Final Exam Flashcards
(217 cards)
1
Q
What is a toxicant?
A
a compound causing toxicity (natural or man-made)
2
Q
What is a xenobiotic?
A
foreign substance
3
Q
What is an antidote?
A
This is a substance that prevents/relieves the effects of a toxicant.
4
Q
How are poisons classified?
A
The lower the dose the more toxic!
toxic dose with <1mg/kg being extremely toxic and > 15 g/kg being relatively harmless
5
Q
Dose-response curve?
A
Assumes a cause/effect relationship and that response is proportional to dose
- in general more toxin is bad!
6
Q
What factors influence toxicity?
A
Exposure, subject (spp.) & environment
7
Q
What’s the difference between concentration and dose?
A
Concentration: amount of chemical per volume
dose: amount given to an animal
8
Q
What animals have genetic defects affecting metabolism?
A
o Cats are deficient in glucuronidation- affecting phase 2
o Dogs are deficient acetylation
o Pigs are deficient sulfonation
9
Q
Metabolism can…
A
detox compound & increase elimination.
- bioactivation
10
Q
Bioactivation & list some examples
A
conversion of parent compound into something more toxic
Ex. ethylene glycol toxicosis, benzopyrene (petroleum), aflatoxin & acetaminophen
11
Q
What is the process of toxicity?
A
Delivery from exposure site to target → Rxn of the ultimate toxicant with the target molecule → Cellular dysfunction & resultant toxicities → Repair (apoptosis, tissue regeneration) or disrepair (tissue necrosis, fibrosis, cancer
12
Q
What makes an organ sensitive to toxin?
A
Receptor type and amount, amount of transporters present
13
Q
How do toxicants cause toxicity?
A
- Damage cells
- Ex. Acetaminophen, arsenic - Organ system dysfunction
- Ex. insecticides, rodenticides
14
Q
What are 5 life-threatening problems that require immediate attention?
A
Respiratory distress, CNS, Cardiovascular, Hemorrhage, Thermoregulation
- ID toxin is helpful nOT crucial so treat the pt not the poison!
15
Q
When is ventilation needed?
A
hypoventilation/hypercapnia (PCO2 >45mmHg), metabolic acidosis (venous pH <7.35) hypoxia (PaO2<65mmHg)
16
Q
How do you treat hypoxia?
A
Treat with 40% O2 (brief start w/100%): 100% O2 for a short period of time, because it will cause damage to lung epithelium
17
Q
how do you prevent aspiration of vomitus?
A
positioning
18
Q
How do you control CNS hyperactivity? (Seizures)
A
Diazepam, phenobarbital, methocarbamol, gabapentin
19
Q
How do you control CNS depression?
A
analeptics & doxapram
20
Q
How do you control tachycardia & arrhythmias?
A
lidocaine, propanolol
21
Q
How do you control hypertension?
A
nitroprusside, hydralazine
22
Q
What are the four major themes for completing a history?
A
health history, current clinical history, diet & environment
23
Q
What is the goal of GI decontamination?
A
reduce absorption of toxin & facilitate transport out of GI system. Done with emesis & activated charcoal
24
Q
What medication induces vomiting in cats?
A
xylazine; may cause hypotension & bradycardia
25
What medication induces vomiting in dogs & pigs?
apomorphine; may cause prolonged vomiting
26
When should you induce emesis?
Perform if toxic dose ingested, no vomiting has yet occurred & activated charcoal is not an option
27
When should you NOT induce emesis?
caustic chemicals, sharp items, volatile chemicals, risk of aspiration pneumonia
28
When should you give activated charcoal?
known substance, recent ingestion or undergoes enterohepatic circulation, pt. can tolerate or no need to administer oral rx immediately
29
When should you not give activated charcoal?
protracted vomiting, caustic/basic substance that charcoal doesn’t bind, intestinal FB (physical GI damage), obstructed airway, chronic exposures
30
What doesn't bind activated charcoal?
acids/alkalis, alcohols/glycols, metals, oils, petroleum, detergents, cyanide
31
MOA for strychnine?
competitive antagonist to glycine receptors (spinal cord & medulla) causing
32
Strychnine clinical signs
stiff neck and gait, “grinning” (facial muscles tighten), tetanic seizures, sawhorse stance
33
Strychnine DX
CS, elevated CPK and LDH in serum, increased anion gap- lactic acidosis, hyperkalemia, leukocytosis
34
Strychnine TX
Decontamination, ammonium chloride (ion trapping), seizure control +/- ventilate with pentobarbital
35
Ammoniated Feed Toxicosis- MOA
imidazole and/ or non-protein nitrogen added to cattle feed and byproduct causes too much ammonia--> blood
* Ruminants are most susceptible*
36
Ammoniated Feed Toxicosis- CS?
