Environmental/Toxicological Emergencies Flashcards

Question

What do Oxidants continuously generated ## Footnote #3

Answer 1

1. hydrogen peroxide (H2O2), 1. superoxide free radicals (O2−), 1. hydroxyl radicals (OH−)

Answer 2

superoxide dismutase, catalase, glutathione peroxidase, glutathione, **metHb reductase** (also known as cytochrome b5 reductase or nicotinamide adenine dinucleotide diaphorase)

Answer 3

component of over-the-counter drug formulations, is metabolized rapidly to acetaminophen and could result in toxicity in small animals

Answer 4

(1) It is **conjugated to a sulfate** compound by a phenol sulfotransferase, (2) it is **conjugated to a glucuronide** compound by a uridine diphosphate-glucuronosyltransferase, (3) it can be **transformed and oxidized by the cytochrome P-450** system that converts it to the reactive intermediate, N-acetyl-P-benzoquinone-imine (NAPQI)

Answer 5

-- Cats are limited in their **ability to conjugate glucuronide** because they **lack a specific form of the enzyme glucuronyl transferase** needed to conjugate acetaminophen -- cats are estimated to have one-tenth the capacity to eliminate acetaminophen compared with dogs

Answer 6

-- additional **metabolite of acetaminophen** -- plays a **role in erythrocyte oxidative damage**

Answer 7

**Lower levels of metHb reductase** in dogs and cats relative to other species further **increase potential for erythrocyte oxidative injury**

Answer 8

-- Benzocaine sprays for laryngeal spasm in cats and over-the-counter creams for pruritus in dogs and cats have been associated with methemoglobinemia -- **Metabolites of benzocaine are likely responsible for oxidative damage to Hb** -- effects of HzBs associated with benzocaine toxicity are generally mild and rarely associated with hemolysis

Answer 9

-- toxic substances in skunk musk are thought to be thiols, which can react with oxyhemoglobin to form metHb, a thiyl radical, and H2O2

Answer 10

-- Exposure to these substances could occur in small animals that receive vasodilatory drugs that release nitric oxide, including **nitroglycerin and sodium nitroprusside** -- metHb is reduced by metHb reductase in red blood cells, but some evidence indicates that **nitric oxide decreases metHb reductase activity**

Answer 11

-- Oxygen therapy is the mainstay of treatment for CO toxicity -- **increasing the amount of oxygen in the blood decreases the half-life of CO as dissolved oxygen** competes with CO for Hb binding -- CO is then displaced from Hb and exhaled through the lungs

Answer 12

-- involves diuresis or medications that increase the rate of elimination or decrease the production of toxic metabolites -- Induction of vomiting followed by the administration of activated charcoal should be considered -- treatment with methylene blue should occur when methemoglobin exceeds 20-30%,

Answer 13

-- preferred treatment for acetaminophen toxicity -- NAC augments the endogenous glutathione stores as it is hydrolyzed to cysteine (one of the components of GSH) -- **increases the fraction of acetaminophen excreted as the sulfate conjugate** -- NAC is most effective if administered within 12 hours of ingestion of acetaminophen

Answer 14

-- an antioxidant and **can augment metHb conversion** to Hb through nonenzymatic reduction

Answer 15

-- histamine-2 receptor antagonist, is theoretically useful in cases of acetaminophen toxicity because it inhibits the P-450 oxidation system in the liver, limiting the production of NAPQI

Answer 16

-- an essential metabolite that is vital to hepatocytes and has been reported to be hepatoprotective, have antioxidant properties, and decrease the osmotic fragility of erythrocytes

Answer 17

constellation of clinical signs secondary to 1. thermal injury, 1. particulate matter inhalation, 1. toxicant inhalation.

Answer 18

1. upper airway injury, 1. lower airway injury, 1. pulmonary parenchymal injury, 1. systemic injury, 1. systemic toxicity.

Answer 19

consequence of impaired oxygen delivery, mitochondrial dysfunction, and direct neurological damage from systemic toxicity.

Answer 20

inspiration of superheated particulate matter (soot) -- soot → carbonaceous particles cause direct damage via their high temperature. -- can carry large variety of toxins, -- facilitate the transport of toxins to the alveoli through the inhaled air.

Answer 21

-- direct thermal damage to the oral cavity, nasopharynx, nasal cavity, larynx, trachea and eventually the lower airways -- resulting in edema and inflammation of these tissues. -- soft tissue edema in the upper airway apparatus is the risk for airway obstruction -- usually peaks 24 hours postexposure

Answer 22

-- direct thermal injury of the lower airway is unusual -- injury typically secondary to chemical inhalation. -- inhalation of smoke containing chemical irritants incites the production of neuropeptides that leads to a severe inflammatory response by **activating vagal nerve sensory fibers** containing **proinflammatory peptides, neurokinins, and calcitonin gene-related peptide**. -- causes **bronchoconstriction, pulmonary vasoconstriction, and airway fluid accumulation**

Answer 23

-- elevated levels of nitric oxide = impairing pulmonary hypoxic vasoconstriction, further **exacerbating ventilation–perfusion mismatch and dead space ventilation.**

