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ACVECC prep > Toxicology and Extracorporeal therapies (SACCM + Dobratz) > Flashcards

Toxicology and Extracorporeal therapies (SACCM + Dobratz) Flashcards

1
Q

For which toxicoses can ILE be considered as a life saving antidote?

A
  • Macrocyclic lactones (ivermectin, moxidectin)
  • Baclofen - muscle relaxants
  • Ca channel blocker and B blockers
  • Cholecalciferol
  • Bromethalin
  • NSAIDS (Ibuprofen, Naproxen)
  • Marijuana
  • Methamphetamine, cocaine
  • Local anesthetics
  • TCAs
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2
Q

List indications and contraindication to induce emesis

A
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3
Q

When is activated charcoal contraindicated

A
  • Heavy metals (Fe, Zn), xylitol, alcohols (EG, ethanol, methanol) ? don’t reliably bind to AC
  • Symptomatic patients who are at risk for aspiration pneumonia
  • AC with a cathartic should be used cautiously in hypovolemic, in dehydrated patients or those with excessive free water loss (e.g., diabetes mellitus, renal disease, diabetes insipidus)
  • Endoscopy
  • GI obstruction, hemorrhage or perforation
  • Recent surgery
  • Ileus
  • Ingestion of caustic substance or hydrocarbons
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4
Q

What are indication for multidose of AC?

A
  • Enterohepatic circulation

- XR (extended release) / LA (long acting) / SR (sustained release)

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5
Q

Complications of activated charcoal

A
  • Hypernatremia
  • aspiration pneumonia
  • the use of AC could confuse the diagnosis of intoxication of substances that can increase the osmolal gap such as ethylene glycol
  • difficult endoscopy
  • constipation
  • corneal abrasion (if contact with eyes)
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6
Q

List catartics that can be used in VM

A
  • sorbitol
  • sodium sulfate
  • magnesium sulfate
  • magnesium citrate
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7
Q

List potential toxins that can cause CNS stimulation

A
  • SSRIs, TCAs, amphetamines, 5-FU, Bromethalin, methylxantines, pyretrins, metaldehyde, strychnine, tremorgenic mycotoxins, sleep aids
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8
Q

List potential toxins that can cause CNS depression

A

Muscle relaxants (baclofen), opioids, sleep aids, marijuana, macrocyclic lactones (ivermectin, moxidectin)

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9
Q

T/F - α-agonist activity (such as imidazole decongestants found in nasal sprays and eyedrops or amitraz collars) can be reversed with the use of α-adrenergic antagonists such as yohimbine or atipamezole

A

TRUE

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10
Q

Explain mechanism of action of SAMe

A
  • Acts as a methyl donor
  • Generates sulfur-containing compounds that are imporant for conjugation reactions used in detoxfication.
  • Acts as a precursor of glutathione
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11
Q

Explain mechanism of action of NAC for acetaminophen toxicosis

A
  • Limits the formation of toxic metabolite NAPQI by providing alternative glutathione substrate with acetaminophen toxicosis (it is a glutathione precursor).
  • Binds with APAP metabolites making them inactive
  • Increases sulfate conjugation by being a sulfur donor.
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12
Q

Explain the lipid sink hypothesis of ILE therapy

A

compartimentalization of the drug in the lipid phase results in a decreased free drug concentration available to tissues

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13
Q

List effects of ILE other than “lipid sink”

A
  • provides energy substrates to myocytes augmenting cardiac performance (remember FFAs are the preferred substrate for myocardial cells)
  • restores myocardial function by increasing intracelular calcium
  • Increasing the overall fatty acid pool, which overcomes inhibition of mitochondrial fatty acid metabolism (e.g., bupivacaine toxicosis).
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14
Q

What are the dosage recommendations of ILE in VM?

A
  • Initial 20% ILE bolus 1.5 to 4 ml/kg (between 0.3 g/kg and 0.8 g/kg IV over 1 minute)
  • followed by 0.25 ml/kg/min CRI (0.05 g/kg/min IV over 30 to 60 minutes)
  • If not response: Intermittent bolusing at 1.5 ml/kg q4-6h for 24 hours can be considered; C19follow-up CRI doses of 0.5 ml/kg/hr (0.1 g/kg/ hr) can be continued until clinical signs improve (not to exceed 24 hours) or until serum is lipemic.
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15
Q

List adverse effects of ILE therapy

A
  • fat embolism
  • fat overload syndrom
  • phlebitis
  • local systemic infection if injection site is contaminated
  • pancreatitis
  • Interaction with lipophilic medications being given to patient
  • worsening of ARDS (decreased PaO2:FiO2 ratio)
  • allergic reactions, anaphylatic reactions
  • interferance with lab tests
  • Fat overload syndrome is reported in humans (not yet in VM) –> associated with excessive administration that overwhelms lipid clearance mechanisms and leads to: hyperlipidemia, hepatomegaly, splenomegaly, icterus, coagulopathy, hemolysis
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16
Q

Which components in regular therapies for toxicities can make a cageside Ethylene glycol test false positive?

A
  • Propylene glycol in Diazepam

- Glycerol in activated charcoal

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17
Q

T/F - Chocolate increases the pyloric sphincter tone and can be recovered inducing emesis up to 8h after ingestion

A

TRUE

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18
Q

Emetis generally empty __% of gastric content

A

40% to 60%

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19
Q

T/F In general gastric lavage is more efficacious than emesis for decontamination

A

FALSE

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20
Q

In which circumstances is recommended to administer milk, water or liquid from water-packed tuna?

A
  • SOME household products
  • corrosive or irritant products
  • exposure to toad secretions
  • taste reactions due to topically aplied products (foaming kitties following flea spray application)
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21
Q

What is a side effect of administration of 3% hydrogen peroxide in cats?

A

25% of cats can develop severe hemorrhagic gastritis, rarely death

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22
Q

What is a consequence of inducing vomiting in a patient that ingested petroleum distillates or hydrocarbons (kerosene, gasoline, motor oil, transmision fluid)?

A

toxicants can easily be aspirated –> severe aspiration pneumonitis

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23
Q

What’s the mechanism of action of Apomorphine and in which species is not effective

A
  • Acts on CRTZ (chemoreceptor trigger zone)

- cats

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24
Q

Xylazine causes emesis in ~___% of cats

A

50%

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25
Q

Over the counter urine ilicit drug screening tests are used for detection of…..
What is the disadvantage?

A
  • They test for: heroin, cocaine, THC, methanphetamines, PCP
  • Can give false positive if patient is on: opioids, trazodone, lidocaine, diphenhydramine, NSAIDS, others
  • Can give false negative for some THC metabolytes
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26
Q

What is the composition of ILE and how are they metabolized

A

Composition:

  • Medium to long chain tryglicerides (soybean oil, saffloer oil, etc)
  • Glycerin
  • Phospholypid emulsifier

Metabolism:
- tipically cleared by skeletal muscle, myocardium, splanchnic viscera and SC tissues where they are broken into glycerol, free fatty acids and choline to be used as energy by the tissues

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27
Q

What is the Log p?

A

Is the measure of the solubility of a compound between two solvents, one hydrophilic and one lipophilic

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28
Q

A compound is considered lipophilic is the log p is > ____

A

> 1

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29
Q

List the 4 RRTs

A
  • Intermitent hemodialysis (IHD)
  • Continuous Renal Replacement therapy (CRRT)
  • Hemoperfusion (HF)
  • Total plasma exchange (TPE)
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30
Q

What are the two main mechanisms of solute removal in RRT

A
  • Diffusion = movement of solute across semi-permeable membrane driven by transmembrane concentration membrane.
  • convection (aka. ultrafiltration) = movement of water and solvent drag across permeable membrane that occurs due to transmembrane pressure gradient. Convection allows for removal of middle (MW 500- to 60,000 Da) and large (MW > 60,000 Da) molecular weight solutes during dialysis
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31
Q

In which modes removal of solute occurs mainly by diffusion

A
  • IHD
  • Continuous Venovenous Hemodyalysis (CVVHD) –> mode or CRRT
  • Peritoneal dyalysis
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32
Q

In which modes removal of solute occurs mainly by convection

A
  • Continuous venovenous hemofiltration (CVVHF) –> mode of CRRT
  • SCUF
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33
Q

Which methods combine diffusive and convective modalities?

A
  • Continuous venovenous hemodiafiltration (CVVHDF)

- Application of ultafiltration during IDH and PD

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34
Q

The permeability of a dialyzer membrane is determined by

A
  • Pore size
  • surface area
  • thickness
  • membrane material
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35
Q

What are benefits of IHD over CRRT

A
  • Rapid solute removal
  • Smaller molecular weight water-soluble intoxicants are removed most efficiently by IHD.
  • IHD + charcoal hemoperfusion (CH) allows for removal of large solutes.
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36
Q

What are benefits of CRRT

A
  • slow and continuous solute removal
  • better tolerated than IHD in hemodynamically unstable patients, however, rapid toxin removal is almost always more ideal, and when performed by an experienced RRT team, IHD rarely leads to hemodynamic instability.
  • better clearance of larger molecular weight solutes due to:
    • diffusive and convective properties
    • membranes used in CRRT are often more permeable than IHD membranes
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37
Q

Solutes with a large Vd that are redistributed into the IV compartment have better clearance with……..CRRT or IHD?

A

solutes with a large Vd that are redistributed into the IV compartment have better clearance with CRRT compared with shorter IHD treatments

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38
Q

Does TCAs go enterohepatic recirculation?

A
  • Toxins with high protein binding capacity

- Toxin with large molecular weight (up to 40.000 Da)

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39
Q

What are potential complications of charcoal hemoperfusion and how can you eliminate this potential side effects?

A
  • Hypocalcemia
  • Hypoglycemia
  • Thrombocytopenia
  • *Due to non selective properties
  • priming volume of commercially available CH cartridges ranges from 150 ml to 240 ml  can lead to hemodynamic instability in < 10 kg animals
  • CH is performed in tandem with HD to decrease or eliminate these potential side effects: blood passes through the dialyzer after contact with HF cartridge  normalization of electrolyte abnormalities.
  • priming the extracorporeal circuit with blood, can be considered when treating smaller patients
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40
Q

Define the mechanism of action of TPE (aka. Plasmapheresis)

A
  • Separates the blood into its various components either by centrifugation or filtration
  • The plasma component of the blood is removed and replaced with a replacement s/n:
    ?colloid (albumin, Hetastarch, or plasma)
    ? or a combination of crystalloid and colloid
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41
Q

What are the advantages of TPE?

A
  • independent of the toxin size and protein binding
  • Removes the inciting toxin and toxic byproducts:
    • mediators of inflammation and other endogenous substances
  • Ideal for treatment of intoxications shortly after ingestion and for those toxins that have a small volume of distribution (Vd), because only the blood compartment is being treated and procedures are performed over a shorter period
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42
Q

What’s the molecular weight of albumin

A

69000 Da

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43
Q

Define volume of distribution

A

sum of all compartmental volumes that account for the total toxin distribution at an equilibrated state

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44
Q

What is the ideal Vd for maximal clearance of a substance with ECT

A

Equal or less than the blood volume because toxin removal occurs directly from the intravascular compartment.
- For toxins with a large Vd, concentration within the intravascular compartment decreases as the solute distributes between the body fluid compartments (intercompartmental equilibration

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45
Q

The speed of equilibration of a toxin depends on:

A

The characteristics of the toxin as well as the Vd

- Ex. a highly lipid-soluble, large-MW toxin with large Vd is likely to have a slower compartmental equilibration time.

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46
Q

Explain how post-treatment rebound occurs and give an example of a toxin that does that:

A

Plasma [ ] of the intoxicant may return to a toxic level as intercompartmental equilibration occurs –> after cessation of toxin removal via ECT, as the toxin redistributes from the other compartments into the IV space
** Ex. Phenobarbital

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47
Q

T/F uremia can alter the tissue binding capacity of some solutes, resulting in a decreased Vd

A

TRUE

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48
Q

What would happen with the Vd of a substance that is highly protein bound in a hypoproteinemic patient

A

The free fraction of drug increases but can re-equilibrate in tissue compartments and result in a higher Vd

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49
Q

What makes ethylene glycol toxicity a good option for IHD and what special consideration needs to be applied during the treatment

A
  • Low molecular weight (62Da) and non-protein binding capacity –> approx. 90 to 100% of the toxin and metabolites can be removed from circulation with a single session of IHD (with traditional medical management the toxic metabolites are not removed)
  • ethanol is added to the dialysate to inhibit ongoing metabolism of EG to its more toxic metabolites (conversion of glycoaldehyde by alcohol dehydrogenase)
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50
Q

T/F Acetaminophen is a small (151 Da), non–protein bound, highly water-soluble compound with a small Vd that could be treated with ECT

A

TRUE

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51
Q

Describe the general pharmacokinetics of NSAIDS

A

small size, highly protein bound (90-95% to mostly albumin) and small Vd - Some undergo enterohepatic recirculation (diclofenac, indomethacin, sulindac, etodolac, ibuprofen, naproxen, piroxicam, meloxicam, carprofen)

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52
Q

What method of ECT would you consider for an NSAID intoxication? What are potential limitations?

A
  • The high protein binding property of the drug favors the use of CH over conventional HD
  • in veterinary medicine, hemoperfusion is almost always performed simultaneously with HD to prevent the potential complications associated with CH.
  • The large extracorporeal volume needed to perform combined HD/HP limits the application for this modality to larger patients.
  • It is difficult to determine when a HP cartridge is saturated, although in the author’s experience this typically occurs 4 to 6 hours after the start of therapy
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53
Q

What are benefits and limitations of the use of ECT in Amanita Phalloides toxicity?

A
  • It is an ideal toxin to remove via ECT due to it’s small Vd, however it’s rapid absorption and short plasma half life limit the benefit of the treatment
  • Has high affinity for AC
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54
Q

What could be indications of using ECT in barbiturate toxicity?

A
  • when severe intoxication with long-acting barbiturates occurs, ECTs can be used to decrease hospital stay and to avoid complications such as aspiration pneumonia that can occur in severely obtunded or comatose patients
  • Given the large Vd, rebound of drug into the intravascular space is likely to occur after treatment with HD/HP, with resultant recurrence of clinical signs. In these situations, multiple or prolonged ECT sessions may be indicated
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55
Q

T/F - barbiturates undergo enterohepatic recirculation

A

TRUE

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56
Q

Differences between IHD and CRRT equipment. Describe the different modes

A

IDH
- has mainly diffusion mode and a bit of convection
CRRT (Prismaflex machine common in VM)
- Predominantely convection
- Combines up to 4 modes of diffusion and convection:
**Slow coninuous untrafiltration (SCUF) (convection)–> ultrafiltrate gets discarded, hemoconcentrated blood goes back to patient
**CVVH (convection)–> A a balanced electrolyte solution replaces the ultrafiltrate
** CVVHD (diffusion)–> similar to IHD but the rate is very slow
**CVVHDF –> combines diffusion and convection, the grade of convection and diffusion can be adjusted independently

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57
Q

List indications for RRT

A
  • Severe electrolyte/acid-base disturbances non responsive to medical management/ AKI (BUN >100mg/dL, creat >10mg/dL)
  • Fluid overload (specially when anuria/oliguria are present)
  • CHF
  • Refractory hyperkalemia
  • compromised patients secondary to uremic toxemia
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58
Q

T/F CRRT is a continuous modality, which most closely mimics endogenous renal function.

A

TRUE

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59
Q

Which RRT modality has a high maximum removal ratio to low molecular weight solutes per unit of time

A

IHD

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60
Q

T/F The physiologic peritoneal membrane is defined to have three different pore sizes, allowing for movement of both small and larger molecular weight solutes

A

TRUE. Large pores, 100 to 200 A˚in diameter, correspond to clefts in the endothelium and allow the transport of macromolecules such as albumin. They are present in very small numbers, accounting for less than 0.01% ofthe total pore surface area. Small pores, 20 to 25 A˚ in diameter, also correspond to clefts in the endothelium. They present in large numbers, representing more than 90% ofthe pore surface area, and allow the passage of low molecular weight substances such as urea. creatinine, and glucose. Ultra small pores, 4 to 6 A˚ in diameter, are aquaporin I channels found within peritoneal capillary and mesothelial cells, and transport only water

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61
Q

Define ultrafiltration

A

Ultrafiltration is the process of plasma water removal from the intravascular compartment (and ultimately from the interstitial and intracellular spaces as redistribution occurs)

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62
Q

List contraindications for peritoneal dialysis

A

Contraindications for PD in veterinary medicine include peritonitis, recent abdominal surgery, and hypoalbuminemia.

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63
Q

T/F In IHD and the CVVHD and CVVHDF modes of CRRT, the dialysate flows countercurrent to the blood to allow for maximum solute removal. In

A

TRUE

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64
Q

Which are the three mechanisms by which fluids and solutes are transported aross the peritoneal membrane

A
  • Diffusion
  • Convection (Solvent drag) –> when solutes are carried along with the bulk flow of water during ultrafiltration (not very relevant in PD)
  • ultrafiltration –> removal of fluid (water) during PD –> desired when performing PD in animals that are overhydrated
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65
Q

T/F Urea has a relatively low molecular weight of 60 and diffuses more rapidly than creatinine, which has a molecular weight of 113

A

TRUE

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66
Q

List possible indications for peritoneal dialysis

A
  • AKI, severe uremia
  • Toxicities where toxin is highly diffusible (EG, ethanol. Barbiturates)
    severe metabolic disturbances (hyperkalemia, hypercalcemia, hepatic encephalopathy)
  • life threatening fluid overload
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67
Q

Dialysis for removal of solutes generally is performed using ____% dextrose. Dialysates containing___% and ___% dextrose are used in moderate to severely overhydrated patients.

A
  • 1.5% dextrose.
  • 2.5%
  • 4.25%
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68
Q

How would you prepare a dialysate solution for PD?

A

Adding dextrose to lactated Ringer’s solution can make a suitable dialysate solution. Osmolality should closely approximate that of the patient, and the dextrose concentration should be at least 1.5%. Adding 30 mL of 50% glucose to 1 L of lactated Ringer’s solution will result in a 1.5% dextrose solution.
- Heparin (250 to 1000 U/L) should be added to the dialysate for the first few days after catheter placement to help prevent occlusion of the catheter by fibrin deposition. This heparin is minimally absorbed by the patient’s circu- lation and is unlikely to prolong clotting times.

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69
Q

Describe the exchange procedure of peritoneal dialysis

A

Dialysate is infused at a dosage of30 to 40 mL/kg during a 10-minute period.12,14,39,57 The dialysate is allowed to remain in the peritoneal cavity for 30 to 40 minutes (dwell time) and then is drained into a collection bag by gravity during a 20- to 30-minute period. A 90% to 100% recovery of dialysate is expected. This process is repeated continually, and the dialysate formula and dwell times are adjusted every 12 to 24 hours according to the animal’s need.

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70
Q

What is a disadvantage of using highly concentrated dextrose solutions for peritoneal dialysis

A

Although more concentrated dextrose solutions allow for effective fluid removal from the patient, these concentrates are more likely to lead to secondary peritonitis and dysfunction of the peritoneal membrane

  • Glucose activates the polyol pathway and the secretion of transforming growth fac- tor-b1 (TGF-b1), monocyte chemoattractant protein-1 (MCP-1), and fibronectin. in vitro data suggest that glu- cose is involved in the development of peritoneal fibrosis. Glucose is likely to be involved in the development of peritoneal neoangiogenesis.
  • A third mechanism by which glucose can damage the peritoneal tissue is by inducing nonenzymatic glycosylation oftissue proteins, which leads to the formation of advanced glycosylation end products (AGEs). The depo- sition ofAGEs in the vascular wall also leads to ultrafiltration failure
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71
Q

Which anticoagulation methods are most commonly used in IHD and CRRT?

A
  • Systemic heparinization –> IHD

- Regional citrate –> for CRRT

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72
Q

Define dialysis disequilibrium syndrome

A

In severely uremic patients, rapid removal of uremic toxins should
be avoided to prevent dialysis disequilibrium syndrome. Rapid removal of osmotically active solutes from the blood compartment creates osmotic pressure gradients between the blood, extravascular, and intracellular compartments. This gradient allows plasma water to shift from the vascular compartment and into the intracellular compartments. When this phenomenon occurs in brain tissue, sec- ondary swelling occurs and this can lead to irreversible neurologic damage or death

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73
Q

The goal of PD for an animal with renal failure is to remove enough urea to maintain the BUN concentration at ____mg/dL

A

70mg/dL

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74
Q

How can you prevent dialysis disequilibrium syndrome

A
  • when severe uremia is present, initial treatments must be designed to achieve slow solute removal. (CRRT?)
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75
Q

What is the normal dialysate volume per exchange cycle in peritoneal dialysis? Why is this important?

A
  • 30-40ml/kg
  • In PD, precise measurements of dialysate inputs and outputs must be recorded to avoid overhydration of the patient
  • If fluid balance becomes positive or returning volume decreases to less than 90% of what was administered, the dialysate should be changed to encourage ultrafiltration
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76
Q

What are disadvantages of CRRT

A

The intensive prolonged treatments required with CRRT and the need to have a dedicated and trained technical staff for the duration of the treatments make it difficult to carry out quality treatments in many veterinary practices. In addition, the cost for premade dialysate can become cost-prohibitive when high dialysate flows were required. In addition, since CRRT is not designed to be a long-term treatment modality, it is necessary to have facilities available to provide longer-term care for patients that remain dependent on RRT

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77
Q

Describe the 4 cathegories of applications for apheresis in human medicine based on the defined or proven benefit that apheresis provides

A

I - considered standard of care for that condition (ex. Myastemia gravis)
II - considered suppoertive therapy in combination with other therapies (ex. Amanita poisoning)
III - condition in which controlled trials are limited or their results inconclusive
IV - condition in which therapy appeared to be ineffective or harmful

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78
Q

How many plasma volumes are removed with each plasmapheresis treatment? Why?

A
  • One
  • For most higher-molecular-weight substances, such as immunoglobulins, the efficiency of patho- logic substance removal is not increased when more than 1 or 1.5 plasma volumes are exchanged in a single treatment.
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79
Q

In which disease processes has apheresis been used most commonly in the CC setting in VM?

A
  • Myastenia gravis
  • IMHA

** Although case numbers are low, the anecdotal success in these cases is promising

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80
Q

Mention advantages of TPE in IMHA patients

A

Use of TPE allowed patients that were previously crossmatch incom- patible due to severe agglutination to receive blood transfusions. likely because of a reduction in antibody load
- Use of TPE allowed for successful control of disease with the same immunosuppressive protocols that had been previously unsuccessful in those patients

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81
Q

Explain the arachidonic acid pathway

A

After a tissue has been damaged, arachidonic acid is released from cell membranes, precipitating a chain of events known as the arachi- donic acid cascade. Two enzyme groups metabolize arachidonic acid: the lipoxygenases (LOX) and the cyclooxygenases (COX). Products from the LOX cascade include leukotrienes and chemotactic factors. Products of the COX cascade include prostacyclin, thromboxanes, and prostaglandins.

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82
Q

List functions of the prostaglandins

A

Important in maintaining local blood supply to tissues

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83
Q

Define constitutive vs inducible prostaglandins

A
  • Continuously produced (constitutive) prostaglandins are required for the normal function of the brain, kidneys, gastrointestinal tract, primary hemostatic system, and reproductive system.
  • Inducible prostaglandins are produced in response to tissue injury. They escalate the inflammatory response and increase peripheral nerve sensitization; they also have protective actions and play a role in tissue repair
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84
Q

What is the difference between COX 1 and COX2 prostaglandins?

A
  • most COX-1–induced prostaglandins are constitutive and have homeostatic effects, some are also produced in response to tissue injury.
  • although many prostaglandins produced by COX-2 are inducible, there are constitutive COX-2 prostaglandins found in the brain, intestine, and kidneys in many species. COX2 appears to be constitutive in canine pyloric and duodenal mucosa and these products are important for healing of gastoduodenal ulcers
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85
Q

Mention COX dual acting medications and COX2 selective medications

A
  • Dual acting –>Aspirin, ketoprofen, tepoxalin

- COX2 selective: carprofen, meloxicam, deracoxib, firocoxib

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86
Q

Explain the mechanism of gastric ulceration secondary to COX medications

A
  • COX1 induced prostaglandins in gastric mucosa have protective effects –> mucous production and enhance local blood flow –> COX 2 is stimulated when damage to the gastric mucosa occurs and produces prostaglandins important in mucosal healing –> NSAIDS can inhibit all these
  • Some NSAIDs, such as aspirin, can cause direct injury to the gastric mucosa by disrupting surface phospho- lipids, allowing gastric acid to penetrate directly to the cells in the wall of the stomach
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87
Q

What could be an explanation of why the gastric mucosa is more susceptible o NSAID even at lower doses when compared to other tissues?

A

NSAIDs are weak acids that become lipid soluble in the highly acidic environment in the stomach. This allows them to penetrate easily into gastric cells, where they become trapped in the relatively more alkaline environment. This leads to a high local concentration of NSAIDs in the gastric mucosa and may be an explanation for adverse effects occurring in the gastrointestinal system at lower doses than in other organ systems.

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88
Q

Which NSAID medication seems to have the lowest incidence of gastrointestinal ulceration?

A

Carprofen

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89
Q

List the effects of COX inhibitors in the kidneys

A
  • Inhibition of prostaglandins production by the juxtaglomerular apparatus –> inhibitis prostaglandin mediated local vasodilation of afferent arteriole in cases where GRF is decreased –> decreased renal blood flow –>AKI
  • Inhibition of renin release by the JGA (this process is mediated by COX1-COX2 enzymes
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90
Q

T/F NSAID use has been associated with an increase in liver enzymes and hepatocellular injury in some patients. This toxicity depends on dose and duration of treatment

A

FALSE - NSAID use has been associated with an increase in liver enzymes and hepatocellular injury in some patients. This toxicity does not depend on dose or duration of treatment and therefore is classified as an idiosyncratic reaction. –> typically occurs within the first 3 weeks of administration, but can happen after months/years.

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91
Q

What are the effects of COX-1 and COX-2 in coagulation?

A
  • COX-1 –> promotes production of TXA2 –> more platelet agregation and vasoconstriction
  • COX-2 –> promotes production of PGI2 (prostacyclin) –> vasodilation and inhibits platelet aggregation
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92
Q

T/F Aspirin is the most effective NSAID for reducing platelet aggregation because it binds permanently and decreases TXA2 production for the life of the platelet.

A

TRUE. Platelets lack a nucleus and are unable to synthesize new COX enzymes

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93
Q

Which medications can reach toxic plasma concentrations when combined with an NSAID

A

Protein-bound drugs –> other antiinflammatory agents, warfarin, phenytoin, penicil- lins, and sulfonamide antibiotics. NSAIDs can also increase plasma levels of digoxin and can decrease the efficacy of furosemide.

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94
Q

T/F - Drugs that induce cytochrome P450 metabolic pathway in the liver (e.g., phenobarbitone) can decrease NSAID metabolism, increasing their analgesic efficacy

A

FALSE -Drugs that induce cytochrome P450 metabolic pathway in the liver (e.g., phenobarbi- tone) can increase NSAID metabolism, reducing their analgesic efficacy

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95
Q

Which findings in the UA are idicative of renal damage and can help differentiale renal from pre-renal azotemia?

A
  • isostenuria can be indicative of acute renal insuficiency
  • casts in urine sediment can indicate renal tubular injury as an early sign of toxicity
  • proteinuria can indicate glomerular damage
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96
Q

In general, how many half lifes are going to determine treatment duration in a case of NSAID overdose?

A

In most cases of medication overdose, treatment duration depends on the half-life of the drug that has been ingested; treatment should continue until at least three half- lives have passed.

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97
Q

List the half life of NSAID medications –> fill table

A
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98
Q

Which antinausea medication is contraindicated in a case of NSAIDs toxicity and why?

A

Metoclopramide should be avoided because this dopamine antagonist could decrease renal blood flow.

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99
Q

NSAIDS-induced renal injury is characterized by:

A

Papillary necrosis and interstitial nephritis

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100
Q

What is the mechanism of action of misoprostol?

A

PGE1 analog

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101
Q

What is the proposed toxic substance within grapes, raisins and currants?

A

Two dogs that ingested potasium bitartrate (cream or tartar) developed acute azotemia and isostenuria, one ingested 2 tea spoon of cream of tartar, the second one ingested homemade play dough made with cream of tartar. Second dog died and necropsy revealed changes similar to the ones reported in raising toxicosis –> cortical tubular degeneration,
necrosis, and mineralization, with some evidence of regeneration.
- Potassium bitartrate is the salt of tartaric acid, and both potassium bitartrate and tartaric acid are uniquely present in high concentrations in grapes and tamarinds.
- Interestingly, the ASPCA Animal Poison Control Center has had reports of severe vomiting and acute renal failure in dogs following large exposures to tamarinds, which are also uniquely high in tartaric acid.

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102
Q

What are the effects of lily toxicity in cats

A
  • proximal tubular epithelial cells necrosis, edeme and tubular obstruction in the kidneys
  • pancreatitis
  • vomiting, lehtargy and hypersalivation appear within 1 to 5 days (some as soon as 1-3h)
  • seizures, ataxia (40% of cats)
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103
Q

T/F A common finding in cats with Lily toxicosis is a more markedly elevated serum creatinine concentration compared to a more moderate blood urea nitrogen

A

TRUE

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104
Q

Approximately ______% of dogs will remain asymptomatic following grape or raisin exposure. Dogs which developed AKI reportedly had a _____% survival rate. The median time until resolution of azotemia in surviving dogs was 16 days for BUN and ____days for creatinine.

A
  • 25-60%
  • 53%
  • 30 days
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105
Q

The prognosis for cats which have been given supportive care shortly after exposure to Lilys is good, up to 100% survival in one study. Cats developing AKI have reportedly had a grave prognosis, _______% mortality in several studies. Survival rate for cats treated with dialysis is reportedly ______%

A
  • 50-100%

- 50%

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106
Q

What’s the mechanis of action of benzodiazepines

A
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107
Q

What’s the mechanis of action of imidazopyridines, oyrazolopyridines, cyclopyrrolones?

A
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108
Q

What’s the mechanis of action of penothiazines, alpha-agonist and barbiturates?

A
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109
Q

Is there an specific therapy for sedatives overdose?

A

only reversals for opioids, benzodiazepines and alpha-2 agonist. Other than than is supportive and sympthomatic care.

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110
Q

What is the LD50 of Diazeman and Midazolam

A

> 20mg/kg (dogs) and 1600mg/kg IV respectively

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111
Q

what is the LD50 of acepromacine?

A

257mg/kg PO / 61mg/kg IV (mice)

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112
Q

what is the LD50 of Pentobarbital?

A

85mg/kg PO or 50mg/kg IV (dogs)

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113
Q

T/F Flumazenil can also revert effects of imidazopyridines, pyrazolopirimidines and cyclopyrrolones

A

TRUE

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114
Q

List alpha-2 agonist reversals

A
  • Atipamezol
  • Yohimbine
  • Tolazoline

**last 2 are less specific and have more side effects

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115
Q

Fill table of skeletal muscle relaxants of clinical and toxicologic importance and their mode of action

A
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116
Q

What are the indications of AC use for muscle relaxant toxicity?

A

For patients that ingest baclofen or carisoprodol, only one dose of activated charcoal with a cathartic is necessary because these drugs do not undergo enterohepatic circulation. For the remaining muscle relaxants, efficacy of multidose activated charcoal regimens has not been established

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117
Q

What would be your drug of choice to control seizures in a patient with baclophen or carisoprodol toxicity?

A
  • Diazepam, despite also being a γ-aminobutyric acid agonist, is the drug of choice for baclofen- and carisoprodol-induced seizures
  • if carisoprodol has been ingested, barbiturates are not recommended for seizure control because they may compound the CNS depression
118
Q

What is the prognosis of muscle relaxants ingestion?

A

The prognosis for toxicity with most of these muscle relaxants in veterinary medicine is unknown. For symptomatic patients with baclofen toxicity, resolution of clinical signs may take several days in severe cases, but if adequate supportive care and monitoring are available, the prognosis is generally good

119
Q

Fill table with opiate receptor and specific function/side effect

A
120
Q

what are the natural opioids and which ones are the synthetic?

A
  • Natural = codeine, morphine

- Synthetic = fentanyl, methadone, hydrocodone, hydromorphone, heroin

121
Q

What is the mechanism of action of opioids?

A

Opioid receptor activation results in inhibition of adenyl cyclase activity, activation of receptor-operated potassium currents, and suppression of voltage- gated calcium currents. These effects cause hyperpolarization of the cell membrane, decreased neurotransmitter release, and reduced pain transmission

122
Q

Functionally, opioids can be classified into four groups:

A
  • morphine-like opioid agonists
  • opioid antagonists
  • mixed agonist-antagonists
  • partial agonists
123
Q

T/F - Morphine, oxymorphone, hydromorphone, butorphanol, and buprenorphine are well absorbed after intrave- nous, intramuscular, subcutaneous, oral, and rectal administration. However, first-pass metabolism is significant and results in low bioavailability and a less predictable effect after oral ingestion

A

TRUE

124
Q

T/F Low lipid-soluble drugs (e.g., codeine, fentanyl, and heroin), onset of action occurs more rapidly, and the pharmacologic effects resolve earlier.

A

FALSE - highly lipid-soluble drugs (e.g., codeine, fentanyl, and heroin), onset of action occurs more rapidly, and the pharma- cologic effects resolve earlier. Drugs that are less lipid soluble, such as morphine, move less rapidly and therefore take longer to be effec- tive and may have a longer duration of action

125
Q

T/F - All opioids are metabolized primarily in the liver via glucuronidation. Cats are deficient in this metabolic pathway, and therefore the half-life of certain drugs may be prolonged

A

TRUE

126
Q

In normal dogs, the lethal dose for morphine is

A

100mg/kg

127
Q

How can opioids contribute to increased ICP?

A

Opioids may lead to hypoventilation and hypercapnia, which cause cerebral vasodilation and increased intracranial pressure.

128
Q

Why a fetus may suffer severe depression after administering a dose of opioids to the mother?

A
  • In the developing fetus, opiates pass more easily into the CNS because the blood-brain barrier is not fully developed.
  • Small amounts of opioids also are distributed into the milk of nursing mothers.
129
Q

List 4 medications that can potentiate the effects of opioids

A
  • Monoamide oxidase inhibitors (MOAs)
    — fentanyl, meperidine, tramadol,
    methadone, and dextromethorphan are weak serotonin reuptake inhibitors and have been involved in serotonin toxicity reactions with MAOIs
  • Phanotiazines
  • Erythromycin
  • Cimetidine
130
Q

What is a classic triad of clinical signs seen with opioid toxicity?

A

There is a classic triad seen with opioid toxicity: CNS depression, respiratory depression, and miosis in dogs. Cats typically develop mydriasis.

131
Q

Why miosis occurs in dogs with opioid toxicity

A

from µ-related stimulation of the visceral nuclei of the oculomotor nuclear complex and the parasym- pathetic nerve that innervates the pupil

132
Q

T/F - Opioids may alter the thermoregulatory response. Hyperthermia is seen commonly in dogs, whereas hypothermia may occur in cats

A

False - Opioids may alter the thermoregulatory response. Hypothermia is seen commonly in dogs, whereas hyperthermia may occur in cats

133
Q

Why opioids cause respiratory depression?

A
  • reduction in responsiveness to CO2 in the brainstem respiratory center as well as the centers that regulate respiratory rhythm.
  • Areas of the medulla oblongata that control ventilation (nucleus tractus solitarius and nucleus ambiguus) have many opioid binding sites, and these respiratory neurons are inhibited by opioid receptor agonists.
134
Q

Why opioids cause panting?

A

by resetting the thermoregulatory center, so the animal attempts to lose heat by increasing the respiratory rate, despite a normal to low body temperature

135
Q

Why morphine and meperidine should be avoided in animals with mast cell disease or envenomation?

A

when given IV , may cause histamine release leading to peripheral dilation (arterial and venous) and bradycardia. Cutaneous signs include itching, warmth, and urticaria

136
Q

Why opioids cause nausea?

A

They stimulate chemoreceptor triggering zone

137
Q

What are the GI effects of opioids?

A
  • Decreasedlower esophageal sphincter tone
  • Increase tone and decreased propulsive activity of small intestines
  • Decreased motility
  • lower small intestinal secretions and enhance intetsinal fluid absorption
  • *constipation
  • Morphine has been associated with spasm of sphincter of Oddi –> contraindicated in obstructive biliary or pancreatic disease
138
Q

What are the urinary effects of opioids?

A
  • At high doses, opioids may increase ureteral tone, bladder tone, and external sphincter tone, leading to urinary retention.
  • µ-agonist increase ADH release –> reduced urine production, increased USG
139
Q

Is oral decontamination recommended In patients thathave had oral exposure to opioids?

A

yes, particularly those drugs that can have delayed absorption such as loperamide and sustained-release morphine products.

140
Q

Which opioid receptor does not provide analgeisa?

A

sigma –> responsible for autonomic stimulation, dysphoria, hallucinations

141
Q

Explain Naloxone mechanism of action, onset and duration of effect and dose

A
  • competitively binds opioid receptors κ, δ, and, particularly, µ. It has a greater affinity for receptors than do the agonists.
  • It is highly lipophilic and moves rapidly into the CNS.
  • usually has an onset of action of 1 to 2 minutes when given intravenously.
  • duration of action ~ 45 to 90 minutes.
  • dose for dogs and cats = 0.01 to 0.04 mg/kg. IV,, IM, SC, IO, ET
  • Naloxone may have a shorter duration of action than most
    opioids, and repeated doses or a continuous infusion may be necessary.
142
Q

Why cocaine has symphatomimetic effects?

A
  • due to reuptake inhibition of norepinephrine, serotonin and dopamine
  • There is stimulation of endogenous catecholamine release having direct effects in the myocardium and CNS
143
Q

List differentials for cocaine toxicity

A
  • Amphetamines
  • methamphetamines
  • serotonergic drugs
  • caffeine
  • mycotoxins
  • strichnine
  • metaldehyde
  • Pheochromocytoma
144
Q

What is the mechanism of action of methamphetamines?

A
  • sympathomimetic stimulant due to inhibition of MAO(Monoamide Oxidase) and direct cathecholamine release:
    • inhibitis reuptake of serotonin
    • direct stimulation of dopamine and serotonin receptors
145
Q

What is the toxic component in marijuana? What is Hashish?

A
  • Toxicity is due to the psychoactive compound delta-9-tetrahydrocannabinol (THC).
  • “Hashish” refers to the highly concentrated resin from the flowering portion of the plant.
146
Q

Following ingestion, THC is converted in the liver and lung to ________, the primary metabolite

A

11-hydroxy-delta- 9-THC

147
Q

Which are the major canabinoid receptors and where are they located?

A
  • CB1 –> Located in CNS

- CB2 -> Located in peripheral tissues

148
Q

T/F All clinical effects of THC are thought to be due to activity at CB1 receptors

A

TRUE

149
Q

Which neurotransmiters are inhibited by CB1 receptor activation in Marijuana toxicity?

A

acetylcholine, glutamate, GABA, norepinephrine, dopamine, 5-HT

150
Q

T/F While results of urine drug tests must be interpreted with caution, it is generally accepted that a positive test most likely indicates true THC toxic- ity and a negative test does not exclude the possibility of exposure.

A

TRUE. dog urine may contain altered THC metabolites not detected via human drug-screening kits, making their use controversial

151
Q

What is the mechanism of Xylitol toxicity in dogs and how is it correlated with the dose ingested?

A
  • doses over 0.1g/kg –> massive release of insulin and hypoglycemia for 12-48h
  • doses >0.5g/kg –> hepatic necrosis and fulminant liver failure in 9 to 72h post-ingestion
152
Q

Which are the 2 main methylxantines that cause most of the clinical sings in chocolate toxicity

A
  • caffeine

- theobromine

153
Q

T/F “White” chocolate is not chocolate at all, so is considered non-toxic

A

TRUE

154
Q

What is a possible additional side effects of chocolate toxicity secondary to the high fat content of most chocolates?

A

Pancreatitis

155
Q

Which are member of the Allium genus?

A

onions, leeks, chives and garlic (cebollas, puerros, cebollines y ajo)

156
Q

What are hematology findings in Allium toxicity cases?

A
  • Hemolysis
  • Anemia
  • Heinz bodies
  • Methemoglobinemia
157
Q

Mention 2 main complications after bread dough ingestion in dogs

A
  • abdominal distention
  • GI obstruction
  • respiratory and vascular decompensation
  • Ethanol production due to yeast fermentation –> signs of alcohol toxicity (CNS depression, ataxia, severe cases can require mechanical ventilation
158
Q

If an owner reports that his dog got into snail and slug control products, what is the most likely toxin ingested? What are possible clinical signs? What is the expected recovery time with adequate treatment/supportive care?

A

Metaldehydes

  • signs: muscle tremors, hyperestesia, tachycardia, hyperthermia, severe neuro signs (seizures), respiratory failure
  • Full recovery can take up to 3 days in severely affected animals, most of them recover within 24h
159
Q

What are local effects of household cleaning products containing acids?

A
  • local coagulative tissue necrosis
  • mouth –> pain, dysphagia, vomiting, ulcers
  • eyes: corneal ulceration/melting
160
Q

What decontamination approach would you advise in a patient that ingested acid containing products

A

Acids are some of the few toxins where decontamination is not advocated due to the risk of worsening corro- sive injury. Initially, administering water or milk to the patient may dilute the product and limit the effects of exposure. Following this, treatment is mostly sympto- matic and geared towards pain management. For dermal or ocular exposures, flushing with copious amounts of water for over 15 minutes is recommended.

161
Q

Why alkalis ingestions may not immediately be apparent?

A

These agents will cause severe corrosive injury without associated pain, which is why clinical signs may not immediately be apparent. Clinical signs that do develop are often related to the underly- ing mucosal damage caused to the gastrointestinal tract, which can be severe enough to cause perforation.

162
Q

Pennies minted in the United States after 1982 are made primarily of_______and coated with a thin layer of _______. After a penny is ingested by an animal, the gastric juices will cause _____to leach out of the coin and enter the systemic circulation, where it will cause ________

A
  • Zinc
  • Copper
  • Zinc
  • IV hemolysis
163
Q

What would be your approach for a patient that ingested batteries

A
  • Water administration to delay the chance or internal corrosive damage (most of batterias contain components alkaline in nature)
  • Feeding a bulky diet may help the bateri to pass
  • Sx or endoscopy for removal
164
Q

What is a complication of multiple magnets ingestion

A
  • They can attract to each other from different segment of bowel and cause pressure necrosis and subsequent septic peritonitis
165
Q

which channels are inhibited by Ca channel blockers and B-blockers?

A

L- type voltage sensitive calcium channels

166
Q

Which are the three voltage operated calcium channels?

A
  • N-type –>neuronal
  • T-Type –> transient
  • L-type –> long-lasting –> they have a prolonged opening time and are high conductance (large amounts of Ca can pass rapidlythrough them and cause sudden changes in intracellular Ca)
167
Q

Where are L-type Ca channels found in higest concentration?

A

Atria, vascular smooth muscle, skeletal muscle

** in cardiac and skeletal muscle the density of L- channels is higher in the t-tubules than in the surface sarcolema….??

168
Q

What are the three major groups of Ca channel blockers based on their structure?

A
  • phenylalkylamines (e.g., verapamil)
  • benzothiazepines (e.g., diltiazem)
  • dihydropyridines (e.g., amlodipine).
    • The structural differences between the classes allow them to associate with distinct binding sites on the calcium channel, resulting in varying potency and tissue affinities
    • All three types of calcium channel blockers exert the majority of their effects on cardiac myocytes, pacemaker cells, and vascular smooth muscle
169
Q

Which phase of the action potential is described below:
- Within Purkinje cells and myocytes, opening of the L-type calcium channels in response to membrane depolarization increases calcium conductance

A

Phase 2 of the action potential

170
Q

Describe Calcium rol in the cardiac and vascular smooth muscle excitation-contraction

A
  • In cardiac smooth muscle = within Purkinje cells and myocytes, opening of the L-type calcium channels in response to membrane depolarization increases calcium conduc- tance (phase 2 of the action potential). This inward flow of calcium triggers the release of additional calcium into the cytoplasm from the sarcoplasmic reticulum. Intracellular calcium binds to troponin, changing its conformation and enabling cross bridging of actin and myosin and subsequent contraction of the muscle to occur
  • In vascular smooth muscle = opening of calcium channels increases the cytosolic calcium concentration. This calcium interacts with calmodulin, leading to phosphorylation of the myosin light chain and subsequent actin-myosin binding. This results in smooth muscle contraction and vasoconstriction
171
Q

What’s the effect of Ca channel blocker in arteries/arterioles vs venous system?

A

Calcium channel blockers prevent the rise in intracellular calcium needed for formation of the calcium-calmodulin complex and thus cause dilatation of systemic and coronary arteries and arterioles. Veins have less smooth muscle in their wall, thus, at therapeutic concentrations, calcium channel blockers have minimal effects on the venous system.

172
Q

Explain how an overdose of Ca channel blockers can cause hyperglycemia

A

The beta cells (B2) of the pancreatic islets, which produce insulin, also contain L-type calcium channels. Calcium influx into pancreatic islet cells via L-type channels is required for insulin release. High doses of calcium channel blockers may induce insulin resistance, which causes serum glucose levels to rise, while intracellular glucose stores fall.

173
Q

Mention 2 tissues/organs other than the heart where B1 receptors are located

A

Kidneys and adipose tissue.

174
Q

Complete:
- B1 receptors are present in the ________ and ______, where, if stimulated, they contribute to an increase in heart rate and conduction velocity. In addition, they are in the ___________, where stimulation results in increased contractility.

A
  • sinus and av nodes

- myocardium

175
Q

Where are B2 receptor located

A

Smooth muscle of:

  • bronchial wall
  • vascular walls (coronary, hepatic, skeletal arteries)
  • Pancreas
  • GI tract
  • Reproductive tract
176
Q

List two B1-B2 receptor blockers and two specific B1-receptor blockers

A

B1-B2:

  • Propanolol
  • Sotalol

Specific /B1:

  • Esmolol
  • Atenolol
177
Q

Explain how B1 receptor stimulation produces cardiac contraction (systole)

A

β-receptor in the cardiac nodal cell membrane or in the cardiomyocyte cell membrane stimu- lates the membrane-bound enzyme, adenyl cyclase, which raises the intracellular concentration of cyclic AMP. Cyclic AMP activates protein kinases that phosphorylate the L-type calcium channel, increasing myocellular calcium entry, which then triggers the release of more calcium from the sarcoplasmic reticulum. This calcium interacts with the myocardial contractile machinery and produces systole.

178
Q

Explain how diastole occurs after B1 stimulation

A

Protein kinases phosphorylate a protein, phospholamban, which causes the sarcoplasmic reticulum to take up calcium more rapidly, allowing relaxation (diastole).

179
Q

T/F In the smooth muscle of the gastrointestinal tract and vascular system, inhibition of β2 receptors results in contraction.

A

TRUE

180
Q

Complete:
- In the kidney, β1 -receptors mediate _______release; inhibition suppresses catecholamine- stimulated ____ release, thus decreasing ________ synthesis

A
  • renin
  • renin
  • aldosterone
181
Q

calcium channel blockers are approximately ___% protein bound.

A

80%

182
Q

Lipid soluble compounds require _____ biotransformation before excretion, and therefore can accumulate in animals with decreased ____ blood flow or insuficiency. An example of a lipid-soluble b-blocker is ______

A
  • hepatic
  • hepatic
  • Propanolol
183
Q

water soluble compounds are excreted by _____ and can accumulate in patients with ____ insuficiency

A
  • kidney

- Renal

184
Q

Give an example of a B-blocker that is water soluble but does not accumulate in animals with renal disease. Explain why

A

Esmolol is water soluble but does not accumulate in animals with renal disease because it is metabolized by erythrocyte esterases.

185
Q

T/F β non-selective agents are safer than β1 selective agents for diabetic patients or cats with asthma.

A

FALSE. Is the opposite.

186
Q

Explain why administration of a B blocker can result in a lethal decrease in contractility and HR in a patient with heart failure.

A

In patients with heart failure, chronic increases in circulating catecholamine concentrations and increased sympathetic nervous system activity cause down-regulation of β-adrenergic receptors. Fewer receptors are present to which a β-blocker may bind. Despite decreased numbers of receptors, many patients with com- promised myocardial function rely on stimulation of remaining β-receptors to maintain myocardial contractility. In these circum- stances, acute administration of medium to high doses of a β-blocker can result in lethal decreases in contractility and heart rate.

187
Q

Explain the development of hyperkalemia after b-blocker overdose

A
  • Lower aldosterone due to decreased catecholamine-induced release of renin in B cells of the kidneys
  • Decreased uptake of K by the cells –> Normally, agonist binding to the β2-adrenergic receptor stimulates the formation of cyclic AMP, which acts through protein kinase A to phosphorylate and activate the Na+/K+-ATPase pump, leading to the influx of potassium into cells. Competitive inhibition of the β2 -receptor by β-blockers decreases Na+ /-K+ -ATPase function and thus reduces potassium uptake by cells resulting in hyperkalemia.
188
Q

What’s the mechanism of development of pulmonary edema in Calcium channel and b-blockers toxicity?

A

Studies have shown that calcium blockage inhibits alveolar fluid clearance by interfering with transepi- thelial sodium and potassium transport. Combined with excessive
fluid therapy during resuscitation, selective precapillary vasodilation may result in pulmonary transudation.

189
Q

Is activated charcoal indicated for Ca channel and B-blockers toxicity?

A

Yes, can be administered every 4 to 6 hours for two to four repeated doses if a sustained-release product was ingested.

190
Q

List metications that could potentially be used in a patient with Ca channel or B-blocker toxicity

A
191
Q

Would you consider the use of extracorporeal therapy in a patient with Ca channel blocker or b-blocker toxicity?

A

Elimination of calcium channel blockers and lipid-soluble β-blockers (e.g., propranolol) via extracorporeal removal procedures (e.g., hemodialysis, hemoperfusion) is ineffective because these compounds are highly protein bound and have large volumes of distribu- tion. It may be possible to remove water-soluble β-blockers (e.g., atenolol and esmolol) using hemodialysis.

192
Q

T/F β-Agonists bind only receptors that are not occupied by a β-blocker.

A

TRUE - In animals with moderate to severe β-blocker intoxication, β-agonist drugs may not be effective because most adrenergic receptors are blocked.

193
Q

T/F During non-stress conditions the cardiac cells prefer to use free fatty acid as their primary energy substrate. During toxicity events the myocardial energy substrate switches to carbohydrates

A

TRUE

194
Q

Draw a cardiomyocyte during treatment of b-blocker and calcium channel toxicity with Ca, epinephrine, glucagon and insulin.

A

(1) Ca2+ enters the cell through voltage gated L-type Ca2+ channels. It is then pumped into the sarcoplasmic reticulum via the sarcoplasmic endoplasmic reticulum Ca2+ -ATPase (SERCA). In the sarcoplasmic reticulum the Ca2+ becomes bound to the high-capacity Ca2+ binding protein calsequestrin (CalS). The stored Ca2+ is released from the sarcoplasmic reticulum when the Ca2+ activated Ca2+ channel is opened. The released Ca2+ pairs with troponin to cause muscle contraction via actin and myosin fibers.
(2) EPI (epinephrine) binds and stimulates β-receptors that are not occupied or blocked by a β-blocker (BB). This in turn activates the attached Gs protein that activates adenylate cyclase (AC). AC catalyzes the conversion of adenosine triphosphate (ATP) to cyclic adenosine monophosphate (cAMP). This then activates protein kinase A (PKA), which stimulates the opening of dormant Ca2+ channels thus enhancing the release of Ca2+ from the sar- coplasmic reticulum.
(3) Glucagon bypasses the β-receptor and acts directly on the Gs protein, stimulating conversion of ATP to cAMP. Thus glucagon can enhance myocardial contractility, heart rate, and atrio- ventricular conduction.
4) Insulin improves the outcomes of β-blocker and calcium channel blocker toxicity via its positive inotropic effects and its positive effects on myocardial carbohydrate metabolism”

195
Q

What is the function of the SERCA pump?

A

The sarcoplasmic endoplasmic reticulum Ca2+ -ATPase (SERCA). Pumps Ca into the sarcoplasmic reticulum.

196
Q

Explain how Ca channel blocker toxicity can cause hyperlactatemia and metabolic acidosis

A

In high concentrations, calcium channel blockers inhibit mitochondrial calcium entry at the sarcolemma and mitochondrial membrane, which in turn can decrease pyruvate dehydrogenase activity. Pyruvate cannot enter the Krebs cycle and lactate accumulates, producing a metabolic acidosis.

197
Q

Which drug class inhibits the enzyme monoamine oxydase?

A

MOAIs (Monoaminde oxydase inhibitors) inhibit breakdown of serotonin by inhibiting this enzyme.

198
Q

Which drug class increases serotonin release?

A

Amphetamines

199
Q

Which drug class inihbitis the reuptake of serotonin?

A

selective serotonin reuptake inhibitors (SSRIs), tricyclic antidepressants (TCAs)

200
Q

Where in the body is serotonin mostly synthetized and stored?

A

Enterochromafin cells and myenteric plexus of the GI tract

201
Q

Where is serotonin stored in the platelets and what is it’s effect?

A

Dense granules, platelet agreggation

202
Q

what are effects of serotonin in the peripheral nervous system?

A

Vasoconstriction, uterine contraction, intestinal peristalsis, bronchoconstriction.

203
Q

T/F serotonin can cross BBB

A

FALSE

204
Q

Where is serotonin produced in the brain?

A

midline raphe nuclei of the lower pons and medulla

205
Q

How is serotonin formed in the body?

A

hydroxylation and decarboxilation of the essential aa tryptophan by tryptophan hydroxylase

206
Q

How is serotonin inactivated and eliminated from the body?

A

After release into synaptic cleft there is an active reuptake mechanism and serotonin get inactivated by the monoamide oxidase to form 5-hydroxyindoleacetic acid. This substance is then eliminated in the urine.

207
Q

T/F serotonin excess can lead to activation of other pathways through the release of noradrenaline, dopamine and glutamine

A

TRUE

208
Q

List drug classes implicated in serotonin syndrome

A
209
Q

What are the most common reported initial clinical signs for animals with TCA ingestion?

A

Hyperexcitability and vomiting… followed by ataxia, lethargy and tremors.

210
Q

What’s the mechanism of animals developing bradycardia and cardiac arrhythmias after TCAs ingestion

A

Disruption of Na-K pump.

211
Q

What are clinical signs seen on serotonin syndrome?

A
  • neurologic (mydriasis, restlessness, ataxia, somnolence, tremors, transient blindness, hyperstesia, seizures, paresis, coma)
  • GI (vomit, diarrhea, abdominal pain, ptyalism, flatulence, bloat)
  • Cardiac (tachycardia, arrhythmias)
  • Hyperthermia
212
Q

What is the toxic dose of TCAs?

A

~15mg/kg (therapeutic doses fallin in the range of 2-4mg/kg)

213
Q

what are the toxic doses and the minimum lethal dose of SSRIs in dogs and cats?

A
  • Toxic doses dogs: (0.3-50mg/kg)
  • *Mild: 1-3mg/kg –> lethargy, salivation
    • Moderate: 8-10mg/kg –> tremors, lethargy
    • Severe: >25mg/kg –> seizures
  • 100mg/kg dogs; 50mg/kg cats
214
Q

Does TCAs go enterohepatic recirculation?

A

yes –> charcoal q6h indicated

215
Q

T/F diuresis does not enhance excretion of TCAs because they are highly protein bound

A

TRUE

216
Q

Why hypertension and tachycardia occur in MAOs toxicity and how would you treat it?

A

Excessive concentration of epinephrine and norepi. / Tx with short acting B-blocker (esmolol 200-500mcg/kg IV) or Nitroprusside (0.5 - 3 mcg/kg/min)

217
Q

Which serotonin receptor antagonist agents can be used for treatment of serotonin syndrome? - mention mechanism of action and dose

A

Cyproheptadine
5HT1A and 5HT2 receptor antagonist
1.1mg/kg dogs, 2-4mg/kg cats q4-6h
if oral route not possible or patient received AC —> tablets can be crushed and given rectally

Chlorpromazine
5HT2 receptor antagonism
0.2-0.5mg/kg IV, IM, SQ q6h
can cause sedation and hypotension

218
Q

T/F ILE can be considered in severely affected animals with serotonin syndrome that do not respond to standard therapy

A

TRUE, not enough evidence to support regular use.

219
Q

What are the Vit K dependent factors

A

2, 7, 9, 10

220
Q

Explain the mechanism of action of anticoagulant rodenticides

A

Activation of coagulation factors II, VII, IX, and X (the vitamin K– dependent factors) requires reduced vitamin K (hydroquinone) for posttranslational γ-carboxylation. Activation of these factors leads to oxidation of reduced vitamin K to inactive epoxide. The enzyme vitamin K reductase catalyzes the conversion of inactive epoxide back to active hydroquinone. Anticoagulant rodenticides antagonize the action of vitamin K epoxide reductase, so levels of hydroquinone decrease.

221
Q

Why usually a lag period of 3 to 5 days occurs between exposure and appearance of clinical signs in anticoagulant toxicities?

A

As the vitamin K–dependent factors become depleted.

222
Q

treatment with vitamin K1 must be administered for only 2 weeks after ingestion for the first-generation anticoagulants but must be administered for 4 weeks after ingestion of the second-generation anticoagulants. Explain why and list the second generation anticoagulants?

A

warfarin-based rodenticides (first generation) now are used rarely; they have been replaced by the second-generation anticoagulants. Second-generation anticoagulants include the coumarin-based generics: brodifacoum, difenacoum, and bromadiolone and the indandiones: diphacinone (also called diphenadione) and chlorophacinone. The second- generation anticoagulants retain the same basic nucleus, but the chemical structures were selected for increased potency (single lethal feeding potential), longer duration of activity, and efficacy against resistant rodents.

223
Q

Complete:

- A PT should be obtained for all patients _____hours after ingestion if they have not received any doses of vitamin K.

A

48 hours –> Factor VII levels will be depleted after 48 hours, resulting in a prolongation of the PT; however, this is not enough time for depletion of the other factors that would result in clinical bleeding

224
Q

what’s the half life of FVII

A

6.2 hours

225
Q

In a study evaluating dogs receiving gastrointestinal decontamination within 6 hours of anticoagulant rodenticide ingestion, what was the % of dogs that required vitamin K1 therapy based on PT prolongation after 48h of ingestion?

A

Only 8.3% of dogs required vitamin K1 therapy, and none of them had adverse events develop during the time period between ingestion and starting vitamin K1 therapy.

226
Q

T/F anticoagulant rodenticide intoxication is unlikely in a patient with a severe prolongation of the aPTT and a mild prolongation of the PT

A

TRUE

227
Q

What are PIVKA and what’s their usefullness in Vit K toxicity cases?

A

Proteins Induced by Vitamin K Antagonism
thought previously to be a more specific test for diagnosing
However, it can be elevated with other disease processes, particularly severe liver disease and/or malabsorption and maldigestion syndromes. One study found that performing a PT and a PIVKA simultaneously added no additional diagnostic information.

228
Q

How can you can obtain a definitive diagnosis of anticoagulant rodenticide intoxication and learn the type of rodenticide ingested

A

anticoagulation rodenticide screens using spectrophotometry (available at veterinary laboratories), which can demonstrate quantitatively the presence of the toxin in whole blood

229
Q

T/F Animals with less severe clinical signs and a normal PTT may benefit from frozen plasma that no longer contains labile clotting factors but retains functional vitamin K–dependent clotting factors.

A

TRUE

230
Q

T/F There is better bioavailability of vitamin K1 when given SQ

A

FALSE - There is better bioavailability of vitamin K1 when ingested, so therapy should be switched from subcutaneous to the oral route as soon as possible

231
Q

Complete:
- _____________(vitamin D3) is absorbed rapidly and transported to the liver by specific binding proteins. It first is converted within the hepatocytes to ___________and then to ___________ within the kidney.

A
  • cholecalciferol
  • 25-hydroxycholecalciferol
  • 1,25-dihydroxycholecalciferol
232
Q

What are the primary pathologic effects of the hypercalcemia in a Vitamin D toxicosis? What is the mechanism of it?

A

Acute kidney injury

    • Hypercalcemia –> how?
    • soft tissue mineralization
    • Dehydration/hypoperfusion

Cardiac arrhythmias:

    • mineralization of the heart
  • *changes in the ratio of intracellular-to-extracellular ion concentrations
    • increase in the depolarization threshold.
233
Q

What’s the mechanism of PU/PD in hypercalcemia?

A

Inhibition of ADH

234
Q

Complete

- A serum calcium level should be checked ____hours after acute ingestion of Cholecalciferol

A

48h

235
Q

Other differential diagnoses for increased ionized calcium levels include hypercalcemia of malignancy, hypoadrenocorticism, chronic kidney disease, primary hyperparathyroidism, osteolytic bone disease, and ingestion of vitamin D ointments (psoriasis creams) or supplements.

A
  • Neoplasia/hypercalcemia of malignancy
  • Hypoadrenocorticism/Addison’s
  • CKD
  • Primary hyperparathyroidism
  • Osteolitic bone disease
  • Ingestion of Vitamin D ointments or supplements (ex. psoriasis cream)
  • Idiopathic in cats
236
Q

Why is 0.9%NaCl the fluid of choice for treatment of hypercalcemia?

A

The high sodium concentration of 0.9% NaCl (154 mEq/L) induces a calciuresis. Additional Na competes in renal tubule for Ca reabsorption + is a calcium free solution (dilutional effect)

237
Q

Explain medications used for hypercalcemia treatment and mechanism of action/considerations

A

Furosemide

    • Mechanism: enhances renal calcium loss
    • Considerations: should be administered only after fluid deficit correction

Glucocorticoids

    • Mechanism: causes reduced bone absorbtion, decreased intestinal absorbtion and increased renal excretion
    • Considerations: glucocorticoids given only after other diagnoses of hypercalcemia have been excluded

Salmon calcitonin

    • Mechanism: In addition to inducing a calciuresis, salmon calcitonin inhibits osteoclast activity and thus reduces the resorption of calcium from bones
    • Considerations: there is a risk of anaphylaxis with salmon calcitonin therapy and therefore bisphosphonate therapy typically is preferred over calcitonin.

Biphosphonate therapy (pamidronate)

    • Mechanism: inhibits osteoclastic bone resorption and reduces calcium concentrations within 48 hours of administration
    • Considerations:
238
Q

What is the prognosis in Vit D toxicosis based on degree of azotemia?

A
  • No to mild azotemia: fair to good

- Hypercalcemia and AKI: poor

239
Q

Explain pathophysiology of bromethalin toxicity

A

Uncoupoling of oxidative phosphorilation and decreased production of ATP –> decreased cellular energy –> inhability of ATP dependent transport pump to function –> malfunction of Na/K/ATPase pump –> build up of IC Na –> cerebral edema –> increased ATP.

240
Q

What is the LD50 for bromethalin in dogs and cats?

A
  • Dogs: 2.4 - 4.7mg/kg

- Cats: 0.3 - 1.8 mg/kg

241
Q

What are delayed manifestations of bromethalin intoxication?

A

Clinical signs with lower doses may manifest between 1 and 3 days; signs include hind limb ataxia, paresis or paralysis, and CNS depression

242
Q

T/F Bromethalin undergoes enterohepatic recirculation

A

TRUE - Repeated doses of activated charcoal should be administered (3 to 5 g/kg q6-8h) for 48 hours

243
Q

Mention strategies to maintain cerebral perfusion pressure and oxygen delivery to the brain

A
  • administration of mannitol to reduce cerebral edema
  • elevation of the head at a 15- to 30-degree incline
  • prevention of jugular compression
  • maintenance of normocapnia
244
Q

What’s the prognosis in bromethalin toxicity?

A

No reports exist of dogs ingesting more than 5 mg/kg bromethalin, developing neurologic signs, and surviving. However, there is a report of a dog that survived after ingesting a lower dose of bromethalin (less than 2.5 mg/kg), which led to tremors, ataxia, and muscle weakness.

245
Q

Mention two miscellaneous (uncommon) rodenticides and their mechanism of action

A

Zinc phosphide
- MOA: after contact with gastric acid zinc phosphide is hydrolyzed to phosphine gas and free radicals –> the lower the gastric pH the more phosphine gas generated –> phosphine gas (active form) inhibits cytochrome C oxidase and causes disruption of mitocondrial respiration and production of ROS (it’s corrosive, directly toxic to heart, adrenal glands, kidneys)–> Clinical signs start 15min to 4h after ingestion –> GI signs more common, but also possible: neurologic, respiratory, cardiovascular

Strychnine
- MOA: Strychnine prevents the uptake of glycine at inhibitory synapses of Renshaw cells in the CNS. This inhibition of an inhibitory pathway is termed disinhibition and results in a net excit- atory effect from an excessive afferent input and efferent response. Onset of stimulant activity, including apprehension and muscle con- tractions, occurs within minutes to hours of ingestion. Signs progress to convulsions, extensor rigidity, and death –> Animals often die from respiratory muscle paralysis and hypoventilation; mechanical ventilation of the paralyzed patient therefore may prove.

246
Q

What special precaution needs to be considered in the management of a patient with Zinc phosphide ingestion?

A
  • Caution is recommended strongly because veterinary hospital staff treating animals can be poisoned from phosphine gas. The unpleasant odor of phosphine (smells like acetylene, garlic, or rotting fish) may be detectable on the breath, vomitus, or carcass.
  • moving the animal outside, inducing vomiting, and standing upwind of and above animal level to reduce exposure to phosphine gas. The animal then should be removed from the vicinity and the area flushed with copious amounts of water (while remaining upwind). If the animal vomits in an enclosed area, the area should be vacated and the fire department contacted. If practical, windows and doors should be opened, and if personnel are exposed to the phosphine gas, they should seek medical attention immediately if they are experiencing symptoms.
247
Q

What toxin can cause teal or blue-green pigmented vomit other than rodenticide?

A

Paint ball toxicity

248
Q

Do rodenticides undergo enterohepatic recirculation?

A

No

249
Q

List first and second generation rodenticides

A

1st generation:

  • Chlorphacinone
  • Diphacinone
  • Warfarin
  • Dicoumarol

2nd generation:

  • Brodifacoum
  • Bromadiolone
  • Difenacoum
  • Difethialone
250
Q

Vitamin K is necessary for activation of which antithrombotic factors?

A

C, S, Z

251
Q

______ has the potential of being the earliest clinical indicator of clinically relevant anticoagulant rodenticide ingestion

A

Protein C

252
Q

Metastatic mineralization of tissues in a patient with Vit D toxicosis can occure at calcium x phosphorus products over ____mg/dl

A

60mg/dL

253
Q

What is the toxic and possible lethal dose of Vit D3 in dogs?

A
  • Toxic: as low as 0.5mg/kg

- Lethal: 2mg/kg

254
Q

Which are the primary contributors of morbidity and mortality in patients with cholecalciferol toxicity?

A
  • AKI

- GI mineralization

255
Q

How would be the profile of a confirmatory test for cholecalciferol toxicity?

A
  • High iCa
  • High phosphorus
  • Low PTH
256
Q

What is the prognosis of phosphine toxicity?

A

Guarded to grave if clinical signs present

  • can cause hepatic and kidney injury within 48 to 72h
  • death may results as a consequence of:
    • combination of cardiogenic and non-cardiogenic PE
    • neurological signs
    • acid-base disturbances
    • renal failure
257
Q

What is the mechanism of action of Aldicarb rodenticide? What is the treatment and prognosis?

A
  • reversible inhibitor of acetylcholinesterase
  • Atropin might help clinical signs by blocking muscarinic receptors but patient will need ventilation and intensive supportive care to prevent respiratory arrest since there is no antidote to prevent stimulation of nicotinic receptors.
258
Q

Where can EG be found?

A
  • primarily antifreeze (concentration of EG greater than 95% in some products)
  • also in paint, adhesives, wood stain, windshield deicers
259
Q

lethal dose of EG

A
  • Dogs: 6.6ml/kg

- Cats: 1.5ml/kg

260
Q

Draw the MOA of EG toxicity

A
261
Q

What are the hallmarks of EG toxicity and the mechanism of injury?

A

AKI:

  • Direct injury of renal tubular epithelium by glycolic acid
  • deposition of Ca oxalate crystals in tubular lumen

metabolic acidosis
- gain of acid –> high AGAP metabolic acidosis

262
Q

Which is the metabolite thought to be mainly responsible for the CNS depression caused by EG toxicity?

A

Glycoaldehyde

263
Q

Explain why hypocalcemia develops in EG toxicity

A

Utilization due to crystal formation –> Ca binds to oxalic acid and forms Ca oxalate crystals

264
Q

what are the mortality rates in dogs and cats with EG toxicity?

A
  • dogs: 59-70%

- cats: 96-100%

265
Q

Describe the 3 phases of EG toxicity

A
  1. within several hours –> vomiting, lethargy, PU/PD, ataxia, muscle fasciculations, seizures coma –> in dogs neuro signs can resolve within 12h (false recovery)
  2. 12-24h after ingestion –> cardiopulmonary signs develop (tachyarrhytmias, tachypnea, hypocalcemia
  3. 24-72 hours after ingestion –> Oliguric/anuric AKI
266
Q

A rise in serum osmolality can occur as early as _____ after EG ingestion, facilitating early recognition and treatment if recognized. The osmolal gap peaks at ____ after ingestion, but remains elevated for up to ____ after ingestion.

A
  • 1 hour
  • 6 hours
  • 18 hours
267
Q

How do you calculate osmolality and what is the normal osmolal gap?

A
  • freezing point osmometry or vapor pressure osmometry (uncommonly available)
  • (2Na+K)+(glu/18)+(BUN/2.8)
  • Normal osmolal gap <10mOsm/L
268
Q

In EG toxicity, The anion gap rises within _____ after ingestion and peaks at _____, but remains elevated for approximately _____

A
  • 3 hours
  • 6 hours
  • 48 hours
269
Q

Why EG toxicity can cause an erroneous hyperlactatemia and why is this important?

A

An erroneous hyperlactatemia may be reported by enzymatic point-of-care (POC) machines and can be attributed to the measurement of glycolate, a chemically similar metabolite of EG [8]. As lactic aci- dosis also results in a high anion gap metabolic acidosis, this could result in a missed diagnosis of EG intoxication.

270
Q

How soon after EG ingestion can Ca oxalate crystals be seen in the urine?

A

3-6 hours after ingestion

271
Q

What are the most common type ox Ca oxalate crystals observed in urine in a patient with EG toxicity?

A

Calcium oxalate monohydrate crystals are the most common type observed and have a distinct appearance, looking like long, clear, six-sided or “picket fence” shaped structures, versus the square envelope shape of the dihydrate crystals.

272
Q

What is the rationale behind analyzin the urine, mouth or paws of a patient with a Wood’s lamp in a suspected EG ingestion

A

Wood’s lamp to look for fluorescence can be performed as many antifreeze solutions are made with sodium flu- orescein dye in order to detect radiator leaks. Since this is not found in all solutions, and is only excreted in the urine for 6 hours following ingestion of antifreeze [9], a negative test does not exclude the diagnosis of EG intoxication.

273
Q

What is the gold standard test for EG toxicosis? What’s the disadvantage?

A

Gas chromatography (not readily available) and EG levels are usually not detectable in serum or urine 48 to 72h after ingestion.

274
Q

Which components can crossreact with the Kacey EG test strips?

A
  • Propylene glycol (carrier inseveral meds–> diazepam, AC)
  • glycerol
  • ethanol
275
Q

Whats the mechanism of action of Fomepizole (4MP) and ethanol in EG toxicity

A

Preventing metabolism of EG is accomplished by competitively inhibiting the function of alcohol dehydrogenase (ADH) with ethanol or fomepizole (4-methyl-1H-pyrazole, or 4-MP). These two antidotes have a higher affinity for the enzyme than EG, which allows excretion of the toxin unchanged into the urine.

276
Q

What are the disadvantages of ethanol over Fomepizole?

A
  • CNS depressant
  • increases serum osmolality
  • induces diuresis
277
Q

Describe your treatment protocol for ethanol and fomepizole in a patient with EG toxicity

A

Fomepizole:

  • Dogs: 20 mg/ kg 5% IV initially, followed by 15 mg/kg IV at 12 and 24 hours and 5 mg/kg IV at 36 hours.
  • In cats, a higher dose is required at 125 mg/kg IV initially, then 31.25 mg/kg IV at 12, 24, and 36 hours.

Ethanol:
- Because of ethanol’s short half-life, ideally it should be administered as a CRI with a 1.3 mL/kg IV bolus of 30% ethanol followed by a CRI of 0.42 mL/kg/h for 48 hours

278
Q

What is the mechanism of action of acetaminophen

A
  • Appears to exert its analgesic effects via central cyclo-oxygenase (COX) inhibition. APAP crosses the blood–brain barrier and inhibits the central COX enzyme pathway, with only weak peripheral COX inhibition
  • Seems to act in the previously called COX3 (now recognized as central COX1 variant) localized in the dog’s brain
  • Other theories of APAP’s mechanism of action include blockade of substance P’s nocic- eptive actions via N-methyl-D-aspartate inhibition and activation of serotonergic nociception pathways centrally
  • Has analgesic and antipyretic effects but not antiinflammatory
  • Appears to inhibit the peroxydase portion of prostaglandin H2 synthase
  • Can act as a selective COX 2 inhibitor in some tissues
279
Q

T/F Since APAP primarily inhibits central COX enzymes, it lacks the adverse local gastric and renal effects of NSAIDs

A

TRUE

280
Q

How is acetaminophen metabolized in dogs and cats. Explain how toxicity develops

A
  • Glucuronidation is the main metabolic pathway in dogs, followed by sulfuric acid conjugation. In contrast, cats primarily use the sulfation pathway.
  • If the glucuronidation and sulfation pathways are saturated, residual APAP is metabolized by CYP2E1 and CYP1A2 (cytochrome p450) oxidation to the toxic compound N-acetyl-p- benzoquinone imine (NAPQI), which is converted into non-toxic metabolites by glutathione
  • If glutathione stores are depleted to less than 70% of normal, NAPQI remains in its toxic form and binds to hepatic cell membranes, causing necrosis and hepatotoxicity.
  • Glutathione depletion also leads to oxidative damage to the heme in red blood cells, causing methemoglobinemia in dogs and cats and Heinz body anemia in cats.
281
Q

What is the proposed pathophysiology of APAP-induced nephrotoxicity in dogs and cats

A

Renal glutathione depletion and damage of renal proteins and cell death secondary to NAPQ1

282
Q

Why are cats more sensitive to APAP

A

They lack a specific form of glucuronyl transferase, hepatic acetaminophen-directed uridine 5′-diphosphate, which is needed to conjugate APAP to glucuronic acid.
- Cat erythrocytes are also more susceptible to oxidative damage by NAPQI due to the increased number of sulfhydryl groups on feline heme compared to other species.

283
Q

T/F It has been suggested that a metabolite other than NAPQI, para-aminophenol (PAP), may cause methemoglobinemia in dogs and cats.

A

TRUE

284
Q

Toxic doses of APAP in cats tend to occur with ingestion of _________, which represents one regular strength OTC human tablet. However, there are reports of cats developing clinical signs after ingestion of as little as ____.

A
  • 50 - 100mg/kg

- 10 mg/kg

285
Q

T/F Although weak, APAP does inhibit COX enzymes and, in theory, high doses could affect gastrointestinal mucosal integrity

A

TRUE

286
Q

What is the rationale of using Ascorbic acid (vit c) for APAP toxicity?

A

Ascorbic acid reduces methemoglobin to hemoglobin, but its effectiveness in patients with acetaminophen tox- icity is questionable. Recommended doses include 10 mg/kg PO or IV every 6–12 hours [7] or 30 mg/kg IV every 6 hours.

287
Q

T/F Ranitidine is an H2 antagonist that at high concentra- tions binds to cytochrome p450 and prevents oxidation of acetaminophen

A

TRUE

288
Q

Why methylene blue should be used wth caution in cats with APAP toxicity

A

Methylene blue reduces methemoglobin to hemoglobin but it should be used cautiously in cats as a treatment for APAP toxicosis [27]. At high doses, it has the poten- tial to induce methemoglobinemia by oxidizing heme [27]. Methylene blue is generally not recommended as a treatment for methemoglobinemia in cats.

289
Q

List medications that could be considered in a patient with APAP toxicity

A
290
Q

NAPQI is converted into non-toxic metabolites by ________. These metabolites are further converted into _______ and ______ conjugates that are excreted in urine along with _____ and ______ in dogs and cats respectively.

A
  • Glutatione
  • Cysteine
  • mercapturic acid
  • APAP-glucuronide
  • APAP-sulfate
291
Q

ILE components

A
292
Q

Alternate forms of ILE

A

ACVECC prep (19 decks)

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