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Clinical Medicine > Exam 3 Study Guide > Flashcards

Exam 3 Study Guide Flashcards

1
Q

Peripheral vascular disease - PVD

A

General term of disrupted arterial or venous blood flow to the extremities

Causes are multifactorial – smoking, cardiac disease, DM, HTN, ↑ cholesterol & triglycerides, obesity, & sedentary lifestyle

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2
Q

Arterial Insufficiency

A

lack of blood flow to a region

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3
Q

Venous Insufficiency

A

inadequate drainage of venous blood

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4
Q

Arterial ulcer clinical presentation

A

lower extremities (Lateral malleoli, dorsum of foot & toes), size is partial to full thickness, wound base is necrotic & pale, lacks granulation, dry gangrene, drainage is minimal, painful and skin is cool to the touch.

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5
Q

> 1.0 <1.3 ABI reading

A

Normal

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6
Q

0.8-1.0 ABI reading

A

Mild peripheral arterial occlusive disease

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7
Q

<0.6 ABI reading

A

Intermittent Claudication

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8
Q

0.5-0.8 ABI reading

A

Moderate peripheral arterial occlusive disease

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9
Q

< 0.5 ABI readings

A

Severe occlusive disease

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10
Q

< 0.26 ABI readings

A

Resting ischemic pain

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11
Q

<0.02 ABI readings

A

Gangrenous extremity

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12
Q

Venous Ulcers

A

Inadequate drainage of venous blood resulting in edema, skin abnormalities & ulcerations

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13
Q

Venous ulcers clinical presentation

A

mostly located on Medial malleolus, small, shallow, irregular margins, wound bed is red and granulation tissue present, moderate to large quantity of drainage, generally painless, skin temp may be elevated.

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14
Q

Pitting edema grading scale 1+

A

up to 2mm depression, rebounding immediately.

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15
Q

Pitting edema grading scale 2+

A

3-4mm of depression, rebounding in 15sec or less

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16
Q

Pitting edema grading scale 3+

A

5-6mm of depression, rebounding in 60sec

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17
Q

Pitting edema grading scale 4+

A

8mm of depression, rebounding in 2-3 minutes.

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18
Q

Diabetic Neuropathy

A

weight-bearing surface of the foot, anesthetic, round & over a bony prominence, size is variable, wound bed is discolored, granulation is central with less necrotic tissue, drainage is minimal unless infected, rimmed by callus, painless.

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19
Q

Autonomic Neuropathy

A

Decreased or absent sweat and oil production, dry and inelastic skin, increased susceptibility to skin breakdown and injury, heavy callus formation.

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20
Q

Pressure Ulcers

A

Results from unrelieved pressure, friction, shear or stress, associated with poor mobility, dehydration, hypotension, decreased sensation, incontinence.

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21
Q

Pathogenesis of pressure ulcers

A

compression of capillaries occluding blood flow to and lymphatic drainage from tissues, occurs with pressure higher than 32 mmHg, muscle and tendon tolerate less pressure than skin.

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22
Q

Clinical presentation of pressure ulcers

A

circular pattern over bony prominence, greatest ischemia near bone, generally not painful

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23
Q

Stage 1 pressure wound

A

intact skin, non-blanchable erythema, warm skin temp, firm or boggy tissue feel, pain and itching

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24
Q

Stage 2 Pressure wound

A

partial-thickness wound with loss of dermis, shallow open ulcer or open/ruptured serum filled blister, red or pink wound bed but adipose is not visible

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25
Q

Stage 3 Pressure wound

A

Full thickness tissue loss, but not through fascia, undermining or tunneling may be present

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26
Q

Stage 4 pressure ulcer

A

Full-thickness loss, undermining, tunneling, or sinus tracts, exposed or easily palpable bone, tendon, or muscle.

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27
Q

Unstageable pressure ulcer

A

full-thickness skin or tissue loss, extent of tissue damage cannot be determined due to slough or eschar.

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28
Q

External risk factors for pressure ulcers

A

pressure with shear or moisture

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29
Q

intrinsic risk factors for pressure ulcers

A

Maceration, decreased skin resilience, malnutrition, decreased circulation, decreased sensation. Impaired mobility/activity, incontinence, altered level of consciousness

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30
Q

Phases of wound healing

A

Inflammation, repair, remodeling

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31
Q

Inflammation phase 1

A

normal immune response, injury to 10 days. Goals are to limit the extent of tissue damage, limit the spread of infection, remove necrotic tissue, debris, and pathogens.

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32
Q

Proliferation phase 2 timing and goals

A

day 3 to day 20, rebuilding structure and framework of the wound, fragile.

