Final Exam Flashcards

1
Q

Fescue Basics & Toxicity

A

o Tall fescue
o Common problem in large animals

Toxicity
o Toxic principal – ergovaline
o Peripheral vasoconstriction
o Suppression of prolactin secretion

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2
Q

Fescue Clinical Signs

A
Summer slump
•	Hyperthermia
•	Decrease feed intake
•	Weight loss
•	Abortions
Winter – fescue foot
•	Vasoconstriction -> ischemic necrosis of distal limbs
•	Loss of appetite 
•	Lameness
•	Abortions
Repro problems any time of year
•	Horses > cows > sheep
•	Prolonged gestation
•	Dysmature young
•	Agalactia
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3
Q

Ergot Basics, specific alkaloids, & Mech of Action

A

o Claviceps fungus found in grass & grains
o Replace seed w/ sclerotia body (hard black)
o Problem in PNW

Mech of Action
o Ergoeptide alkaloids – ergotamine & ergonovine
o Peripheral vasoconstriction
o Affects humans, cattle, swine

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4
Q

Ergot Clinical Signs, Diagnosis, Treatment

A
Clinical Signs
o	Feed refusal
o	Dry gangrene (ischemic necrosis) of distal extremities
o	Lameness
o	Neuro symptoms
o	Small week piglets & claves
o	Agalactia
o	Abortion

Diagnosis
o Look for sclerotia
o Analyze feed for ergopeptide alkaloids

Treatment
o symptomatic

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5
Q

Selenium Basics, Diagnosis, Treatment

A

o Acute or Chronic
o From high selenium forage
o Horses most sensitive

Diagnosis
o Source
o Analysis of blood (antemortem)
o Liver & kidney postmortem

Treatment
o Symptomatic

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6
Q

Selenium Clinical Signs

A

o Vary between species & duration of exposure

Acute
• Cardiac, lung, liver, kidney, skeletal muscle
• Poliomyelomalacia in swine

Chronic
•	Bob-tailed dz
•	Hair-loss on mane & tail
•	Anorexia
•	Hoof deformities
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7
Q

Selenium Deficiency

A

White muscle dz
o cows, goats, sheep, horse

Masseter muscle myopathy
o horses

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8
Q

Paraquat Basics & Toxicity

A
o	Herbicide
o	Desiccant
o	Very popular
o	Color, odor, & emetic added to deter humans
o	All animals susceptible but dogs often
Toxicity
o	Acute oral exposures
o	Less than 20% absorbed
o	Accumulates in lungs
o	T1/2 = 24hrs
o	Most excreted unchanged in urine
o	Uses MOA & produces free radicals
o	O2 is substrate
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9
Q

Paraquat Clinical SIgns

A

Acute
• GI: V, D, abdominal pain
• Pulmonary: inflammation, necrosis, edema, dyspnea
• Death

Chronic
• ~5-7d
• continued pulmonary changes -> fibrosis
• renal issues

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10
Q

Paraquat Gross & Histo Lesions

A

Gross
• Acute hemorrhage, necrosis, edema of lung & GI
• Chronic fibrosis in lung

Microscopic
• Acute hemorrhage, necrosis, edema of lung & GI
• Chronic interstitial lung fibroplasis & renal necrosis

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11
Q

Paraquat Diagnosis & Treatment

A
Diagnosis
•	History
•	GI, lung, & renal lesions
•	Urine analysis antemortem
•	Liver, kidney, lung postmortem

Treatment
• Decontaminate (AS): emesis, *AC, cathartic 

• Anti-emetics, analgesics 

• GI protectants: sucralfate, H2-antagonists, omeprazole 

• IV fluids
• Oxygen?? 
(need to breath but O2 is substrate for parquat)

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12
Q

Polytetrafluoroethylene (PTFE) Basics, Toxicity, Treatment

A

o Nonstick surfaces, lightbulbs, heat lamps, irons, ironing board covers, baking sheets, ovens, heaters
o Birds most susceptible
o Polymer fume fever

Toxicity
o Above 500F PTFE releases fumes & particulates
o Acute respiratory distress

Treatment
o Remove from environment
o O2

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13
Q

Slaframine Basics, Diagnosis, Treatment

A

o Fungus on red clover, alfalfa, legumes
o Slaframine is gland M3 agonist
o Excessive salivation

Diagnosis
o Test for Slaframine in Feed source
o Salivation

Treatment
o Remove access to feed

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14
Q

Zearalenone Basics

A
o	Produced by Fusarium
o	Metabolized to zearalenol which binds to estradiol 18B receptor
o	Found on grains
o	Weak estrogen
o	Swine > cows
o	Test for Zearalenone in food
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15
Q

Strychnine Basics & Mech of Action

A

o Common in PNW
o Rodenticide
o Died grain or liquid
o All animals susceptible

Mech of Action
o Rapid absorption & wide tissue distribution ->
o reversible antagonism of inhibitory NT glycine at postsynaptic sites in spinal cord + medulla ->
o reflex stimulation, extensor muscles predominate ->
o muscle rigidity similar to tentanus

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16
Q

Strychnine Clin Signs, Diagnosis, Treatment

A
Clinical Signs
o	Acute onset
o	Extensor rigidity
o	Tonic seizures induce by stimuli
o	Death is common

Diagnosis
o History
o clinical signs
o Chemical analysis of stomach contents

Treatment
o	Control tonic seizures & rigidity w/ pentobarbital
o	Decontaminate (mostly if asymptomatic)
o	O2
o	Fluids
o	Lower temp
o	Put in quiet place
o	Monitor acidosis
o	Watch for 24hrs
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17
Q

Metaldehyde Basics

A

o Slug & snail bait (molluscicide)
o Often combined w/ acetylcholinesterase inhibitors
o DUMBSLED = Ds, urination, miosis, bradycardia, salivation, lacrimation, emesis & dyspnea
o All species susceptible; most commonly dogs
o Usually not as fatal as strychnine

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18
Q

Metaldehyde Clin Signs

A
  • Early ‘apprehension’ phase
  • muscle tremors (face, body
  • sensitive to external stimuli
  • dose high enough -> tonic/clonic seizures -> death (respiratory failure)
  • Hyperthermia
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19
Q

Metaldehyde Diagnosis & Treatment

A

Diagnoisis
o Muscle tremors
o History
o Chem analysis of stomach contents

Treatment
o Decontaminate; emetic, AC, etc
o Control tremors / seizures – length of sedation (hrs to days)
o Supportive care: IV fluids / acid-base / oxygen / control T
o Prognosis better (24-48 hrs) depends on dose and success of decontamination

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20
Q

Penitrem A & roquefortine Basics

A
o	Penicillium mold species
o	Tremergenic mycotoxins
o	Moldy foods, decaying organic material, walnuts - cheese – bread, egg shells, coffee grounds, carrot peels, corn
o	All species susceptible 
o	hard to estimate dose
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21
Q

Penitrem A & roquefortine Clin Signs

A

o Onset rapid

  • Initial ‘apprehensive’ phase
  • intention tremors, ataxia
  • tonic/clonic seizures
  • sensitivity to external stimuli
  • nystagmus
  • 50% will vomit 

  • cerebellar component

Death if dose is high enough or no treatment provided

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22
Q

Penitrem A & roquefortine Diagnosis & Treatment

A

Diagnosis
o History
o Chemical analysis of Stomach contents, Serum, bile, urine

Treatment
o Decontaminate; emetic, cholestyramine, cathartic, lavage 

o Control tremors / seizures w/ methocarbamol or diazepam 

o Supportive: IV fluids / acid-base / T / oxygen / ataxic patient
o Prognosis – variable (depends on dose and success at decontamination) – 24 to 48 hrs 


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23
Q

Bromethalin Basics

A
o	Rodenticide
o	Dogs most common
o	Cats 10X more sensitive
o	Long T ½ = 6 days
o	Important to do math
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24
Q

Bromethalin Mech of Action

A

o Uncoupler of oxidative phosphorylation in mitochondria of CNS ->
o drop in ATP ->
o build up of extracellular fluid ->
o fluid filled vacuoles between myelin sheaths, edema ->
o pressure impairs nerve conduction and increase in intracranial pressure ->
o paralytic syndrome / convulsant syndrome

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25
Q

Bromethalin Clinical Pathology, Diagnosis, Treatment

A

Clinical Pathology
o More likely to see lesions after 24hrs
o Edema postmortem
o Vacuolation w/in myelin sheaths

Diagnosis
o History
o Abrupt onset of lethargy, paralysis, convulsing
o Maybe chem analysis of stomach contents acutely
o Chem analysis of fat postmortem

Treatment
o	Decontaminate
o	AC every 6-8hrs for 24hrs
o	Maybe cholestyramine
o	Control temors & seizures
o	support
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26
Q

Bromethalin Clinical Signs

A

o Lag phase up to 2-5 days

Paralytic form
•	Any toxic dose
•	hind limb paresis / paralysis 

•	abdominal distension, ileus 

•	more common in cats

Convulsant form
• Dose greater than LD 50
• V, muscle tremors, tonic/clonic seizures
• Hypersensitivity to external stimuli

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27
Q

1080 Sodium monofluoroacetate Basics & Mech of Action

A

o Banned in US
o All animals susceptible
o Secondary poisonings occur

Mech of Action
o Affects krebs cycle & ATP production

28
Q

1080 Sodium monofluoroacetate Clinical Signs Dogs, Cats, Livestock

A

o Lag phase 30 min to 2 hrs

Dogs
• GI & CNS
• Cycles of vocalizing, running, deficating, seizures intensify
• Respiratory & cardiac arrest

Cats
• GI & CNS depression or excitation

Livestock
• Cardiac

29
Q

1080 Sodium monofluoroacetate Diagnosis & Treatment

A

Diagnosis
o History
o Clinical signs
o Chem analysis of urine & kidney

Treatment
o Doesn’t really work
o Maybe pentobarbital + Na bicarbonate

30
Q

Methionine Basics, Clinical Signs, Treatment

A

o given to dogs for lawn care
o transient hind limb paralysis / abnormal posture
o metabolite is homocysteine

Clinical Signs
o vomiting, ataxia / acidosis, lethargy, diarrhea, weakness, PD, hypermetria, disorientation, tremors, anorexia, vocalization 


Treatment
o Fluids & confinement
o bicarbonate
o emetics if asymptomatic within 2-4 hours

31
Q

Methylxanthines; what are they?

A

Theobromine
o Cacao beans
o Chocolate foods

Caffeine
o Coffee, tea etc
o Coffee beans (chocolate covered?)
o No-Doz

Theophylline
o Bronchodilator
o Tea

32
Q

Methylxanthines Toxicity

A
o	All animals susceptible, dogs common
o	Variation in chronic dose for different individuals
o	Long T1/2
o	Enterohepatic recirculation
o	Chocolate delays gastric emptying
o	Pancreatitis can be concern due to fat
o	DO THE MATH
33
Q

Methylxanthines Clinical Signs & Diagnosis

A
Clinical Signs
o	CNS excitation, excessive urination, CV effects, GI
o	Increased HR & BP
o	Muscular excitability
o	V, D, urination, bloat
o	Hyperactivity, tremors
o	Tachycardia, hypertension
o	Tonic/clonic seizures
o	Cardiac arrhythmias

Diagnosis
o Exposure
o Clinical signs in order of GI -> PU/PD -> tremors -> CV

34
Q

Methylxanthines Treatment

A

Asymptomatic
• Emesis up to 6hrs post ingestion
• AC 3x in 24hrs
• Cathartic

Symptomatic
•	Control tremors w/ benzos
•	Monitor ECG, BP, HR, CNS, Na levels
•	IV fluids
•	Anti emetics
•	Send home after 8-12 hrs
35
Q

Glow Jewelry

A

o Dibutyl phthalate
o Biggest risk to cats
o Acute salivation & catnip like behavior change
o Rinse mouth, eyes, etc
o give Zinc sulfide or strontium aluminate

36
Q

Basics of Lead

A

o Found in paint, batteries, sinkers/shot
o All animal susceptible
o Often in cattle & acute
o Often chronic in raptors & waterfowl
o Young animals have increased absorbtion in GI
o Excreted in bile

37
Q

Mech of Action of Lead

A

o Bind to protein on RBCs
o Premature release of immature RBCs in dogs & cats
o Increased vascular permeability -> edema of CNS/PNS & demylination of peripheral nerves
o GI irritation
o Renal changes
o Liver necrosis

38
Q

Clin Signs of Lead in Dogs, Cats, Cows, Horses, Birds

A

Cats/Dogs
• GI first then maybe CNS
• Vs, Ds, anorexia, abdominal pain
• Hysteria hyperexcitability

Cows
•	CNS & PNS maybe GI
•	Blindness, wandering, twitching
•	Acute death in calves
•	Hyperthermia

Horses
• Never seen!
• Lethargy & laryngeal paralysis

Birds
•	Chronic GI & PNS symtoms
•	Lethargy anorexia
•	Ds, crop stasis
•	Wing paralysis
39
Q

Lead; clin path & lesions

A
Clin Path
o	nRBCs + regeneration
o	chronic anemia in birds
o	maybe renal tubular nephropathy
o	maybe elevated liver enzymes
Lesions
o	Cerebral edema
o	Pale-cooked muscle
o	Polioencephalomalacia
o	Liver & kidney necrosis
40
Q

Lead Diagnosis, Treatment, Prognosis

A
Diagnosis
o	Exposure
o	Radiographs
o	Lead analysis of whole blood
o	Liver & kidney postmortem
Treatment
o	Decontaminate; emetics or surgery
o	Chelation w/ succimer
o	CaEDTA (in cows)
o	Maybe penecillamine
o	Thiamine hydrochloride
o	Control seizures

Prognosis
o SA do well
o LA & birds do not

41
Q

Non-protein Nitrogen Basics & Toxicity

A

o Urea most common
o Fertilizer
o Anhydrous ammonia fertilizer can cause pulmonary

Toxicity
o All species susceptible
o Ruminants most common
o Excessive ammonia levels in vivo

42
Q

Non-protein Nitrogen Mech of Action

A

o Urea + water -> NH3 + CO2 (urease)
o Rumen flora take ammonia and carbs -> amino acids + protein
o Microflora overwhelmed -> rumen buffers to NH4 ->
o Increased NH4 -> pH rises (> *8-10); overwhelm buffering capacity & increase NH3 concentrations
o NH3 gets absorbed -> overwhelms buffer and urea cycle -> hyperammonemia (toxicosis)
o Rumen alkalosis / metabolic acidosis -> hyperkalemia-induced cardiac failure

43
Q

Non-protein Nitrogen Clinical Signs, Diagnosis, Treatment

A

Clinical Signs
o Onset <4hrs
o Usually after new feed introduced
o Salivation, Abdominal pain – grinding 
teeth 

o Muscle tremors, Ataxia, weakness, dyspnea 

o Convulsions, bloat, death 

o Rapid clinical progression 


Diagnosis
o	Many animals affected
o	Rumen pH >8-10
o	Collect eyeball immediately after death & freeze to confirm high ammonia
o	Analyze supplement
Treatment
o	Often not possible
o	Treat w/ in 20 mins of signs
o	Cold water & Vinegar to convert NH3 to NH4
o	Correct acidosis w/ fluids & bicarb
44
Q

Organophosphates & Carbamates Basics & Mech of Action

A

o Acetylycholinesterase inhibitors
o Insecticides
o Affects all animals

Mech of Action
o	Bind Acetylcholinesterase ->
o	Phosphorylate or carbamylate ->
o	inactivate
o	build up of acetylcholine leading to overstimulation ->
o	muscarinic, nicotinic, & CNS
45
Q

Organophosphates & Carbamates Clinical Signs & Treatment

A
Clinical Signs
o	Not all symptoms all the time
o	DUMBSLED
o	Nicotinic = tremors
o	CNS excitation & seizures
o	Death due to respiratory failure
o	Pancreatitis in dogs/cats
o	Colic & Ds in horses
Treatment
o	Decontaminate
o	Atropine for muscarinic signs
o	Oximes bind unbound pesticide
o	O2
46
Q

Organophosphates & Carbamates Diagnosis

A

Che inhibition screening tool
• No inhibition for carbamates because too fast = false (-)
• Inhibition due to anemia or others = false (+)

Chemical residue of GI, skin, etc

47
Q

Organophosphates & Carbamates: Delayed neuropathy syndrome Vs Intermediate Syndrome

A

Delayed neuropathy syndrome
o Inhibition of neuro toxic esterase 

o Signs 1-2 weeks after exposure 

o Polyneuritis = ascending paralysis 


Intermediate Syndrome
o Lipophilic compounds 

o Long term accumulation at receptor induces tolerance / down regulation of cholinergic receptors
o Anorexia, neuromuscular weakness, ventro-flexion of the neck

48
Q

Dead Birds

A

DRC-13 or Starlicide
o nephrosis that kills at roosting site

Avitrol
o neurotoxin

49
Q

Natural pyrethrins, pyrethrum & Synthetic pyrethroids Basics & Toxicity

A

o Insecticides, flea tick repellent
o Dogs very sensitive to bifenthrin
o Cats very sensitive to permethrin
o Products w/ 65% or greater

Toxicity
o Low mammalian toxicity
o Should not use on cats or dogs in a cat home
o Spot on treatment can cause epidermal paresthesia -> inflammatory contact dermatitis (especially pyrethroids)

50
Q

Natural pyrethrins, pyrethrum & Synthetic pyrethroids Clinical Signs & Diagnosis

A
Clinical Signs
o	CNS excitation
o	Salivation
o	Tremors, twitching
o	Temporary blindness
o	Convulsions

Diagnosis
o history
o Chemical residue analysis

51
Q

Natural pyrethrins, pyrethrum & Synthetic pyrethroids Treatment

A

o Decontaminate by sedating, bathing w/ mild soap, AC-cathartic-gastric lavage w/ stomach tube
o Control tremors/seizures w/ methocarbamol
o Control body tmep
o IV lipid rescue therapy for permethrin
o Apply Vit E to application site
o Prognosis good w/in 24-72 hrs bad in cats

52
Q

Chlorinate Hydrocarbons Basics & Toxicity

A

o Insecticides
o Limited use in US
o Environmental contamination

Toxicity
o Affects most mammals
o Lipid soluble, stable -> persists in environment & body
o Diffuse nervous stimulant

53
Q

Chlorinate Hydrocarbons Clin Signs, Diagnosis, Treatment

A

Clinical Signs
o Onset 30-60 mins
o Early premonition period
o muscle tremors of head, neck, entire body
o tonic/clonic seizures (continuous, intermittent) 

o Excessive response to external stimuli 


Diagnosis
o History
o Tremors/seizures
o Chemical analysis of fat, serum, milk, liver, brain, GI contents

Treatment
o	Control tremors, seizures 
o	Decontaminate 
o	Maintain hydration, acid-base status, temperature, etc. 
o	Prognosis variable
54
Q

Cyanobacteria Basics & Clinical Signs

A

o Blooms all year round
o Stagnant, low O2, high nutrients, high light, warm clam water

Clincal Signs
o	Acute onset
o	Muscle tremors 

o	DUMBSLED 

o	Seizures / paralysis 

o	Death due to respiratory paralysis
55
Q

Cyanobacteria Toxins

A

Anatoxin-a
• mimics acetylcholine (nicotinic)
• 20X more potent than ACh

Anatoxin-a(s)
• inhibits acetylcholinesterase (nicotinic and muscarinic)
• more potent than anatoxin-a

