Canine dx 20
1.diabetes mellitus
Polyuria and polydipsia Increased appetite Weight loss
Ketoacidosis: vomiting, inappetence, lethargy
2.hyperadrenocorticism (coushing dz)
The 4 P’s: polyuria, polydipsia, polyphagia, panting Truncal
alopecia Potbellied appearance Thin skin/cutaneous atrophy
Calcinosis cutis 3 types: Pituitary dependent
hyperadrenocorticism (PDH)
Adrenal dependent hyperadrenocorticism (ADH)
Iatrogenic
3.collapsing trachea
Toy and small breeds
Middle aged
“Honking” cough exacerbated by excitement or activity
Retch at end of cough
Severe cases: cyanosis or exercise intolerance
Serum chemistries and urinalysis Fructosamine gives estimation
of blood glucose over the previous 2 weeks
None are very sensitive in early disease
Chemistry profile: ALP elevation, hypercholesterolemia CBC:
stress leukogram (neutrophilia, lymphopenia, eosinopenia),
thrombocytosis
Urinalysis: hyposthenuria, +/- proteinuria
Urine cortisol: creatinine If normal, rules out
hyperadrenocorticism If abnormal, further testing needed
ACTH stimulation test: test of choice for iatrogenic
hyperadrenocorticism
Low-dose dexamethasone suppression test (LLDS): higher
sensitivity for hyperadrenocorticism Endogenous ACTH
Differentiates PDH from ADH
Limited usefulness because of high rate of false low values
High-dose dexamethasone suppression test PDH: 75% will
suppress, 25% will not ADH: will not suppress
Abdominal ultrasonography PDH: bilateral normal-to-plump
adrenals ADH: single enlarged adrenal gland, contralateral is
small or non-visible
Thoracic radiographs: may be hard to catch dynamic collapse
Fluoroscopy
Endoscopy: requires anesthesia
Stable, non-ketotic diabetics: Long-acting insulin (NPH, Prognosis is good Measure fructosamine to rule out stress
Vetsulin) Increase dietary fiber, Rx diabetic diet Ketoacidotic or hyperglycemia Glucosuria can cause elevated urine specific
ill: Hospitalization with supportive care Treat potassium or gravity
phosphorus derangements Short-acting regular insulin until
ketosis resolved
PDH Guarded to good prognosis Stereotactic radiosurgery and
Trilostane: inhibits enzyme key to cortisol production Lysodren: radiotherapy are promising treatments for pituitary tumors
causes necrosis and destruction of cortisol-secreting portions of
adrenals Surgical: hypophysectomy or bilateral adrenalectomy
Requires referral, limited availability Lifelong hormonal therapy
post-op Radiation, especially stereotactic radiotherapy or
radiosurgery
ADH
Surgical: adrenalectomy, requires referral Medical Trilostane
or lysodren Lysodren may result in neoplastic adrenal gland
necrosis
Iatrogenic
Change to oral, short-acting steroid Gradually decrease dosage
over several weeks Do ACTH stimulation test to see if steroids
can be discontinued
Medical Always radiograph to rule out pulmonary edema as cause of
Short course of corticosteroids Cough suppressant Weight loss cough
if overweight
Tracheal stent
If refractory to medical management Requires referral
4.immune-mediated hemolytic anemia IMHA
Lethargy, weakness, pallor Tachypnea Icterus Variable CBC: anemia, +/- elevated reticulocytes, spherocytes, Immunosuppression: prednisone, azathioprine, cyclosporine, Prognosis is guarded
organomegaly polychromasia, anisocytosis mycophenolate Regenerative anemia expected with IMHA, but bone marrow
Discolored urine from hemoglobinuria or bilirubinuria Saline slide agglutination test Blood transfusion needs 3-5 days to respond
Coombs test: for antibodies against RBCs Prevent thromboembolism: aspirin, low molecular weight or
Imaging to look for neoplasia unfractionated heparin
Infectious disease testing

5.intervertebral disk disease IVDD

PAIN in neck or back – arched back or head held down Ataxia,
paraparesis, or paraplegia Tetraparesis