Bovine Bonkers- hyperexcitability & SLUD
37
Ammoniated Feed Toxicosis- DX?
CS/HX, feed analysis, increased ammonia/ glucose/BUN & acidosis
38
Ammoniated Feed Toxicosis- TX?
Remove feed, sedation (prevent self-mutilation), milking out cows +/- cold H20 + vinegar
39
Salt Tox MOA
decreased water intake/lots of salt-->blood becomes hypernatremia--> fluids in the brain movie into the hypertonic cerebral circulation (brain dehydration)-->drinking water provided and blood becomes hypotonic relative to the brain-->osmotic edema and swelling if water is not returned slowly!
40
Salt tox CS
primarily salivation/increased thirst, progressing to circling, head pressing, seizures, blindness, partial paralysis
41
Salt tox DX
blood sodium levels, high sodium levels in brain diagnostic in swine & cattle (> 2000 ppm)
42
Salt tox TX
slow rehydration starting with hyperosmotic fluid, furosemide to prevent pulmonary edema
43
What are mycotoxins & the three subgroups?
Fungal secondary metabolites
i. Slaframine
ii. Fumonisin
iii. Tremorgenic Mycotoxins- produced by Penicillium, Aspergillus, Claviceps, etc.
44
Slaframine MOA
Acts as a muscarinic cholinergic agonist (esp. in exocrine glands) ~ “Ach mimic”
45
Slaframine CS
```
Most common in horses & cattle
copious salivation (slobbers), +/- bloat, diarrhea, frequent urination, feed refusal
```
46
Slaframine TX
Remove source, atropine
47
Fumonisin MOA
MOA: inhibits sphingosine N-acetyltransferase causing increase sphingosine level cytotoxic
48
Diseases linked to Fumonisin?
i. Equine leukoencephelomalacia (ELEM): affecting CNS
| ii. Porcine pulmonary edema (PPE): affecting respiratory system
49
Fumonisin TX
isolate, can change feed +/- Ultrasorb S (mycotoxin deactivator)
50
Porcine pulmonary edema (PPE) CS?
inactivity/tachypnea/bradycardia (pigs); wipe out of large swine population.
& die of hypoxia, indicated by cyanosis
51
Porcine pulmonary edema (PPE) DX?
Increases liver enzyme and in serum/tissue sphingoid bases
| - post mortem: pulmonary edema & hepatic lesions
52
ELEM CS?
CNS- terminal frenzy before death (mania, profuse sweating), prior to anorexia/ataxia/blindness
LIVER- HE & jaundice
Brain- liquefaction (unilat)
53
What is one toxic principle of tremorgenic mycotoxins?
Penitram A
54
Tremorgenic mycotoxin MOA?
multiple mechanisms including GABA receptor antagonist-like, acts on varied neurotransmitters to cause excitation
55
Tremorgenic mycotoxin CS?
muscle tremor, ataxia, tetanic seizures *tremors in vertebrates*
56
Alprazolam MOA
Benzodiazepone, that acts at limbic, thalamic, and hypothalamic level of CNS
57
Alprazolam CS
ataxia, depression, vomiting, tremors, tachycardia, hypothermia, diarrhea, paradoxical hyperactivity
58
Alprazolam TX
induce emesis, use gastric lavage with activated charcoal if toxic dose, flumazenil
59
What is flumazenil?
Benzodiazepine antagonist; blocks GABA receptor and can be used as an alprazolam tox "antidote"
60
Zolpidem MOA?
inhibits neuronal excitation by binding to benzodiazepine site oN GABA receptors (rapid absorption from GI)
61
Zolpidem CS
ataxia, vomiting, lethargy, disorientation, hyper-salivation, paradoxical excitement
62
What breeds are susceptible to ivermectin toxicosis?
Border collies, Shelties & Australian shepherds
| - MDR1 gene mutation causes bioaccumulation in brain & tissues.
63
Ivermectin MOA?
GABA receptor agonist that decreases ability to respond to other stimuli
64
Ivermectin TX?
decontamination w/ activated charcoal, lipid emulsion, picrotoxin
- seizures? don't use benzodiazepines OR use short acting like propofol & phenobarbital
65
Organophosphate Pesticides MOA
reversible inhibition of acetylcholinesterase activity- can become irreversible with time
continuous stimulation of neuron (muscarinic & nicotinic receptors)--> death
66
Organophosphate Pesticides CS?
Muscarinic: salivation, lacrimation, urination, GI distress/defecation, emesis, myosis
Nicotinic: muscle fasciculations, tremors, weakness, paralysis
CNS: respiratory depression, ataxia, clonic-tonic seizures, delayed neuropathy
67
Organophosphate Pesticides DX?
HX/CS, reduced rbc ACHE, atropine challenge- if no response/change means OP poisoning
68
OP TX?
GI decontamination, atropine (corrects muscarinic receptor), glycopyrrolate, oximes (protopam/2-PAM : to reactivate anticholinesterase, diazepam/barbiturates for seizures & time!
69
organophosphate-induced delayed neurotoxicity/ neuropathy
OP inhibited NTE- neuropathy, will get degeneration over time of motor axons due to excessive anti-cholinesterase degeneration (occurs after 2 weeks of exposure)
Results: Hindlimb weakness, paralysis
no treatment
70
Pyrethrin MOA
Bind voltage-gated sodium channels and causes hyperactivity
| * cats are sensitive due to inefficient glucuronidation
71
Pyrethrin CS? Cat vs. Dog
Cat-drooling, paresthesia, muscle tremors/seizures/hyperthermia Dog- paresthesia
72
Pyrethrin TX
Methocarbamol, diazepam, bathe multiple times with dishwashing liquid, lipid infusion, IV fluids to protect kidneys from myoglobin breakdown products in cats-created d/t trembling
73
Bromethalin MOA
block oxidative phosphorylation in CNS leading to dysregulation
74
Bromethalin CS
ataxia, hindlimb paralysis, hyper-excitability, severe muscle tremors, seizures
75
Bromethalin DX
cerebral edema and cerebellar degeneration
76
Bromethalin TX
Emesis, charcoal, furosemide for cerebral & pulmonary edema, treat seizures, lipid infusion
77
Acetaminophen MOA?
metabolized by glucuronidation, sulphonation & oxidation pathways~ bioactivated to NAPQI (N-acetyl-p-benzoquinone imine).
78
What spp. is extremely sensitive to acetominophen?
Cats because they cannot glucoronidate
79
Acetaminophen CS?
Cats: cyanosis, methemoglobinemia, depression & edema of paws/ face
Dogs- Hepatotoxicity- hepatic necrosis nausea, v/d/shock
Other- hemolysis, Heinz bodies
80
Acetaminophen TX:
N-acetyl cysteine OR cimetidine (cats), ascorbic acid, antioxidants, silymarin (milk thistle) & s-adenosylmethionine
81
Xylitol MOA
Dose dependent insulin release causing lethal liver injury & hypoglycemia (dogs)
82
Xylitol CS
vomiting, lethargy, ataxia, collapse & seizures, liver enzymes, BG & hypokalemia (d/t endogenous induced insulin)
83
Xylitol TX
activated charcoal is NOT effective or recommended (poor binding ability) & monitor BG/liver function (supplement accordingly)
84
What toxins do some cyanobacteria or blue green algae produce?
Microcystin- impairs phosphatase affecting cell regulation/signaling and affects the liver.
Anatoxin- affect CNA & will see ataxia/ disorientation with toxicosis
85
Cyanobacteria CS & DX
v/d/pale mm, ataxia, seizures
DX: blood in stool, elevated liver enzymes & hx
86
Cyanobacteria TX?
Atropine ( helps with anatoxins), fluid & seizure control
87
Where in the kidney is the most common site of toxin-induced injury?
PCT
88
Acute renal failure
transient damage to tubule/glomerulus/ vasculature causing decreased GFR & azotemia
- CS: vomiting, GI bleed, anuria
89
Chronic renal failure
secondary changes triggered by initial injury (not all chemicals effect one organ)
Signs: edema, hypocalcemia, reduced rbc
90
Ethylene Glycol MOA
metabolites produced by action of alcohol dehydrogenase
- Glycolic acid--> metabolic acidosis
- Glyoxylic acids--> CNS signs
- Oxalate/Oxalic acids--> renal damage & hypocalcemia (crystal formation in kidney)
91
Ethylene Glycol CS (3 Stages)
1. Drunkenness, nausea, vomiting, PU/PD (Dogs)
92
What stage of ethylene glycol toxicosis does the animal normally present?
Stage 3
93
Ethylene Glycol DX
Ethylene glycol blood concentration blood, Azotemia (stage 3), low USG & crystalluria (calcium oxalate monohydrate)
Chemistry: hyperglycemia, hypocalcemia & increased anion gap
94
Ethylene Glycol TX
Fomepizole to block alcohol dehydrogenase (EG metablized via other pathways) or more trasitional ethanol & sodium bicarbonate (difficult to maintain/less exact)
*** DO NOT USE IF PT IN RENAL FAILURE***
95
Cholecalciferol MOA
Liver metabolizes cholecalciferol to 1,25 dihydroxycholecalciferols causing a massive increase in serum calcium!
96
Cholecalciferol CS
Delayed!
| anorexia, thirst, PU, dark diarrhea, bradycardia, ventricular arrhythmia, hypertension & mineralization of tissues
97
Cholecalciferol Dx
- clinical signs
- hypercalcemia
- Low PTH
- Renal damage: low USG & azotemia
- Hydroxycholecalciferols in bile & kidneys
- Histo: mineralization in multiple organs
98
How to differentiate cholecalciferol from ethylene glycol?
EG has higher kidney calcium compared to cholecalciferol
EG Ca: P ratio in kidney higher than cholecalciferol
99
Cholecalciferol TX
- Gi decontamination (emesis & activated charcoal 6-8 hr.)
- reduce dietary calcium& phosphorous
- Saline & furosemide (promotes excretion of calcium)
- Prednisolone (reduces bone & kidney resorption & reduced calcium absorption)
- Pamidronate- bisphosphonate, (blocks osteoclast from releasing calcium)
- sucralfate for GI ulcers
100
Grape & Raisin MOA?
Unknown
101
Grape & Raisin CS?
Variable! vomiting, followed by acute renal failure signs
102
Grape & Raisin DX?
hypercalcemia, hyperphosphatemia, increased Ca:PO4, elevated BUN/creatinine
103
Grape & Raisin TX?
- Emesis, lavage, or activated charcoal (grape remain in GI with slow absorption)
- Fluid therapy + supportive therapy
104
Ergot Alkaloids MOA?
dopamine & serotonin receptor agonist--> hallucinations, reproductive problems, lack of thermoreg.
- Dopamine is inhibitory causing decreased prolactin so poor reproduction
- alpha-2 adrenergic agonist affects smooth muscle contraction & vasocontraction at extremity- abortion and ischemia
105
Ergot Alkaloids CS?
poor reproductive performance (abortion in horses & pigs see infertility)
- Summer slump- reduced feed intake, weight gain, heat intolerance, retain winter coat
- Fescue foot- lameness, gangrene of extremities, necrotic tissue on extremity (sores on ears, feet, tail d/t vasoconstriction)
106
Ergot Alkaloids TX?
metoclopramide or domperidone (dopamine antagonists- primarily to correct reproductive issues), remove source
107
What species are most sensitive to ionophore toxicosis?
Horses>Cow>Poultry
| - usually caused by a feed-mixing error
108
Ionophore MOA?
increase intracellular sodium/calcium leading to mitochondrial swelling and cell death
109
Ionophore CS? in horses & cows
anorexia, colic, profuse sweating on flank, recumbent, incoordination, diarrhea (cattle), respiratory difficulty (cattle)
110
Ionophore DX?
increased muscle enzymes (CK) myoglobinuria, elevated AST/LDH/BUN/bilirubin, hypokalemia, hypocalcemia, chemical analysis of feed
- Necropsy: pale cardiac muscle; muscle has striation/ vacuolization
111
Tetanus MOA
-spores in puncture wounds, produce toxins that blocks the release of GABA & glycine--> overstimulation of muscles leading to muscle stiffness & tetany (can animal die from exhaustion)
112
Tetanus CS?
stiffness, twitching, lockjaw (all facial muscle lock up), unsteady gait, bloat (ruminant)
113
Tetanus TX?
antitoxin (only useful at early stages), supportive therapy
114
Bobtail Disease
Chronic Selenium Toxicosis: occurs with shampoo, forage or plants (locoweed)
- Horses are sensitive to locoweed
CS- lameness, hoof deformity, muscle wasting
-TX- none (remove from source)
115
White Muscle Disease
Selenium deficiency, causing degeneration of muscle tissue (cardiac and skeletal) ~ mostly livestock
- Clinical signs: Weakness, prostration (Lie down), muscle wasting
- TX: selenium replacement and Vitamin E
116
Phenoxyacetic Acid Herbicides moa?
unknown, however dogs are more susceptible
117
Phenoxyacetic Acid Herbicides CS?
vomiting, diarrhea, oral/GI ulceration, ataxia, weakness, seizures at high doses, myotonia with serious toxicosis, rumen acidosis, renal tubular degeneration, hepatic necrosis
• GI effects (often only sign in dogs)
118
Phenoxyacetic Acid Herbicides TX?
emesis, lavage, bathe, activated charcoal, cathartic, ion trapping using basic compound (since this is a weak acid- making urine more basic, traps compound in urine, so it is excreted with sodium bicarbonate)
119
What are three common respiratory toxins?
1. ventilatory muscle paralysis- botulism, tetanus, OP, strychnine, venom
2. Respiratory center depression- barbiturates, opiates, hypnotics, sedatives & antidepressants
3. Aspiration pneumonia: ethylene glycol, petroleum & bleach
120
Paraquat MOA?
non-selective herbicide that induces oxidative damage
- lungs are sensitive and will absorb at a higher affinity than O2)
121
Paraquat CS?
lung damage, renal failure, pulmonary fibrosis, vomiting, burning skin, acute pulmonary edema
122
Paraquat tx?
no oxygen unless hypoxic (b/c can worsen lung issues), emesis, charcoal, lavage
123
Polytetrafluoroethylene (PTFE
oBurning of Teflon from cooking pans,
o MOA - respiratory tract irritant
oClinical signs - choking, dyspnea, ataxia, edema, hemorrhage, rapid death
oTreatment - fresh air, oxygen, diuretics
124
What species is mostly effected by PTFE?
birds
125
First generation anticoagulant- Warfarin
o Short half-life (15 hours), low potency, requires multiple feedings
o Can be used in human medication (blood thinning), found in sweet clover (affecting LA) & with rodenticides (less common)
126
Second Generation - Brodifacoum
oLong half-life (20 days), high potency, kills in single feeding
127
Anticoagulant MOA
- inhibits Vitamin K epoxide reductase
| - when it is blocked vitamin K cannot be used to make clotting factors.
128
Anticoagulant CS
Initially okay w/ delayed onset (3-5 days) due to native anticoagulants. depression, anorexia, anemia, dyspnea, nosebleeds, bleeding gums, bloody feces, hemorrhage (chest/abdomen), hematoma, prolonged bleeding from injection
129
Anticoagulant DX
history of exposure, evidence of coagulopathy, response to Vitamin K therapy
o Testing: increased PT/PTT
130
Anticoagulant TX?
emetic (recent exposure) adsorbent, cathartic therapy & Vitamin K
- low dose treat for 2 wk for first generation & 1 month for second generation
131
Gossypol toxicosis MOA?
increases with time & accumulates b/c lipophilic.
- iron chelation causing anemia & reducing protein availability, binds to dehydrogenase leading to increased oxidative damage and decreased energy
132
Gossypol toxicosis CS?
- Low concentration: weight loss, weakness, dyspnea
- Other levels: moderate anemia, edema secondary to heart failure, myocardial necrosis, congestive heart failure, sudden death (dairy cows/lamb)
133
Gossypol toxicosis DX
HX of cotton ingestion, cardiac necrosis, edema, vacuolization, chemical analysis
134
Gossypol toxicosis TX
feed high protein diet with Vitamin A/iron/lysine supplementation, remove sources from diet & symptomatic treatment
135
Cantharidin (Blister beetle or Spanish fly) toxicosis
inhibits protein phosphates and mucosal irritant
| ** usually affects horses**
136
Cantharidin toxicosis CS?
colic, frequent urination, diaphragm contraction with heartbeat, shock, irritation/ ulceration of epithelia (muzzle in water- irritated in mouth so constantly drinking water) & cardiac toxicity
137
Cantharidin toxicosis DX?
alfalfa hay consumed, beetles in hay or stomach, hypocalcemia, increased BUN, ulceration of mucous membranes, cardiac necrosis & sudden death “with no struggle”
o Necropsy: hemorrhage & ulceration of the bladder.
o Can perform mass spectrometer
138
Cantharidin toxicosis TX?
GI decontamination and protection with sucralfate, antibiotics
139
Methylxanthines MOA?
antagonist of adenosine receptors --> CNS stimulation (overstimulation), vasoconstriction, tachycardia
oPrevents calcium reuptake --> increased skeletal/cardiac muscle contractility
oInhibits phosphodiesterase--> increase cAMP and cGMP
140
Methylxanthines CS?
vomiting, diarrhea, diuresis, hyperactivity (bounce), panting, tachycardia, hypertension, ataxia, tremors, seizures, coma, death from arrhythmia or respiratory failure
141
Methylxanthines DX?
history, stomach content analysis, plasma/serum/urine/liver analysis
142
Methylxanthines TX?
o GI decontamination: induce emesis, repeated administration of activated charcoal (every 3 hr)
o EKG: arrhythmias with lidocaine (not in cats) or metoprolol (cats)
o maintain respiration, fluid diuresis
143
Nitrate toxicosis MOA?
