Toxicology Module 2 Flashcards
(21 cards)
What is heat stroke? What are the stages leading to it?
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
What are 3 recognised causes of heat related illness?
- Vehicular
- Exertional
- Environmental
Over 41C requires active cooling
What are the mechanisms of heat loss?
- Conduction: through direct transmission to in solid contact solid material
- Convection: heat loss to gaseous or liquid phase materials that then move away from body
- Evaporation: energy loss due to conversion of liquid to gas
- Radiation: infrared radtion into the immediate environment
How can dogs lose heat?
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
What is the pathophysiology of heat stroke?
- Excessive heat generation in skeletal muscle
- Pro-inflammatory cytokines are released (IL1, IL6)
- If uncontrolled spills in to blood and starts to have effects on organs distant to original injury
- Effects of pro-inflam factors: altered endothelial permeability, vasodilation, increase body T and hyperalgesia, microthrombus gen
- SIRs
- MODs
What are the cytokines involved in heat shock
- IL1, 6
- PRRs –> Pattern recognition receptors - stimulated by molecules asspciated with tissue damage - PAMPs (pathogen associated molecular patterns and DAMPs (danger associated)
- 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
what are heat stroke risk factors?
- Obesity
- Breed
- Ambient Temp
- Humid environment
- Lack of fitness
- Lack of acclimatisation
- Prior HS
Clinical signs of heat stroke
- 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
- Resp signs - BOAS, aspiration, ARDs, hypoxia
- GIT signs - Decreased visceral perfusion, v+/d+ of acute haem diarrhea with sloughing
- Renal signs - pathology ranging from intestinal + glomerular congestion to renal tubular necrosis, AKI
- Coagulation - thrombosis, direct endothelial damage
Treatment of heat shock
- O2
- Decrease core temp: clipping, active cooling, airmovement, spraying fur, cool IV fluids, lavage body cavities
- Support SIRs: fluids, plasma, ab cover
treatment of hypothermia
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
What is drowning?
A process resulting in primary resp impairment from submersion/immersion in a liquid medium
What is the pathophysiology of drowning?
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
What is the Dive Reflex?
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
What is the treatment for drowning injury?
- Optimise tissue oxygenation - lung protective ventilation
- Acid/base abnormalities stabiliastion
- Stabilise CV - fluids to restore circulating fluid volume - monitor RR, BW, UO, BP
- Stabilise neuro - maintain BP, correct ICP, avoid hypercarbia
What are prognostic indictors for drowning?
Poor if presents - unconscious, v-tach, fixed pupils, severe acidosis
Should start getting worse/better after 4-8hrs
What are the 4 types of burn injuries?
- Chemical
- Electrical
- Radiation
- Thermal
What are the mechanisms of electrical/lightening injury?
- Electrophysiological effect on excitable cells - muscle spasms, arrhythmias, resp arrest - profound sympathetic release
- Heat generation - burns, coag of tissues, proteins, thrombosis, necrosis
- electroporation - voltage applied across plasma membrane creates short lived pores that lead to osmotic flux
Treatment of electrical burns?
- Judicious fluids
- O2 supplementation
- Hexarinse if oral ulcers
- Analgesia
- Early enteral nutrition
- lubricate eyes
What is the rule of 9ths?
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
What is the thermal injury classification?
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
Treatment of thermal burns?
- Conservative: fluids, pain relief
- Enzymatic debridement - topical agents - No GA
- Surgical - early and agg is amenable to closure/grafting, may require staging and revision
- Cooling of burn wounds to reduce spread - decreased edema and increased speed of epithelialisation - tap water + cold water
- Nutrition - high calorie, high protein
- Antibiotics - topical unless septic
- Topical therapies - aloe, sulphadiazine, honey, hyperbaric O2, vaccume assissted closure
