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NURS 2500 > CLASS 9 - TISSUE INJURY, PVD/PAD AND SKIN EXEMPLARS > Flashcards

CLASS 9 - TISSUE INJURY, PVD/PAD AND SKIN EXEMPLARS Flashcards

1
Q

What is tissue integrity?

What does it mean when tissue integrity is impaired?

A

State of structurally intact and physiologically functioning body tissues

Impaired tissue integrity reflects varying levels of damage to one or more tissues

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2
Q

What are the 2 types of cell injury?

A

Lethal + sublethal

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3
Q

What is sublethal injury? Is it reversable? Is it a normal physiological response or pathological? What is the goal when treating sublethal cell injury? What can it progress to?

A

Alters function of the cell w/o causing death.
Potentially reversible.
May be normal physiological response or pathologic
Goal is to remove injurious stimulus and limit injury
May progress to lethal injury

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4
Q

What are the 4 types of adaptive changes cells can make to sublethal injury?

A

ATROPHY (decrease in size)
HYPERTROPHY (overgrowth / increase in size)
HYPERPLASIA (increased #)
METAPLASIA (new type)

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5
Q

What are the 2 types of maladaptive changes cells can make to sublethal injury?

A

Dysplasia (abnormal change)

Anaplasia (increased amt of immature cells)

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6
Q

What are the 7 causes of lethal cell injury?

A
  1. Ischemia (hypoxic injury)
  2. Physical injury (heat, cold, radiation, electrothermal, mechanical)
  3. Chemical injury (free radicals)
  4. Infectious (Microbial) injury (virus, bacteria, protozoa)
  5. Immunological injury (autoimmune, antigen-antibody response)
  6. Neoplatic growth (benign or cancerous)
  7. Normal substances w unintended contact (ex - gastric acid leaks into abdominal cavity)
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7
Q

How does ischemia lead to lethal cell injury? How long does it take neurons to die? Cardiac muscle? What is a short term compensation this? Long term?

A

decreased arterial blood flow insufficient for tissue O2 demands leads to tissue hypoxia and impaired waste product removal.
Leads to cell death if not corrected.
Neurons > 5 mins til death begins
Cardiac muscle > 20 mins
short term compensation = anaerobic metabolism
Long-term: angiogenesis

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8
Q

what is angiogenesis?

A

“collateral circulation”

development of small arterial vessels from other arteries that re-route the blood around a blocked artery

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9
Q

What is treatment aimed at to reduce the adverse effects of tissue ischemia?

A

aimed at improving / restoring blood flow and increasing oxygen levels in the blood.

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10
Q

What is cell apoptosis? Is this a physiological or pathological response? Explain this process.

A

Programmed cell death, highly regulated and normal. Removes unnecessary, aging, or damaged cells to prevent the passing on of faulty genes.
Following death, the cell remnants are removed by pahgcytes. There is usually no symptoms or inflammation.
Physiological response.
Active process (requires ATP).

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11
Q

What is cell necrosis?

A

Severe, irreversible cell injury. Pathological response that leads to uncontrolled cell death. Cell will ultimately rupture and their products will remain in the blood, causing inflammation and collateral cell damage.

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12
Q

What are the 4 types of necrosis?

A

Coagulative
Liquefactive
Caseous
Gangrene (dry or wet)

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13
Q

Describe coagulative necrosis

A

Result of ischmia or free radicals. May have viable cells around it.

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14
Q

Describe liquefactive necrosis.

A

Bacterial (tissues dissolved by WBCs)

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15
Q

Describe Caseous necrosis.

A

C for cheese.

Tissue is no longer recognizable, looks like cheese.

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16
Q

Describe gangrene necrosis.

A

build-up of decomposing dead tissue. Referes to an appendage or limb w ischemic necrosis.

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17
Q

describe dry gangrene

describe wet gangrene

which type has the higher risk of injury to the patient? why?

A
  • looks dry and shrivelled. chronic/slow process, may not require debridement, may auto-amputate.
  • acute + quick. possibly caused by bacteria.

wet gangrene has a higher risk of injury t the patient, and has an even higher risk of more active destruction if there is a bacterial infection involved in addition to the original injury.

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18
Q

Define debridement.

A

The medical removal of dead, damaged, or infected itssue to improve healing in the remaining healthy tissue.

  • surgical removal (scraping, cutting away)
  • enzymatic creams and dressing to break down dead tissue
  • mechanical irrigation (syringe of NS)
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19
Q

What is regeneration?

What types of cells do not regenerate?

A

Replacement of lost cells and tissues w cells of the same type.
Permanent cells such as cardiac muscle and neurons of the CNS do not regenerate.

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20
Q

What are the 3 ways in which tissue repair can occur? Define them.

A
  1. PRIMARY INTENTION - 2 well approximated margins Imatched edges, precise) such as a surgical incision or paper cut
  2. SECONDARY INTENTION - wound w a wide or irregular margin that can’t be approximated (ulcers, erosion, trauma). Granulation occurs from the margins inward and the centre outward until the defect is filled in; results in a much larger scar than primary intention.
  3. TERITARY INTENTION - delayed primary intention for sanitary reasons (ex - contaminatd wound like a dog bite). Wound is deliberately left open and is later surgically closed.
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21
Q

What are the 3 ISTAP Skin Tear Classifications? Define them.

A

Type 1: No Skin Loss - linear or flap tear which can be repositioned to cover the wound bed.

Type 2: Partial Flap Loss - cannot be repositioned to cover wound bed.

Type 3: Total Flap Loss - exposes entire wound bed.

22
Q

What are the 6 forms of measurement on the Braden Scale for Predicting Pressure sore risk? Define them.

A
  1. SENSORY PERCEPTION - ability to respond meaninfully to pressure-related discomfort
  2. MOISTURE - degree to which skin is exposed to moisture
  3. ACTIVITY - degree of physical activity
  4. MOBILITY - ability to change and control body position
  5. NUTRITION
  6. FRICTION AND SHEAR
23
Q

Staging of Pressire Ulcers:

Describe the characteristics of a “Suspected Deep Tissue Injury”

A

Purple / maroon localized area of discolored intact skin or blood-filled blister due to damage of underlying soft tissue from pressure and/or shear

24
Q

Describe the characteristics of a Stage I Pressure Ulcer

A

Intact skin w non-blanchable redness of a localized area; usually over a bony prominence

25
Q

Describe the characteristics of a Stage II Pressure Ulcer

A

Partial thickness loss of dermis
Presents as a shallow open ulcer w a red/pink wound bed; no slough
May also present as an intact or ruptured serum-filled blister

26
Q

Describe the characteristics of a Stage III Pressure Ulcer

A

Full thickness tissue loss; subcut fat may be visible but not tendon, muscle, or bone.

27
Q

Describe the characteristics of a Stage IV Pressure Ulcer

A

Full thickness tissue loss w exposed bone, tendon, or muscle.

28
Q

Describe the characteristics of an Unstageable Pressure Ulcer

A

Full thickness tissue loss in which the actual depth of the ulcer is completely obscured by slough and/or eschar in the wound bed.

29
Q

Describe serous exudate. What types of wounds is it seen in? When is it normal?

A

thin, clear, watery plasma seen in partial thickness wounds and venous ulceration.
Normal in the acute inflammatory stage.

30
Q

Describe sanguineous exudate. What types of wounds is it seen in? When is it normal?

A

bloody drainage seen in deep partial-thickness and full thickness wounds during angiogenesis. A small amoung is normal in the acute inflammatory stage.

31
Q

Describe serosanguineous exudate. What types of wounds is it seen in? When is it normal?

A

Thin, watery, pale red-pink plasma w RBCs. Small amounts may be seen in the acute inflammatory or acute proliferative healing phases.

32
Q

Describe purulent exudate. What types of wounds is it seen in? When is it normal?

A

Thick, opaque drainage that is tan, yellow, green, or brown. Never normal and is often associated w infection or high bacteria levels.

33
Q

What are the 5 descriptors you can use whn describing the amount of wound exudate on an intact dressing (meaning you do not remove the dressing)? Define them.

A
  • None: wound tissues are dry
  • Scant: wound tissues moist but there is no measurable drainage
  • Small / Minimal: wound tissues are v moist or wet, drainage covers less than 25% of the dressing
  • Moderate: Wound tissues are wet, drainage involves more than 25-75% of the dressing
  • Large / copious: wound tissues are filled w fluid that involves over 75% of the dressing
34
Q

What are the 4 descriptors you can use when describing old (removed) wound dressing exudate? Define them.

A
  • Dry: primary dressing is unmarked by exudate; dressing may adhere to wound
  • moist: small amts of exudate are visible when the dressing is removed; the primary dressing may be lightly marked
  • saturated: primary dresing is wet and strikethrough occurs
  • leaking: dressings are saturated and exudate is leaking from primary and secondary dressings onto the patient’s clothes.
35
Q

What are some of the risk factors for delayed wound healing?

