Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

VTS ECC 2024 > Muscoskeletal/integumentary > Flashcards

Muscoskeletal/integumentary Flashcards

1
Q

Necrotizing soft tissue infection (NSTI)

what are 3 things it can cause?

A

term used to describe a subset of soft tissue infections involving skin, subcutaneous tissue, muscle, and fascia that cause vascular occlusion, ischemia, and necrosis.
– associated with virulent bacterial and fungal organisms
– NSTIs are progressive and rapidly spread along tissue planes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Necrotizing soft tissue infection (NSTI) examples

Name at least 3

A
  1. Fournier gangrene,
  2. Ludwig angina,
  3. flesh-eating disease,
  4. hemolytic streptococcal gangrene,
  5. necrotizing fasciitis (NF),
  6. myonecrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Toxic shock syndrome (TSS)

A

acute, severe, SIRS initiated by a microbial infection at a normally sterile site,
– usually exotoxin-releasing Staphylococcus or Streptococcus spp.
– manifests as an acute, early occurrence of circulatory shock and MODS that can include renal and/or hepatic dysfunction, coagulopathy, acute respiratory distress syndrome, and/or an erythematous rash
– TSS occurs in a subset of type II NSTIs and is associated with severe systemic disease including septic shock and MODS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

NSTI four categories based on type of infection

A
  1. Type I NSTI is polymicrobial,
  2. Type II NSTI is monomicrobial,
  3. Type III NSTI is associated with Gram-negative, often marine-related organisms,
  4. Type IV NSTI is associated with fungal infection.

Most of the veterinary cases reported could be categorized as type II NSTI due to trauma or wounds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

NSTI

Type I infections: Polymicrobial

A

Mixed anaerobes and aerobes
* Usually isolate four or more organisms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

NSTI

Type II infections: Monomicrobial

A

Commonly β-hemolytic Streptococcus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

NSTI

Type III infections: Gram-negative monomicrobials

A
  • Clostridia infections
  • Includes marine organisms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

NSTI

Type IV infections: Fungal

A

Such as Candida infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Pathophys of NSTI

A

toxicity of virulent streptococci releases exotoxin superantigens, cell envelope proteinases, hyaluronidase, complement inhibitor, M-protein, protein F, and streptolysins – which amplifies cytokine release and induction of a SIRS and septic shock.
– Microbial invasion associated with localized thrombosis
→ liquefactive necrosis of the superficial fascia and soft tissue is a key pathologic process of NSTI.
– Occlusion of nutrient vessels → extensive undermining of apparently normal-appearing skin, followed by gangrene of the subcutaneous fat, dermis, and epidermis, evolving into ischemic necrosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

NSTI

Clostridial toxin effects

x4 effects

A

Clostridial toxins can cause:
hemolysis, platelet aggregation, leukocyte destruction, and histamine release,
– in addition to damage to the vascular endothelium, collagen, and hyaluronic acid.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Diagnosis of NSTI: CS

A

– clinical signs of NSTI and TSS can be nonspecific
– Fever and general malaise are commonly evident
– Surgery or a recent traumatic event may be included

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Diagnosis of NSTI: Lab findings

A

– Fine-needle aspirate from an affected tissue site can help confirm an infectious origin and differentiate between type I and type II NSTI.
– Cytology as well as Gram stain, culture, and susceptibility testing are recommended.
– Blood work findings cannot be used to diagnosis NSTI but can reflect infection or SIRS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Diagnosis of NSTI: Imaging

A

Subcutaneous air seen on plain film radiographs is rare but characteristic of necrotizing lesions with gas-producing organisms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Diagnosis of NSTI: Definitive diagnosis

A

Definitive diagnosis of TSS requires positive streptococcal or staphylococcal culture findings and evidence of septic shock.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

NSTI Treatment

A

– septic and circulatory shock treatment
– analgesics
– Antimicrobial therapy should not be delayed beyond the first hour following recognition of a NSTI or TSS
– Clindamycin remains effective during the stationary phase and turns off exotoxin synthesis
– surgical debridement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Why are fluoroquinolones not reccomended for NSTI treatment?