MRI: safe, fast, and best quality
CT: safe and faster than MRI but lower quality Myelography:
invasive and seizures may occur during recovery
If pain only (no neuro signs): strict cage rest and analgesia with
opiates or NSAIDs
Nonambulatory or unresponsive to conservative treatment:
surgical decompression by experienced neurologist or surgeon
Hemilaminectomy for thoracolumbar disks Ventral slot for
cervical disks
Steroids are increasingly unpopular for pain control Falling out
of favor with surgeons and neurologists because of numerous
adverse effects and poor efficacy Better results with NSAIDs
Hansen type I occur in chondrodystrophoid breeds and the
nucleus pulposis extrudes through the annulus Hansen type II
are usually nonchondrodystrophoid breeds with hypertrophy
or bulging of the annulus Prognosis: If ambulatory: excellent If
nonambulatory with deep pain awareness: guarded (without
surgery) to excellent (with surgery) If nonambulatory with no
deep pain awareness: 50% chance of regaining function if
surgery occurs within 24 hours

Lumbar disc dz extended flashnotes Chondrodystrophoid breed (dachshund, beagle, etc) with acute
paraplegia
Presentation: DDX: Rx of choice: Prognosis:
Acute onset paraplegia, chondrodystrophoid breed Fibrocartilagenous embolism, spinal column tumor, Strict cage rest Grades I and II – Good
Differences in severity* affect treatment, monitoring, prognosis discospondylitis, abdominal pain,  Grades I and II Grades II-IV – Fair
 Grade I degenerative myelopathy, spinal fracture/luxation,  4-6 weeks Grades IV-VI – Guarded
 Acute back pain meningomyelitis, meningitis  Allow scarring, fibrosis-prevents further extrusion Grade VI > 48 hours – Poor
 No neurologic deficits Test of choice: Hemilaminectomy Prevention:
 Kyphosis MRI – a high-field MRI is a safe and fast way to localize a  Allows lateral decompression and a window to Keep chondrodystrophoid breeds from jumping up and down
 Tense abdomen ruptured disk remove extruded disc from furniture
 Grade II Myelography  Grades I and II if no response to cage rest Cage rest for 4-6 weeks if back pain occurs to prevent further
 Grade I findings  ± computerized tomography (CT) if necessary  Grades III, IV, V, and VI extrusion
 Spastic paraparesis  Only if MRI unavailable  If Grade VI > 48 hours, will probably not be of benefit Pearls:
 Ataxia  Irritates spinal cord  This procedure should be done by a well-experienced 80% of disc disease occurs between T10 and L3 vertebrae
 Ambulatory  Dogs usually seizure during recovery surgeon or neurosurgeon Intercapital ligaments betw T1 and T11 connect rib heads
 Loss of proprioception Plain radiography Fenestration preventing dorsal disc extrusion
 Grade III  Supports diagnosis of disc disease  Controversial prophylactic measure Withdrawal reflex
 Severe paraparesis  Narrowed intervertebral disc space (if unanesthetized, disc  Annulus is cut laterally  Not an indicator of deep pain presence or absence
 Unable to stand up and walk spaces may  Allow nucleus pulposis to extrude laterally instead of the  Must get a conscious response from dog to indicate presence
 Voluntary movement is present with support narrow from muscle spasms alone) spinal canal of deep pain
 Grade IV  Presence of calcified disc(s)  Does not decompress spinal cord nor treat an extruded disc perception
 Paraplegia  Do not rely on plain radiography alone for surgical localization  Used in conjunction with hemilaminectomy  Yelp
 No voluntary movement Pain management  Tries to bite
 Grade V  NSAID and corticosteroid Types of disc disease
7.heart worm
Cough and exercise intolerance
Abdominal distension
Weight loss/poor body condition
Presentation: NO signs in most HW-infected dogs.
COUGHING is most common complaint
(when clinical signs exist).
Also-Exercise intolerance, weight loss, syncope, death
-Ascites - manifestation of right-sided heart failure
-Dyspnea - manifestation of pulm. hypertension (PTE)
Classic case: INCIDENTAL finding at routine work up
-orCoughing, exercise intolerant, outdoor dog
8.pyometra
Intact middle-aged female 3-4 wks past estrus
+/- Mucoid, purulent, or hemorrhagic vulvar discharge
Polyuria/polydipsia
Vomiting, anorexia, abdominal pain
Enlarged, palpable uterus
Annual screening with antigen SNAP test
Detects protein secreted by adult female worm 5 mos post-
infection
False negatives if: Antigen/antibody complex formation
No adult female worms (e.g., immature females or
males only), Light parasite load
Microfilaria test: recommended annually
Types of tests: Modified Knotts, Filter test, Direct smear of anti-
coagulated blood
Thoracic radiography shows:
Enlarged, tortuous, +/- blunted pulmonary arteries
Pulmonary parenchymal disease
Right heart enlargement
Echocardiography shows: Pulmonary artery dilation, Right
heart dilation
Visible heartworms in pulmonary artery
Caval syndrome: heartworms visible in right ventricle +/- right
atrium
Differential Dx: Congestive heart failure (CHF) or PTE due to
causes other than HW
Coughing-Bordetella, Left CHF, primary bronchointerstitial
disease
Test of choice: HW antigen test-detects adult female worms
Filter or modified Knott’s for microfilariae
For dogs with moderate to severe HW infection, do
echocardiography
Assess for pulmonary hypertension, caval syndrome
Abdominal radiography: distended, tubular, enlarged,
fluid-filled uterus
Vaginal cytology: degenerative neutrophils +/-
phagocytized bacteria
Abdominal ultrasonography: enlarged fluid-filled uterus;
differentiates from pregnancy
Doxycycline Prognosis:
Daily, 30 d prior to adulticide Good to guarded depending on severity
Heartworm prevention: macrocyclic lactones Poor to grave for caval syndrome
Prevent new infections Doxycycline therapy to reduce Wolbachia (intracellular bacteria
Eliminate susceptible larvae and microfilaria (pretreat with essential for worm survival)
diphenhydramine and corticosteroids if microfilaria positive) makes worms more susceptible to adulticide therapy
Treat monthly, starting 2 mos prior to adulticide 7% of infected dogs are negative on SNAP and positive for
Adulticide: melarsomine dihydrochloride microfilaria
3-dose protocol: IM once, wait 1 mo, then 2 doses given 24 h
apart, Kills 98% of heart worms
STRICT exercise restriction during adulticide therapy and
continuing for 6-8 wks after final dose
Corticosteroids
Tapering anti-inflammatory dose to control clinical signs of
pulmonary thromboembolism
Start 1-2 mos prior to adulticide if symptomatic or microfilaria
positive
Surgical extraction of adult worms
Indicated for dogs with caval syndrome
Rx of choice: 1.) Melarsomine, 3 dose adulticide protocol
 2.5 mg/kg IM today
 Two more doses, 24 hours apart, given 1-3 months later
2.) EXERCISE RESTRICTION extremely important, 4-6 weeks
after each dose Prognosis: Good in mild to moderate HW infections
3.) Consider prednisone or NSAIDs to reduce melarsomine Fair-Guarded in severe cases.
injection site inflammation Poor to Grave even with treatment in dogs with caval
Pre-adulticide treatment 1-3 months syndrome, PTE or CHF
Doxycycline, 10mg/kg BID 4 weeks- Why? Prevention: Monthly macrolides-Ivermectin, selamectin,
 Kills endo-symbiotic Wolbachia bacteria living inside HW moxidectin, milbemycin
larvae WIDE window of efficacy- up to two-month “reachback effect”
 Decreases lung pathology associated w/ dead worms during Eliminates developing larvae that have been in dog as long as 2
adulticide Rx months
Monthly HW preventive- most clinicians start asymptomatic Pearls: Caval syndrome - see in some heavily-infected dogs
dogs at time of Dx-Why?  Adults obstruct tricuspid valve (RAV), posterior vena cava
 “Susceptibility Window”  ACUTE ONSET-severe lethargy, dyspnea, pallor, weakness
 Melarsomine adulticide does not kill HW larvae < 4 months  +Jugular pulses, systolic murmur (R) of tricuspid regurgitation
old  + Hemoglobinemia, hemoglobinuria
 HW-infected dog likely to have larvae < 4 months old in blood  Rx by surgical extraction or dog likely to die w/in 2 days
 If larvae < 4 months survive adulticide Rx, can re-infect dog
 So use monthly HW preventive to kill youngest larvae
 Ivermectin, selamectin (Revolution®), moxidectin = “Slow
microfilaricides”
 Fewer adverse rxns, because microfilariae die off slowly
 Milbemycin (Interceptor®)= “fast microfilaricide” Take
precautions
 10% have adverse rxns because larvae die off fast
 Can see shock, depression, hypothermia, vomiting
 Pre-treat with dexamethasone and diphenhydramine
 Hospitalize and observe 8 hours after giving milbemycin
Stabilization: Prognosis: guarded to good if uterus is intact
IV fluids Rule out pyometra in any systemically ill intact female
Broad-spectrum antibiotics
Analgesics
Surgical:
Ovariohysterectomy
9.flea allergy
Acute onset of moderate to severe pruritus History and physical exam Acute: Prognosis is good with long-term management
More common in warmer seasons but can be year round Flea comb to find fleas/flea dirt Tapering dose of corticosteroids for pruritus 15% of dogs do not have evidence of fleas
Excessive self-grooming and hair loss, especially rear half of Positive response to flea eradication Topical/oral flea adulticide
body Chronic:
+/- Visible live fleas Ongoing use of oral/topical flea adulticide
Oral monthly flea development inhibitors (lufenuron)
Environmental control: frequent vacuuming, removal of
outdoor organic debris

10.lamenes overview
Hip dysplasia: "bunny hopping" gait, lameness, difficulty Radiography Hip dysplasia: Hip dysplasia: PennHIP method is more accurate for Dx at an
rising, positive Ortolani sign (hip laxity) Hip dysplasia: Surgical: triple pelvic osteotomy, femoral head ostectomy, total earlier age than OFA method
Panosteitis, HOD, OCD: young, medium to giant breeds, hip replacement (see bodacious links below)
more common in males, acute lameness, fever Medical: NSAIDs, weight loss, joint supplements Panosteitis, HOD: prognosis is excellent but flare-ups may
Panosteitis: Panosteitis, HOD: analgesics occur, repeat radiography may
OCD: surgical debridement or medical Rx with joint be necessary to diagnose
supplements and analgesics OCD: prevent by avoiding excessive food and calcium and
Legge-Perthes disease: surgical femoral head ostectomy or vitamin D supplements
total hip replacement, Legge-Perthes disease: prognosis with surgery is good to
analgesics excellent

long bone pain

HOD: swollen and warm distal limb, metaphyseal pain
OCD: Shallow acetabulum
Flattening of femoral head
< 50% of femoral head covered by acetabular rim
Thickened femoral neck
Panosteitis:
multiple long bones have increased medullary opacity,
periosteal new bone
HOD:

joint effusion, decreased range of motion

Legge-Perthes disease (avascular necrosis of femoral
head): 3-12-mo-old small or toy breeds, pelvic limb
lameness
11.ethylene glycol EG toxicity
At 1-2 hrs: stupor, stumbling, ataxia, nausea, PU/PD
At 24-72 hrs: clinical signs relating to renal failure
(anorexia, lethargy, PU/PD, vomiting)
EG blood screening test
Detects for 30 min to 12 hrs after ingestion
Urinalysis
Calcium oxalate crystals seen 3-18 hrs after ingestion
Isosthenuria as renal failure develops
Best window of Rx is less than 8-12 hrs post ingestion Prognosis fair to good if aggressive intervention within 8-12 hrs
Decontamination: emesis, activated charcoal (need a lot of ingestion, otherwise poor
because it has low affinity for EG) to grave
Fomepizole (prevents conversion to toxic metabolites) False positives on EG test: propylene glycol or glycerol in
7% Ethanol solution parenterally activated charcoal, semi-moist
Supportive care: fluids, hemodialysis or peritoneal dialysis if dog foods, injectable diazepam
oliguria or anuria present

High anion gap metabolic acidosis

Osmole gap: greater than 20 mOsm/kg strongly correlates
with blood EG level
Azotemia, hyperphosphatemia, hypocalcemia,
hyperglycemia
EG extended flashnotes Dog, acute onset lethargy, disorientation, vomiting, seizures. Hx
of anti-freeze exposure
Presentation: VERY COMMON DDX: Rx of choice: Prognosis:
 All animals susceptible Encephalitis, cranial trauma, intracranial neoplasia, Immediate treatment for EG toxicity is critical Good: Dogs treated within 5 hours, cats within 3 hours
 Cats highly sensitive, 1 teaspoon can be fatal pancreatitis, gastroenteritis, ketoacidotic “Due to rapid progression and irreversibility of renal lesions, Guarded to poor: Very large doses presenting with seizures,
 Dogs most frequently exposed diabetes mellitus, renal failure, other toxicities (barbiturates, any patient suspected of consuming EG nystagmus
 Sources aspirin, methanol, isopropanol, should be tested and decontaminated unless/until exposure Prevention:
 Car radiator fluid (ANTIFREEZE #1) propylene glycol, raisins, grapes, NSAIDs, lilies) has been ruled out;  Do not keep animals in the garage
 Puddle under car when leaks or after change Test(s) of choice: empirical treatment with fomepizole or ethanol is indicated if  Lock antifreeze containers away from chewing dogs
 Found in toilets of cabins in Northern  REACTTM Ethylene Glycol Test Kit the index of suspicion is high and  Immediately clean spills or leaks with cat litter
hemisphere to prevent freezing over winter  False positives from propylene glycol, glycerol, sorbitol, a confirmatory test is not available in time. Pearls:
 Antifreeze also found in mannitol, or thimerosol The greatest window of opportunity for intervention is <8–12  Renal tubules regenerate over time
 Aircraft deicing products  Do not use isopropyl alcohol to disinfect area before blood hours post exposure in dogs,  Ethylene glycol itself is not toxic
 Portable basketball posts draw <2 hours post exposure in cats.”  EG is metabolized by liver to toxic metabolites via alcohol
 Windshield wiper fluids  Fomepizole may block a positive result Cote, Clin Vet Advisor, Dog and Cat. 2nd ed. pp. 369-71 dehydrogenase
 Paints  Propylene glycol is found in some injectables, activated  Supportive care (IV fluids, NaBicarb CRI, treat seizures,  Glyoxalate, glycolate, oxalate
 Photography developer solutions charcoal suspensions warmth) o Calcium oxalate crystal formation in renal tubules and
 Risk factors  Serum osmolality: requires colloid osmometer  Decontaminate microvasculature
 Outdoor, free range, garage access  > 20 mOsm/kg strongly suggestive of ethylene glycol toxicity  Induce vomiting if within 4 hours and conscious o Renal tubular damage
 Northern colder climates  Chemistry  Activated charcoal o High anion gap metabolic acidosis
 Water sources for pets are frozen  Increased BUN, creatinine, glucose, phosphorus  ± gastric lavage – under anesthesia o Citric acid cycle inhibition
 Ethylene glycol does not freeze and is sweet tasting  Hypo- or hypercalcemia  Prevent metabolism of ethylene glycol into toxic metabolites o Phosphorylation inhibition
 Summer radiation flushing  High anion gap metabolic acidosis  Fomepizole (4-methylpyrrazole, 4-MP, Antizol-Vet)
 Engine leak (MOST COMMON) o Anion gap = (Na+ + K+) – (Cl- + HCO3-) o Inhibits alcohol dehydrogenase
 Clinical signs - Triphasic o > 25 mEq/L significant for diagnosis o Can cause sedation and hypothermia