56
Q

Cyanobacteria Diagnosis & Treatment

A
Diagnosis
o	History
o	Acetylcholinesterase inhibition in blood
o	Algae ID
o	Test water & GI for toxin

Treatment
o Support
o Adequate respiration
o Cholestyramine

57
Q

Perennial Ryegrass Staggers Basics & Toxicity

A

o Common in NW
o endophyte grows on lower leaf sheath & seed of Lolium
o Symbiotic
o Late summer & fall grazing or anytime if over grazed

Toxicity
• Lolitrems
• Purkinje cell problem
• High morbidity / low mortality

58
Q

Perennial Ryegrass Staggers Clinical Signs, Diagnosis, Control

A
Clinical Signs
•	Fine muscle tremors
•	rhythmic palsy of head, neck and limbs
•	exaggerated when forced to move or eyes covered 
•	look almost normal when at rest

Diagnosis
• History
• Analyses of food for lolitrem

Control
• Remove source
• Avoid overgrazing

59
Q

Equine Leukoencephelomalacia Basics & Clinical Signs

A
o	Moldy corn
o	Fumonisins
o	Problem in E & MW
o	Hepatotoxic to all species
o	Can cause esophageal cancer in humans
Clinical Signs
•	Onset 1-4 wks
•	Low morbidity / high mortality 
•	Blindness, head pressing, aimless walking, stupor, 
•	glossopharyngeal paralysis 
•	delirium, recumbency, seizures, death
60
Q

Equine Leukoencephelomalacia Lesions & Diagnosis

A

Clin Lesions
• Necrosis of subcortical white matter
• Hepatic necrosis, fibrosis, biliary hyperplasia

Diagnosis
• Corn screening
• Analyze food for fumonisin
• No treatment

61
Q

Nicotine Basics, Signs, Diagnosis, Treatment

A

o Cigarettes, chewing tobacoo, e-cig cartriges
o Short T1/2
o Nicotinic acetylcholine receptor agonist

Clinical Signs
• Initial Vs
• Hyperactivity, tremors, seizures
• Death due to respiratory paralysis

Diagnosis
• Nicotine residue

Treatment
• Decontamination
• Control CNS excitation
• O2

62
Q

Ivermectin Basics, Toxicity

A

o Antiparasitic
o Relatively safe
o Cats & dogs w/ MDR1 mutations
o Bad for turtles/tortoises

Toxicity
• Long T1/2
• Inhibits GABA & glutamate-gated chloride channels

63
Q

Ivermectin Signs, Diagnosis, Treatment

A
Clinical Signs
•	Ataxia, depression, lethargy, weakness
•	Reversible blindness
•	Tremors, seizures
•	Coma & death (uncommon)
•	Can persist for days-weeks

Diagnosis
• Chemical analysis of feces, fat, liver, bile (only shows exposure)

Treatment
•	Decontaminate
•	Multiple AC
•	Cholestyramine
•	NO benzos
•	Support
•	IV lipid therapy
64
Q

Salt; Basics & Mech of Action

A

o Electrolyte supps, play dough, ice melts, etc
o Not enough water or too much water after hypernatremia

Mech of Action
•	Fluid shifts from intracellular to intravascular ->
•	Cells shrink & die ->
•	Neuro signs ->
•	Passive diffusion of Na into CSF & neurons ->
•	Inhibition of glycolysis ->
•	More neuro signs ->
•	Rehydrate ->
•	Na trapped in CNS ->
•	Cerebral edema & hemorrhage
65
Q

Salt; Signs, Diagnosis, Treatment

A

Clinical Signs
• V, D, anorexia
• Wandering, circling, head press, blind, tremors, seizures
• Cerebral edema & malacia
• eosinophilic perivascular cuffing lesions in pigs

Diagnosis
• Increased Na levels in serum & CSF

Treatment
•	Remove source
•	NO AC
•	SLOW rehydration
•	OR remove fluids if edema is an issue