A

Fluoroquinolone administration, specifically enrofloxacin, is not recommended, because it may have limited activity against streptococcal infection and may cause bacteriophage-induced lysis of S. canis, enhancing its pathogenicity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Other treatments for NSTI

A

– Hyperbaric oxygen therapy may enhance host antimicrobial activity and the action of various antibiotic agents by facilitating their transport across the bacterial cell wall.
– Hemofiltration, plasmapheresis, and plasma exchange have been used in people to remove circulating inflammatory mediators and toxins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

outermost layer of the skin

A

– epidermis
– remains in direct contact with the external environment under normal circumstances.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

2nd layer of skin

A

dermis
– contains sebaceous glands, blood vessels, arrector pili muscles, and hair follicles.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is below the integumentary?

A

subcutaneous space, aka hypodermis,
– contains connective tissue, fat, and potentially large blood vessels such as veins and arteries along with nerves.

21
Q

Phases of Wound Healing

4 phases

A
  1. Inflammatory phase
  2. Debridement phase
  3. Proliferation (repair) phase
  4. Maturation phase
22
Q

Inflammatory phase

4 classic signs

A

protective tissue response and results in four classic signs:
calor (heat), dolor (pain), rubor (redness), and tumor (swelling)

23
Q

Mechanims of the Inflammatory phase

6 steps

A
  1. Following endothelial damage, activation of tissue factor (factor III) also helps in blood clotting
  2. Vasoconstriction with platelet aggregation prevent hemmorhage
  3. Once bleeding slows or stops, vasoconstriction is followed by vasodilation, which allows for fibrinogen and clotting factors to leak into the wound.
  4. Clot dries and a scab is formed which helps to protect the underlying tissues from further desiccation, contamination, and hemorrhage
  5. With vasodilation white blood cells and endothelial cells are able to enter the wound
  6. inflammatory mediators such as histamine, proteolytic enzymes, prostaglandins, cytokines, leukotrienes, and serotonin also leak into the wound and cause a localized inflammatory response can last up to 5 days
24
Q

Debridement phase

when does this typically start?

A
  1. leukocytes that enter the wound signal the beginning of the debridement phase
  2. begins within the first 6–12 hours following injury
  3. Neutrophils begin phagocytosis
  4. neutrophils begin to degenerate and release enzymes that result in chemotaxis of monocytes
  5. monocytes can develop into macrophages which further assist in the removal of foreign material and necrotic tissue and pathogens
25
Q

Proliferation phase

when does this typically occur

A
  1. occurs 3–5 days after injury
  2. process of creating new blood vessels, known as angiogenesis
    3.increased deposition of collagen, formation of granulation tissue, epithelialization, and wound contraction
  3. macrophages also secrete cytokines and growth factor which help to develop granulation tissue.
  4. also signal fibroblast proliferation
  5. fibroblasts stimulate the production of collagen, elastins, and proteoglycans which help the granulation tissue to become more fibrous, allowing for an increase in wound strength.
26
Q

Maturation phase

A
  1. final phase of wound healing.
  2. can take years to fully complete.
  3. collagen is deposited around the wound site and is remodeled as the wound begins to contract, which will reduce the size of the healing wound
27
Q

Wound Classification: Class I (clean wounds)

A

occurred under clean conditions, such as surgical incisions

28
Q

Wound Classification: Class II (clean contaminated wounds)

what is the most common cause?

A

clean wounds without any visible infection that have been contaminated and are at a higher risk for infection
– Surgical contamination from the patient’s own bodily fluids is the most common cause

29
Q

Wound Classification: Class III (contaminated wounds)

A

most commonly seen with acute injuries
– contain high levels of contamination due to outside objects coming into contact with the wound
– GSW, bite wounds

30
Q

Wound Classification: Class IV (dirty or infected wounds)

A

wounds that retain a foreign object such as gravel, bullets or other debris and/or contain obvious signs of infection or abscesses

31
Q

Abrasions:

how does this type of wound heal?