Answer 24

-- classically delayed symptom -- Increased transvascular fluid efflux, lack of surfactant, and loss of hypoxic pulmonary vasoconstriction result in impaired oxygenation -- **Atelectasis develops and fibrin deposition in airways is promoted by the procoagulant status and concurrent reduced antifibrinolytic activity**

Answer 25

-- activated neutrophils -- perpetuate the inflammatory injury to the pulmonary parenchyma

Answer 26

-- volatile compounds present in smoke can cause disruption of the **corneal tear film** and consequently ocular irritation and direct corneal damage and ulceration as well as direct thermal injury. -- Left ventricular dysfunction → secondary to **direct myocardial damage** -- **Sympathetic compensation** is activated and leads to tachycardia and increased systemic vascular resistance, resulting in increased myocardial oxygen demand -- carbon monoxide (CO) further compromises oxygen carrying capacity and oxygen delivery and predisposes to development of arrhythmias, congestive heart failure, and systemic hypotension

Answer 27

-- HC is a colorless gas → **gaseous form of cyanide** -- generated by the combustion of substances such as wool, silk, cotton, and paper as well as plastic and other polymers --With Cyanide intoxication, the **liver may not be capable of metabolizing the cyanide**, particularly when large concentrations are present

Answer 28

-- the level of the mitochondria, where it **inhibits the electron transport chain, impairing cellular ATP production** -- additional effects of HC toxicity include **neurotoxicity, tachypnea** through direct stimulation of chemoreceptors (aortic arch and carotid bodies), arrhythmias, and death.

Answer 29

CO has a half-life of 320 minutes in patients breathing room air; -- reduced to approximately 70 minutes when the patient is provided 100% oxygen at atmospheric pressure

Answer 30

-- humidified supplemental oxygen therapy -- Oxygen therapy improves oxygen delivery and effectively decreases the half-life of CO -- prophylactic use of antimicrobial therapy is not indicated -- not reccomened to use corticosteriods -- inhaled β2-agonists may provide bronchodilation and antiinflammatory effects and promote alveolar fluid clearance.

Answer 31

-- Antidotes **Amyl nitrate and sodium thiosulfate** -- **convert hemoglobin to methemoglobin and favor reduction of cyanide levels** as it preferentially binds to methemoglobin. -- leads to reduced oxygen carrying capacity as a consequence of methemoglobin formation and should be reserved for only those patients highly suspected of cyanide toxicity -- **Hydroxocobalamin (vitamin B12a)** actively binds cyanide to form cyanocobalamin, which is directly excreted via the kidney

Answer 32

-- severe central nervous system (CNS) disturbance --associated with MODS

Answer 33

form of “hyperthermia associated with a systemic inflammatory response leading to a syndrome of multiorgan dysfunction in which encephalopathy predominates.”

Answer 34

-- balance between **heat load** (environmental heat and heat generated through metabolism and exercise) and **heat-dissipating mechanisms** controlled in **hypothalamus**

Answer 35

Heat load Heat dissapation

Answer 36

1. convection, Bair hugger heat support, Hot shower 1. conduction, Heating a pot on the stove 1. radiation, Earth is heated by the Sun 1. evaporation. Sweating, respiration

Answer 37

radiation and convection through the skin

Answer 38

-- increased cutaneous circulation as a result of increased cardiac output and sympathetically mediated peripheral -- involves a trade-off with blood supply to the viscera (intestines and kidneys)

Answer 39

-- via respiratory tract through panting -- predominant mechanism of heat loss when ambient temperature is equal to or greater than the body -- Respiratory evaporative heat loss may be diminished by humid climatic conditions, confinement in a closed space with poor ventilation, and obstructive upper respiratory tract abnormalities

Answer 40

-- from the skin may occur as a result of hypovolemia from any cause, poor cardiac output, obesity, extremely thick hair coat, or lack of acclimatization to heat

Answer 41

1. thermoregulation 1. acute-phase response, 1. increased expression of intracellular heat shock proteins.

Answer 42

variety of **proinflammatory and antiinflammatory cytokines**. 1. Proinflammatory mediators induce leukocytosis, 2. promote synthesis of acute-phase proteins, 3. stimulate the **hypothalamic-pituitary-adrenal axis**, 4. activate endothelial cells and white blood cells. -- they are **protective when the body is balance between the proinflammatory and antiinflammatory response systems**

Answer 43

-- protect the cell and the body against further heat insults and **prevent denaturation of intracellular proteins** -- also help to **regulate the baroreceptor response during heat stress**, -- thus **preventing hypotension and conferring cardiovascular** protection

Answer 44

failure of thermoregulation followed by an exaggerated acute-phase response and alteration of heat shock proteins

Answer 45

initial production and release of **interleukin-1** and **interleukin-6** from the muscles into the circulation and increased systemic levels of endotoxin from the GI tract. -- results in the release of numerous proinflammatory and antiinflammatory cytokines as well as activation of coagulation and inhibition of fibrinolysis

Answer 46

-- poor cerebral perfusion, direct thermal damage, cerebral edema, CNS hemorrhage, or metabolic abnormalities such as hypoglycemia or hepatoencephalopathy

Answer 47

-- tepid water and blowing fans over the body -- massage the muscles to maintain circulation -- External conduction cooling techniques include application of ice packs over major vessels (e.g., jugular veins), tap water immersion, ice water immersion, and use of cooling blankets -- room temperature intravenous fluids may be helpful.