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33
Q

what happens during proliferation phase 2

A

new tissue from fibroblasts turn into collagen, re-epithelialization &/or contraction

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34
Q

Maturation/remodeling phase 3 timing and goals

A

day 9 up to 2 years, obtain complete wound healing & strength

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35
Q

whats happening during Maturation/Remodeling phase 3

A

epithelial cells continue to turn into type 1 collagen, granulation tissue is replaced by less vascular tissue, scar formation

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36
Q

role of oxygen in wound healing

A

oxygen is needed at the cellular level, decreased oxygen means increased likely hood for infection

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37
Q

What can limit perfusion

A

edema, necrosis, vasoconstriction

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38
Q

what can improve perfusion

A

warmth, avoid smoking, hydration, controlling pain & anxiety

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39
Q

Role of moisture in wound healing

A

dry wounds delay healing, wound hydration is most important external factor

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40
Q

Primary Skin Lesion

A

1st to appear, visually recognizable structure

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41
Q

Secondary skin lesion

A

when changes occur to a primary lesion (Scale, crust, thickening, erosion, ulcer, scar, fissure)

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42
Q

Signs and symptoms of skin lesions

A

Pruritis (itching)
Xerosis/Xeroderma (dry skin)
Urticaria (hives)
Rash (eruption of skin)
Blisters (could be friction or bacteria)
Changes in appearance of nails
Changes in skin pigmentation, turgor, texture

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43
Q

Causes of skin disease

A

Hereditary factors
Physical trauma
Systemic origin
Burns
Dehisced surgical wounds
Neoplasm
Reaction to radiotherapy
Contact with infective organism or injurious agent
Reaction to medication

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44
Q

Atopic Dermatitis

A

Most common type of eczema - chronic inflammatory skin disease. Results of dry irritable skin with impaired immune function

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45
Q

Diagnosis of atopic dermatitis

A

increased IgE and food allergies

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46
Q

Treatment of atopic dermatitis

A

Education, hygiene, moisture, avoidance of irritant, topical or systemic pharmacology.

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47
Q

Contact Dermatitis

A

Presents pruritis, erythema, and edema, primary treatment is to remove the causative agent, secondary treatment is avoidance, lubrication, topical agents.

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48
Q

Stasis Dermatitis

A

Development of areas of very dry, thin skin, often with small shallow ulcerations, result of vascular insufficiency. Initially presents with edema of legs, tissue becomes hypoxic & dies. Itching, heaviness in legs, brown-stained skin, open shallow lesions

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49
Q

Impetigo (bacterial infection)

A

superficial skin infection. Can be caused by staph or strep, hot and humid weather, close contact, poor hygiene, and trauma. Treatment with antibiotics

50
Q

Cellulitis (bacterial infection)

A

Rapid spreading acute inflammation & infection of skin & subcutaneous tissue (strep or staph). Present in adults with DM, malnutrition, steroid therapy, presence wounds/ulcerations, lymphedema, obesity.

51
Q

Herpes Simplex

A

Type 1 - Cold sore
Type 2 - Genital warts

52
Q

Herpes Varicella-Zoster Virus (VZV)

A

Varicella (chicken pox) – fluid filled vesicles
Herpes Zoster (shingles) – blister like lesions
14 to 21 days

53
Q

Verrucae (warts)

A

Common benign infection of skin & adjacent mucous membranes (HPV), transmission through direct contact. white/black dots.

54
Q

Fungal infections

A

Invade stratum corneum, hair & nails
Superficial infections, live on not in skin.

55
Q

Tinea corporis

A

Ringworm

56
Q

Tinea capitis

A

Scalp

57
Q

Tinea cruris

A

jock itch

58
Q

tinea pedis

A

athletes foot

59
Q

Candida

A

yeast infection

60
Q

Seborrheic Keratosis (benign tumor)

A

basal cells, waxy smooth or raised yellow to dark tone lesions

61
Q

Nevi (moles) (benign tumor)

A

pigmented or nonpigmented lesions of melanocytes

62
Q

Actinic Keratosis (premalignant)

A

results years of sun exposure, abnormal well defined crusty like skin

63
Q

Bowen Disease (premalignant)

A

can occur any where, persistent brown to reddish brown well-defined lesions

64
Q

Basal Cell Carcinoma

A

Slow growing epithelial skin tumor originating from undifferentiated basal cells (Lack keratin). Rarely metastasize. Prolonged sun exposure, immunosuppression, & genetics.

65
Q

Squamous Cell Carcinoma

A

2nd most common, invasive, risk is UV damage of DNA of epidermal nuclei

66
Q

Malignant Melanoma

A

Neoplasm of melanocytes, can occur anywhere. there are 4 subtypes.

67
Q

Psoriasis (autoimmune)

A

Chronic inherited, recurrent, inflammatory disease, triggered by mechanical, UV or chemical injury, stress, smoking & endocrine changes

68
Q

Signs and symptoms of psoriasis

A

Dry, Itchy, cracking lesions

69
Q

Functions of the epidermis

A

protection and regulation

70
Q

function of dermis

A

provides strength, support, and blood to epidermis, “true skin”

71
Q

Hypodermis

A

stabilization, loose adipose and connective tissue, provides padding especially over bony areas

72
Q

Gauze indications

A

More reasons not to use than to use. Can be used as a secondary dressing, especially if changed frequently or if exudate is heavy

73
Q

Gauze Disadvantages

A

No specific contraindications, but there are generally much better choices. Wet-to-Dry = Pain & Trauma

74
Q

Impregnated Gauze indications

A

Good as a primary dressing over new sutures to prevent them catching or sticking

75
Q

Impregnated Gauze disadvantages

A

Not very absorptive, may be greasy to wound bed

76
Q

Transparent Films indications

A

Facilitates a moist environment, While in place, can protect skin from shearing, friction, & incontinence.

