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tissue Integrity: trauma, thermal injuries Flashcards

1
Q

what concepts are directly linked to sepsis?

A
  • functional ability
  • family dynamics
  • fluid and electrolyte
  • acid-base balance
  • sleep
  • cellular regulation
  • intracranial regulation
  • hormonal regulation
  • glucose regulation
  • nutrition
  • perfusion
  • gas exchange
  • clotting
  • immunity
  • inflammation
  • infection
  • mobility
  • tissue integrity
  • sensory perception
  • pain
  • fatigue
  • stress
  • anxiety
  • cognition
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2
Q

important note about peds

A

Peds compensate well & then decompensate suddenly, respiratory failure happens 1st

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3
Q

important note about adults

A

Adults don’t compensate well d/t comorbidities & aging, cardiac failure occurs 1st

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4
Q

causation examples of cell injury (5)

A
  • nutritional deficits (ex. vitamin/iron/calorie deficiencies)
  • mechanical forces (fractures, tissue tears)
  • chemical injury (drugs, biologic agents, toxicities)
  • radiation injury (damage to cells at the molecular level)
  • extreme temperatures (heat, freezing)
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5
Q

types of radiation injuries

A
  • ionizing radiation (=> electron displacement, broken cellular bonds, effects cellular replication) ex. cancer treatment, nuclear radiation, radioactive agents
  • ultraviolot radiation (UVR) (=> burn + ROS formed => DNA damage or necrosis
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6
Q

electrical injury due to exposure to a source (ex. lightning)

A
  • Electrical current damage to endogenous circuits (cardiac) = arrhythmia; brain (seizure)
  • Heat destruction of tissues: 1st affected are body fluids & nerves + entry/exit wound
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7
Q

cellular injury pathophysiology (4 main mechanisms)

A
  • inflammation
  • hypoxia
  • cellular calcium dysfunction
  • free radicals
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8
Q

hypoxia (low tissue oxygen)

A
  • tissue deprivation of oxygen

- injury within minutes to high O2 demand tissues (brain to 4mins, heart, kidney 15 to 20 mins)

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9
Q

causes of hypoxia (4)

A
  • low air content (normal: 21%)
  • construction/obstruction (bronchoconstriction, vasoconstriction, thrombus, disease)
  • altered cellular permeability (ex. inflammation/injury) ex. shock, burns
  • hypermetabolic states (insufficient increase to meet higher demands) ex. fever, burns
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10
Q

inflammation

A
  • release and activation of inflammatory mediators

- damage caused by excessive inflammation that may cause edema, ischemia, necrosis

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11
Q

ischemia

A

impaired oxygen delivery to tissues due to poor perfusion

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12
Q

sequelae (3)

A
  • electrolyte pump dysfunction will cause increase intracellular calcium (electrolyte dysfunction causes a fluid shift and an increase in cellular edema resulting in more decreased functions)
  • hypoxia causing mitochondrial dysfunction starting anaerobic metabolism and creating a byproduct of lactic acid resulting in metabolic acidosis
  • free radical formation will cause injury to the cells causing cell organ damage and leakage and destruction of vital enzymes/organelles
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13
Q

causes of calcium cell dysfunction (3)

A
  • cellular hypoxia (inside cell)
  • inflammation causes a fluid shift of calcium into the cell
  • parathyroid gland is stimulated to take calcium from the bones because blood lacks calcium. Calcium is taken into the cell resulting in an increase of calcium in the cell and in circulation too

*due to the calcium imbalance there can be a problem with depolarization of the cells and altered metabolic process (the normal process is decreased calcium in the cell and depolarization of the cells)

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14
Q

free radicals

A

molecules containing an unpaired electron, they are unstable and reactive

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15
Q

what do free radicals react with

A

lipids, enzymes, DNA

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16
Q

what do free radicals create

A

reactive oxidative stress (ROS) which creates oxidative stress (damage to cells)

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17
Q

why is unstable oxygen molecule (OH) a free radical

A

because it seeks to pair up with another electron. it causes cell damage by pairing up with another molecules electrons

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18
Q

what are free radicals the byproduct of

A

normal respiratory processes and metabolic processes. only when free radicals are in excess due to altered cell metabolism will cause oxidative stress (damage to cells)

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19
Q

what are free radicals balanced by

A

antioxidants which are acquired by food (fruits and vegetables and endogenous scavenger (catalase)

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20
Q

antioxidants

A
  • pair up with the electron and prevent oxidative stress
  • Antioxidants < free radicals = oxidative stress = damage to lipids, DNA, and enzymes = tissue injury and inflammation due to injury = cell damage
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21
Q

acute causative agents

A
  • radiation, drugs, pathogens
  • cause oxidative stress by the release of NO to cause the release of reactive nitrogen species resulting in more oxidative stress
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22
Q

oxidative stress

A

damage to individual cells via electron displacement/dysfunction that will cause a decrease in organ function (ex. insulin resistance) and cytokine release (inflammation that causes cell damage)