A

open partial‐thickness wound of the epidermis with exposure of the dermis.
– wound usually has minimal trauma or contamination and usually heals through second intention

32
Q

Lacerations:

A

– open irregular wound caused by tearing, that can be superficial or involve underlying structures
– most commonly repaired through primary closure
– sharp objects

33
Q

Avulsions

A

– open wound created by tearing of the tissue, where the tissue is also torn away from its underlying structures
– degloving injuries

34
Q

Contusions:

A

– closed wound that does not break through the skin but can cause damage to the underlying tissue and capillaries, resulting in bleeding under the skin and bruising
– blunt trauma
– can occur in any tissue and contusions of the lungs or heart are not uncommon with blunt force trauma

35
Q

First vs second intention healing

A

– First intention healing: appositional healing, where the wound is sutured together with fresh wound edges.
– Second intention healing: relies on the body’s own contraction and epithelialization for wound healing, no surgical closure

surgical vs non-surgical

36
Q

Delayed primary wound closure

A

– aka third intention healing or tertiary wound healing, utilizes appositional closure as well, but typically not within the first 6–8 hours after injury
– usually occurs before 3–5 days from the date of injury
– utilized for mild to moderately contaminated wounds and allows extra time for irrigation and debridement prior to closure.

37
Q

Secondary wound closure

A

– closure of a wound after granulation tissue has formed, meaning that this form of closure occurs after a 3–5‐day period from the injury
– used for contaminated and dirty wounds and often the new granulation tissue is used in the closure of the wound and may need to be debrided to freshen the edges prior to closure

38
Q

Vacuum‐assisted wound closure

MOA and benefits

A

– aka negative‐pressure wound therapy and utilizes subatmospheric pressure to expose the wound bed and stimulate granulation tissue formation
– VAC can retain a moist wound environment and help to improve circulation while reducing inflammation by decreasing the amount of inflammatory cytokines and reducing wound edema
– helps to decrease the duration of open wounds while reducing wound size and volume

39
Q

Contraindications for the use of VAC

x3

A
  1. wounds that are neoplastic in nature,
  2. wounds that have veins or arteries exposed that could lead to hemorrhaging,
  3. or patients with coagulopathies
40
Q

Total body surface area (TBSA)

A

refers to the total amount of the body that has been damaged.
– rule of 9 s” commonly utilized in human medicine breaks the body up into percentages of 1%, 9% or 18% of the TBSA

41
Q

First‐degree burn:

A

– a superficial burn and is painful.
– only affect the epidermis.
skin can appear red and may contain a small amount of swelling but blistering will not be present

42
Q

Second‐degree burn:

A

– also called partial‐thickness burns and affect both the epidermis and the dermis
– Small vessels of the dermis can be damaged and leak plasma fluid.
– Blisters are commonly seen with second‐degree burns.
– also painful

43
Q

Third‐degree burns:

A

– affect the epidermis, dermis, and subcutaneous layer (hypodermis) and are known as full‐thickness burns
– also affect the adipose tissue and destroy nerve tissues and nociceptors
– skin can develop a leathery, firm, and depressed appearance and may be white or even black
– top layers injured may not be painful but deep structures are painful and sensitive

44
Q

Partial‐ or full‐thickness burns are at risk for

A

Eschar, a black, firm crust composed of degenerated tissue.
– usually develops within the first 7–10 days post injury and can sometimes be attached to newly developing skin

45
Q

Metabolic derangements with burns/wounds

A

– hypovolemic shock often occurs If more than 20% of a patient’s TBSA is burned or if the wounds are classified as second or third-degree.
– result of capillary thrombosis and plasma leakage, massive amounts of fluid are retained in the wound, often leading to burn wound edema
– results in the loss of fluid and electrolytes, with the most dramatic losses occurring within the first 12 hours

46
Q

8

Systemic abnormalities with burn pts:

A
  1. including anemia,
  2. hypoproteinemia,
  3. hypernatremia/hyponatremia,
  4. hyperkalemia/ hypokalemia,
  5. acidosis (metabolic and respiratory)
  6. coagulopathy,
  7. oliguria,
  8. prerenal azotemia.
47
Q

Antimicrobial therapy with burn pts

A

– Sepsis is one of the greatest threats to burn patients with extensive TBSA involvement because bacteria can colonize and proliferate in wounds that have lost the protective skin barrier
– remove all necrotic tissue and purulent exudates from the wound surface as aggressively as possible through serial debridement
– Systemic antimicrobials are not indicated unless the patient is immunocompromised, has pneumonia or pulmonary injury, or sepsis is suspected

Topical antibiotics are the antimicrobial treatment of choice

48
Q

Aloe vera cream for burn wounds

A

antithromboxane effects that prevent vasoconstriction and thromboembolic seeding of the dermal vasculature

VTS ECC 2024 (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions