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Auburn ECC > Environmental/Toxic > Flashcards

Environmental/Toxic Flashcards

1
Q

2 possible causes of acute hepatic necrosis with xylitol toxicity?

A

ATP depletion

Increased generation of ROS

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2
Q

Cocaine MOA

A

Inhibits presynaptic neuronal uptake of dopamine, NE, and serotonin = enhanced sympathetic transmission (tachycardia, arrhythmias, hypertension) & CNS (excitement & euphoria)

Blocks fast sodium channels = local anesthetic activity

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3
Q

Toxin in mountain laurel (rhododendron) and MOA

A

grayanotoxins: bind sodium channels in excitable cell membranes of nerve, heart, skeletal muscle which increases membrane permeability of sodium ions in the excitable membranes, thus maintaining the cells in the state of depolarization

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4
Q

N-acetylcysteine MOA?

A

Increased synthesis and availability of glutathione (NAC –> cysteine)

For acetaminophen:
Substrate for sulfation (less toxic metabolites)
Direct binding and detoxification of NAPQI

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5
Q

MOA of anticoagulant rodenticide

A

Inhibits vitamin K epoxide reductase which is needed to convert inactive vitamin K to active vitamin K

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6
Q

What is the difference between first and second generation anticoagulant rodenticides?

A

Second generation products are longer acting so vitamin K therapy should be continued for at least 4 weeks

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7
Q

MOA of bromethalin rodenticide

A

Uncoupling of oxidative phosphorylation with a resultant decrease in ATP production. Decrease in cellular energy leads to inability of the Na/K-ATPase pump to function. This leads to a buildup of intracellular sodium followed by water movement into the cells and resultant cerebral edema and elevated intracranial pressure.

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8
Q

MOA of zinc phosphide rodenticide

A

Once it comes into contact with gastric acid it is hydrolyzed to phosphine gas and free radicals. When it is ingested with food there is enhanced susceptibility to zinc phosphide due to increased gastric acid.

Phosphine gas disrupts mitochondrial respiration as well as produces free radicals such as reactive oxygen species

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9
Q

Describe the pathophysiology of carbon monoxide poisoning

A

Carbon monoxide competitively and reversibly binds to hemoglobin at the same sites as oxygen but with an affinity that is 230-270 times greater, resulting in marked anemic, hypoxia.

Carboxyhemoglobin shifts the oxygen-hemoglobin dissociation curve to the left, resulting in less offloading at the tissue level.

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10
Q

How does hydrogen cyanide cause toxicity?

A

It interferes with utilization of oxygen by cellular cytochrome-oxidase and thereby causes histotoxic hypoxia.

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11
Q

Describe some of the changes to the respiratory tract that can be seen with smoke inhalation

A

Direct thermal injury can cause mucosal edema, of which laryngeal edema is of greatest concern.

Noxious gases can be inhaled (or gases are converted to acids within the respiratory tract).

Decreased lung compliance due to alveolar atelectasis due to impaired pulmonary surfactant activity as well as pulmonary edema.

Progressive mucosal edema can cause mucosal sloughing.

Smoke inhalation can cause a reflex bronchoconstriction which may worsen airway obstruction.

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12
Q

How does smoke inhalation increase the likelihood of bacterial pneumonia?

A

It may impair alveolar macrophage function. There are also stagnant luminal contents which create a favorable environment for bacteria.

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13
Q

What are the three possible outcomes in pure, uncomplicated carbon monoxide poisoning?

A
  1. complete recovery with possible transient hearing loss but no permanent effects.
  2. recovery with permanent central nervous system abnormalities
  3. death
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14
Q

Hyperemia of the mucous membranes in a case of smoke inhalation can be caused by what?

A

carboxyhemoglobinemia

cyanide toxicosis

systemic vasodilation

local vasodilation due to mucosal irritation

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15
Q

Why is oxygen supplementation beneficial in carbon monoxide poisoning?

A

the half-life of CO is 250 minutes i patients with normal respiratory exchange breathing room air, but is reduced to 26-148 minutes at an FiO2 of 100%.

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16
Q

How is cyanide toxicity treated?

A

IV sodium nitrite followed by IV sodium thiosulfate.

In the case of smoke inhalation, sodium thiosulfate should be used alone as sodium nitrite results in the formation of methemoglobin which could further compromise oxygen carrying ability

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17
Q

Describe some of the treatments for airway management following smoke inhalation

A

Tracheostomy if laryngeal obstruction

Empiric bronchodilators

Supplemental humidified oxygen which regular saline nebulization and coupage

Gentle activity is encouraged

Mucolytics may be used

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18
Q

True or false, mycoplasma species lack a cell wall

A

True, all members of the class lack a cell wall, thus they are damaged easily outside the host, and are difficult to identify with most staining techniques

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19
Q

In what locations are nonhemotropic mycoplasma infections found?

A

Respiratory tract, ocular, urogenital, nervous system, and systemically

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20
Q

True or false, mycoplasma are considered normal flora of the UPPER respiratory tract in dogs and cats

A

True

For the lower respiratory tract, they have been isolated from the lungs of healthy dogs buts not healthy cats

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21
Q

Why are ureaplasmas (a form of mycoplasma) found more commonly in the urogenital tract?

A

They require urea for a carbon source

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22
Q

True or false, mycoplasma has been found to cause disease in the lower urinary tract in cats

A

False, because of the lack of a cell wall, mycoplasma is at a high risk for osmotic damage from highly concentrated feline urine

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23
Q

What is the gold standard for diagnosis of a nonhemotropic mycoplasma infection?

A

Cultures

As the organism is slow growing it may be difficult to culture, it may require special growth media and transport

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24
Q

What are the benefits of PCR over culture for diagnosis of nonhemotropic mycoplasma infection?

A

Has improved sensitivity over culture, able to identify nonviable organisms, faster results

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25
Q

Which bacteria (actinomyces or nocardia) are part of the normal flora of the oropharynx, gastrointestinal tract, and urogenital tract?

A

Actinomyces

Nocardia is found in the environment and is inoculated via penetrating wound or from inhalation

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26
Q

Describe the staining and morphology of actinomyces and nocardia

A

Gram positive, rod shaped

Actinomyces is non-acid fast, nocardia is partially acid-fast

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27
Q

What is the empiric antibiotic treatment of choice for actinomycosis? for nocardiosis?

A

Actinomycosis - penicillins

Nocardiosis - TMS

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28
Q

Which has a better prognosis, actinomycosis or nocardiosis?

A

Actinomycosis, reported cure rates of 90% in the dog

Vs. nocardia which has 50% mortality rate and 38.5% euthanasia rate from lack of clinical response

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29
Q

How do the biologic requirements of actinomyces and nocardia differ?

A

Actinomyces is facultative or an obligate anaerobe

Nocardia is aerobic

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30
Q

How low should actinomycosis be treated?

How long should nocardiosis be treated?

A

Actinomycosis should be treated for 6-12 months

Nocardiosis should be treated for 1-3 months for simple cutaneous infections, up to 1 year for severe systemic infections

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31
Q

What are the clinical sighs of aldicarb toxicity?

A

Muscarinic overstimulationSLUDGESalivation, lacrimation, urination/urinary incontinence, defecation/diarrhea, gastric cramping, and emesisAdditional symptoms of the cholinergic toxidrome include miosis, bronchorrhea, bradycardia, and lethargyNiconitic overstimulation: tachycardia, hypertension, muscle fasciculations, tremors, respiratory depression, respiratory failure

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32
Q

Minimum lethal dosage of EG in dogs vs cats?

A

4.4-6.6 ml/kg dogs, 1.5 ml/kg cats

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33
Q

List the pathway for ethylene glycol.

A

EG, glycoaldehyde, glycolate, glyoxylate, oxalate(al-co-oxy-oxa)ADH converts EG to glycoaldehyde AND glycoaldehyde to glycolate

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34
Q

What is the rate limiting step in EG pathway?

A

glycolate to glyoxylate

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35
Q

What are the most toxic metabolites of EG on a per weight basis?

A

glyoxylate and glycoaldehyde; HOWEVER, b/c of its longer half life and greater systemic accumulation, GLYCOLATE is thought to be the major mediator IN VIVOR

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36
Q

The CNS effects that occur during the first 12 hours of exposure to EG thought to be due to…

A
  1. aldehyde metabolites2. hyperosmolality3. metabolic acidosis
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37
Q

Clinical signs during 30 min to 12 h exposure to EG?

A

Depression, incoordination, ataxia, seizures, paresis, vomiting, coma, PU/PD, proprioception deficits, LMN signs, muscle fasciculations, hypothermiaLike me when drunk:)

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38
Q

Clinical signs from 12 h to 24 h exposure to EG?

A

Sometimes resolution CNS signs (cats sometimes remain severely depressed), tachycardia, tachypnea, hypothermia, muscle fasciculations

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39
Q

Clinical signs 24-72h post exposure to EG?

A

Severe GI signs, oliguria/anuria, seizures, death, anorexia, oral ulcerations, ptyalism

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40
Q

Rise in osmolal gap ocurs as early as __ hr in cats and dogs and typically peaks by ___ hrs dogs.

A

1 hr, 6 hrs

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41
Q

How long does the osmolal gap remain elevated after EG ingestion?

A

up to 18 h

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42
Q

What is the normal osmolal gap?

A

10 mOsm/kg

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43
Q

What method is best to determine the osmolal gap?

A

freezing point depression

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44
Q

What normally develops in 3 hr of ingestion of EG?

A

high anion gap normochloremic metabolic acidosis

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45
Q

Why does EG cause hypocalcemia?

A

chelation of calcium with oxalic acid to form calcium oxalate crystals

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46
Q

Hyperglycemia is seen in over 70% of patients with EG toxicity. Proposed mechanims?

A
  1. aldehyde induced inhibition of glucose metabolism2. increased epinephrine3. increased endogenous cortisol4. uremia
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47
Q

When are calcium oxalate crystals seen?

A

w/i 3 hr in cats, 4-6 hr dogs

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48
Q

What can be done to the urine to help determine if EG toxicity?

A

Wood’s lamp the urine - will fluoresce up to 6 h after ingestion of toxin

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49
Q

What can cause a false positive EG test?

A
  1. propylene glycol2. glycerol3. lactate dehydrogenas4. lactic acid5. less than 50 mg/dl EG
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50
Q

What causes acidosis with EG toxicity?

A
  1. Metabolic products of EG (glycolic acid aka glycolate)2. Increased lactic acid production caused by NAD depletion during EG metabolism
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51
Q

Disadvantages to using ethanol to tx EG tox?

A
  1. exacerbates hyperosmolality2. exacerbates osmotic diuresis3. worsens metabolic acidosis by enhancing formation of lactate from pyruvate
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52
Q

How does ethanol cause hypoglycemia?

A

Metabolized to acetaldehyde which impairs gluconeogenesis

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53
Q

Advantages of 4MP?

A
  1. Greater affinity for ADH than ethanol2. Not associated with CNS depression, hyperosmolality, or osmotic diuresis
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54
Q

What’s different b/t cats and dogs regarding use of 4MP?

A

Cats require much higher doses, up to 6 times higher

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55
Q

What therapies are used to prevent metabolism of glycoxylic acid (glyoxalate) to toxic end products?

A

Thiamine (converts it to alpha hydroxy and beta ketoadipate) and pyridoxine (converts it to glycine then hippurate, needs benzoate)

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56
Q

Signs of muscarinic overstimulation?

A

PNS: vomiting, diarrhea ptyalism, urination, bradycardia, miosis, bronchorrhea, tenesmus

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57
Q

Signs of nictotinic overstimulation?

A

SNS: tachycardia, hypertension, mydriasisCNS: agitation, coma, respiratory depression/failureNM jxn: muscle fasciculation, weakness, paralysis

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58
Q

Anastasio, JVECC, 2011. What were the most common clinical signs of acute aldicarb toxicity?

A

vomiting (M 93%), ptyalism (M 86%), diarrhea (M 80%), tremors (N 73%)others: dull mentation, bradycardia (M), increased resp effort, miosis (M), ataxia (N), hyperthermia, tachycardia (N), mydriasis (N), tenesmus (M), resp failure (N)

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59
Q

DDx for acute aldicarb toxicity?

A
  1. intoxication (other carbamate, OPs, nicotine, phenothiazines,mushrooms with muscarine)2. envenomation (spider, scorpion, neurotoxic snake)3. Infectious dz (botulism, lepto, encephalitis, meningitis)4. Neuro dz (epilepsy, cerebral vasculitis, subarachnoid or subdural hemorrhage or hematoma)5. metabolic dz (uremia, hypo or hyper glu, myxedema coma, thyrotoxicosis)
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60
Q

What is methiocarb?

A

molluscicide and insecticide, carbamate, less toxic than aldicarb

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61
Q

How do you make a definitive diagnosis of aldicarb toxicity?

A

gas chromatography or mass spectrometry on tissue, urine, vomit, stomach contents

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62
Q

How is measuring AChE activity helpful with aldicarb tox?

A

<25% diagnostic if C/S fitNot reliable in cats b/c of presence of pseudocholinesterase in feline erythrocytes

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63
Q

What was most common lab abnormalities with aldicarb tox?

A
  1. lactic acidosis2. hyperglycemia
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64
Q

How does atropine help with aldicarb tox?

A

parasympatholytic - helps with muscarinic sings (not nicotinic)

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65
Q

What are side effects of atropine?

A

GI stasis, constipation and prolonged retention of toxin, dry mouth, thirst, mydriasis, tachycardia, dysphagia, if severe then dyspnea, ataxia, muscle tremors, resp failure, death

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66
Q

How is aldicarb excreted?

A

kidneys

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67
Q

What about aldicarb causes respiratory failure?

A

peripheral - profound NM weakness d/t nictonic overstimcentral - depression of medullary resp centerothers: aspiration pneumonia, bronchorrhea, bronchoconstriction

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68
Q

How could diphenhydramine be helpful with aldicarb tox?

A

blocks nicotinic receptor overstimulation (only been shown effective due to OP tox, not carbamate tox)

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69
Q

How is 2-PAM helpful?

A

oximes decrease toxicity of cholinesterase inhibitors by reactivating cholinesterases (used for OP tox, not really needed for carbamate b/c spontaneous hydrolysis occurs that rapidly reactivates AChE); HOWEVER, may be synergistic with atropine with carbamate toxicity from human studies

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70
Q

What was survival in aldicarb tox paper?

A

91%

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71
Q

What 6 systems are evaluated on the SSS?

A

pulmonarycardiovascularlocal woundGI systemhematologic systemCNS

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72
Q

In humans, SSS > ___ is considered severe?

A

8

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73
Q

Immediate adverse effects of antivenom.

A

Bradycardia, 2nd degree AV block, agitation, injection of pinnae and sclera, vomiting, fever, nausea, tachycardia, trembling, anaphylaxis

74
Q

OPCA is ___ times as otent as ACP

A

5.2

75
Q

Size of ACP vs OPCA

A

150 kDa vs 50 kDa

76
Q

Intralipid is from what fat?

A

soybeal oil based emulsion of long chain triglycerides

77
Q

Fat overload syndrome can cause…

A

fat embolism, hyperlipidemia, hepatomegaly, icterus, splenomegaly, thrombocytopenia, increased clotting times, hemolysis

78
Q

Adverse effects on pulmonary system from ILE.

A

increased PAP, increased venous admixture, decreased PaO2/FiO2, increased A-a, intrapulmonary shunting

79
Q

ILE improvement theories

A
  1. Improved myocardial performance by providing energy substrate2. Drug sequestration or lipid sink theory
80
Q

The higher the log P value, the more lipophilic a drug or chemical becomes. T/F

A

TP>1

81
Q

How does heparin treat complications of ILE?

A

Heparin causes the release of LPL and hepatic lipase from endothelium, an can potentially act as the rate limiting step in metabolism of triglycerides

82
Q

Side effects of cholinesterse inhibitors.

A

Pharnygeal and bronchial secretions, increased pharyngeal and bronchial secretions, diarrhea and enhanced GI peristalsis, increased urination, resp depression, arrest if desensitization blockade (abundance Ach at synapse)

83
Q

What is a cholinergic crisis?

A

result of cholinergic overload at NM jxn secondary to inhibition of cholinesterase

84
Q

Atropine MOA in cholinergic crisis.

A

competes with acetylcholine for the postsynaptic muscarinic receptor (does nothing for nicotinic receptors but helps with bronchospasm and bronchorrhea)

85
Q

Neurotoxin from Clostridium tetani

A

tetanospasm - prevents release of inhibitory neurotransmitters and results in unopposed muscle excitation and dysautonomia

86
Q

Beneficial effects of Mg for tetanus?

A

Nonspecific calcium channel blocker (decreases calcium entry into presynaptic terminals and decreases release of ACh)Decreases sensitivity of postsynaptic motor endplates to ACh - relaxation

87
Q

What is the earliest sign of Mg toxicity?

A

deep tendon hyporeflexia

88
Q

Effects of venom A?

A

Irreversible, pre-synaptic acting neurotoxin composed of acidic peptide and basic protein. Acidic: noncompetitive CCB blocks ACh releaseBasic: acts like PLA2 to hydrolyze acetyl bond on phospholipids

89
Q

Effects of venom B?

A

edema, tissue necrosisproteolytic enzymes and cytotoxinshyaluronidase and collagenase spread venom, protease cause coagulopathy

90
Q

Most common signs of cats vs dogs with essential oil products. Genovesse, JVECC, 2012

A

Cats - behavioral changes, seizures, tremorsDogs - lethargy92% clinical signs, 50% resolved with bath, 50% needed more care

91
Q

What are terpenes?

A

essential oils that are rapidly orally and dermally absorbed d/t lipophilic nature

92
Q

Salbutamol (albuterol) inhaler toxicity dogs…

A

tachycardia, hypokalemia, oral burns!! (pressurized hydrocarbons cause frostbite)

93
Q

Incidence of neurotoxicity from rattlesnake envenomation?Julius, JVECC, 2012

A

5.4%

94
Q

Findings from Julius, JVECC, 2012, Neurotoxicity in cats/dogs from rattlesnake envenomation.

A
  1. incidence 5.4%2. No diff b/t type of antivenom or #vials and neurotox, LOH, or survivial3. 11.8% PPV, half survived4. Overall mortality 18%5. Cats * longer LOH6. Cats overrepresented with neuro signs7. Diphenhydramine and colloids assc’d with survival
95
Q

Crotalidae polyvalent immune Fab (ovine) antivenom made from…

A

Eastern and Western diamondbacks, Mojave rattlesnake, cottonmouth

96
Q

ACP antivenom made from….

A

horses inoculated with Eastern and Western diamondback, Central and South American rattlesnakes, Fer-de-Lance

97
Q

What is myokymia?

A

muscle fasciculation associated with envenomationMOA: interaction of venom components with calcium or calcium binding sites on the nerve membrane

98
Q

MOA of Mojave toxin?

A

inhibits ACh release at PRESYNAPTIC terminal of the NM jxn, causing inhibition of NM transmission and eventually complete NM blockade

99
Q

MOA for hypokalemia from snake envenomation?

A

release of endogenous epinephrine that stimulates beta receptors on the cell surface, thereby stimulating Na-K-ATPase pumps, leasing to intracellular shift of potassium

100
Q

Toxic dose 5FU

A

5 mg/kg, lethal at 40 mg/kg

101
Q

Signs os 5FU toxicity

A

CNS (seizures, depression, ataxia, tremors), respiratory (cyanosis, distress), GI (diarrhea, vomiting, salivation), cardiac arrhythmias, death, severe myelosuppression, ocular signs

102
Q

5-FU MOA

A

metabolism of 5FU into fluorouridine triphosphate that then interferes with RNA synthesis and fxn; inhibits thymidylate synthase via FdUMP which leads to depletion of thymidine 5’ monophopshate and thymidine 5’ triphosphate thus accumulating deoxyuridine mono- and tri- phosphate - goes into new DNA and doesn’t work well leading to cell death

103
Q

How do you treat seizures from 5-FU?

A

phenobarb, meperidine, anesthesia - diazepam not effective

104
Q

What is the neurotoxin MOA coral snakes?

A

postsynaptic alpha-neurotoxins; block the nicotinic acetylcholine receptors of NM jxns and cause a curare-like effect characterized by vasomotor instability, CNS depression, and muscle paralysis

105
Q

Coral snake venom inhibits….plt aggregation.

A

ADP

106
Q

What lab parameters were elevated in all coral snake dogs?

A

AST and CK

107
Q

T/F - Both dogs and cats show hemolysis after coral snake envenomation.

A

F - only dogs

108
Q

Clinical signs of marijuana toxicity

A

CNS depression, ataxia, mydriasis, increased sensitivity to motion or sound, hyperesthesia, ptyalism, tremors, acute onset urinary incontinence

109
Q

Toxic compound marijuanan.

A

delta-tetrahydrocannabinol (delta-THC)

110
Q

MOA permethrins

A

modulate sodium ion channels, causing them to say open for a longer period of time, resulting in repetitive discharging of excitable cells

111
Q

How do you know of a drug is lipid soluble?

A

partition coefficient, log P reported to indicate lipophilicity, higher values = greater lipophilicity

112
Q

MOA for lipids

A
  1. Lipid sink2. Cardioprotective by provision of FAs which are major substrate of cardiac ATP production, + cardiac inotropic effects
113
Q

Potential adverse effects of lipids

A

acute allegic rxns, anaphylactoid reactions, fat overload syndrome (liver, fat embolism, thrombocytopenic, coagulopathy), sepsis, neuro signs, thrombophlebitis

114
Q

Osmolality of 20% lipids

A

350 mOsm/kg

115
Q

Lipid antidote

A

heparin

116
Q

Most common clinical sign from SSRI intoxication

A

CNS depression (JVECC, 2012)neuro and GI most common overall signs

117
Q

How is serotonin made?

A

from tryptophan via enzymes tryptophan hydroxylase and tryptophan decarboxylase

118
Q

Where is serotonin made?

A

most in CNS and enterochromaffin cells, some platelets95% stored in GI enterochromaffin cells and plts

119
Q

Where is serotonin stored in CNS?

A

presynaptic vesicles of serotonergic neurons, pineal gland, and catechoalminergic neuronsmetabolized by monoamine oxidase (MAO)

120
Q

What SSRI was associated with dose effect on clinical signs?

A

fluoxetine (JVECC, 2012)

121
Q

What is the toxin in mountain laurel (rhododendron) and MOA.

A

grayanotoxins - bind to sodium channels in excitable cell membranes of nerve, heart, skeletal muscle which increases membrane permeability of sodium ions in the excitable membranes, thus maintaining the cells in the state of depolarization

122
Q

Salicylate toxicity MOA

A

uncouples oxidative phosphorylation and disturbs Krebs

123
Q

Antidote for salicylate toxicity

A

none

124
Q

Principle tx of salicylate toxicity

A
  1. urinary alkalinization to increase rate of excretion2. hemodialysis effective
125
Q

Mechanism of GI signs in salicylate toxicity

A

Direct antagonism of prostaglandins which normally serve to increase epithelial cell turnover and mucus/bicarb secretion

126
Q

What acid base disturbance seen with severe salicylate toxicity?

A

respiratory alkalosis or mixed (metabolic acidosis with respiratory alkalosis)Toxin directly stimulates respiratory center causing tachypnea and respiratory alkalosis –> kidneys get rid of bicarb which makes it worse for impending metabolic acidosis (lactate and ketoacids)

127
Q

What type of metabolic acidosis seen with salicylate tox?

A

increased AG metabolic acidosis (lactate and ketoacids accumulate d/t uncoupling of oxidative phosphorylation)

128
Q

What lung problem can occur with salicylate toxicity?

A

noncardiogenic pulmonary edema

129
Q

Goals of urinary alkalinization with salicylate toxicity?

A

NaHCO3 to keep urine pH 7.5-8 and blood pH 7.35-7.5Increases renal excretion 10-20X

130
Q

Why is it important to prevent hypokalemia with salicylate toxicity?

A

Potassium reabsorption prevents excretion of an alkaline urine b/c of the exchange of potassium for hydrogen in the distal tubule (intercalated type A cell)

131
Q

What is the rational for empirically supplementing glucose with salicylate toxicity

A

neuroglycopenia can occur despite a normal blood glucose

132
Q

Amphetamine toxicity MOA

A

indirect-acting sympathomimetic amines and clinical signs d/t enhanced adrenergic stimulation and serotonin syndrome. Hyperdynamic sage can cause severe hyperthermia with rhabdomyoloysis, CNS signs, AKI, metabolic abnormalities

133
Q

Cocaine MOA

A

inhibits presynaptic neuronal uptake of dopamine, NE, and serotonin, and causes blockade of fast sodium channels = neuro and cardio signs

134
Q

Phencyclidine MOA

A

dissociative that antagonizes NMDA operated calcium channels; causes marked CNS depression or stimulation; increased ICP, also acts on delta-receptors causing dysphoria and hallucinations

135
Q

What 2 drugs may antagonize the effects of amphetamines and cocaine by antagonizing or blocking catecholamines

A

chlorpromazine, haloperidol

136
Q

Why do dogs become PU/PD after ingestion of cholecalciferol?

A

inhibition of ADH

137
Q

MOA of cardiac arrhythmias after cholecalciferol ingestion?

A
  1. mineralization of heart2. changes in ratio of IC to EX ion concentratione3. increase in depolarization threshold
138
Q

Tx cholecalciferol ingestion?

A

Tx hypercalcemia - saline diuresis to induce calciuresis, furosemide, glucocorticoids, salmon calcitonin (can cause anaphylaxis), pamidronatecalcitonin and pamidrongate inhibit osteoclastic activity

139
Q

LD50 bromethalin dogs vs cats

A

dogs 4.7 mg/kg, cats 1.8 mg/kg

140
Q

MOA bromethalin

A

uncouples oxidative phosphorylation, Na, K ATPase pumps fail, in goes water – cerebral edema and neuro predominate as clinical signsEnterohepatic recirculation, lots of charcoal

141
Q

Histopathologic evidence of bromethalin toxicity?

A

diffuse white matter vacuolation (spongy degeneration) with microgliosis

142
Q

What enhances zinc phosphide toxicity?

A

food b/c gastric acid secretion; once ingested and in acidic environment zinc phosphide hydrolyzed to phosphine gas and free radicals

143
Q

Strychnine MOA

A

prevents uptake of glycine at inhibitory synapses of Renshaw cells in CNS; inhibition of an inhibitory pathway called disinhibition, results in net excitatory effect from excessive afferent input and efferent response

144
Q

Risks of gastric lavage

A

hypoxia, dysrhytmias, laryngospasm, perforation of GI tract or pharynx, fluid and electrolyte abnormalities, aspiration pneumonia, aspiration pneumonitis

145
Q

Contraindications to gastric lavage

A

loss of protective airway reflexes (unless patient indubated), ingestion of a strong acid or alkali, ingestion of a hydrocarbon with a high risk of aspiration potential, risk of GI hemorrhage due to an underlying medical or surgical condition, hyponatremia if lavage with water

146
Q

If gastric lavage performed at 60 minutes post ingestion, mean recovery of markers?

A

8.6-13%

147
Q

Theories for ILE

A
  1. Lipid sink - sequestration of lipophilic compounds in the newly created lipid compartment2. Myocardial energy substrate improving cardiac performance3. Increasing cardiac calcium to restore myocardial fxn4. Increasing the overall fatty acid pool, which overcomes inhibition of mitochondrial fatty acid metabolism (eg, bupivicaine toxicity)
148
Q

List drugs/toxins that are not absorbed by activated charcoal.

A
  1. Hydrocarbons2. Lithium3. Ferrous sulfate (conflicting reports)4. Potassium5. Ethanol
149
Q

Urinary alkalinization is useful for what toxins?

A

SALICYLATES, PHENOBARBITAL, methotrexate, chlorpropamide, 2.4-dichlorophenoxyacetic acid, diflunasil

150
Q

Contraindications to urinary alkalinization?

A

Renal failure, heart failure (sodium load) - relative

151
Q

Complications of urinary alkalization?

A

Hypokalemia most common, hypocalcemia, coronary vasoconstriction (alkalemia shifts curve to left), cerebral vascoconstriction

152
Q

When should whole bowel irrigation be considered?

A

Sustained release or enteric coated drugs in patient presenting 2 hours after ingestion

153
Q

Contraindications for WBI?

A

bowel obstruction, perforation, ileus, recent surgery, hemodynamic instability, vomiting, GI hemorrhage

154
Q

How do you perform WBI?

A

Enteral administration (NG tube) of large amounts of polyethylene glycol electrolyte solution, osmotically active, liquid stool, no net absorption or secretion so no significant changes in water or electrolytes occur

155
Q

MOA zinc phospide rodenticides

A

After ingestion, phosphine gas produced by hydrolysis of zinc phospide in acidic moist stomach; phosphine gas rapidly absorbed across gastric mucosa then who knows…possible inhibition cytochrome C oxidase, inhibition serum acetyl cholinesterase activity, formation of reactive hydroxyl radicals, inhibition of catalase and peroxidase resulting in lipid peroxidationFood increases absorption b/c dec gastric acidity

156
Q

Tx zinc phosphide tox?

A

increase stomach pH (aluminum hydroxide, calcium carbonate, magnesium) then make vomit or do gastric lavage, charcoal probably not helpful, but give anyway

157
Q

What kind of drug is PPA

A

sympathomimetic amine, acts as an alpha-adrenergic receptor agonist and indirectly through increased release of stored norepi by alpha- and beta-adrenergic receptors

158
Q

PPA toxicity (JAVMA, 2011, findings)

A

Dose dependent side effects, 61% dogs showed signs including agitation, vomiting, mydriasis, lethargy, tremor/twitching, panting, bradycardia, tachycardia, hypertension, erythema, one dog died that ate 145 mg/kg (therapeutic dose 1-1.5 mg/kg)

159
Q

What is the toxin in bath salts?

A

methylene-dioxypyrovalerone (MDPV) - inhibit NE and dopamine reuptake and act as central system stimulants, clinical signs extreme sympathetic stimulation

160
Q

What’s used in humans to treat frostbite?

A

aspirin and prostacyclin

161
Q

SSRI toxicosis cats, JVECC, 2013, findings.

A
  1. 24% clinical signs2. Sedation > GI > CNS stimulation = CV = hyperthermia3. No deaths4. venlafaxaine had most clinical signs5. No assc’n b/t dose ingested and clinical signs
162
Q

Where is serotonin made normally?

A

raphe nuclei

163
Q

Systemic effects of serotonin?

A

vasoconstriction, plt aggregation, intestinal peristalsis, bronchoconstriction

164
Q

SSRI MOA

A

block reuptake of serotonin in presynapse, increasing serotonin at synaptic cleft

165
Q

What is the MOA of aldicarb?

A

CarbamateInhibits acetylcholinesterase leading to hyper excitability of cholinergic receptors

166
Q

What are the three types of calcium channels and which is the most sensitive to beta blockers?

A

Neuronal (N) type
Transient (T) type
Long-lasting (L) type - most sensitive

167
Q

Where are L type calcium channels found in the highest concentrations?

A

Atria
Vascular smooth muscle
Skeletal muscle

168
Q

What are the three major types of calcium channel blockers and what are their primary effects?