*oxidative stress also causes electrolyte imbalances (fluid shift from circulation into the cells, capillary leakage, increased cell permeability, altered depolarization and repolarization

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23
Q

antioxidant agents (3)

A
  • vitamin A
  • vitamin C
  • flavonoids
24
Q

agent exposure to drugs and biological agents (4)

A
  • overdose (ex. tylenol, contains toxic metabolites, cytotoxic - hepatotoxic leads to damage to liver cells)
  • narrow TI (ex. aminoglycosides, toxic levels are reached really easy and can cause cell damage really easy)
  • substances (ex. arsenic, depends on arsenic type can cause specific cell alterations, causes long term cell injury)
  • carbon monoxide (CO) (unable to exhale CO, increased affinity for red blood cells and displace O2 causing hypoxia)
25
Q

arsenic poisoning

A
  • type dependant, depending on the type of arsenic it can cause different cell alterations and damage
26
Q

cause of cellular necrosis (4)

A
  • decreased ATP production (targets mitochondria and alters cell metabolism to decrease cell functions
  • arsenic imitate/replaces cell phosphate (phosphate is used for ATP production)
  • inhibits pyruvates (used for aerobic metabolism)
  • directly induces oxidative stress
27
Q

treatment to arsenic poisoning

A
  • limit exposure

- chelation therapy (agents that bind to arsenic to decrease further damage to cells)

28
Q

radiation: polonium (chemical agent)

A
  • unstable and radioactive
  • binds to cellular electrons causing destruction, leading to necrosis
  • extremely potent, effective in very small doses
  • very difficult to detect as the signs are very common in many diseases (nausea vomiting, diarrhea) but the symptoms progress to bone marrow damage, low white blood cells count, hair loss (all due to attacking the cells that multiply very quickly)
29
Q

treatment of polonium radiation

A

dimercaprol (chelating agent used to remove heavy metals from the body) and supportive treatments such as blood product administration

30
Q

how long is the radioactive half life

A

140 days

31
Q

how does radiation cause damage

A
  • ionizes the cells directly pulling apart the cell structure
  • ionizes water molecules causing ROS formation
  • directly cause DNA damage via electron binding
32
Q

what does polonium damage lead to

A
  • bone marrow failure (one of the first things noticed on lab results) which is extremely destructive
33
Q

UV radiation and skin damage`

A
  • UV (UVR radiation)
    • UVC (naturally doesnt enter into earths atmosphere)
    • UVA (weak rays, 1000 : 1 (UVA to UVB), pass through glass)
    • UVB (sunburn rays, do not pass through glass, most skin damaging)
      • cellular damage to melanin, langerhans cells, immune cells
      • reactive oxygen formation (oxidative stress causing tissue injury)
34
Q

sunburns (damage due to UV radiation)

A
  • epidermal and or dermal layers affected
  • visualized by erythema (redness)
  • the degree of damage varies depending on the duration and intensity of exposure
  • superficial effects lead to systemic effects (fever, chills, malaise, dehydration)
35
Q

sunburn prevention

A
  • sunscreens
  • Benzones absorbs UVR (benzophenone, oxybenzone)
    • mechanisms: distributive shift of electrons-release-repeat
    • bioavailibility: very low, detected in plasma and urine
  • Zinc or Zinc like reflect UVR
    • mechanism: physical protective layer
36
Q

thermal burns

A
  • most common thermal burns are associated with flames, liquids, hot solid objects, steam
  • usually not uniform in depth (mixture of deep and superficial components)
  • burn wounds are dynamic as they can progress to deeper wounds (can require several days for final classification)
  • regeneration (healing) is dependent on presence of dermal tissue (no dermal tissue = grafting)
37
Q

burn classification (4)

A
  • superficial (epidermis)
  • partial thickness (epidermis and dermis)
  • full thickness (full dermis and subcutaneous tissue)
  • 4th degree (involves underlying structures)
38
Q

superficial burns

A
  • epidermis layer only
  • do not blister
  • painful (most painful burns)
  • healing time 6 days
39
Q

partial thickness burns (epidermis and dermis)

A
  • classifies into 2 categories (superficial and deep)
  • superficial:
    • blisters in 24 hours (between epidermis and dermis)
    • painful, red, weeping
    • healing time 7-21 days
  • deep:
    • more dermis involved
    • blisters may occur
    • less painful and waxy appearances
    • healing upto 9 weeks
40
Q

full thickness burns

A
  • full dermis and subcutaneous tissue
  • no blisters
  • waxy to black appearance (eschar formation)
  • no pain, no tactile sensation, loss of function
41
Q

4th degree burns

A
  • underlying structures involved (muscle, bone, joints)
42
Q

DOs with superficial burns (4)

A
  • stop the burning with cool water for at least 20 minutes, use a cold compress to decrease vascular flow, decrease inflammation, decrease nociceptor stimulation (pain)
  • pain relief with NSAIDs, tylenol, glucocorticoids (lidocaine) and use soothing lotions if dry, itchy, peeling skin (ex. aloe vera)
  • protect by loosely covering the burn area with a sterile gauge bandage
  • rehydration with fluids and electrolytes (gatorade)
43
Q