A
  • poor nutrition
  • heart failure
  • smoking
  • corticosteroids (suppress WBC activity)
  • infection (local tissue destruction)
  • anemia (pooor energy supply)
  • advanced age
  • obesity (decreased perfusion)
  • diabetes
  • cold temp
  • excessive moisture (bacterial growth)
36
Q

What are the clinical manifestations of Peripheral Artery Disease (PAD) of the Lower Extremities?

A
  • Ischemic pain + intermittent claudication
  • paresthesia of toes and feet, neuropathy (associated with diabetes)
  • atrophy of skin and underlying muscles
  • skin changea: thin, shiny, taut
  • pain at rest
  • coolness, pallor, pain on elevation
  • ulcers to toes, metatarsal heads, heels, and lateral ankle
  • ulcers w pale ischemic base, well-defined edges, and no bleeding
37
Q

what are the complications associated w PAD of the lower extremities?

A
  • injury, infection, gangrene, pain

- delayed / absence of healing, amputations

38
Q

What are the potential causes of Chronic Venous Insufficiency (CVI) and Leg Ulcers?

A
  • varicose veins and prothrombic syndrome
  • ambulatory venous hypertension
  • increased venous capillary hydrostatic pressure –> edema
  • RBC breakdown
  • Venous leg ulcers (venous stasis ulcers)
  • painful, debilitating, chronic
39
Q

What are the clinical manifestations of CVI?

A
  • leathery lower legs
  • persistent edema
  • eczema or stasis dermatitis, pruritis
  • often above medial malleolus
  • often worse in dependent position
  • painful w edema, infection, cellulitis
40
Q

Describe malignant melanoma.

A
  • Most deadly skin cancer + most rapid progress, less common.
  • affects 1-2% of people but kills 20%.
  • Arises from pigment producing melanocytes
  • caused by UV radiation, intense sun exposure + burns
  • resemble moles and may develop from them.
  • found on: trunk, back, legs, soles, palms
41
Q

What can melanoma appear very similar to and be mistaken for?

A

Seborrheic keratosis (common benign skin growth) or the common skin mole.

42
Q

Describe basal cell carcinoma. What does it look like?

A
  • typically looks like a skin-coloured papule (may be darker in colour
  • often has pearly round border
  • central red ulcer
  • may bleed easily if rubbed, may be crusted + flat

common skin cancer, slow growth, rarely causes death.

43
Q

What benign skin growth can Basal Cell Carcinoma (BCC) appear similar to?

A

Sebaceous hyperplasia.

44
Q

Describe Squamous Cell Carcinoma (SCC).

A
  • red, scaly patch
  • may crust or bleed; open sores that don’t heal.
  • sharp margins
  • located on hands, face, head, and mucous membranes
  • caused by cumulative UV exposure, progresses slowly + can be lethal.
45
Q

What skin condition does Squamous Cell Carcinoma appear similar to?

A

Actinic Keratosis (pre-malignant which may develp into SCC).

46
Q

What are the 4 ways in which we can obtain laboratory samples of skin neoplasms?

A

skin scraping
curettage
punch biopsy
excision

47
Q

what is cellulitis? what are the clinical manifestations? is this a common condition?

A

bacterial infection involving inner layers of the skin (dermis + subcut fat)

  • erythema, tenderness
  • swelling, warmth
  • blanches w pressure
  • febrile, lethargy
  • increased w obesity, edema, PVD
  • common in legs after break in skin + IV sites.
48
Q

what are 2 concerns associated w cellulitis?

A
  • bone infection (osteomyelitis)

- necrotizing fasciitis

49
Q

What are some common skin lesions in children?

A
  • diaper dermatitis
  • intertrigo (warm, moist skin folds)
  • impetigo (contagious, bacterial)
  • atopic dermatitis
  • measles
  • german measles
  • chicken poz
50
Q

Describe the following common skin lesions:

  • folliculitis
  • primary contact dermatitis
  • allergic drug rxn
  • tinea corporis or tinea pedis
  • psoriasis
  • herpes
  • herpes zoster
  • erythema migrants of lyme disease
A
  • folliculitis: razor burn
  • primary contact dermatitis: irritant
  • allergic drug rxn: erythema/symmetry/hives/pruritis/swelling
  • tinea corporis or tinea pedis: ringworn of body or foot; funal infection, contagious + itchy
  • psoriasis: scaly, red patches
  • herpes: HSV-1 oral, HSV-2 genital
  • herpes zoster (shingles) - vesicles along sensory nerve tract
  • erythema migrants of lyme disease - bullseye rash

NURS 2500 (22 decks)

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