Disease Management Flashcards
1
Q
Atypical myopathy pathophysiology
A
sycamore ingestion - seeds or seedlings
impairs lipid metabolism
acute degeneration in postural and respiratory muscles
degeneration of myocardium –> cardiac failure
or
CHF –> pulmonary oedema
+
respiratory muscle necrosis –> reduced ventilation
if alive after 5 days prognosis good, otherwise high mortality
2
Q
atypical myopathy - signs
A
reluctance to move
weakness
stiffness
lethargy
red urine - myoglobinuria
hypothermia
tachycardia and irregular heart rhythm
pain - varying severity
sudden death - if very acute may be only sign seen
3
Q
atypical myopathy diagnosis
A
history - grazing, access to sycamore, sudden onset, multiple horses affected, time of year, poor weather
CK, AST and LDH - released from damaged muscle, may not show extent at early stages
myoglobinuria
hyperlipidemia and hyperglycemia - from stress,impaired lipid metabolism and impaired hepatic gluconeogenesis
4
Q
atypical myopathy ddx
A
rhabdo
colic
lameness - arthritis, laminitis
endotoxemia
neuro signs - tetanus, rabies, botulism, spinal cord disease, grass sickness, meningtitis
myoglobinuria (or hematuria) - trauma, exercise, cystitis, calculi, systemic hemolysis, urethral deficits, bladder tumour, renal hemorrhage
PSSM (polysaccharide storage myopathy) - genetic
vitamin E/selenium deficiency
poison
immune-mediated myolysis
prolonged recumbancy
5
Q
atypical myopathy - management aims
A
limit further muscle wastage
restore circulating volume
correct acid base balance and electrolytes
provide alternative energy substrates to muscle cells
analgesia
6
Q
atypical myopathy - management
A
immediate treatment critical
24/7 supportive care requires
fluids - high volume - protect kidneys from myoglobin injury and NSAID effects, correct dehydration and acid base, continue until urin yellow and horse not dehydrated
nutrition - carb energy, good quality hay, grass alfafa, impaired liver metabolism, vitamin e supplements, selenium, B2, C and carnitine
warmth
minimise stress
drain bladder
physiotherapy
if recumbent turn regularly and maintain in sternal
7
Q
atypical myopathy - prevention
A
check for sycamore
fence off
pick up seeds
turn out horses for shorter times
more forage provision
reduce stocking density so enough good grazing
field mates removed and tested if suspected case
antioxidant, B vit and amino acid supplements
8
Q
grass sickness - premises factors
A
soil - loam and sand worse that chalk, high nitrate and titanium increased risk, low zinc and chromium increased risk
high grass iron
climate - more days of sun, lower temp
recent cases on premises
many horses on premises
mechanical dropping removing
soil disturbance
9
Q
grass sickness - horse risk factors
A
grazing horses
young horses - higher incidence up to 10yo
native scottish breeds
stallions - slightly more than mares
recent movement
recent diet change
recent stress
recent ivermectin treatment
10
Q
grass sickness - protective factors
A
high clostridium botulinum C antibodies
co grazing with ruminants
regular grass cutting
manual dropping removal
supplementary forage feeding
11
Q
grass sickness forms and prognosis
A
acute - nearly always fatal - gastric refluc, SI distension, secondary LI impaction
subacute - nearly always fatal - secondary SI impaction
chronic - up to 50% fatal if prolonged supportive care, intensive nursing
12
Q
grass sickness - signs - acute
A
dull
tachycardia >60pm
drooling saliva
mild-moderate colic signs
muscle tremors
patchy sweating
SI distension - dilated loops on US
nasogastric reflux - high volume, due to functional ileus
dehydration - high TP on bloods
may have fever
external appearnace may not reflect severity - can be standing quite comfortably
bilateral ptosis - all forms (dropping eyelids) - neuro degeneration
dry scant feces with mucus and epithelial debris - all forms
fluid filled stomach on US - all forms
13
Q
grass sickness - signs - chronic
A
weight loss
dysphagia
rhinitis sicca
diffuse weakness
low head carriage
muscle tremors
elephant on ball stance
ptosis
dry scant feces with mucus and epithelial debris
fluid filled stomach on US
14
Q
grass sickness - ddx
A
other colics that increase HR - surgical, enterior enteritis, inflammatory enteritis, primary ileus impaction, gastric impaction
oesophageal choke - drooling
botulism
hemoabdomen
hypocalcemia
equine motor neurone disease
15
Q
grass sickness diagnosis
A
history and signs pretty accurate
eyedrop test - phenyephine eye drops - resolves ptosis in grass sickness - false positives if sedated, seom breeds, botulism or if very sick horse, false negatives in excited horses
ex lap - rule out surgical colic
monitor progression of signs over time - only if welfare permits, give supportive care at same time, not if suspect surgical colic
microscopic exam of ileal biopsy - formalin fixed, 1cm full thickness - time delay on results
16
Q
grass sickness - treatment
A
nursing
NSAIDs - bute - analgesia and encourage eating
omeprazole
antimicrobials - if suspect aspiration pneumonia, severe rhinitis sicca or if there’s diarrhoea
probiotics/prebiotics - address GI dysbiosis - not much evidence
appetite stimulatns - steroids, diazepam - not much evidence
fluids - hydration
17
Q
grass sickness - co grazing horses
A
house all for 2-4 weeks or until heavy rain if poss
house high risk or move to another pasture if not possible to house all
manual feces collection
avoid ivermectin
supplementary forage
feed additives - unproven, aim to improve gut flora
18
Q
grass sickness - potential causes
A
c botulinum c - probably not
myotoxins - maybe
19
Q
pig exam
A
history - housing, facilities, other pigs, vax history, worming, other animals, feed, bedding
demeanor
PUPD
lameness
asymmetry
body marks
temp
RR
HR
MM
20
Q
MMA pigs - metritis mastitis and agalactiae
A
24-72h post farrowing
complex if all 3
mastitis usually caused by trueperella pyogenes
piglets not feeding
recumbancy and lethargy
not eating
dry feces
fever
laboured breathing
treatment -
feed and supplement piglets and warm them
milk sow
anti inflammatories for sow
don’t need oxytocin, cervix closed
ddx -
erysipelas - notifiable
retained foetus or membranes
21
Q
pig parasites
A
ascaris suum - milk spot
SI –> liver migration –> milk spot on autopsy
travel to lungs –> coughed up –> ingested
decreased weight gain, penumonia in pigs under 4 months
sarcopted scabii - mange
mite
buroows into skin –> inflammation and red spots and pruritis
usually seen at slaughter
matestrongylus apri - lungworm
outdoor
migrate LN in intestines –> lungs –> lung damage –> chronic bronchitis –> secondary bacterial infections
eggs survive well in soil even if cold
from infected earthworms
22
Q
pig parasite control
A
flubendazole - lungowrm and milk spot, adults larvae and eggs
ivermectin - ascaris and lung worms, adults and older larvae
fenbendazole - ascaris and lungworm, adults and egg
23
Q
pig parasite diagnosis
A
fecal flotation
necropsy
skin scrape for sarcoptes
haematopinus suis - visible, blood sucking
ascarids - intermittent shedding, blood ELISA available
24
Q
pig vaccinations
A
Porcine parvovirus -
Only affects pregnant sow in damage to unborn litter – no signs for adult themselves
Can lead to smaller litters due to embryonic death
Progressive mummification
Stillborn pigs
Delayed farrowing – esp with small litters
Most common cause of SMEDI
Porcine reproductive respiratory syndrom (PRRS) -
Main signs in young piglets – scour, weakness, high mortality, weak or underdeveloped piglets
Growing pigs – respiratory disease, depressed lung immunity, secondary bacterial infections – may see blue ears
Adults – depression, inappetence, vomiting, skin discolouration (Extremities), agalactia – non-specific. Abortions, premature farrowing, failure to farrow, stillbirths and late mummification
Porcine circovirus associated disease -
Primarily growing pigs
High mortality
Post weaning mulisystemic wasting disease -
Rapid loss of condition – 7-12 weeks old
Enlarge superficial lymph nodes – esp superficial inguinal
Profuse watery scour
Respiratory disress
High mortality rates
Porcine dermatitis neprhopathy syndrome -
Usually later than PMWS
Immune mediated
Sudden onset haemorrhage of skin