Nitrate converted to nitrite, which causes vasodilation & oxidized ferrous iron in hemoglobin to ferric state--> methemoglobinemia (O2 starved tissues)
144
What spp. is most susceptible to nitrate toxicosis?
Pig>cattle>sheep>horses
145
What are plants that cause nitrate toxicosis?
lambsquarters, black nightshade, pigweed
146
Nitrate toxicosis CS?
depending on level of methg: cyanosis (15%)
ataxia, seizures, coma (50%)
death (>70%)
147
Nitrate toxicosis DX?
methemoglobinemia, nitrate in feed/water, necropsy (eyes)
148
Nitrate toxicosis TX?
1-2% methylene blue IV (urine will turn green), ascorbic acid (cats, horses), feed cattle corn to increase nitrite reduction by rumen flora
149
Examples of cardiac glycosides?
Digitalis, digoxin
Plant examples: Foxglove, oleander (SE region), lily of the valley
150
Cardiac glycosides MOA
inhibit sodium/potassium ATPase through competition (found on cardiomyocytes)- leading to increased intracellular calcium
151
Cardiac glycosides CS
staggering, trembling, dyspnea, increased intracellular sodium and calcium, hyperkalemia, tachycardia, arrhythmia
- over time can become bradycardia & weak pulse
152
Cardiac glycosides TX
GI decontamination, propranolol (for arrhythmias), insulin w/ glucose (treat hyperkalemia), Digoxin fragment antibodies- designed from toxin in foxglove (antidote) “digibind”
153
What is digibind?
Digoxin fragment antibodies- designed from toxin in foxglove (antidote for digoxin and similar cardiac glycosides)
154
Cyanide toxicity MOA
inhibition of cytochrome C oxidase (no ATP production)- shuts down oxidative respiration
155
Cyanide toxicity CS
super oxygenated (cherry red) blood that is slow to clot, bitter almond smell, sudden death, dyspnea, weakness, tremors
- Rapid onset of toxicosis (20 min)
156
Cyanide toxicity TX
```
Find a cyanide recipient:
1. give sodium nitrate to bind cyanide (inducing methemoglobinemia)
2. Then, sodium thiosulfate to increase formation of nontoxic thiocyanate by rhodanese --> eliminated in urine
OR
One step approach:
Cyanokit:
- Vit B12 (higher affinity for cyanide)
- sulfanegan sodium (bind cyanide)
- cobalt-EDTA
```
157
What spp are sensitive to NSAIDs?
Dog- ibuprofen
| Cat- Aspirin d/t lack of glucoronidation
158
NSAIDs MOA
- inhibit cyclooxygenase (COX1&2) and damage GI and liver
| - Uncouples oxidative phosphorylation at high doses-increased lactic acid, metabolic acidosis
159
NSAIDs CS
Acute- vomiting, anorexia, fluid imbalances, seizures, acidosis with anion gap, renal failure
Chronic- gastric irritation, ulceration
- Cats: Heinz body (oxidative damage), anemia (cats), thrombocytopenia (cats)
160
NSAIDs DX
HX/CS, increased anion gap due to acidosis (specific to salicylates such as aspirin), increased liver enzymes, jaundice, prolonged clotting time, acute renal failure (see renal tubular cell cast)
161
NSAIDs TX
induce emesis, activated charcoal (multiple doses), ranitidine (H2 blocker), sucralfate & misoprostol (prostaglandins analog), supportive care +/- transfusion with hemorrhage
162
What is the #1 priority pollutant?
Arsenic
163
Arsenic MOA?
o pentavalent reduced and metabolized in rumen to reduce metabolic energy & CNS problems
o trivalent inhibits oxidative phosphorylation and causes blood/mucosal issues
164
Arsenic CS?
Dog- intense abdominal pain, gastroenteritis, vomiting
weakness, staggering gait, PU/PD, oliguria, anuria, dehydration
- Blood related: cold extremities
“black foot disease” d/t tissue necrosis
- CNS related: salivation, trembling, depression, posterior paresis
165
Arsenic DX:
Neocropsy: brick red abomasum, fluid GI contents, soft yellow liver, red congested lungs & kidney damage
analysis- liver or kidney has arsenic > 5 ppm, HX, stomach contents or vomitus with arsenic (must take samples early because rapidly absorbed/excreted)
166
Arsenic TX:
o GI contamination: if acute~ emesis, activated charcoal/ cathartic
o chelation therapy- dimercaprol, sodium thiosulfate (binds arsenic) prior to clinical signs
o supportive therapy
167
Zinc MOA?
zinc enters the stomach- acid eats & releases zinc--> free zinc damages GI mucosa (corrosive effect & oxidative damage causing hemolysis)
168
Zinc CS?
v/d/ PU/PD, hemoglobinuria, hemolytic anemia, jaundice, pancreatitis & lesions along GI, liver/kidney/pancreas
169
Zinc DX:
serum & liver zinc values, decreased PCV, regenerative anemia, thrombocytopenia, oxidative damage, elevated liver/kidney/pancreatic enzymes, hemoglobinuria, radiographs for hardware, formation of Heinz body
170
Zinc TX:
remove foreign body, emesis (if possible), omeprazole (proton pump inhibitor) or H2 blockers +/- GI protectants
171
Soap/Shampoo
o Clinical signs: GI distress, vomiting, diarrhea
o Treatment: simple dilution with milk or water, fluid treatment
o Rarely lethal
172
Scouring Powder/ Bleach
Alkaline- corrosive effect on skin/mm, that can cause liquefactive necrosis
- Clinical signs: vomiting, drooling & abdominal pain
- TX: milk, water & gastro protectant
* Avoid emesis or lavage because caustic & poor binding effect (have risk of aspiration pneumonia)*
173
Disinfectant CS
Acute: corrosive burns, vomiting, nausea, abdominal pain, hyper-salivation, panting, respiratory depression, hypotension, ataxia, depression
Severe: shock, cardiac arrhythmia, methemoglobinemia, hepatic/renal damage, acute renal failure, pulmonary edema
174
Disinfectant TX
dilute with gastro-protectants, activated charcoal or cathartic, 1% methylene blue for methemoglobinemia
No emesis/lavage because of aspiration pneumonia
175
Automatic Dishwasher Detergents:
o High alkalinity & extremely causative ~ most concerning b/c of pH
o Clinical signs: vomiting, diarrhea, salivation, GI pain, oral/GI erosions
o Treatment: dilute with milk or water, analgesics +/- steroids
176
Toilet Bowl Cleaner:
oAcidic
o CS: vomiting, salivation, dysphagia, abdominal pain, GI ulceration, dyspnea
o TX: dilution with milk/water, metoclopramide, steroids
***No emesis, lavage, activated charcoal-->contraindicated***
177
What spp. is primarily affected by zearalenone?
Pigs>livestock
| * chickens are resistant*
178
Zearalenone MOA?
Estrogen receptor agonist (higher affinity)
179
Zearalenone CS?
Symptoms depend on sex & maturity
- decreased male libido, infertility (decreased litter size), enlarged/swollen uteri, shrunken/cystic ovaries
*vulva swelling/reddening* vaginal/rectal prolapse, regressed testes (feminization), abortions, pseudopregnancy
o Vulva swelling can be reversed once removed from the contaminated feed source!
180
Zearalenone TX?
change feed, activated charcoal (d/t enterohepatic recirculation) or high fiber to reduce elimination times
181
Venom
actively injected toxin, used for hunting and defense - “If it bites you, you die”
- LMW substance--> Cause pain, inflammation, hypotension
- Peptides--> Direct toxic effects and allergy
- Enzymes
182
Poison
passive secretion as passive defense mechanism
183
Bee venom MOA
* melittin acts as detergent and hemolytic causing pain
| * phospholipase A2 destroys membranes
184
Wasp venom MOA
use alarm pheromones & kinins produce pain
185
Ant venom MOA
piperidine causes dermal necrosis, formic acid causes burning sensation and pain
(also has antibacterial properties)
186
Hymenoptera Venom CS
local swelling, red plaques, edema, regional allergy or anaphylaxis (rare), shock, hemolysis, renal/hepatic injury
- delayed hypersensitivity is possible
187
Hymenoptera Venom TX
removal of stinger by scraping, cold compress, antihistamines, corticosteroids, epinephrine for shock/systemic toxicosis
188
What is the gold standard for anaphylactic shock?
epinephrine
189
What toxin do ticks produce?
Holocyclotoxin impairs acetylcholine release, causing paralysis/muscle weakness
- dermacentor may act on sodium channels.