DONTs with superficial burns (2)

A
  • no ice (leads to further damage to skin)

- no butter or oils (traps heat and enhances burning

44
Q

blisters

A
  • indicate that the dermis is involved
  • occur in between the epidermis and dermis
  • keep blisters in tact unless the placement makes it hard to do stuff
45
Q

rule of 9s

A
  • way to determine the extent of the burn
  • epidermal burns are not counted by the rule of 9s, must be deeper
  • hypovolemia present in burns greater than 15%
  • severe burn effects observed in >40% burns
46
Q

rule of 9s percentages in adults

A 
arm = 9%
head = 9%
neck = 1%
leg = 18%
anterior trunk = 18%
posterior trunk = 18%
47
Q

rule of 9s percentages in children

A 
arm = 9%
head and neck = 18%
leg = 14%
anterior trunk = 18%
posterior trunk = 18%
48
Q

burn zone

A
  • burns cause direct cell membrane disruption causing cell injury
  • the more burn zone, the bigger the inflammatory response
  • inflammation leads to more vascular injury and permeability, causing hypoxia/cellular Ca dysfunction/oxidative stress and further effects (insulin resistance, fluid shift (edema, hypovolemia, hypoproteinemia = further fluid shift out of vessels), coagulation due to stimulation of platelets)
  • necrosis of affected tissue
49
Q

results of burns (4)

A
  • hemodynamic instability
  • hypermetabolic state
  • respiratory system dysfunction
  • immune dysfunction (risk of infection/sepsis)
50
Q

hemodynamic instability

A
  • first phase is hypovolemic shock
    • loss of fluids and protein from cellular, interstitial, vascular compartments
    • => fluid shift and total fluid loss
  • decreased cardiac output causing respiratory dysfunction (hypoxia, hypoxemia, cell damage, necrosis)
51
Q

hypermetabolic state

A
  • response to the injury is release of catecholamines, cortisol, inflammatory mediators (bradykinin and histamine, nitric oxide, cytokines, hydrogen sulfide (produces in liver in response to burn stress))
  • 2nd phase: hypervolemic/hypermetabolic state (24-72 hours post burn, lasts upto 2 years)
    • overcompensation causing high CO, high cellular metabolic rate, fever
    • metabolic crisis: protein catabolism due to injury, extreme glucose mobilization but insulin resistance due to injury, electrolyte imbalance (higher if more skeletal damage)
52
Q

immune dysfunction

A
  • depletion and loss of WBC
  • integument loss
  • infection risk upto 50%

due to the burn, the patient is in an immune dysfunction

53
Q

treatment focus of burns (5)

A
  • ABC’s
  • oxygenation (high O2 flow, intubate)
  • hemodynamic stability (requires 2 IV lines)
    • fluid balance and electrolyte balance
    • 1st fluid resuscitation
    • albumin replacement
    • assess for hypermetabolic state carefully and perform continuous monitoring
  • thermoregulation (cool the burn area, post-acute phase keep the room warm to prevent hypothermia
  • treat lactic acidosis
  • nutrition (enteral feeds with protein demands 50% above normal (normal = 1g/kg))
  • manage hyperglycemia with insulin
  • prevent infection (sterile dressings, isolation)
  • escharotomy (surgical incision through the eschar to release the constriction, thereby restoring distal circulation and allowing for adequate ventilation. Escharotomy is usually done within 48 hours to avoid compartment syndrome)
  • manage hypermetabolic state and performing wound grafting ASAP
  • manage hormonal imbalace caused by hypermetabolic response (ex. growth hormone, testosterone…)
54
Q

additional treatment for electrical burns (3)

A
  • exit wound treatment
  • arrhythmias are possible
    • asystole which is treated with TEA (Transcutaneous pacing. Epinephrine Atropine)
    • heart block
    • vfib (defibrillate, epinephrine, propranolol)
  • seizure
  • treat associated injuries (fractures = 50-60%, head injuries = 25%, inhalation injuries)
55
Q

inhalation injuries

A
  • risk of cyanide poisoning due to the release of cyanide through the materials burning (cyanide blocks mitochondrial respiration, therefore no ATP and hypoxia)
  • inhaled cyanide = cyanide with hydrogen
  • very common symptoms that progress to more serious (seizures, pulmonary edema, changes in LOC)
56
Q

extreme temperatures (freezing)

A
  • Vasoconstriction
    • SNS + reflex action of blood vessels
    • => tissue hypoxia => necrosis
  • Decreased blood flow (stasis)
    • => thrombosis (clots form in non-flowing blood)
    • => tissue hypoxia
  • Inflammation
    • => capillary permeability => fluid shift = edema => ROS = pain + tissue hypoxia + Ca dysfunction = necrosis

pharm (2 decks)

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