Protein loss from nephritis –> oedema of legs
High mortality
Non-specific porcine circovirus associated disease -
Usually respiratory or enteric
Often complicated with bacteria
Acute systemic disease
High temp, depression, anorexia, coughing, dyspnoea, scour (varying degree)
Discolouration of extremities
Secondary infections – streptococci, pasteurella – distort signs
Significant mortality but not as much as the other types
Peracute PCVAD -
Sudden death due to fluid accumulation in lungs
PCV2 -
Reproduction failure in naive adults
Abortion, mummification, stillbirths
Not common in UK
Mycoplasma hyopneumoniae -
Enzootic pneumonia
Component of PRRS
Coughing and laboured breathing
Slow and uneven growth
Death rare in uncomplicated cases but secondary infections increase mortality
Routinely monitored in slaughter pigs
E coli enteritis -
Newborn piglets most at risk – prevent through vax of sow
Diarrhoea – severe and watery in first 3 days of life
Hygiene in farrowing area crucial for prevention
Clostridial enteritis -
Often in conjunction with e coli
Sows farrowing on contaminated soil
Piglets – scour with blood in, from a few hours after to birth to 1 week old
Haemorrhage can occur into gut with some strains – death before chance for diarrhoea to show
Erysipelas -
Bacterial
All pigs vulnerable
Found in environment and carried by wild animals
Adults – high temp, depression, lethargy, diamond shapes on back and sides
Pregnant – abortion
Boars – sterility for up to 8 weeks
Peracute, acute and mild forms – sudden death due to septicemia, to signs and diamond lesions, to just skin lesions with no other signs
Longer term – arthritis (crippling), necrosis of skin, death due to lesions on heart valves (endocarditis)
Arthropic rhinitis -
Pasteurella multocida
Young piglets – under 8 weeks old
Slow growth
Secondary bacterial lower resp disease
Distortion of snout and loss of filter effect of nose
Lots of sneezing and epistaxis in severely affected
25
pig vaccine target groups
Porcine parvo – breeding pigs before service
PRRS – breeding and growing
PCVAD – growing or breeding to protect piglets
Mycoplasma – growing
E coli – breeding, to protect piglets
Clostridia – breeding, to protect piglets
Erysipelas – breeding and growing
Atrophic rhinitis – breeding, to protect piglets
Haemophilus parasuis (glassers disease) - breeding, to protect piglets
Lawsonia intracellularis – growing
Aujeszkys disease virus – breeding and growing
Strep suis – breeding, to protect young and weaners (meningitis in sucklers or weaners)
Actinobaccilus pleuropneumoniae – growing
Salmonella typhimurium – growing
Swine influenza – breeding, to protect piglets and weaners
26
pig - kune kune feed
grazers
overfeeding and obesity common problems --> osteoarthritis --> lameness
communal troughs --> bullying --> weight loss
no kitchen scraps
parsnips poisonous maybe
less grain than standard pigs
27
pig castration
must be by vet if over 7 days old
may be advisble to leave to 6 weeks
must use anaesthetic - local or GA - over 7 days
must be surgical - not rubber ring or burdizzo
kune kunes prone to inguinal hernia, if happens may have incomplete castration
monitor after for infection, excessive bleeding or swelling
28
walking a pig
license needed
issued by APHA vet
only valid for specified route
carry license when walking
annual review
should be kept in environment where can get enough exercise without walking either way
29
pig - nose ring
digging/rooting - natural behaviour
if stop it bad for welfare --> behavioural issues
create fenced area where can root
30
pigs - food scraps
illegal
disease spread - african or classical swine fever, foot and mouth
31
detusking boar
wire
take to gum line
appropriate handling and sedation
32
apocrine anal gland tumours
deep, firm masses
near anal glands
older dogs
spaniels, malamutes, german shepherd, mixed breeds
constipation
hypocalcemia - poor appetite, weight loss, kidney disease, PUPD
spread to local lymph nodes and other organs
remove whole tumour, if not possible reduce size
remove affected lymph nodes
+ chemo and radiotherapy
33
AHDB mobility scoring - cattle
0 - good mobility
even weight bearing and even rhythm, flat back, long fluid strides
routine foot trimming and mobility scoring
1 - imperfect
uneven steps, shortened strides, affected limb not immediately obvious
routine foot trimming, observation
2 - impaired
uneven weight bearing, affected limb obvious, obviously shortened strides
prompt treatment, lift foot to establish cause, attended to as soon as practically possible
3 - severely impaired
unable to walk at brisk human pace, lame leg obvious, back arched, very lame
urgent attention, treat, limit walking distance, keep on straw or grass - cull in severe cases
34
dutch 5 step
1 - red
measure and trim largest claw - inner on hind, outer on fore
coronary band to toe - 8cm
clip and even out depth
visualise v part of white line at toe
2 - yellow
match opposing toe
3- green
dish out axial parts of both claws
allows muck to flow between toes and out
don't model toe - changes weight bearing
4 - blue
remove diseased horn
create height difference to keep affected claw off floor
block sound claw
NSAIDs, soft floors, short walking distance
5 - purple
remove loose horn from heel
check between claws
35
blocks - types
wood
rubber
plastic
slippers
36
blocks - duration
minimum 4 weeks
may come off on its own, cut or grind off
37
foot bandage durations - cattle
healing wound - keep dirt off - 2 days max
alicylic acid on leasion - 7 day max
cover digit amputation - change every 2-3 days
38
IVRA - toe amputation - cattle
tourniquet - elastic
procaine
any vein
lateral plantar vein
saphenous
plantar digital veins
radial
medial palmar digital
39
laminitis - causes - equine
sepsis associated - secondary to systemic inflammation - severe GI disease, pneumonia, retained membranes
endocrine - most common - insulin dysregulation, PPID, EMS, excessive pasture consumption
supporting limb laminitis - associated with fracture or joint sepsis in contralateral limb, not as common
40
laminitis - signs - equine
tachycardia/tachypnoea
bilateral forelimb lameness
leaning back on heels
bounding digital pulses
increased hoof wall temp
pain on hoof testers
palpable depression on coronary band
may be subclinical but with divergent hoof rings
may also see - lying down, non weight bearing on one leg, reluctance to walk, tying up - various
owner less likely to suspect if don't think horse is overweight or if not a pony
41
laminitis - equine - obel grading
0 - 4
0 - no abnormalilities at walk or trot
4 - difficulty weight bearing, reluctance to move
42
laminitis - equine - treatment
analgesia and anti-inflammatories -
NSAID - bute, flunixin, suxibuzone, leloxicam - try out until one works
butorphanol, pethidine, morphine - if NSAIDs not working, only in clinic
foot support -
deep bedding
box rest
shoe removal
frog supports - small ponies only
styrofoam support - only in heavier horses
hoof cast - make sure even weight distribution, only leave on for couple of weeks
ACP - sedate, decreased ambulation
cryotherapy - use immediately if sepsis associated, hoof temp kept below 10c for 72 hours, ice and water in old fluid bags fine
43
laminitis - equine - diagnostics
radiographs -
diagnostic and monitoring
latero-medial and dorso palmar of both forelimbs
looking at rotation of pedal bone, thinning sole, sinking of pedal bone
farriery -
trial and error - casts, clogs, imprint shoes
aim to take pressure off painful area and support pedal bone
44
laminitis - equine - salvage procedure
DDFT tenotomy - for unresponsive cases that have lost potential for future athletic use
cut the DDFT so not pulling at pedal bone
45
apocrine anal gland tumours
spaniels, german shepherds, mixed breeds
older dogs
deep, firm masses
near anal sacs
constipation
paraneoplastics hypercalcemia --> poor appetite, weight loss, kidney disease, PUPD
spread to local LNs and other organs
treat -
ideally remove whole tumour
reduce size if can't remove whole
remove affected LNs
chemo and radiotherapy in addition
poor prognosis
46
basal cell tumours
wirehaired pointed griffons, kerry blue and wheeaten terriers
middle to older aged
benign
head, ears, neck, forelimbs
firm solitary masses, elevated, domed, often hairless and ulcerated, sometimes dark colour
caried size
may still be uncomfortable even though benign - broken skin, tissue necrosis, drain fluid or pus
surgical removal to cure
47
basal cell carcinoma
more common in cats
in dogs - older, st bernarns, terriers
malignant
anywhere on body
flattened or raised
spread --> new ulcers
can also spread to other organs
rarely metastatic in cats
treat - surgical removal, ensure get good margins
48
fibromas
dobermans, boxers, goldens but all breeds
aged dogs
head and legs
can look like skin tags
isolated, usually raised, often hairless, originate under skin surface
firm rubbery feel or soft and mushy
benign
treatment optional, recommend complete surgical removal if change in appearance or grow large
49
benign histiocytoma
young dogs - under 3.5 yrs
english bulldogs, schottish terriers, greyhounds, boxers, boston terriers
head, ears and limbs
solitary, raised, usually hairless, sometimes ulcerated
freely movable
diagnosis - FNA, or biopsy
often resolve on their own
surgical removal if causing issues for the dog
50
malignant histiocytoma
uncommon
bernese mountain dogs
males
average onset 7 years old
starts at internal organs - liver, LNs, lungs - not usually skin
rapid progression - illness, pain, eventual death
chemo can be used but not much point
poor prognosis - rarely over 6 months
51
lipomas
common in dogs
obese females
doberman, labs, mini schnauzers, mixed (but all really)
trunk or tops of legs most common
soft, discrete lumps
move freely
may merge with healthy fat tissue next to it
FNA to diagnose
remove if causing isse
best to remove earlier when a more manageable size
52
liposarcoma
rare
if occur then usually older dogs
chest and legs
malignant but low spreading potential
wide margin surgical removal recommended
reoccurence common
53
mast cell tumours
most common malignant tumour of dogs
any age - 8-10 years old most common
anywhere on body or on internal organs
limbs most common - back of upper thigh
may have multiple locations
tumour size affects prognosis - over 3cm poor survival time
more likely to spread if on mms, feet, prepuce, or lower surface of body
also if rapid growing or not fully removed at surgery
mast cells - reactive so can flare if messed around with
cats - can look like lipoma and easily removed with narrow margins
54
benign melanoma
benign more common than malignant
middle aged to older dogs
schnauzers, dobermans, goldens, setters, vizlas
spots or patches, raised or flat, generally solitary but can be multiple
pigmented - usually dark coloured
surgical removal to cure
55
malignant melanoma
older animals
schauzers, scottish terriers
more often males
lips, mouth, nail beds most common
rare in haired skin, if on haired skin then lower abdomen and scrotum
raised, generally ulcerated, may be darkened (on lips or mouth dark to light grey or pink)
on nail bed - swelling of toe, may lose nail and destroy underlying bone
festering toe in older dog - indication for xray and tissue sample including bone for biopsy
treat - complete surgical removal, toe amputation standard for on toe
spreads easily
56
squamous cell carcinoma
older dogs and cats
lightly pigmented skin and spending time in sun
mulitple lesions on thinly haired areas
most common digital tumour in dogs
in cats more often ear tips, eyelids or nasal planum
digital - swollen digit, abnormal nail, nail bed infection
57
characteristics of malignancy
large and variably shaped nuclei
increased division
disorganised arrangment
variation in size and shape
loss of normal features
58
stains
diff quick -
different cell types - RBCs pink/yellowish red/ platelets violet, neutrophils blue nucleus with pink cytoplasm and violet granules, eosinophils blue nucleus and cytoplasm with red granules, basophils purople nucleus with violet granules, monocytes violet nucleus with light blue cytoplasm, fungi dark blue
H&E -
blue nuclei with pink extracellular matrix - visualisation of structure, distribution and morphological changes
histochemical stains -
eg muricarmine
attached to mucus - lungadenocarcinoma - mucus producing
immunohistochemical stains -
react with antibodies, either for one cancer type or multiple, can indicate prognosis
59
classes of intoxicated patients
asymptomatic with known exposure - aim to decontaminate and prevent signs developing
symptomatic - either known exposure or just suspected - decontaminate, stabilise, diagnostic investigation, supportive care
60
intoxication resources
veterinary poison information service - toxic dose info, suggested treatment
BSAVA/VPS guide to common canine and feline poisons
ingredient lists/data sheets
61
phone triage - intoxication
signalment
suspected toxin
timing
suspected dose
time of arrival
instructions for owners - prevent further exposure, bring packaging
prep - set up medication, supportive care, contact VPS if needed
62
intoxication - decontamination
topical - rinse eyes, wash skin/coat with mild detergent
emesis - sooner better, longer time for solid toxins as stay in stomach longer
don't use emesis if non toxic dose, if already vomited, risk of aspiration, resp distress, severe electrolyte or acid base imbalance, or if toxin is caustic
apomorphine - licensed in dogs
xylzine in cats - preferred but unlicensed
examine vomitus
gastric lavage - GA with cuffed ETT, if emesis contraindicated, useful in tortoises
adsorbants - activated charcoals - binds to toxins so not absorbed, feed food with repeated doses until feces black (NB may effect efficacy of oral meds)
doesn't work for alcohol or xylitol
63
supportive care - intoxication
fluids - replace losses and maintain renal perfusion
analgesia - opioids
antiemetics - maropitant and andansetron
gastroprotectants
64
allium intoxication
garlic, onions, leeks
cats more sensitive than dogs
toxic dose -
cats - 5g/kg
dogs - 15-30g/kg
oganosulphoxides --> change to organic sulphur when digested --> oxidative damage to RBCs --> heinz body anemia
signs -
inappetance
vomiting
diarrhoea
heinz body anemia
methemaglobinemia - chocolate blood
jaundice - RBC lysis
treament -
emesis
fluids
symptomatic/supportive care - probiotics, antioxidant therapy (vit c)
too late for emesis once showing signs
prognosis good
65
intoxicants - anti-parasiticides
pyrethroids -
cats and snakes
damages sodium channels in nerve membranes
neuro signs
active cooling for seizures, lipid infusion, decontamination and supportive care
fipronil -
rabbits
affects GABA receptors in CNS
neuro signs
stasis treatment if needed, decontamination, supportive care
ivermectin -
tortoises
flaccid paralysis
respiratory support, decontamination, supportive care
decontamination including washing
seizure control - may need pentobarb or propfol
fluids
nutritional support
prognosis guarded to poor
66
intoxicants - avocado
persin
usually birds
myocardial necrosis, mammary necrosis, hemorrhage in mammals
signs -
GI signs - anorexia, vomiting, diarrhoea
mastitis
cardiac insufficiency
takes a while to cause signs, once signs usually too late
if no signs - decontamination and GI symptomatic treatment
poor prognosis if cardiac signs
67
intoxicants - chocolate
theobromine and caffeine
cocoa powder worst
CNS stimulation --> increased muscle contractility in skeletal and cardiac muscle
signs - vomiting
death if heart muscle affected
treatment -
decontamination
fluids then antiemetics
sedation if severe CNS signs - seizure
beta blockers
prognosis good if treated
68
intoxication - ethylene glycol
antifreeze, screen wash, brake fluid, fountains in winter
cats more sensitive than dogs
converted to toxic metabolites --> renal damage and hypocalcemia
converted by alcohol dehydrogenase
signs -
stage 1 - non specific - vomiting, ataxia, tachycardia, PUPD, CNS in cats (convulsions, rapid progression to coma)
stage 2 - signs in dogs start at stage 2 - cardiopulmonary signs
stage 3 - renal signs
metabolic acidosis, oxaluria, hyperglycemia, hyperkalemia, hyperphosphatemia
calcium oxalate crystals in utine - picket fence
treat -
emesis only works if immediate - like just now seen it
don't use charcoal
ethanol - competitive inhibitor for alcohol dehydrogenase
intensive fluids
monitor renal enzymes
prognosis good in dogs if catch right away, always poor in cats, poor in dogs if renal signs
69
intoxicants - grapes/raisins
dogs more than cats
cats show GI signs rather than kidney
dried seems worse than fresh
unknown toxic dose, very variable
diffuse renal tubular degeneration --> kidney failure
signs -
vomiting and diarrhoea - sometimes with blood
hypersalivation
ataxia
weakness and lethargy
progression to renal failure - 24-72 hours
treat -
decontamination
aggressive flids
antiemetics
supportive care for diarrhoea
monitor kidney parameters
prognosis variable
70
intoxicants - herbicides/fertilisers
lots of types -
phenoyacetic acid herbicidesm- weed killers - acididc
diquats
glyphosphate
iron based moss killers
signs associates with iritation - mouth ulcers
can cause renal and hepatic toxicity with some products
hypersalivation
vomiting
diarrhoea
ulceration of mm
treat -
don't use emesis - more irritation
activated charcoal
washing
fluids
analgesia
GI protectants
feeding tube if severe - won't want to eat if bad ulcers
prognosis favourable, mostly just uncomfortable
71
intoxicants - lilies
cats
necrosis of renal tubular cells
signs -
vomiting
anorexia
depression
PUPD
renal failure
treat -
topical decontamination
emesis hard - usually only a tiny bit
activated charcoal
fluid
monitor renal parameters
supportive - anti emetics, appetite stimulatns, feeding tube if not eating
prognosis favourable unless renal signs, then very poor
72
intoxicants - metaldehyde
slug bait pellets
GABA effects (maybe)
signs -
CNS - hyperaesthesia, spasm, muscle rigidity, tremors, twitching, convulsions
hyperthermia
tachycardia
tachypnoea
resp depression
cyanosis
treat -
emesis if asymptomatic (but usually quick acting)
gastric lavage if suspect large amount and recent (propofol GA will prob help with CNS signs anyway)
diazepam - seizures
active cooling
supportive care - fluids, liver support (SAMe)
prognosis favourable if mild signs, poor if seizuring
73
intoxication - NSAIDs
aspirin, paracetamol, ibuprofen
aspirin - stimulates resp centre --> hyperventilation and resp alkalosis --> metabolic acidosis over tiem
paracetamol - overdose - toxic metabolite --> methemaglobin and heinz body anemia, no safe dose in cats
ibuprofen - GI signs - non selective COX inhibitor
signs -
depression
vomiting
anorexia
hyperthermia
tachypneoa
hematemesis
malaena
abdominal tenderness
paracetamol - brown mm (RBC damage), hypothermia, facial and paw oedema in cats
treat -
aspirin - decontamination and supportive
paracetamol - n-acetylcystein (triggers good pathways, vit c and methylene blue
ibuprofen - prostglandin analogue (misoprotol)
decontamination
oxygen
fluids
entiemetics if needed
gastroprotectants
monitor renal and hepatic markers, electrolytes and acid base - watch closely while treating
NB - owners may be reluctant to tell you what they had as may have given it themselves to avoid coming in
74
intoxicants - rodenticides
anticoagulant or vitamin D types
1st gen (eg warfarin) less toxic than 2nd gen
important to get label
anticoagulants - inhibit hepatic vit K enzymes --> depletion of clotting factors and impaired prothrombin synthesis --> can't clot, bleed out
vitamin D - hypercalcemia --> tissue mineralisation and renal failure
signs -
initially non specific - weakness, lethargy, depression
depend on site of bleeding - may see petechiae, hemoabdomen, hemothorax
treat -
decontamination
anticogulant - vitamin k immediately in symptomatic cases, if acute or asymptomatic wait and check PT after 48-72 hours
if severe anemia - blood transfusion
vitamin D - fluids, diuretics, biphosphonares or calcitonin to promote calcium excretion
prognosis -
depends on how much and what stage you see them at, if already bleeding then poor
vitamin D prognosis usually poor as advanced by the time you see them
75
intoxicants - polytetrafluroethylene
teflon - non stick plans overheated in closed rooms
birds
keep birds 2 doors from kitchen and ventilate kitchen
fumes inhaled --> rapid onset hypoglycemia
also hepatotoxic but not the immediate issue
signs -
vomiting
ataxia
depression
eventual coma
convulsions
collapse
liver failure signs and coagulopathy - not common, in cases where small dose so survive long enough
treat -
decontamination if not seizing or collapsed
IV dextrose for hypoglycemia
liver support once past hypoglycemia - SAMe, silybin
prognosis favourable if caught early, poor if liver failrue
76
oncology - diagnostics
cytology -
FNA - solid tumours or enlarged lymph nodes
quick, non invasive, quick results
can be done awake
sample not always representative
some masses don't exfoliate
can't do staging
contraindications - cleeding disorders, bladder tumours
histopathology -
biopsy
more invasive, expensive, needs sedation
FNA advised first, but excisional biosy without FNA ok in mammary tumour
risks - bleeding
contraindications - bleeding disorders, comorbidities that make GA more risky
always do FNA first in - mass of unkown origin, poorly definied masses, inflamed or oedematous masses, rapidly growing masses, ulcerated masses
heat diffusion imaging -
heat waves used to detect thermal rection of cancer cells
1-4 - increased risk of malignancy, FNA advised
5-10 - likely benign
limited use in deep subcut masses or large masses
staging -
abdominal ultrasound - liver and spleen mets - can't distinguish benign from malignant
thoracic xray - nodular interstitial pattern in lungs (lung mets) - only visible if bigger than 3-5mm
CT - preferred - can detect mets down to 1-2mm
77
oncology - margins
narrow - <1cm - benign masses
wide - 2+cm plus a fascial plane for intermediate mast cell tumour, 3-4cm + fascial plane for high grade tumour (any)
radical exclusion - amputation
78
chemotherapy - indications
primary treatment - lymphoma
secondary after surgery - metastatic disease and most other malignant tumours
79
chemotherapy - side effects
extravasation - pain, swelling and redness at site of catheter - remove catheter and try and suck out as much as poss, cold compress, contact oncologist
GI - diarrhoea, nausea, loss of appetite, delayed ileus (treat with metaclopramide and supportive treatment)
myelosuppression -
lowerst neutrophils at 7 days
risk of sepsis - prophylactic amoxycillin
febrile neutropenia - emergency - isolation, broad spectrum IV antibiotics including a fluroquinolone
80
electrochemotherapy
referral
IV chemo with an electric current through tumour so it absorbs more
indicated in inoperable tumours as palliative care or in advanced disease
good for nasal squamous cell carcinomas in cats, melanomas, sarcomas
81
oncology - radiotherapy
palliative - 4 treatments, 1 a week
needs GA
good in malignant melonoma or pain relief for inoperable osteosarcomas
treatment for brain and bone cancer - 12 fractions for 4 weeks
82
oncology - multi modal analgesia
paracetamol - dogs
NSAIDs - if no contraindications and not on steroids
gabapentin - esp neuro pain
monoclonal antibodies - targets nerve growth factors
amantadine - good for pain refractory to NSAIDs (may become restricted - human antiviral)
ketamine - low dose sub cut, monthly or weekly
antidepressants
83
mulitcentric lymphoma
very common
malignant
check all lymph nodes - peripheral lymphadenopathy
kethargy
weight loss
anorexia
vomiting
if signs - usually poorer prognosis
need to know type of lymphoma
test -
PARR clonality - lab - differentiate T or B cell
flow cytometry
IHC
treatment -
chemo
steroids - low cost palliative option
choice depending on comorbidities and tolerance of animal to coming in and owner facilities
T cell less bad
B cell - 90% remission with CHOP
84
feline alimentary lymphoma
most common cat neoplasia
vomiting
weight loss
diarhoea
present like IBD
low grade - diffuse looking
high grade - more systemically ill, feel a mass, intestinal thickening, enlarged LNs
diagnosis -
US - thickening of intestinal walls - also happens in IBD
hypocobalaminemia - 78% cases
ex lap - full thickness sample
endoscopy - partial thickness
(higher risk of wound breakdown in unhealthy patients)
treatment -
steroids and chlorambucil
(same as IBD so if not sure which can just do this is cost for tests or health not good for GA id prohibitive)
85
canine osteosarcoma
big dogs
lameness not responding to analgesia
limb swelling/mass
may cause pathological fractures because weak bone
tests -
xray - sunburst
FNA - only needs sedation
biopsy - needs GA and risk of fracture
CT - check for mets, micro mets usually present when seen
treat -
analgesia - key - very painful, multi modal
usually euthanised quite soon
palliative radiotherapy - 4 treatments once a week under GA
amputation - palliative, gets rid of pain but probably not going to cure because mets
chemo - still need chemo after amputation, very aggressive cancer
86
bladder neoplasia
hematuria
straining to urinate
don't FNA - can seed the tumour
US guided suction biopsy to get sample for cytology or free catch urine cytology
CADET BRAF test - PCR for BRAF mutation, done on urine, 80% detection
usually transitional cell carcinomas
surgery usually not possible
may block urine as they grow
treat secondary UTI
chemo - NSAIDs (cheap option), metronomic chemo (NSAID + chlorambucil)
87
dog spleen masses
hemoabdomen due to rupture
abdominocentesis to confirm
2/3 spleen masses neoplastic
not always malignant
if acute bleed - weak, floppy, tired
PUPD
GI signs
may see enlarged abdomen - hard to tell in big dogs
if no trauma and hemoabdomen - usually splenic mass
staging -
US - liver
thoracic radiograph - lungs
check heart if possible - right auricular appendage
splenic hemagiosarcoma - poor prognosis
benign masses - remove because of chance of rupture, good prognosis with splenectomy
post op chemo if hemangiosarcoma - IV or oral options, NSAIDs on their own if cost prohibitive, better than nothing
88
main causes of sheep lameness
interdigital dermatitis - scald
footrot
CODD
toe granuloma - strawberry toe
toe abscess
shelly hoof - white line disease
89
foot rot - sheep
healthy --> scald --> footrot
painful
smelly grey exudate
underun horn
dichelobacter nodosus - causes both scald and footrot - gram -ve, dumbell shaped, anaerobic
survives well in wet environment
soil reservoir
more in wet times of year and wet parts of country
spring and autumn
persist in interdigital space and seed in soil
moist, soft or injured interdigital skin --> inflammation and necrosis --> infection with d nodosus --> scald --> footropt
fusobacterium necrophorum - secondary infection
treat -
best within 3 days of onset - regular inspeciton important
antibiotic injection
spray interdigital space and foot - oxytet
analgesic for pain
focus on individuals
don't trim
vaccine - footvax - prevention in face of outbreak, not a nice one, thick
footbath - 10% zinc sulphate, formalin, or others, antiobiotic baths
prevention not treatment
90
CODD - sheep
severe lameness
lesion at coronary band going down under horn to toe
avulsion of horn
exposed laminae, affects pedal bone
treponema spp (spriochete), s nodosus, f necrophorum
infectious
treat -
oxytet injection or spray
analgesia - NSAIDs (cascade)
91
shelly hoof - sheep
white line
detachment of horn wall - usually abaxial wall
impaction in separation space --> acts as foreign body --> exposed laminae --> lameness, pain
very painful
can lead to abscess
more common with flocks bathed in formalin than not bathed
92
toe granuloma - sheep
granulation tissue formed in response to injury or untreated footrot
looks a bit like a strawberry
bleeds a lot
regrow if removed
causes - excessive foot trimming, predisposed if bathed with formalin
cull
93
toe abscess - sheep
infection into white line --> abscess under wall or sole horn
pus from coronary band
smelly
hot hoof
painful
acute lameness
94
post dipping lameness - sheep
erysiplothrix rhusiopathiae
usually when dip used and left top stand
bacteria enter through skin abraions
dullness
lame
pyrexic
signs within a few days
large numbers of sheep affected - esp bad in lambs
prevention - refresh dip frequently
95
joint ill - sheep
lambs <4 weeks (usually signs 10-14 days)
usually strep dysgalactiae
swollen hot joints
lameness
recumbency
outbreaks
prevention -
iodine on umbiliucs
colostrum
lambing hygiene
treat -
penicillin
NSAIDs
can lead to permanent joint pathology
96
pathophysiology - canine cognitive dysfunction
risk factors - female neutered, low BCS, low quality diet, concurrent disease
amyloid beta accumulation forms plaques around vessels of brain - neurotoxic
decreased oxygenation
oxidative brain damage
build up of free radicals
decreased neural glucose metabolism
glutamate mediate toxic neuron damage
decreased catecholaime, serotonin, and GABA
97
canine cognitive dysfuntion - structural features
heamorrhage in cerebral vascularature
meningeal calcification
reduction in overall brain mass
increased ventricular size
inflammation and degeneration of glial cells
98
canine cognitive dysfunction - signs
often missed
changes in socialisation - decreased interest in play, greeting behaviours, more needy, increased agression
sleep change - changed cycle, more day sleeping
vocalisation
house soiling - esp cats - linked to memory
disorientation - stuck in corners, staring into space, difficulty recognising pets and humans they known, can't find or drop food, increased reaction to visual and audio stimuli
altered activity - pacing, snapping at air, weird licking, increased appetite, decreased interest in treats, decreased play
anxiety - vocalisation, fear, separation anxiety
reduced learning and memory - decreased ability to perform learned tasks
99
canine cognitive dysfunction - diagnosis
signalment -
dogs > 8yo
cats >10yo
no apparent signs until well after cerebral changes
exclusion of other causes
identification of stress factors
exam - general, neuro, ortho, pain assessment
canine cognitive dysfunction rating scale, canine dementia scale
100
canine cognitive dysfunction - ddx
endocrine - hyperthyroid, cushings, addisons, insulinoma
blindness/deafness
hepatic
pain
GI disease
Urogenital disease
neuro disease - sleep disorders, partial seizures, peripheral neuropathy
side effects of meds
101
canine cognitive dysfunction - management
aim to delay onset and progression - can't sure
early recognition and intervention key
client education
consistency at home - reduce stress
cognitive and environmental enrichment - variety, training, play, meeting new people and pets, new stimuli, exporing, for cats need 3d entertainment and hunt and chase games
soiling - increased access to outdoors, indoor toilet areas, low side litter trays, ramps
mobility - ramps, non slip floors, slings, cart or pram for walks, easy access
sleep - consistent day night cycle, reduce night disturbance, safe rest spaces, final interacitve session before sleep
diet - prescription diets, antioxidants (vits B, C, E), omega 3, mitochondrial co-factor, supplements
mobility - physio, hydro, analgesia
102
canine cognitive dysfunction - medical management
selegiline - selective monoamine oxidase B inhibitoy - enhances catecholamine activty, decrease free radicals, dont use with other serotinergics rugs (SSRI)
propentofyline - phophodieterase inhibitors - increase CNS blood flow
anxiolytics and behaviour modification drugs - mermantine, sertraline, fluoxetine, tramadone, gabapentin - anxiety, compulsion, sedation
melatonin - aids sleep
pheromones - adaptil, feliway - anxiety
situation use of sedatives - phenobarb, trazadone, benzos
103
causes of urinary incontinence
structural abnormalities -
urethral length - shorter has greater risk of becoming incontinent (middle aged female dogs most common)
diameter of urethra - interferes with passage of urine through urethra (uroliths, strictures, neoplasia)
imbalance between storage capacity of bladder and urethral tone -
reduction of urethral tone - bladder nexk positioning (more incontinence if in pelvis rather than abdomen), neutering (reduces oestrogen), innervation (upper motor neurone bladder)
storage capacity of bladder - innervation (lower motor neurone bladder), inability of detruser muscle to contract
104
urethral sphincter mechanism incontinence
adult and geriatric patients
reduction of tone of muscle of internal and external sphincters
due to -
anatomical abnormalities - short urethra, pelvic bladder
neutering - reduced oestrogen
degenerative - loss of collagen
other risk factors - breed (german shepherds, rottie, doberman, english bulldog, springer, weimerarmer - large breeds), obesity
treat -
aim to increase sphincter tone
propalin - phenylpropalolamine - increased contractility - 1st line treatment
incurin - estriol - oestrogen replacement, 2nd line only in females
split into doses through day
need to treat a couple months before know if working
surgier - debulking agent into urethra via endposcope, cuff around urethra, move bladder neck and urethra cranial
no guaranteed cure, and may get a bit better but still leak some so need to establish owner expectations
105
primary hyperaldosteronism (conn's syndrome) - pathophysiology
most common adrenocortical disorder in cats
adrenal masses - functional adenoma, benign or malignant
or bilateral adrenal hyperplasia
aldosterone - regulated blood pressure by managing blood sodium and potassium
regulated by RAAS
systemic hypertension --> damage to heart, eyes, brain
muscle weakness due to low potassium
106
primary hyperaldosteronism (conn's) - signs/signalment
hypokalemia
cervical ventroflexion - neuromuscular wekness
systemic hypertension
flaccid paresis
breathing difficulty - rarer
ocular signs - around 50% cases
may also have hyperprogesteronism --> ksin fragility
cardiac complications
cats
medican age 13yo
no sex or breed disposition
107
primary hyperaldosteronism (conn's) - testing
plasma renin ration - low - not a common test
plasma aldosterone concentration - low - most commonly used
urinary aldosterone to creatinine ratio - high - easier collection
dynamic testing - fludocortisone - reduces aldosterone secretion in healthy cats but little to no effect if have hyperaldosteronism
imaging - adrenal changes, mets
108
primary hyperaldosteronism (conn's) - treatment
unilteral adrenalectomy - if only one side
medical management - if not possible to do surgery or before surgery -
aldosterone receptor blocker - sprirolactone
potassium supplement
amlopidine - calcium blocker, treats hypertension
109
feline hypersomatotropsim - pathophysiology
excessive growth hormone secretion from pituitary
growth hormone - increases free fatty acidis in the blood for energy to grow, increases glucose use and decreases insulin action
increased growth (acromegaly) and compensatory insulin secretion
especially insulin like growth factor - IGF-12
usually functional adenoma in pituitary
less freuqently hyperplasia
110
feline hypersomatotropism - signs/signalment
males more than females
median age 11yo
PUPD
Polyphagia
systolic cardiac murmur
plantigrade stance
respiratory stridor
broad facial features
hyperglossia - increased snoring because more soft tissue
growth of flat bones of skull and manible
cardiomegaly
nephropathy
neuro - blindness, depression, circling - usually later stages
NB - cushings in cats has similar signs
111
feline hypersomatotropism - testing
IGF-1 - false negatives can come from exogenous insulin treatment, repeat testing 6-8 weeks into treatment, also false negatives from not eating
basal plasma growth hormone - only used for research processes
MRI or CT - structural pituitary changes strength evidence, not a screening test, doesn't differentiate whether benign or neoplastic tumour
echo - left ventricle and artial hypertrophy and enlargement
112
feline hypersomatotropism - treatment
surgery - transphenoidal hypophysectomy - remove pituitary mass, immediate decrease in growth hormone, usually also sorts the diabetes
medical -
somatostatin analogues
radiation - most widely used
conservative - high dose insulin plus low carb high protein diet - symptomatic only, ignores underlying mechanism
113
primary hypoparathyroidism - pathophysiology
parathyroid hormone - controls calcium levels --> low serum calcium and high serum phosphorus
114
primary hypoparathyroidism - signs/signallment
more common in females
mini schnauzers and poodles
low serum calcium and high serum phosphorus with normal renal function - hypocalcemia
extracranial seizures
mild to severe - cramping and behavioural changes to generalised tremors
115
primary hypoparathyroidism - treatment
acute - manage hypocalcemia
IV calcium - slow bolus clacium gluconate over 15-20 mins
keep ECG attached
chronic -
vitamin D oral supplement - activated vitamin D, don't have PTH to activate it themselves
calcitriol - gold standard, but only human ones available and can't split them so dosing hard
alfacidiol - best current option, low dose to start then gradual increase
to start also give calcium then taper off
aim to maintain calcium at low end of reference range - if too high then get hypercalcemia and high phosphate causing calcification of kidneys
treatment quite time consuming
116
diabetes insipidus - pathophysiology
central or nephrogenic - ADH production inhibitied at hypothalamus or receptors at kidneys not working
lack of response to ADH
causes -
neoplasia
hypothalamic-pituitary malformations
vascular
iatrogenic following surgery on pituitary
congenital
other endocrine disease
dilute urine with PUPD - primary polyuria, secondary polydipsia
can be partial - some ability of kidneys to concentrate but not to full extent
117
diabetes insipidus - testing
water deprivation test - only if otherwise healthy, deprive water for 8 houRs and monitor urine, of DI then will still be colourless and low SG
despopressin trial - differentiate central and nephrogenic - water deprivation trial with despopressin IV, if still low SG then central
118
diabetes insipidus - treatment
desmopressin tablets - care not to use if chance its actualy psychogenic polydipsia
transphenoidal hypophysectomy - surgery, for central DI
low sodium diet - with desmopressin tablets or nasal spray for nephrogenic
don't always need therapy so long as lots of water access and not causing problems for owner
119
pituitary dwarfism/congenital GH deficiency
rare
german shepherds
profound dwarfism
hyperpigmented skin
soft wooly coat
unilateral or bilateral cryptorchidism
heart murmur of persistent ductus arteriosus
predisposed to secondary infections
can develop secondary hypothyroidism and impaired renal function
Test -
GH stim test
basal plasma GH and IGF-1, prolactin, thyriotropin and LH - low
treat - progestens or pig growth hormone
120
farm animal toxicology - lead
usually younger cattle - curious
old car batteries, engine oil, old pains, asphalt roofing, environmental pollution
acute encephalopathy, cerebral and GI signs
signs -
early stages - standing alone, depression, hyperaesthesia, muscular fasciculations
progression - ataxia, blindness with pupillary reflexes present, head pressing, manic behaviour, convulsions, coma, death
abdominal pain
rumen atony --> bloat
diarrhoea
froth at mouth
may see sudden death
treat -
seizure control - IV pentobarb
chelation - calcium EDTA slow drip
thiamine subcut daily
oral magnesium
prognosis poor
milk may not be suitable for human consumption
121
farm animal toxicology - ragwort
in silage - won't just eat it in the field, doesn't taste good
signs -
chronic weight loss
diarrhoea
jaundice
peripheral oedema and ascites
dull/depressed
signs resulting from liver failure
ddx - liver fluke, lead poisoning
management -
no effective treatment
remove contaminated feed
control ragwort on pasture
122
farm animal toxicology - photosensitising agents
photodynamic substance enters skin --> reacts with UV --> inflammation/photochemical reaction (primary type - eg st johns wort)
or liver function imparied to phyloethrin build up --> liver damage --> photosensitivity (secondary type, less common, ragwort)
worse in summer - more UV
signs -
oedema
erythema
dermal effusions
vesicles
skin necrosis - esp on less pigmented areas
crusting, ulceration and skin sloughing
painful and sensitive - essentially bad sunburn
may have concurrent hepatic signs
diagnosis -
signs
increased GGT and AST
liver biopsy
management -
move animals inside
antibiotics for secondary infection
debride necrotic skin
control flies
remove causative agent if known
analgesia
prognosis good in primary type unless extensive skin loss, poor in secondary
123
farm animal toxicology - acorn/oak
tannins
very common - fall on pasture after autumn storms
signs -
anorexia
depression
rumen stasis --> bloat
constipation --> fetid tarry diarrhoea
occassionally sudden death
often die in 4-7 days even with treatment
also may have severe nephron damage even if survive - not always economically viable to treat
ddx -
severe ostertagia infestation
mucosal disease
diagnosis -
signs and exposure history
acorns in rumen on pm
management -
no specific treatment - supportive - lots of IV fluids, expensive
remove cattle from pasture with oaks, fence off areas under trees
124
farm animal toxicology - bracken
chronic - ingestion over severeal weeks
sparse pasture/not a lot of available grass
suppress bone marrow --> secondary infection
carcinogenic over long periods --> bladder tumour or squamous cell carcinoma in oesophagus or rumen
signs -
anorexia
retinal atrophy - sheep
pyrexia - secondary infection
petechia; hemorrhage
ocassional sudden death
increased HR and RR
weakness --> recumbancy --> death
bladder tumours --> hematuria
ddx -
anthrax - sudden deaths
bladder tumours from other cause
cystitis
pyelonephritis
redwater fever - babesiosis
diagnosis -
signs - esp widespread petechiae
exposure history
management -
di-batyl alcohol
broad spectrum antibiotics
give enough food so don't eat it in the first place
treatment not usually successful
125
farm animal toxicology - rhodedendron
sparse pasture after winter snows
garden cuttings dumped over fences
sodium channel agonist - stems and leaves worst
signs -
weakness
depression
recumbancy
abdominal pain
brixism
vocalising
rumen atony --> bloat
ruminal regurgitation - vomiting
rumen contents round muzzle
death within hours - goats worst, tend to get out and be curious
ddx -
hypocalcemia - weakness and recumbancy with rumen atony and bloat
management -
pethidine
NSAIDs
supportive care
adequate feeding to prevent incidence
126
farm animal toxicology - copper
contamination or inadvertent supplementation (high copper feeds)
more common in heep
build up of liver copper over time --> sudden release to blood --> acute intravascular hemolytic crisis
acute and chronic presentations
acute -
severe gastroenteritis
colic signs
diarrhoea
severe dehydration
death within 3 days
chronic -
weakness
depression
isolation
inappetence
fetid diarrhoea with mucus
dehydration
jaundice mm
increased HR and RR with abdominal effort
no rumen turnover
recumbency --> death
ddx - other causes of hemolytic anemia - babesia, post parturient hemoglobinuria, kale poisoning
diagnosis -
signs and history of exposure - esp jaundice
increased serum copper
increased AST and GGT
pm - severe gastroenteritis, erosion of abomasal mucosa, diffuse jaundice in chronic cases and swollen dark grey kidney, red urine in bladder, friable enlarged liver
elevated kidney copper - more reliable than liver copper
management -
remove copper source
measure AST to identify at risk animals
ammonium tetratheiomolybdate - IV or SC, 3 times, 2 days apart
careful management of copper supplements after deficiency diagnosed
127
farm animal toxicology - nitrate
kate, turnips, cabbage, fertiliser - too much or for too long
nitrates --> nitrites (by rumen flora) --> methemaglobinuria
signs -
chronic - decreased weight gain
acute - within hours if sudden exposuret or large amount -
cyanosis
weak rapid pulse
recumbency --> death
abortion common in survivors
ddx - causes of sudden death - hypomagnesemia, lightening
treatment -
IV methylene blue
slow introduction of brassicas and never more than 70% of diet
128
farm animal toxicology - organophosphate
overdose or accidental exposure - used to control sheep parasites
block cholinesterase --> continual acetylcholine action
signs -
hypersalivation
colic
diarrhoea
muscle fasciculations
stiffness
paralysis
depression
dyspnoea
sweating
death
ddx - other poisoning
diagnosis -
recent exposure history
cholinesterase levels in blood - bit niche
managament -
atropine sulphate - repeated as necessary, slow IV
correct storage, disposal and dosing of organophosphates
129
farm animal toxicology - urea (non-protein nitrogen)
used as source of non-protein nitrogen in feed
released into rumen as ammonia
after sudden access or withdrawal then free access or washed out feed blocks after heavy rains leading to urea in puddles or contaminated water
very rapid - 15mins to hours after digestion
signs -
ear and facial muscle twitching
bruxism
frothy salivation
bloat
abdominal pain
frequent urination
staggering
vocalisation
seizures
often found dead at source of urea
ddx -
other causes of sudden death - botulism, hypomagnesia, anthrax, clostridial disease
diagnosis -
signs and history of sudden exposure
blood ammonia - live animals only
pm - bloat, congested mm, pulmonary oedema, hemorrhages on heart - needs done quickly after death
management -
stomach tube - relieve bloat
cold water followed by vinegar
supportive - isotonic saline
thorough ration mixing
gradual introduction in feed
do no interrupt urea supply, if interrupt re introduce slowly
130
equine metabolic syndrome (EMS)
collection of risk factors for endocrinopathic laminitis -
insulin dysregulation
obesity or regional adiposity
"easy keepers" - put on weight easily
+/- hypoadiponectinemia
+/- hyperlectinemia
leads to laminitis, hypertension, pro inflammatory state
diagnostics -
basal insulin
oral glucose test
IV insulin tolerance test
131
pars pituitary intermedia dysfunction (PPID) - pathophysiology
age related degenerative condition
loss of dopimergic inhibition --> hypothalamus unable to regulate pars intermedia --> hypertrophy or hyperplasia of PI --> increased hormone production --> array of effects on body
PI hormone - ACTH
EMS + PPID --> insulin dysregulation + carbs in diet --> hyperinsulinemia --> laminitis
132
pars pituitary intermedia dysfunction (PPID) - signs
hypertrichosis - excessive hair growth - pathognomonic
hair colour changes
patchy shedding
lethargy
poor performance
skeletal muscle atrophy
rounded abdomen
abnormal sweating - increased or decreased
PUPD
regional adiposity
infertility or absent cycle
laminitis
susceptible to secondary infections
133
pars pituitary intermedia dysfunction (PPID) - diagnostics
basal ACTH
TRH stim
134
pars pituitary intermedia dysfunction (PPID) - management
no cure - aim to reduce clinical signs
peroglide mesylate (prascend) - dopamine agonist - may have side effects, lethargy and decreased appeitite, stop for a few days then start again at lower dose
recheck signs and basal ACTH at 1-2 months
6 monthly evaluation once seeing results
if not improving - increased dose
diet and exercise plan - aim to bring back to normal BCS - lower risk of laminitis
regular dental and parasite checks
regular farriery - esp if laminitic
clipping and skin health
geriatric health checks for concurrent issues
135
insulin dysregulation/hyperinsulinemia - equine - management
central feature of EMS and accounts for at least 33% horses with PPID
associated with laminities - welfare concern
diet - aim to reduce post prandial hyperinsulinemia, feeds low in non-structural carbohydrates, retrict intake in obese animals and increase exercise if possible
most of diet should be hay with low eater soluble carbs, fed little and open
soaking hay - reduces water soluble carbs
exercise - only if no signs of lameness, improves insulin sensitivity
pharmaceuticals - severe or non-responsive cases
non licensed
if not responsive with diet and exercise in 4-6 weeks
gliflozin - rapidly reduces insulin, blocks blood glucose reabsorption - human type 2 diabetes medication
levothyroxine - synthetic thyroid hormone, increases basal metabolic rate
metformin - anti-glycemic, improves insulin sensitivity - controversial and only effective in small % for short duration
farriery -
essential in laminitic cases
acute cases - treat as emergency
chronic - decrease stress on damaged lamelkae, increase ground weight bearing surface, position breakover appropriately, restore alignment of pedal bone
xray to assess status
136
foot care in chronic laminitis - equine - common issues
disease causes weak laminar growth
tension in ddft
chronic pain
tearing of laminae
sensitisation of tissue
chronic infections
seedy toe
absecesses
137
common presentations - NTCA neuro
abnormal head position
weakness and ataxia
seizures
paralysis and paresis
138
abnormal head position - NTCA Neuro
head tilt (torticollis) or twisting of neck and hyperextension (opisthotonus)
head tilt -
common presentation of neuro disease
usually otitis, aural polyps or aural neoplasia
central or peripheral
signalment -
younger - more likely infectious
older - neoplasia
rabbits - e cuniculi
rats - pituitary adenoma
testing -
neuro exam
serology - e cuniculi in rabbits and guinea pigs, toxo gondii in ferrets
MRI - neoplasia
CSF analysis - not often done in NTCA
opisthotonus -
paramyxyoviruses (newcastles, ferlavirus in snakes)
arenavirus - snakes
adenovirus - lizards
thiamine deficiency
star gazing
prognosis usually poor - often euthanise without investigation
testing -
PCR for some viral diseases
history - thiamine deficiency - frozen fish not defrosted properly
treat -
viruses - usually just fatal, all housing destroyed
arenavirus - control snake mites - fipronil
pigeon paramyxovirus - annual vacx
newcastle - vax available but short immunity and expensive
139
e cuniculi - rabbits
also sometimes guinea pigs
most common cause head tilt in rabbits, sometimes guinea pigs
test - serology, IgG and IgM
treatment -
fenbendacole - 28 days - gets rid of signs but not parasite
panacur - licensed for prevention at times of stress, not great evidence
supportive care - benzos for stress, treatment for GI stasis, prophylactic antibiosis (secondary pasteurella from stress induced immune suppression)
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pituitary adenoma - rats
head tilt
very common
predisposes to mammary tumour
treat -
cabergoline (galistop) - inhibits prolactin, reduces tumour size
supportive - environmental modification - ramps, deep bedding, aim to cusion falls (ataxia and loss of balance)
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nutritional causes - weakness and ataxia - NTCA neuro
hypocalcemia - most common - all species ubt more in herbivorous and insectivorous reptiles, and birds
thiamine deficiency - fish eaters
biotin deficiency - egg eating species
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infectious causes - weakness and ataxia - NTCA neuro
bornavirus - birds
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weakness and ataxia - NTCA neuro - emergency management
warmth - usually hypothermic, lose heat easily - incubator, bear hugger, heat pads (care for burns, can't always move away)
fluids - oral if can swallow and no dehydrated, parenteral if not
glucose - birds and mammals - reptiles prone to refeeding syndrome and cope well with low glucose (can use critical care)
calcium - reptiles, african grey parrots - prone to hypocalcemia - oral if can swallow, IV if can't or having seizures
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weakness and ataxia - heavy metal toxicity - NTCA neuro
lead and zinc
waterfowl and psittacines
signs -
non-specific - weakness, depression, weight loss
GI signs - anorexia, crop stasis, regurgitation, diarrhoea
urinary - PUPD, hematuria, billiverdinuria
neuro - circling, twitching, seizures
diagnosis -
xray - metal density in GIT, may not see, inc usually chronic exposure
hematology - non-regenerative anemia, basophilic
toxicology - blood lead, or zinc levels increased
treat -
chelate or remove metal - chelation calcium EDTA BMSA, D-penicillamine injections (can be stressful)
supportive care - heat, fluid, nutrition
antiseizure meds
bulking agents - psyllium husk - move through GIT where can't manually remove
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weakness and ataxia - NSHP/Hypocalcemia - NTCA neuro
seizures in parrots
progressive weakness in reptiles
emergency management -
calcium
analgesia - opioids in reptiles, butorphanol in birds, NSAIDs an option but care for dehydration or renal disease
benzos for seizures
supportive care -
environmental modification - make sure can't fall and injure themselves
oral calcium and vit D supplements
fluid and nutritional supported feeding
analgesia - oral NSAIDs once checked renal values and corrected dehydration
long term correct husbandry - UVB and heat
guarded prognosis, probably euthanasia esp if collapsed.
owner needs to be able to commit to nursing for long time
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weakness and ataxia - avian bornavirus - NTCA neuro
proventricular dilatation disease
very common
signs -
neuro - ataxia, difficulty perching, blindness, seizures
GI - weight loss, crop stasis, regurgitation, proventricular and intestinal dilatation, maldigestion
may not see signs
diagnosis -
bloods - nonspecific
serology - not reliable
xray - proventriculus dilatation
RT-PCR - on feater calamus or whole blood, can get false negatives
post mortem - most commonly where its found
no cure, few treatments
treat -
antiinflammatory - cyclooxygenase 2 inhibitors - improve quality of life
cyclosporin - may reduce signs, but immunosuppressive so also need antibiotics and antifungals
gabapentin analogue - reduce seizures and ataxia
prokinetiocs - GI support
high quality easily digestible diet
antibiotics and antifungals - secondary infections
minimise stress
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seizures - common causes - NTCA neuro
lead toxicity
hypoglycemia - ferrets with insulinoma, small mammals and birds off food
hypocalcemia - guinea pigs with pregnancy toxemia, anything fed contaminated insects
toxins - medications, teflon in birds
bornavirus
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seizures - emergency management - NTCA neuro
warmth
oxygen
fluids
glucose
benzos
calcium - esp african grey parrots and callitrichids (IV to avoid aspiration)
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seizures - hypoglycemia - NTCA neuro
inappetent small mammals and birds
ferrets with insulinoma
treatment - glucose then investigate underlying cause
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insulinoma - ferrets
2nd most common ferret neoplasia
seizures
diagnosis -
signs
low blood plasma glucose
US - often hard to see, tumours can be very small
histopathology - definitive diagnosis but hard to do in practice
treat -
surgery - if tumour large enough and can image for planning, otherwise risk leaving bits behind
diazoxide - human drug, eliminates insulin secretion
steroids - increase hepatic gluconeogenesis (but side effects and may just stimulate more insulin release)
train ferrets to allow insulin monitoring to enable quick treatment
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seizures - NCTA neuro - toxins
ivermectin - chelonians
fipronil - rabbits
pyrethrins - snakes and lizrds
avocado and teflon - psittacines
treat -
wash off
gastric lavage
activated charcoal - adsorbant
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paresis and paralysis - causes - NTCA neuro
mainly spinal trauma - all species
lead toxicity
mareks disease - chickens
botulism - water fowl
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paresis and paralysis - marek's disease - NCTA neuro
production poultry, sometimes backyard poultry
signs -
asymmetrical limb paralysis - classic form
ocular paralysis, cutaneous form and transient paralysis in other forms
weight loss
pallor
diarrhoea
anorexia
acute - 24-72h depression then death
chronic - secondary infections
diagnosis - signs
prevention - vax
no treatment options
prognosis bad - euthanise
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paralysis and paresis - botulism - NCTA neuro
mainly waterfowl
ingested - stagnent or poorly oxygenated water in summer
ascending flaccid paralysis
diagnosis - history and signs
treat -
remove source of toxin or move bird
supportive - fluids, nutritional support (care re aspiration, not good at swallowing)
botulism antitoxins - rarely used, expensive
could give antibiotics - not usually done
usually recover with time and supportive care
euthanasia indicated if resp and cardiac signs
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anatomical diagnosis - neuro regions
C1-5 - UMN signs both thoracic and pelvic limbs
C6-T2 - LMN signs thoracic, UMN pelvic
T3-L3 - normal thoracic, UMN pelvic
L4-S1 - normal thoracic, LMN pelvic
UMN - ataxia
LMN - weakness
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