Answer 48

-- may result in vasoconstriction and paradoxical inhibition of body cooling -- and thus diminish heat dissipation overall.

Answer 49

-- iced gastric lavage, iced peritoneal lavage, and cold water enemas, although the latter may interfere with rectal temperature monitoring -- risks of aspiration pnemonia, septic peritonitis

Answer 50

-- Direct thermal damage and poor visceral perfusion and/or reperfusion may result in GI mucosal sloughing and ulceration

Answer 51

-- increasing number of NRBCs is associated with more severe injury and worse outcome

Answer 52

-- process resulting in primary respiratory impairment from submersion or immersion in a liquid medium. -- Liquid is present at the victim’s airway, preventing respiration of air

Answer 53

-- cases in which liquid is not aspirated into the lungs -- often experience morbidity from laryngospasm -- **which results in the same hypoxemic and hypercarbic state** seen in those who have aspirated liquid

Answer 54

-- aspiration of liquid into lungs

Answer 55

-- All submersion victims experience hypoxemia -- either from **laryngospasm** in which no aspiration occurs or from aspiration of fluid resulting in **loss of surfactant** that causes **atelectasis and intrapulmonary shunt**

Answer 56

-- results from intrapulmonary shunting of blood -- Bronchospasm, atelectasis due to surfactant washout, aspirated water or matter in the alveolar space, infectious or chemical pneumonitis, and ARDS **all contribute to pulmonary oxygen shunting** pulmonary shunting = **develops when blood passes through the lungs but fails to take part in gas exchange**)

Answer 57

-- both **ventilation-perfusion mismatch** and **intrapulmonary shunt** from alveolar collapse -- V/Q mismatch may be present in submersion victims that aspirate water or particulate matter

Answer 58

-- air is present under the skin and in the soft tissue -- secondary to an underlying defect that allows air to dissect through soft tissue, most commonly in the chest wall or neck -- causes can be traumatic, iatrogenic, infectious, or rarely spontaneous causes.

Answer 59

-- overinflation from ETT -- Air leak from the peritoneum during laparoscopic procedures -- rare causes = positive pressure ventilation

Answer 60

-- can develop if gas-producing bacteria, such as Clostridium sp. and Bacteroides produce gas that accumulates under the skin

Answer 61

-- extremely rare in people -- thought to occur as a result of a break in the alveolar lining due to chronic pulmonary pathology (COPD in people)

Answer 62

-- from free air escaping from the trachea, mediastinum, pleural, peritoneal, or retroperitoneal spaces

Answer 63

fenestrated, which allows free communication between the mediastinum and the pleural space.

Answer 64

-- Mild typically requires no tx and is self limiting -- supplemental oxygen can hasten the resolution by reducing the partial pressure of nitrogen in the distended tissue and mediastinum

Answer 65

-- patient with air leaking into the pleural space is breathing 100% oxygen, the pleural gas will be composed mostly of oxygen without nitrogen -- pressure gradient between the pneumothorax and venous blood becomes larger because 100% oxygen washes out nitrogen from the alveoli

Answer 66

-- decompression via subcutaneous needle centesis, incision, or drain placement may be necessary

Answer 67

-- any form of damage to tissues or organs by electrical energy or electrical current -- two types of current are alternating current (AC) and direct current (DC

Answer 68

-- can result in muscular tetany, in which the muscles contract -- this can prevent the patient letting go of the cord as the muscles in the mouth will contract and clench -- increases the exposure time to the current and overall severity of injury. -- **important to turn off the electricity before removing the cord from the animal** ## Footnote Direct current does not typically cause this type of muscle contraction

Answer 69

-- development of holes in the cellular membrane, known as cellular pore disruption -- **holes are caused by the electric current, which allows the movement of larger molecules such as fluid and ions across the cellular membrane** -- cause **excessive swelling or shrinking of cells,** resulting in osmotic damage and cell death

Answer 70

-- occurs when the electrical current turns into heat, which **increases the temperature of both intracellular (ICF) and extracellular (ECF) fluid**

Answer 71

-- Electrical current **can arc, meaning it will jump to neighboring tissues not in direct contact** with the electrical source -- can result in tissue damage and necrosis of neighboring areas

Answer 72

-- **cellular damage of the myocardium from thermal injury,** pulse deficits and auscultable cardiac arrhythmias may be seen on presentation -- exposed to a **low‐voltage current, such as AC, most likely experience ventricular fibrillation** leading to circulatory arrest, -- while patients exposed to a **high‐voltage current, such as DC, develop asystole**

Answer 73

-- form of **non‐cardiogenic pulmonary edema** -- damage to the central nervous system (CNS), causes a **massive sympathetic outflow from the CNS results in vasoconstriction and subsequent hypertension** -- leads to an **increase in left ventricular afterload, which will result in a decreased stroke volume** of the left ventricle -- **pulmonary edema can arise from an increase in pulmonary capillary pressure, due to blood backing up into pulmonary circulation**

Answer 74

-- arises from **direct stimulation from electrical energy** as opposed to electroporation, but the latter may still **play a part in CNS hypoxia**. -- altered mental status, muscle tremors, seizure activity, or paresis