190
Tick CS
may appear 6-14 days after attachment.
loss of appetite *voice * incoordination, ascending flaccid paralysis, respiratory distress or death (b/c respiratory paralysis)
191
Tick TX:
supportive treatment, anti-emetics, oxygen therapy
| atropine sulfate contraindicated!
192
What toad produce cardiotoxins?
Bufo marinus (cane toad) affecting dogs
193
Toad MOA:
biogenic amines cause vasoconstriction, hypotension, hallucination, gastrointestinal effects
bufogenins inhibit sodium/potassium ATPase activity (similar activity as digitalis)
194
Toad CS:
immediate hyper salivation or foaming at the mouth, head shaking, vomiting, hyperemic gums, arrhythmia, neurological signs, convulsions/seizures, ataxia, hallucinations, rapid death
- can observe hyperkalemia-
195
Toad TX:
water lavage, activated charcoal if no seizures, diazepam/barbiturates if seizures, propranolol/lidocaine/esmolol for arrhythmia, fluid replacement therapy, digoxin-specific antigen binding fragments
196
What spp. is most susceptible to toad toxicosis?
Dogs
197
What spp. is most susceptible to black widow toxicosis? What spp. is most susceptible to brown recluse?
cats; dog
198
What does the black widow venom contain?
Alpha-latrotoxin
199
Black widow venom MOA
alpha-latroxin creates pores in membranes to allow calcium entry and massive amounts of neurotransmitter release leading to sustained muscle spasms
200
Black widow venom CS
muscle cramping/spasms (Latrodectism), rapid weight loss, abdominal rigidity, restlessness, writhing, vocalization, hypertension, tachycardia, respiratory collapse
201
Black widow venom TX
control muscle spasms and pain, calcium gluconate (controversial), anti-venom
202
Brown recluse venom composition & MOA?
Sphingomyelinase D- cleaves heads of phospholipids bilayers causing tissue necrosis
203
Brown recluse CS?
blister-like bulls eye where bitten (non healing ulcer), hemolytic anemia, fever, weakness, leukocytosis
204
Brown recluse TX
dapsone (dermal lesion), fluids and anti inflammatory glucocorticoids, antibiotics to prevent secondary infection, analgesic, aluminum acetate (Burrow’s solution) or hydrogen peroxide to clean lesion, debridement of necrotic tissue or surgical removal (questionable), bandage
205
Eastern Coral Snake Venom & MOA?
Bungarotoxin prevents binding of acetylcholine leading to paralysis and local tissue necrosis
206
Eastern coral snake CS?
myoglobinemia (cats), hemolysis (dogs), salivation, inability to swallow, dyspnea, weakness, hyporeflexia, CNS depression, paralysis
207
Eastern coral snake TX?
Antivenom (expensive), broad-spectrum antibiotics and symptomatic wound care, supportive care
208
Pit Viper Characteristics
Characterized by heat sensing pit and hinged (retractable) fangs, head wider than body (triangle), elliptical/vertical pupil
209
Snake bite CS
immediate distinct fang marks, immediate swelling/pain/bruising of bite, hypotension, shock, tachycardia, tachypnea, anticoagulation, tissue necrosis
210
Snake bite TX
anti-venom, antihistamines, fluids, corticosteroids, glucocorticosteroids
*do not cut, ice, or tourniquet*
211
Enterotoxins MOA
enterotoxins bind to intestinal epithelium to increase permeability and cause fluid loss (diarrhea) and decreased absorption of nutrients
- Bad case of food poisoning
212
Endotoxin MOA
lipopolysaccharide from gram negative cell walls that activates inflammatory processes & causes release of prostaglandins and histamine -> circulatory collapse, pancreatitis, activation of clotting cascade, uncoupling of oxidative phosphorylation in heart -> lethargy, fever, hypothermia, diarrhea, abdominal pain, shock, foul feces
213
Endotoxin TX:
emesis, support cardiovascular function, correct fluid/electrolyte imbalance, prevent bacteria
214
Botulism in horses
"Forage poisoning in adult horses
| "shaker foal syndrome" in foals
215
Botulism MOA
prevents release of acetylcholine at neuromuscular junction leading to flaccid paralysis
216
Botulism CS
decreased tongue and tail tone, dropping food from mouth, salivation, weakness, weak vocalization, progressive paresis, bradycardia, constipation, urinary retention
217
Botulism TX
supportive therapy, oxygen therapy, warm water enemas, bladder expression, antibiotics, antitoxin (will not neutralize toxin already in neurons)