A

Phenylalkylamines (verapamil) - primarily chronotropic and dromotropic effects

Benzothiazepines (diltiazem) - Chronotropic and dromotropic effects

Dihydropyridines (amlodipine) - systemic vascular resistance and coronary resistance

169
Q

Describe the cardiac effects of calcium channel blockers

A

They inhibit the inward flow of calcium needed to initiate depolarization of the SA and AV node. This leads to slowed SA node activity, decreased conduction of impulses through the AV node, and resultant bradycardia

A negative inotropic effect is seen due to decreased calcium released from the sarcoplasmic reticulum and a decreased force of contraction

170
Q

Describe the vascular effects of calcium channel blockers

A

Calcium channels are in the vascular smooth muscle cells and are needed for vasoconstriction. Calcium channel blocks result in dilatation in systemic and coronary arteries and arterioles. Less of an effect is seen on veins as they have less smooth muscle in their walls.

171
Q

Describe the pancreatic effects of calcium channel blockers

A

Beta cells of the pancreatic islets which produce insulin also contain L type calcium channels. Calcium channel blockers may induce decreased insulin release leading to increased glucose levels in the blood and decreased glucose in the cells

Lack of intracellular glucose may impair cardiovascular function (the heart has to switch to fatty acid metabolism)

172
Q

Describe the two types of beta receptors - where are they found, and what do they do

A

Beta 1 receptors: located primarily in the heart, kidney, and adipose tissue. Stimulation of these receptors results in increases in heart rate, myocardial contractility, AV conduction velocity, and automaticity of subsidiary pacemakers

Beta 2 receptors: located primarily in the smooth muscle of the bronchial and vascular walls where they produce relaxation. They are also located in the pancreas, GI, and reproductive tracts

173
Q

What beta receptors do the following drugs affect?

propranolol, atenolol, esmolol, sotalol

A

Propanolol - Beta 1 and 2
Atenolol - Beta 1
Esmolol - Beta 1
Sotalol - Beta 1 and 2

174
Q

Describe the cardiac effects of beta blockers

A

Decreases transmembrane calcium flow by decreasing cyclic AMP synthesis, thereby decreasing atrial and ventricular contractility, slowing of the heart rate, and slowing the spread of excitation through the AV node and ventricles

175
Q

Describe the pulmonary, pancreatic, GI, vascular, and renal effects of beta blockers

A

Pulmonary - bronchoconstriction or bronchospasm
Pancreatic - inhibition of insulin release leading to decreased glycogenolyis, lipolysis, and gluconeogenesis
GI - contraction of the smooth muscle
Vascular - contraction of the smooth muscle
Renal - suppression of catecholamine-induced renin release resulting in decreased aldosterone synthesis

176
Q

Describe the pharmacokinetics of calcium channel blockers

A

Rapidly and almost completely absorbed via the GI tract
Have extensive first pass metabolism
Reach peak serum concentration in 20-45 minutes (or 4-12 hours for sustained release products)
80% protein bound
Metabolized the liver (cytochrome P450 CYP3A)
Certain classes are strong inhibitors of hepatic microsomal enzymes
Elimination half life varies, 2 to 30 hours
Excretion is primarily through urine

177
Q

Describe the pharmacokinetics of beta blockers

A

More lipid soluble ones (propranolol) require haptic biotransformation before excretion
Lipid soluble compounds have large volume of distribution and CNS faster and more extensively
Water soluble ones (atenolol) are excreted by the kidney
Esmolol is water soluble but does not accumulate as it is metabolized by erythrocytes

178
Q

What clinical signs /physiologic derangements are seen with beta blocker or calcium channel blocker overdose?

A 
Bradycardia
Negative inotropy and chronotropy leading to decreased cardiac output
Hypotension
Tissue hypoperfusion
Cardiovascular shock
179
Q

How do the following drugs work in treatment of beta blocker and calcium channel blocker overdose?

Atropine
Adrenergic agents (dopamine, epic, norepi, etc)
Vasopressin
Glucagon
Intravenous lipid emulsion
A

Atropine - vagolytic that can be given to reverse bradycardia and AV blockade

Adrenergic agents (dopamine, epic, norepi, etc) - used to counter hypotension, can pick alpha and beta activity based on what effects are being seen clinically

Vasopressin - used for refractory hypotension, stimulates V1 receptors

Glucagon - binds to receptor that are distinct from L type calcium channels and adrenergic receptors, stimulates adenyl cyclase which results in cAMP formation, and promotes release of Ca from sarcoplasmic reticulum, it also stimulates the AV and SA node so it has inotropic, dromotropic, and chronotropic properties

Intravenous lipid emulsion - they are variable fat soluble so may be contained in the “lipid compartment” and may also increase cardiac performance

180
Q

How does a calcium channel blocker overdose contribute to metabolic acidosis?

A

Calcium channel blockers inhibit mitochondrial calcium entry at the sarcolemma and mitochondrial membrane, which decreases pyruvate dehydrogenase activity. Pyruvate can’t enter the Krebs cycle and lactate accumulates

Auburn ECC (26 decks)

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