Skin Flashcards

1
Q

How does antibiotic resistance of MRSI occur

A

acquisition of mecA gene which encodes a penicillin binding protien (PBP2a) that has a lower binding affinitiy for beta lactams

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2
Q

What are risk factors for MRSI

A

use of fluoroquinolones; IV catheterization; more than 10 vet staff employed; post-surgery site infection

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3
Q

What are abx commonly used to treat MRSI

A

doxycyclyline and chloramphenicol

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4
Q

How are burns classified

A

on body surface area and depth of tissue

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5
Q

Describe the total body surface area measurements in adapted to animals

A

Rule of nines
Head/Neck, each front limb = 9%
Each pelvic limb, dorsal trunk, ventral trunk = 18%

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6
Q

What is the severity associated with TBSA in burns

A

Local burn < 20% less likely for SIRS
Severe burn > 20-30% Very likely SIRS
> 50% TBSA very poor prognosis

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7
Q

Describe a first degree burn

A

Epidermis only

Painful, hyperemic

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8
Q

Describe second degree burns

A

Epidermis and upper portions of dermis: pain, blistering, hair intact
If deeper portions of dermis but not complete can see yellow white skin, lost of hair (pulls out), pain only with deep pressure

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9
Q

Describe third degree burns

A

Epidermis and entire dermis
black letheary skin; eschar is sensitive to touch
Hair pulls out easily

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10
Q

Describe fourth degree burns

A

epidermis and entire dermis, deeper tissues (connective, bone, vessels etc)
Black letheary skin; eschar is sensitive touch
Hair pulls out easily

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11
Q

Which burn categorization method has been validated in small animals

A

None

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12
Q

What is the local response to burn

A

Cells closest to heat source undergo coagulation and vascular thrombosis
Surrounding tissue affected by blood stasis and edema from capillary leak syndrome
Above plus hypoperfusion lead to ischemia

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13
Q

How does hypoxia worsen with burns

A

Edema from hypoalbuminema and vasoactive substances thromboxane and inducible NO worsen hypoxia

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14
Q

How long before closure of burn may be considered

A

Up to 3 days to declare itself, may be up to 7 days.

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15
Q

How does frostbite result in injury

A

Formation of ice crystals resulting in varying degrees of severity similar to burns

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16
Q

Describe type 1 hypersensitivity reactions- skin

A

angiodema, uticaria, erythema

IgE- antigen complex binds to mast cells and basophils

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17
Q

Describe type 2 hypersensitivity reactions - skin

A

Vesicles, bullae, erosions, mucocutaneous junctions
IgM and IgG cytotoxic
antigen-antibody binding

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18
Q

Describe type 3 hypersensitivity reactions - skin

A

Uticaria, ulceration, pitting edema, wheals, papules, pinnae foot pads; MC junctions
IgG immune complexes deposited in endotheilium of vessels

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19
Q

Describe type 4 hypersensitivity reactions - skin

A

Vesicles bullae, papules, plaques, along trunk axilla, inguinal and pinnae
Antigen bound to T-cells result in tissue necrosis and activation of macrophages

20
Q

What are the three types of soft tissue infections

A

Type 1 Polymicrobial— often MRSA
Type 2 Monomicrobial– often streptococci
Type 3 Anerobic

21
Q

Why are fluoroquinolones not recommended as first line for severe soft tissue infections

A

In vitro induce bacteriophage-mediated lysis with increase expression of superantigens
1 study 50% were resistant

22
Q

What are the phases of wound healing

A

Inflammation/debridement
Repair (proliferation
Maturation

23
Q

What occurs in the inflammation/debridement phase of wound healing

A

First 48-72 hrs
Fills with blood; transient vasoconstriction then vasodilation response to histamine and IL8
Neutrophils initially then macrophages which are essential for wound healing

24
Q

What occurs in the repair (proliferation) phase of wound healing

A

1-3 weeks
angiogensis, fibroplasia, wound contraction and epithealization
Phase change marked by increase number of fibroblasts
Type III to Type 1 collagen

25
Q

How does contraction occur in the repair phase

A

Migration of myofibroblasts

Ceases when tension on surround skin equals the contracting forces or when epithealization is complete

26
Q

What are the benifits of granulation tissue

A

blood supply

increase wounds resistance to infection

27
Q

What occurs in the maturation phase of wound healing

A

Progressive gain of tissue strength revolves around collagen deposition.
Intial portion of phase at 20% after 3 weeks.
Generally will only be 70-80% of normal

28
Q

Which tissue may achieve 100% strength

A

Bladder, Bones

29
Q

What are the types of wound closure

A

Primary- within a few hours of wounding
Delayed primary- within 3 days— before granulation tissue formed
Secondary closure- closure after onset of granulation tissue

30
Q

What are advantages to wound lavage

A

debride and hydrate

31
Q

What is the recommended method of lavage and what pressure is ideal

A

8 psi

35 ml syringe with 19 ga needle

32
Q

What are advantage properities of SSD

A

anti: Gram - , gram + and candida

33
Q

In Burn resuscitation what can be deleterious

A

Delay beyond 2 hours ( increase mortality)

Over resuscitation just as bad as under

34
Q

How does burn shock develop

A

Distrubitive and hypovolemic

IV volume depletion, low pulmonary artery occulusion pressure, elevated systemic vascular resistance and depressued CO

35
Q

How does depressed cardiac output occur with burn injuries

A

Decreased plasma volume increased afterload, and decreased contractility
TNF alpha and impared calcium at the cellular level

36
Q

How does fluid shift after a burn

A

Protein loss to interstitium as microcirculation is lost
Colloid osmotic pressure drops
Transient decrease in interstitial pressure by release of osmotic particles moving fluid to interstitium

37
Q

What results due to fluid shifts after a burn

A

loss of circulationg plasma volume, hemoconcentration, massive edema formation
Decreased UOP, depressed cardiovascular function

38
Q

When is the maximal fluid shift after a burn injury occur

A

at 24 hours

39
Q

What is the formula most widely used to calculate volume resuscitation after a burn

A

Parkland formulat
4 ml/kg x % TBSA = amount LRS to give in first 24 hrs
Give 1/2 over 8 hours then give second have over 1 hours
adjust as needed based on UOP

40
Q

What are colloid recommendations for burns in people based on CCM 2009 review article

A

alubmin increased risk of death
Hypertonic saline 4 x increase AKI, 2 x death
FFP only if coagulatpathy

41
Q

What is a good way and not good way to estimate fluid volume in burn patients

A

No truly great way
UOP > 0.5 ml/kg/hr, if less generally under resuscitated
BAD: HCT- as will often be increased due to protein loss

42
Q

In burn patients what are the benifits of vitamin C

A

reduced fluid requiremtns, burn tissue water content, decreased ventilator days

43
Q

How does inhalation injury affect fluid requirements

A

Increase

44
Q

In people how does inhalation injury alter developement of ventilatory associated pneumonia

A

70% of pateitns develop…. DONT give prophy abx

45
Q

What are preventable complications of burn injuries

A

hypothermia, compartement syndrome, DVT, heparin induced thrombocytopenia
neutropenia, stress ulcers (give prophy), adrenal insufficency

46
Q

How are signs of infection altered with burns

A

Burn patients have a reset of temp (often higher), increased HR and tachypenia therefore it is not always easy to tell