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Clinical Medicine > Exam 3 Study Guide > Flashcards

Exam 3 Study Guide Flashcards

(120 cards)

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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
Stage 3 Pressure wound
Full thickness tissue loss, but not through fascia, undermining or tunneling may be present
26
Stage 4 pressure ulcer
Full-thickness loss, undermining, tunneling, or sinus tracts, exposed or easily palpable bone, tendon, or muscle.
27
Unstageable pressure ulcer
full-thickness skin or tissue loss, extent of tissue damage cannot be determined due to slough or eschar.
28
External risk factors for pressure ulcers
pressure with shear or moisture
29
intrinsic risk factors for pressure ulcers
Maceration, decreased skin resilience, malnutrition, decreased circulation, decreased sensation. Impaired mobility/activity, incontinence, altered level of consciousness
30
Phases of wound healing
Inflammation, repair, remodeling
31
Inflammation phase 1
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.
32
Proliferation phase 2 timing and goals
day 3 to day 20, rebuilding structure and framework of the wound, fragile.
33
what happens during proliferation phase 2
new tissue from fibroblasts turn into collagen, re-epithelialization &/or contraction
34
Maturation/remodeling phase 3 timing and goals
day 9 up to 2 years, obtain complete wound healing & strength
35
whats happening during Maturation/Remodeling phase 3
epithelial cells continue to turn into type 1 collagen, granulation tissue is replaced by less vascular tissue, scar formation
36
role of oxygen in wound healing
oxygen is needed at the cellular level, decreased oxygen means increased likely hood for infection
37
What can limit perfusion
edema, necrosis, vasoconstriction
38
what can improve perfusion
warmth, avoid smoking, hydration, controlling pain & anxiety
39
Role of moisture in wound healing
dry wounds delay healing, wound hydration is most important external factor
40
Primary Skin Lesion
1st to appear, visually recognizable structure
41
Secondary skin lesion
when changes occur to a primary lesion (Scale, crust, thickening, erosion, ulcer, scar, fissure)
42
Signs and symptoms of skin lesions
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
43
Causes of skin disease
Hereditary factors Physical trauma Systemic origin Burns Dehisced surgical wounds Neoplasm Reaction to radiotherapy Contact with infective organism or injurious agent Reaction to medication
44
Atopic Dermatitis
Most common type of eczema - chronic inflammatory skin disease. Results of dry irritable skin with impaired immune function
45
Diagnosis of atopic dermatitis
increased IgE and food allergies
46
Treatment of atopic dermatitis
Education, hygiene, moisture, avoidance of irritant, topical or systemic pharmacology.
47
Contact Dermatitis
Presents pruritis, erythema, and edema, primary treatment is to remove the causative agent, secondary treatment is avoidance, lubrication, topical agents.
48
Stasis Dermatitis
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
49
Impetigo (bacterial infection)
superficial skin infection. Can be caused by staph or strep, hot and humid weather, close contact, poor hygiene, and trauma. Treatment with antibiotics
50
Cellulitis (bacterial infection)
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
Herpes Simplex
Type 1 - Cold sore Type 2 - Genital warts
52
Herpes Varicella-Zoster Virus (VZV)
Varicella (chicken pox) – fluid filled vesicles Herpes Zoster (shingles) – blister like lesions 14 to 21 days
53
Verrucae (warts)
Common benign infection of skin & adjacent mucous membranes (HPV), transmission through direct contact. white/black dots.
54
Fungal infections
Invade stratum corneum, hair & nails Superficial infections, live on not in skin.
55
Tinea corporis
Ringworm
56
Tinea capitis
Scalp
57
Tinea cruris
jock itch
58
tinea pedis
athletes foot
59
Candida
yeast infection
60
Seborrheic Keratosis (benign tumor)
basal cells, waxy smooth or raised yellow to dark tone lesions
61
Nevi (moles) (benign tumor)
pigmented or nonpigmented lesions of melanocytes
62
Actinic Keratosis (premalignant)
results years of sun exposure, abnormal well defined crusty like skin
63
Bowen Disease (premalignant)
can occur any where, persistent brown to reddish brown well-defined lesions
64
Basal Cell Carcinoma
Slow growing epithelial skin tumor originating from undifferentiated basal cells (Lack keratin). Rarely metastasize. Prolonged sun exposure, immunosuppression, & genetics.
65
Squamous Cell Carcinoma
2nd most common, invasive, risk is UV damage of DNA of epidermal nuclei
66
Malignant Melanoma
Neoplasm of melanocytes, can occur anywhere. there are 4 subtypes.
67
Psoriasis (autoimmune)
Chronic inherited, recurrent, inflammatory disease, triggered by mechanical, UV or chemical injury, stress, smoking & endocrine changes
68
Signs and symptoms of psoriasis
Dry, Itchy, cracking lesions
69
Functions of the epidermis
protection and regulation
70
function of dermis
provides strength, support, and blood to epidermis, "true skin"