Answer 75

-- Hypovolemia may result from pulmonary and tissue edema, vasodilation, or impaired cardiac output; however, hypertension may also be seen, resulting from pain or hyperdynamic shock

Answer 76

-- can only be determined in a patient who can potentially maintain their own body temperature -- < 99 °F -- two types of hypothermia: primary and secondary

Answer 77

-- represents **heat loss in the face of normal heat production** and encompasses the **environmental exposure category** -- exposed to subnormal temperatures, rendering them unable to keep up with heat loss ## Footnote Ex: cold water exposure

Answer 78

-- occurs as a result of a disease process, drug administration, or injury causing altered heat production or loss

Answer 79

-- temperature range of 32–37 °C (90–99 °F). Patients with mild hypothermia may develop vasoconstriction, ataxia, and shivering

Answer 80

-- temperature range of 28–32 °C (82–90 °F). --- These patients may exhibit a **decreased level of consciousness and hypotension, and may be shivering** or may no longer have the ability to shiver

Answer 81

-- temperature range of 20–28 °C (68–82 °F). -- These patients typically have **complete loss of the shivering reflex and may have developed cardiac arrhythmia and extreme central nervous system deficits**

Answer 82

-- temperature range below 20 °C (68 °F). -- These patients continue to have **cardiovascular and CNS deficits in addition to coagulopathic deficits, resulting in a hypocoagulable state.**

Answer 83

-- when temperature lowers, signals are sent to the **thermoregulatory center in the hypothalamus** -- **vasoconstriction and piloerection** assist with heat loss restriction -- **As increased heat production is needed, cellular metabolic rates increase and shivering begins to generate more body heat**

Answer 84

-- -- thermoregulatory center’s critical setpoint may also be altered by stressors, including infection, which increases the setpoint, and other illness or stressors which decrease it

Answer 85

-- sympathetic nervous system’s activity increases to conserve metabolic function. -- Heart rate, cardiac output, and mean arterial pressure increase. -- as temperature decreases, responsiveness to catecholamines results in a blunted and eventually decreased sympathetic response. -- Vasodilation, CNS depression, decreased cardiac output, hypotension, and respiratory depression may result.

Answer 86

Reportedly, when body temperature drops below 31 °C (88 °F), thermoregulation ceases

Answer 87

-- thermal regulation is governed by the hypothalamus which is where an actual temperature setpoint is determined. -- drugs such as opioids can affect this setpoint -- Example: the hypothalamus could decrease the temperature setpoint to recognize 36.1 °C (97 °F) as normal -- effect wears off as the therapeutic range of the opioid decreases, allowing the temperature setpoint to return to normal.

Answer 88

-- binding of norepinephrine to alpha‐1 receptors decreases and limits the amount of sympathetic response (vasoconstriction) in the face of heat loss -- decreased catecholamine release also occurs -- cardiac function decreases -- impaired blood flow from increased viscosity -- Hypoxemia results due to decreased minute ventilation and alveolar hypoventilation

Answer 89

-- some hypothermia may be neuroprotective -- however cerebral blood flow reduces significantly for every 1 °C drop in temperature.

Answer 90

-- After warming therapies are instituted, there may continue to be a decrease in the patient’s temperature, known as the “afterdrop,” which is caused by cold peripheral blood passing into the core -- **rewarming shock** is a phenomenon that patients may experience, characterized by **vasodilation as a result of applied heat** -- patients undergo an **extensive metabolic requirement once rewarming is begun**, drawing from crucial cellular stores of metabolites

Answer 91

the balance between heat loss and heat production. -- Metabolic, physiologic, and behavioral mechanisms are used by homeotherms to regulate heat loss and production. -- control center for the body is located in CNS in the preoptic area of the **anterior hypothalamus (AH)**.

Answer 92

-- true fever is the body’s normal response to infection, inflammation, or injury and is part of the acute-phase response -- Nonfebrile hyperthermia is a result of an **imbalance between heat production and heat loss.**

Answer 93

Changes in ambient and core body temperatures are **sensed by the peripheral and central thermoreceptors**, and information is **conveyed to the AH** via the nervous system. -- thermoreceptors sense body is below or above its normal temperature and subsequently cause the **AH to stimulate the body to increase heat production and reduce heat loss through conservation** if the body is too cold or to dissipate heat if the body is too warm

Answer 94

1. Cachectic 1. anesthetized patients, 1. or those with severe neurologic impairment, may not be able to maintain a normal set point or generate a normal response to changes in core body temperature. 1. Neonatal dogs and cats have a poorly developed thermoregulatory center and lack significant muscle mass. They require higher ambient temperatures to maintain normal body temperature.

