Toxicology Module 2 Flashcards

1
Q

What is heat stroke? What are the stages leading to it?

A

Non-pyrogenic increase in body temperature that occurs when thermoregulatory mechanisms are overwhelmed will lead to SIRS and MODS
Heat cramp - loss of NaCL resulting in cramping, not noticed
Heat exhaustion - v+/d+
Heat stroke - MODs and neurological CS

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2
Q

What are 3 recognised causes of heat related illness?

A
  1. Vehicular
  2. Exertional
  3. Environmental

Over 41C requires active cooling

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3
Q

What are the mechanisms of heat loss?

A
  1. Conduction: through direct transmission to in solid contact solid material
  2. Convection: heat loss to gaseous or liquid phase materials that then move away from body
  3. Evaporation: energy loss due to conversion of liquid to gas
  4. Radiation: infrared radtion into the immediate environment
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4
Q

How can dogs lose heat?

A

Over 32C evaporation is the primary mechanism of heat loss
- perspiration in dogs and cats are limited to paw pads
- panting allows large airflow over the mucosa over the mucosal surfaces of both nose and mouth

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5
Q

What is the pathophysiology of heat stroke?

A
  1. Excessive heat generation in skeletal muscle
  2. Pro-inflammatory cytokines are released (IL1, IL6)
  3. If uncontrolled spills in to blood and starts to have effects on organs distant to original injury
  4. Effects of pro-inflam factors: altered endothelial permeability, vasodilation, increase body T and hyperalgesia, microthrombus gen
  5. SIRs
  6. MODs
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6
Q

What are the cytokines involved in heat shock

A
  1. IL1, 6
  2. PRRs –> Pattern recognition receptors - stimulated by molecules asspciated with tissue damage - PAMPs (pathogen associated molecular patterns and DAMPs (danger associated)
  3. Heat shock proteins: help to protect enzyme function in periods of extreme heat - when temp increases suddenly cells release HSPs - they act to maintain the structure of proteins such as maintaining their function
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7
Q

what are heat stroke risk factors?

A
  1. Obesity
  2. Breed
  3. Ambient Temp
  4. Humid environment
  5. Lack of fitness
  6. Lack of acclimatisation
  7. Prior HS
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8
Q

Clinical signs of heat stroke

A
  1. Cardiovascular signs- tachycardia (increased CO to increase cooling) , weak pulses (initially blood direct cutaneously and with fluid loss, v+/d+ will lead to decreased volume), arrhythmias
  2. Resp signs - BOAS, aspiration, ARDs, hypoxia
  3. GIT signs - Decreased visceral perfusion, v+/d+ of acute haem diarrhea with sloughing
  4. Renal signs - pathology ranging from intestinal + glomerular congestion to renal tubular necrosis, AKI
  5. Coagulation - thrombosis, direct endothelial damage
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9
Q

Treatment of heat shock

A
  1. O2
  2. Decrease core temp: clipping, active cooling, airmovement, spraying fur, cool IV fluids, lavage body cavities
  3. Support SIRs: fluids, plasma, ab cover
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10
Q

treatment of hypothermia

A

Warm core first or shock - 0.5-2C per hr
Passive external warming - preventing further loss
Active external rewarming
active core warming: warming/humidified air, warmed IV fluids, body cavity lavage

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11
Q

What is drowning?

A

A process resulting in primary resp impairment from submersion/immersion in a liquid medium

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12
Q

What is the pathophysiology of drowning?

A

Hypoxaemia - caused by laryngospasm or from surfactant washout: hypoxaemia, hypercarbia and acidosis
- quantities of water cause surfactant washout
- progressive hypoxaemia leads to laryngeal relaxation and liquid inhalation
- washout causes interrupted alveolar membrane leading to pulmonary edema
- edema and loss of surfactant and increased capillary alveolar permeability and fluid shiting, plasma, electrolytes and inflammatory cells

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13
Q

What is the Dive Reflex?

A

May give some protection
Cold water <5C trigger, reflex mediated through trigeminal n. to CNS
Vagally bradycardia with peripheral vasoconstriction - cerebral and coronary perfusion is preferentially maintained

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14
Q

What is the treatment for drowning injury?

A
  1. Optimise tissue oxygenation - lung protective ventilation
  2. Acid/base abnormalities stabiliastion
  3. Stabilise CV - fluids to restore circulating fluid volume - monitor RR, BW, UO, BP
  4. Stabilise neuro - maintain BP, correct ICP, avoid hypercarbia
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15
Q

What are prognostic indictors for drowning?

A

Poor if presents - unconscious, v-tach, fixed pupils, severe acidosis
Should start getting worse/better after 4-8hrs

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16
Q

What are the 4 types of burn injuries?

A
  1. Chemical
  2. Electrical
  3. Radiation
  4. Thermal
17
Q

What are the mechanisms of electrical/lightening injury?

A
  1. Electrophysiological effect on excitable cells - muscle spasms, arrhythmias, resp arrest - profound sympathetic release
  2. Heat generation - burns, coag of tissues, proteins, thrombosis, necrosis
  3. electroporation - voltage applied across plasma membrane creates short lived pores that lead to osmotic flux
18
Q

Treatment of electrical burns?

A
  1. Judicious fluids
  2. O2 supplementation
  3. Hexarinse if oral ulcers
  4. Analgesia
  5. Early enteral nutrition
  6. lubricate eyes
19
Q

What is the rule of 9ths?

A

Assessment on burn injuries to judge degree/percentage of body affected

  • Head and neck 9%
  • Each FL - 9%
  • Each hindlimb 18%
  • Thorax 18%
  • Abdomen 18%

<20% local burn injury
>20-30% severe brun
>50% euthanasia indicated

20
Q

What is the thermal injury classification?

A

1st - superficial - epidermis only
2nd - epidermis & superficial dermis - partial thickness
3rd - full thickness - deep partial thickness
4th - full thickness with extension to muscle/tendon/bone

21
Q

Treatment of thermal burns?

A
  1. Conservative: fluids, pain relief
  2. Enzymatic debridement - topical agents - No GA
  3. Surgical - early and agg is amenable to closure/grafting, may require staging and revision
    1. Cooling of burn wounds to reduce spread - decreased edema and increased speed of epithelialisation - tap water + cold water
  1. Nutrition - high calorie, high protein
  2. Antibiotics - topical unless septic
  3. Topical therapies - aloe, sulphadiazine, honey, hyperbaric O2, vaccume assissted closure