71
Hypodermis
stabilization, loose adipose and connective tissue, provides padding especially over bony areas
72
Gauze indications
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
Gauze Disadvantages
No specific contraindications, but there are generally much better choices. Wet-to-Dry = Pain & Trauma
74
Impregnated Gauze indications
Good as a primary dressing over new sutures to prevent them catching or sticking
75
Impregnated Gauze disadvantages
Not very absorptive, may be greasy to wound bed
76
Transparent Films indications
Facilitates a moist environment, While in place, can protect skin from shearing, friction, & incontinence.
77
Transparent Films disadvantages
Can tear skin upon removal.(No deep or highly exudating wounds)
78
Foam indications
Highly absorptive. Help to create an occlusive environment for moist wound healing.
79
Foam disadvantages
Should not be used alone on a dry wound unless used in combination with a “wet” product (i.e. gel)
80
Hydrogels indications
Increase moisture, soften necrotic tissue, support autolytic debridement. Good for stage 2 or 3 dry
81
Hydrogels disadvantages
Only minimally absorptive. Non-adherent (needs a secondary dressing).
82
Hydrocolloids indications
Most occlusive & moisture retentive; best for mild-to-moderately exudating wounds
83
Hydrocolloids disadvantages
Discontinue with increased exudate, hyper-granulation, or infection
84
Alginates indications
Absorb 20-30x their weight., can be used on infected wounds
85
Alignates disadvantages
Permeable to bacteria; require a secondary dressing
86
Hydrofibers indications
very absorbent, do not dry out or stick to the wound.
87
Skin substitutes indications
resemble skin structure and function. Useful for wounds that don’t respond to conventional dressings
88
Skin substitutes disadvantages
Very expensive! May require a secondary dressing or surgical fixation
89
Enzymatic debriders indications
slowly debride eschar
90
Enzymatic debriders disadvantages
Santyl needs added moisture to work (Vashe?)
91
Tape foam
Flexibility and stretch, comfortable, effective for swelling
92
Non adhesive tape
wrapping and securing bandages, adheres to self, does not adhere to skin
93
paper tape
Gentle, less adherent, affordable, breathable, sensitive skin, labeling
94
transparent tape
Sticks to anything, waterproof, easy to tear, strongest adhesive for skin, pliable. Leaves residue however
95
cloth/fabric tape
Sticks to skin, no residue, affordable, breathable, high strength, labeling. not waterproof, difficult to tear.
96
First Degree Burn
thickness is superficial, depth is to the epidermis, characteristics include pain, redness, mild swelling.
97
Second degree burn
Thickness is superficial partial, depth is to the dermis (papillary region), characteristics are pain, blisters, severe swelling.
98
Third degree burn
Thickness is deep partial, depth is to the dermis (reticular region), characteristics are white, leathery.
99
Third and fourth degree burn
Full thickness/subdermal, depth is to the hypodermis, characteristics are charred, insensate, eschar formation.
100
Zone of Coagulation
Cells are irreversibly destroyed, skin grafting, eschar is present and increased risk of infection
101
Zone of Stasis
Cells may die within 1-2 days without treatment.
102
Zone of hyperemia
Minimal cell damage, may recover in a few days without long lasting damage.
103
Heterotopic Ossification
the formation of extraskeletal bone in muscle and soft tissues, 20% burns are at increased risk, most common in elbows, hips, shoulders
104
Heterotopic Ossification signs and symptoms
Pain, tenderness, decreased ROM, a pathologic hard end feel
105
Autograft
The skin is donated by the patient
106
Xenograft
Graft skin is taken from another species
107
Allograft
Graft skin is taken from individual of the same species
108
Epidermal healing
Cells migrate from the surrounding epidermis into the wound, & stop when they bump into other epidermal cells (contact inhibition)
109
Dermal healing
scar formation, categorized by inflammation, proliferation, remodeling.
110
Superficial burn
sunburn, only cell damage to epidermis, skin appears erythematous, dry, free of blisters, & tender to touch.
111
Superficial Partial thickness burn
Epidermis & upper dermis are damaged, presence of intact blisters, extremely painful
112
Deep partial thickness burn
Epidermis is destroyed, dermis is severely damaged, wound bed is white, more white = deeper, very painful
113
Full thickness burn
All epidermal & dermal layers destroyed, possible subcutaneous fat layer, eschar will be present from black, red or white
114
Serous
thin watery appearance with few cells
115
Sanguineous
Maybe called “bloody” Thin, bright red
116
Serosanguineous
Thin, watery, Pale pink
117
Purulent
Thin (seropurulent) or thick Opaque tan to yellow
118
sweet smell
pseudomonas infection
119
ammonia smell
proteus infection
120
Induration
Abnormal hardening of the tissue caused by consolidation of edema.

Clinical Medicine (15 decks)

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