Answer 95

1. shivering 2. increased production of catecholamines/Thyroxine 3. Decrease loss 4. vasoconstriction 5. Piloerection 6. postural changes 7. heat seeking

Answer 96

1. Panting 2. Vasodilation 3. postural changes 4. cool seeking behavior 5. perspiration 6. grooming (cats)

Answer 97

Production of endogenous pyrogens -- fever patients have had their thermoregulatory center setpoint altered as a result of a pyrogen -- still able to dissipate heat

Answer 98

1. Heat stroke 1. Hyperpyrexic syndromes

Answer 99

1. Normal exercise 1. Hypocalcemic tetany (eclampsia) 1. Seizure disorders

Answer 100

1. Lesions in or around the anterior hypothalamus 1. Malignant hyperthermia 1. Hypermetabolic disorders 1. Monoamine metabolism disturbances

Answer 101

normal body response to invasion or injury and is part of the acute-phase response. -- acute-phase response = increased neutrophil numbers and phagocytic ability, enhanced T and B lymphocyte activity, increased acute-phase protein production by the liver, increased fibroblast activity, and increased sleep -- **initiated by exogenous pyrogens** that lead to the release of endogenous pyrogens

Answer 102

-- Exogenous pyrogens have the ability to release endogenous pyrogens, which act directly on the thermoregulatory center -- **interleukin (IL)‐1, IL‐6, and tumor necrosis factor (TNF)**‐alpha examples of fever producing cytokines ## Footnote Ex: bacterial, viral, fungi, protozoa, pharmalogical agents

Answer 103

-- responds to stimulation by an exogenous pyrogen, proteins (cytokines) released from cells of the immune system trigger the febrile response. -- Macrophages are the primary immune cells involved, although T and B lymphocytes and other leukocytes may play significant roles. -- **proteins produced are called endogenous pyrogens or fever-producing cytokines**

Answer 104

1. interleukin 1, 1. interleukin 6, 1. tumor necrosis factor-α

Answer 105

in anterior hypothalamus, stimulate the release of **prostaglandins (PGs), primarily PGE2 and possibly PGF2α**

Answer 106

-- result of **inadequate heat dissipation** -- Exposure to high ambient temperatures may increase heat load at a faster rate than it can be dissipated from the body -- will not respond to antipyretics -- must undergo immediate total body cooling to prevent organ damage or death.

Answer 107

1. **Radiation** : electromagnetic or heat exchange between objects in the environment: Sun warms the Earth 2. **Conduction** : between the body and environmental objects that are in direct contact with the skin, as determined by the relative temperatures and gradients: Pot on Hot stove 2. **Convection**: the movement of fluid, air, or water over the surface of the body: Bair hugger heat support 3. **Evaporation** : disruption of heat by the energy required to convert the material from a liquid to a gas, as with panting: Perspiration/Respiration

Answer 108

associated with moderate to severe exercise in hot and humid climates -- may be more common in hunting dogs or dogs that “jog” with their owners -- heavy exercise may lead to **vasodilation to increase blood flow to skeletal muscles but simultaneous vasoconstriction of cutaneous vessels, thus compromising peripheral heat loss**

Answer 109

-- body temperature will rise with **sustained exercise of even moderate intensity** because of heat production associated with muscular activity -- **Eclampsia results in extreme muscular activity** that can lead to significant heat production and result in severe hyperthermia -- **Sz disorders** from organic, metabolic, or idiopathic causes are encountered often in small animals -- first treatment priority should be to stop the seizures, but when significant hyperthermia is present, total body cooling is also recommended as soon as possible

Answer 110

-- **Hypothalamic lesions** may obliterate the thermoregulatory center -- Malignant hyperthermia leads to a **myopathy and subsequent metabolic heat production secondary to disturbed calcium metabolism that is initiated by pharmacologic agents** such as inhalation anesthetics (especially halothane) and muscle relaxants (e.g., succinylcholine) -- Hypermetabolic disorders may also lead to hyperthermic states.

Answer 111

-- Endocrine disorders such as **hyperthyroidism and pheochromocytoma** can lead to an increased metabolic rate or vasoconstriction, resulting in excess heat production, decreased ability to dissipate heat, or both -- **thyroid hormone** may also act directly on the **hypothalamic set point** resulting in a true fever as part of the hyperthermia

Answer 112

-- a fever will reduce the duration of morbidity and decrease mortality from many infectious diseases. -- decreases ability of many bacteria to use iron, which is necessary for them to live and replicate -- Many viruses are heat sensitive and cannot replicate in high temperatures. -- may inhibit viral replication, increase leukocyte function, and decrease the uptake of iron by microbes (which is often necessary for their growth and replication)

Answer 113

Hyperthermia increases tissue metabolism and oxygen consumption, thus **raising both caloric and water requirements by approximately 7% for each degree Fahrenheit** -- fever in patients with noninfectious diseases such as TBI may carry a worse prognosis -- leads to suppression of appetite center in the hypothalamus; (thirst center usually remains unaffected) -- temps above 107 increases in cellular oxygen consumption that exceed oxygen delivery, resulting in the deterioration of cellular function and integrity. leading to potential DIC

Answer 114

-- liver (hypoglycemia, hyperbilirubinemia) -- kidneys (acute kidney injury) -- hypoxemia, hyperkalemia, skeletal muscle cytolysis, tachypnea, metabolic acidosis, tachycardia, tachypnea, and hyperventilation -- Exertional heat stroke and malignant hyperthermia may lead to severe rhabdomyolysis, hyperkalemia, hypocalcemia, myoglobinemia, myoglobinuria, and elevated levels of creatine phosphokinase