77
Q

Transparent Films disadvantages

A

Can tear skin upon removal.(No deep or highly exudating wounds)

78
Q

Foam indications

A

Highly absorptive.
Help to create an occlusive environment for moist wound healing.

79
Q

Foam disadvantages

A

Should not be used alone on a dry wound unless used in combination with a “wet” product (i.e. gel)

80
Q

Hydrogels indications

A

Increase moisture, soften necrotic tissue, support autolytic debridement. Good for stage 2 or 3 dry

81
Q

Hydrogels disadvantages

A

Only minimally absorptive. Non-adherent (needs a secondary dressing).

82
Q

Hydrocolloids indications

A

Most occlusive & moisture retentive; best for mild-to-moderately exudating wounds

83
Q

Hydrocolloids disadvantages

A

Discontinue with increased exudate, hyper-granulation, or infection

84
Q

Alginates indications

A

Absorb 20-30x their weight., can be used on infected wounds

85
Q

Alignates disadvantages

A

Permeable to bacteria; require a secondary dressing

86
Q

Hydrofibers indications

A

very absorbent, do not dry out or stick to the wound.

87
Q

Skin substitutes indications

A

resemble skin structure and function. Useful for wounds that don’t respond to conventional dressings

88
Q

Skin substitutes disadvantages

A

Very expensive! May require a secondary dressing or surgical fixation

89
Q

Enzymatic debriders indications

A

slowly debride eschar

90
Q

Enzymatic debriders disadvantages

A

Santyl needs added moisture to work (Vashe?)

91
Q

Tape foam

A

Flexibility and stretch, comfortable, effective for swelling

92
Q

Non adhesive tape

A

wrapping and securing bandages, adheres to self, does not adhere to skin

93
Q

paper tape

A

Gentle, less adherent, affordable, breathable, sensitive skin, labeling

94
Q

transparent tape

A

Sticks to anything, waterproof, easy to tear, strongest adhesive for skin, pliable. Leaves residue however

95
Q

cloth/fabric tape

A

Sticks to skin, no residue, affordable, breathable, high strength, labeling. not waterproof, difficult to tear.

96
Q

First Degree Burn

A

thickness is superficial, depth is to the epidermis, characteristics include pain, redness, mild swelling.

97
Q

Second degree burn

A

Thickness is superficial partial, depth is to the dermis (papillary region), characteristics are pain, blisters, severe swelling.

98
Q

Third degree burn

A

Thickness is deep partial, depth is to the dermis (reticular region), characteristics are white, leathery.

99
Q

Third and fourth degree burn

A

Full thickness/subdermal, depth is to the hypodermis, characteristics are charred, insensate, eschar formation.

100
Q

Zone of Coagulation

A

Cells are irreversibly destroyed, skin grafting, eschar is present and increased risk of infection

101
Q

Zone of Stasis

A

Cells may die within 1-2 days without treatment.

102
Q

Zone of hyperemia

A

Minimal cell damage, may recover in a few days without long lasting damage.

103
Q

Heterotopic Ossification

A

the formation of extraskeletal bone in muscle and soft tissues, 20% burns are at increased risk, most common in elbows, hips, shoulders

104
Q

Heterotopic Ossification signs and symptoms

A

Pain, tenderness, decreased ROM, a pathologic hard end feel

105
Q

Autograft

A

The skin is donated by the patient

106
Q

Xenograft

A

Graft skin is taken from another species

107
Q

Allograft

A

Graft skin is taken from individual of the same species

108
Q

Epidermal healing

A

Cells migrate from the surrounding epidermis into the wound, & stop when they bump into other epidermal cells (contact inhibition)

109
Q

Dermal healing

A

scar formation, categorized by inflammation, proliferation, remodeling.

110
Q

Superficial burn

A

sunburn, only cell damage to epidermis, skin appears erythematous, dry, free of blisters, & tender to touch.

111
Q

Superficial Partial thickness burn

A

Epidermis & upper dermis are damaged, presence of intact blisters, extremely painful

112
Q

Deep partial thickness burn

A

Epidermis is destroyed, dermis is severely damaged, wound bed is white, more white = deeper, very painful

113
Q

Full thickness burn

A

All epidermal & dermal layers destroyed, possible subcutaneous fat layer, eschar will be present from black, red or white

114
Q

Serous

A

thin watery appearance with few cells

115
Q

Sanguineous

A

Maybe called “bloody”
Thin, bright red

116
Q

Serosanguineous

A

Thin, watery, Pale pink

117
Q

Purulent

A

Thin (seropurulent) or thick
Opaque tan to yellow

118
Q

sweet smell

A

pseudomonas infection

119
Q

ammonia smell

A

proteus infection

120
Q

Induration

A

Abnormal hardening of the tissue caused by consolidation of edema.

Clinical Medicine (15 decks)

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