps
  • longer post. flap
  • myoplasty: muscle-to-muscle (agonist and antagonist) for stailization
  • myodesis: muscle to bone for transtibial amps
29
Q

how can you differentiate between superficial and deep wound infections

A
  • superficial (NERDS): Non-healing, exudate increase, red/friable tissue, debris present, smells (topical therapy)
  • deep (STONEES): size increasing, temperature increasing, osteomyelitis, new/satellite wounds, erythema, edema, and smell (systemic therapy, 3+ of either of these is indication)
30
Q

how can you prevent surgical wound dehiscence

A

pre-op: no anti-coagulants, good diet, no smoking

post-op: blood volume, maintain warmth for vasodilation, BG

Cardiopulm Patho (4 decks)

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