Answer 115

-- Nonspecific therapy for true fever usually involves inhibitors of prostaglandin synthesis: NSAIDS -- They **do not block the production of endogenous pyrogens** -- Glucocorticoids should be resevered for pts with known causes to be noninfectious: ex immune-mediated -- **Phenothiazines can be effective in alleviating a true fever by depressing normal thermoregulation** and causing peripheral vasodilation

Answer 116

-- will reduce body temperature; **however,** the thermoregulatory center in the hypothalamus will still be directing the body to increase the body temperature. -- may result in a **further increase in metabolic rate, oxygen consumption, and subsequent water and caloric requirements.** -- unless fever is life threatening, this is counterproductive

Answer 117

Infectious vs noninfectious -- Nosocomial infection -- indwelling devices, catheters, compromised immune systems

Answer 118

-- prevent initial absorption or further absorption of a toxin -- specific form of decontamination will depend on the route of toxic exposure

Answer 119

-- corrosive substances (e.g. bleach), strong acids, and strong bases should be treated with **rapid dilution with milk or water** -- emesis is avoided because if vomiting occurred, the substance could cause significant additional damage to the esophagus, leading to esophagitis, strictures, or perforation

Answer 120

-- contraindicated in rodents or rabbits as these species may have weak stomach walls and are unable to vomit. -- comatose, seizuring, severely depressed, dyspneic, hypoxic, or lacking normal swallowing reflexes -- use of emetics after ingestion of strychnine or other central nervous system (CNS) stimulants may precipitate seizures

Answer 121

-- extremely porous form of carbon that, having a large surface area, can act as an effective absorbent -- used to bind to some toxins, thereby preventing absorption in the gastrointestinal tract. -- strong acids or alkalis, alcohols (such as ethanol, methanol, etc.), cyanide, lithium, ethylene glycol, metal (iron), bleach, and xylitol, do not effectively bind to activated charcoal

Answer 122

-- bile acid sequestrant, which binds bile in the gastrointestinal tract to prevent its reabsorption -- is a strong ion exchange resin, exchanging chloride anions with anionic bile acids in the gastrointestinal tract and binding them strongly in the resin matrix for elimination

Answer 123

-- technique used to increase the excretion rate of toxicity‐causing drugs -- **Drugs typically are unable to pass through cell membranes unless they are in a non‐ionized state** -- weak acids are absorbed well when placed into an acidic environment as they will be in a non‐ionized form.

Answer 124

-- consist of soy oil, glycerol and egg phospholipids and are a major component of parenteral nutrition

Answer 125

ILE expands the intravascular lipid phase which acts to **sequester lipophilic toxins** within it, thus reducing the effect site concentration and toxicity until the compound is metabolized and excreted -- **providing myocytes with energy substrates**, thereby augmenting cardiac performance, restoring myocardial function by increasing intracellular calcium concentration and the overall fatty acid pool, thus overcoming inhibition of mitochondrial fatty acid metabolism.

Answer 126

1. First generation 2. 1,3‐Indandiones 3. Second generation

Answer 127

1. warfarin, 1. coumarin, 1. coumatetralyl

Answer 128

1. pindone, 1. chlorophacinone, 1. diphacinone

Answer 129

1. brodifacoum, 1. bromadiolone, 1. flocoumafen, 1. difethialone, 1. difenacoum

Answer 130

First gen depress clotting factors for approximately 7–10 days while second‐generation rodenticides can depress clotting factors for 3–4 weeks.

Answer 131

-- Due to the **short half‐life of factor VII, a prolonged PT** is the most sensitive indication of early toxicity.

Answer 132

-- emesis induction +/- activated charcoal -- Vitamin K1 (phytonadione) is the specific antidote of choice and should be administered to all patients **showing signs of coagulopathy or that have elevated PT measurements**

Answer 133

-- **vitamin K administration will not restore new clotting factors for 12–24 hours**. -- often need to receive whole‐blood transfusions or fresh frozen plasma when they are in need of immediate clotting factors or red blood cells to improve oxygen delivery -- autotransfused back into the patient as a short‐term solution while steps are taken to restore clotting factors with plasma or whole blood

Answer 134

-- antiparasitc agents -- mode of action is via **gamma‐aminobutyric acid (GABA) agonism**. -- MDR-1 mutation dogs have low toxic threshold Tx; anticonvulsants, ILE therapy

Answer 135

-- works by the uncoupling of oxidative phosphorylation in the CNS and liver mitochondria, thereby causing a **decrease in (ATP) production** -- ATP decrease causes a decrease in Na/K ATPase activity, which **results in loss of ability to maintain the osmotic gradient** and membrane potential in the cell. -- leads to **sodium influx into brain cells, consequently causing cerebral edema** and loss of function.

Answer 136

-- treatment is symptomatic and supportive -- IVF, anticonvulsants, HTS or mannitol for cerebral edema -- ILE therapy has been proposed as an antidote for bromethalin toxicity as the agent appears highly lipophilic

Answer 137

-- products are commonly found in dusts, sprays, shampoos, and flea and tick collars -- cause a nearly **identical toxicity to organophosphates** -- cause **reversible inhibition of cholinesterase activity** -- High doses of atropine and support care are typically all that is required for successful recovery

Answer 138

-- **caffeine, theobromine, and theophylline** -- causes adenosine receptor blockage and increases in cyclic adenosine monophosphate (cAMP) -- **increased calcium concentration within the cell which leads to increased muscular contractility**

Answer 139

-- decon with emesis +/- activated charcoal -- IVF, anticonvulsants -- beta‐blockers such as esmolol or propranolol are often necessary to control supraventricular tachycardia or Lidocaine for ventricular arrhythmyias -- trazadone and dexmedetomidine are very useful to control CNS signs such as hyperactivity and restlessness. -- ucath in severe cases b/c methylxanthines can be reabsorbed from the urinary bladder and perpetuate toxicity -- ILE therapy

Answer 140

-- gets metabolized to 25‐hydroxyvitamin D in the liver, which is then **converted by the kidney to active vitamin D3** (1,25‐dihydroxyvitamin D). -- **Vitamin D3 promotes the body’s retention of calcium**. → **tissue mineralization** of blood vessels, kidneys, heart, and lungs -- at risk for tissue mineralization and **subsequent renal tubular injury** when the calcium phosphorus product (Ca × P) is over 60 -- Cats are more sensitive to toxicosis than dogs

Answer 141

-- ionized hypercalcemia, hyperphosphatemia, and azotemia

Answer 142

-- inducing vomiting and administration of activated charcoal -- IVF for renal hydration and **promote calciuresis → 0.9% saline ideal** due to lack of added calcium and promotes calciuresis -- ILE may be beneficial in early exposure -- furosemide will also promote rapid calciuresis

Answer 143

-- automobile antifreeze, rust removers, film processing solutions, and industrial solvents -- EG is **metabolized by the liver to glycoaldehyde, glycolic acid, glyoxalic acid, and oxalic acid** -- Oxalic acid forms insoluble **calcium oxalate crystals** which **precipitate in the renal tubules, ultimately resulting in acute kidney failure**

Answer 144

-- **initial phase** is marked by mild depression, ataxia, polyuria, polydipsia, vomiting, anorexia, hypothermia, and potentially seizures -- **second phase** begins between 12 and 24 hours post ingestion and initially only includes cardiorespiratory signs such as tachycardia and tachypnea -- closely followed by severe depression, vomiting, azotemia, isosthenuria, and eventually acute kidney injury with oliguria by 24–72 hours post ingestion

Answer 145

-- unexplained metabolic acidosis with a **severely increased anion gap** -- Serum osmolality is increased and an increased osmolar gap is present. **Hyperglycemia, hypocalcemia, hyperphosphatemia, and azotemia** -- Hyperkalemia may be noted if anuria is present -- **glucosuria, renal tubular casts, isosthenuria, and calcium oxalate** crytalluria (often monohydrates)

Answer 146

-- Calcium oxalate crystals will form **within five hours of ingestion** in the dog and three hours in the cat

Answer 147

-- anticonvulsants -- Ethanol competes for alcohol dehydrogenase and therefore acts as an antidote -- however causes significant side‐effects, including CNS depression, hypothermia, and increased plasma osmolality, and can easily cause death from alcohol poisoning if overdosed.

Answer 148

-- acute or chronic lead toxicity include old paint, batteries, pipes, fishing sinkers, shotgun pellets, linoleum, putty, golf balls, lubricants, and insulation -- results in **nervous tissue demyelination and interference with GABA, cholinergic function, and heme synthesis**

Answer 149

-- gastrointestinal and nervous systems symtoms -- anxiety, odd behavioral changes, seizures, ataxia, head pressing, polyneuropathy, opisthotonos, mydriasis, and blindness. -- can result in cerebral edema

Answer 150

-- large numbers of nucleated red blood cells (NRBCs) with evidence of severe anemia, anisocytosis, polychromasia, poikilocytosis, target cells, hypochromasia, and potentially **basophilic stippling**

Answer 151

-- administration of a chelating agent. -- Calcium ethylenediaminetetra‐acetic acid (EDTA) -- D‐penicillamine, dimercaptosuccinic acid (DMSA), dimercaprol (BAL), and succimer (DMSA)

Answer 152

--members of the Liliaceae family -- All parts of these plants, including the flowers, are potentially toxic -- exact mechanism of action of lily toxicosis is unknown but **proximal convoluted tubular necrosis occurs.**

Answer 153

-- Metaldyhyde is a **molluscicide (snail/slug killer)** that is highly palatable to dogs and cats -- mechanism of action is unknown but may it act by **decreasing brain GABA**, serotonin, and norepinephrine, **resulting in convulsions** -- causes a rapid onset of severe signs that include seizures, hypersalivation, inco‐ordination, muscle fasciculations, metabolic acidosis, and tachycardia.

Answer 154

-- decontamination with emesis +/- activated charcoal -- fluid therapy, patient cooling, muscle relaxants, anticonvulsants, and sedatives, are necessary to control hyperthermia and CNS stimulation -- dialysis techniques such as hemodialysis and hemoperfusion -- metaldeyde is poorly lipophilic, not responsive to ILE

Answer 155

-- contain either toxic naphthalene or the more inert paradichlorobenzene -- causes **acute oxidative hemolytic anemia, Heinz bodies, and occasionally methemoglobinemia** -- Cats are most sensitive to the toxic effects of naphthalene

Answer 156

-- inducing emesis +/- activated charcoal -- intravenous fluid diuresis -- pRBC transfusion for pts experincinig anemia related hypoxia -- If methemoglobinemia is present, it should be treated with either ascorbic acid (vitamin C)

Answer 157

-- Inhibition of gastric prostaglandin synthesis can result in gastroenteritis, gastrointestinal ulceration, and gastrointestinal perforation. -- Inhibition of renal prostaglandin synthesis can result in acute kidney injury

Answer 158

-- decon w/ emesis +/- activated charcoal -- ILE -- anticonvulsants -- **Naloxone may reduce CNS signs** -- **Due to enterohepatic recirculation of many NSAIDs, patients may benefit from cholestyramine** -- prevent gastrointestinal ulceration, combinations of prostaglandin agonists (e.g. misoprostol), proton pump inhibitors, sucralfate, and H2 blocker -- TPE

Answer 159

-- pet sprays, dips, kennel sprays, powders, yard sprays, and as systemics -- readily absorbed from the skin and gastrointestinal tract and cause **acute irreversible inhibition of acetylcholinesterase activity** -- Acetylcholinesterase is responsible for breaking down acetylcholine and when it is not broken down effectively, the **abundance of acetylcholine can dramatically interfere with autonomic nervous system function**

Answer 160

-- **parasympathomimetic effects (muscarinic stimulation)** such as salivation, lacrimation, vomiting, diarrhea, miosis, and bradycardia -- as it progresses nicotinic stimulation occurs and is followed finally by nicotinic blockade. -- muscle twitching, seizures, respiratory depression, coma, and death occur.

Answer 161

-- decon from topical exposure with bathing -- activated charcoal for oral ingestion -- Large doses of **atropine** 0.2–0.5 mg/kg IV, IM, SC, a antimuscarinic agent competitively inhibits acetylcholine -- **pralioxime chloride (2‐PAM chloride)**, in conjuction with atropine, to **reactivate the acetylcholinesterase** that has been inhibited.

Answer 162

-- derived from the Chrysanthemum cinerariaefolium plant -- Cats an birds most susceptible to actue toxicity -- work by **delaying sodium channel closing**, resulting in repetitive nerve firing -- act as **antagonists of GABA and glutamic acid**.

Answer 163

-- systemic muscle tremors, hyperexcitability, hyperesthesia, hyperthermia, hypersalivation, and, less commonly, vomiting, diarrhea, CNS depression, or generalized seizure activity

Answer 164

-- decon topical exposure with bathing -- emesis +/- activated charcoal for oral ingestion -- IVF for GI/hyperthermia symptoms -- Methocarbamol or dexmed for muscle tremors -- ILE

Answer 165

-- Organic acid → Naturally occurring in plants -- cream of tartar → homemade playdough -- tamarinds, grapes, raisins -- nephrotoxin → risk depends on concentration and amount ingested.

Answer 166

-- 226mg/kg tartaric acid -- more than 1 grape per 4.5kg uncooked grapes

Answer 167

-- **restricted‐use pesticide that antagonizes glycine, one of the body’s main inhibitory neurotransmitters,** -- resulting in **CNS excitation, including spinal reflexes and striated muscles** -- accidentally ingesting **strychnine‐containing rodenticide** or by being poisoned with food laced with strychnine -- anxiousness and muscle tremors, followed by collapse, seizures, extensor rigidity, apnea, and commonly death -- **emesis, ILE**

Answer 168

-- sugar substitute that is commonly found in chewing gum and artificial sweeteners -- results in the **secretion of insulin, thereby potentially causing severe acute hypoglycemia, ataxia, collapse, and seizures** -- insulin release **driving potassium into cells, hypokalemia** can also be observed -- cause a **delayed acute hepatic necrosis and failure approximately 72 hours after initial recovery**

Answer 169

-- decon via emesis -- activated charcoal not effective -- IVF support -- Glucose support -- Anti-oxidant therapy N‐acetylcysteine and S‐adenosyl methionine (SAM‐e) to minimize hepatic injury

Answer 170

-- ingestion of pennies made during or after the year 1983 -- batteries, nuts and bolts, vitamin and mineral supplements, board game pieces, and medicated creams -- exposure of zinc to the acidic environmental of the stomach results in **release of free zinc** which can cause zinc salts -- caustic to the intestinal tract and can have a direct irritant and corrosive effect -- **RBC oxidative damage**

Answer 171

-- gastrointestinal signs -- progress to intravascular hemolysis and anemia, pancreatitis, kidney injury, hepatic failure, and CNS signs -- inflammatory leukogram, regenerative anemia, spherocytosis, **Heinz body formation**, hyperbilirubinemia, azotemia secondary to tubular injury by hemoglobinuria, ELEs, coagulopathy, and increased levels of serum zinc

Answer 172

-- decon with emesis for FB removal -- IVF and gastroprotectants

Answer 173

-- active ingredient in several mole and gopher powder and pellet rodenticide products -- In moist and acidic conditions such as the stomach, zinc phosphide undergoes a chemical reaction to liberate **toxic phosphine gas** -- results in systemic oxidative injury, with target organs including the brain, liver, lungs, heart, and kidneys. -- careful induction of emesis in a well‐ventilated area due to risk of exposure to noxious gas

Environmental/Toxicological Emergencies Flashcards

(199 cards)