 Stage one: 30 min – 12 hrs  Urinalysis o DOGS: 20 mg/kg slow IV infusion Then 15 mg/kg slow IV q 12
 CNS signs  Glucosuria, cellular casts, cells (renal tubular, transitional, h×3
o Lethargy, disorientation, ataxia, knuckling squamous) o CATS: Label dose is NOT effective
o Vomiting, PU/PD, hypothermia, hypotension  Monohydrate calcium oxylate crystalluria – 3-18 hrs post  Must use higher, OFF-label dose in cats
o Seizures, coma, ± muscle fasciculations (grave prognosis) ingestion  Cats <3 hours after ingestion at 125 mg/kg slow IV infusion,
 Stage two: 12 – 24 hrs o Picket fence crystals then
 Appears to have improved  Wood’s lamp 31.25 mg/kg q 12 h × 3 treatments has shown significant
 Quiet, depressed, PU/PD  Detects fluorescein stain in antifreeze success
 Stage three: 24 – 72 hrs  Scan muzzle, paws, vomitus, urine – supports exposure  7% Ethanol (Dogs)
 Weakness, depression, anorexia, tachypnea/dyspnea  Ethylene glycol and glycolic acid levels in serum or urine o Competes with alcohol dehydrogenase
 Ultrasonongraphy o Enhances diuresis
 4 – 6 hours: increased cortical echogenicity o Increases CNS depression
 Later: Halo sign indicating anuria. Grave prognosis  20% Ethanol (Cats)
o If > 3 hours since ingestion of EG by a cat, ethanol is the
15.ophthalmology overview
Cataracts: Ophthalmic exam plus... Cataracts: Cataracts:
Cataracts: Cataract surgery by experienced veterinary ophthalmologist Prognosis good to excellent with surgery
Blood and urine glucose Cherry eye: Cataracts can be associated with diabetes mellitus
Ocular ultrasonography Surgical replacement of 3rd eyelid gland Refer early before secondary uveitis develops
Electroretinography (ERG) Uveitis: Cherry eye:
Uveitis: Topical and systemic corticosteroids or NSAIDs (unless Prognosis good to excellent with surgery
secondary to protozoal or fungal Removal of 3rd eyelid should only be done if cancerous
infection or corneal ulceration!) because high risk of lifelong
Topical atropine to decrease pain of iridocyclospasm keratoconjunctivitis sicca with removal
Cloudy white pupil
Treat underlying cause Uveitis:
Decreased vision
Glaucoma: More than 50% of cases are idiopathic
Cherry eye:
Glaucoma:
Early referral to ophthalmologist recommended
Always treat contralateral eye prophylactically with IOP-
reducing meds
Tonometry: intraocular pressure (IOP) Treat even if blind to address pain
Less than 10 mmHg consistent with uveitis
Greater than 30 mmHg consistent with glaucoma (can be
secondary to uveitis) Acute: decrease IOP and pain
Young (less than 2 yr) Topical or systemic carbonic anhydrase inhibitor
Systemic work-up for underlying cause
English bulldog, beagle, Shih tzu, cocker spaniels Topical beta-adrenergic antagonist or blocker
CBC, chemistry, urinalysis
predisposed Mannitol
Imaging
Smooth, moist, reddish-pink mass at medial canthus +/- Topical or systemic corticosteroids
Glaucoma:
Uveitis: Chronic:
Tonometry: IOP over 30 mmHgGonioscopy: visualization of
Conjunctival hyperemia Topical prostaglandins
iridocorneal angle
Photophobia, blepharospasm Surgery: enucleation
Ocular ultrasonography: evaluate deep ocular structures
Aqueous flare (cloudiness of aqueous humor)
Color change of iris
Midrange to miotic pupils
Glaucoma:
"Big blue eye" (buphthalmos)
Visual impairment
Tortuous episcleral vessels
Proptosed eye OPHTHALMIC EMERGENCY
 ACUTE TRAUMA: Hit-by-car (HBC), fighting, aggressive Differential Dx: Rx of choice: Prognosis:
restraint Buphthalmos 2° to glaucoma STABILIZE & TREAT LIFE THREATENING INJURIES 1st For vision
 Forward displacement of globe w/ entrapment of eyelids Exophthalmos 2° to retrobulbar mass, orbital abscess or  + Lavage eye w/ sterile saline Elements of a guarded to good prognosis:
behind congenital vascular anomaly  + Protect eye w/ topical medications alternating Q 1 hr until  Mild proptosis, eyes w/ positive direct & consensual PLR
 Brachycephalics can proptose w/ MINIMAL trauma Test of choice: eye is treated  Positive menace response and vision on initial exam
 Dolichocephalics require SEVERE trauma to proptose Proptosis diagnosis is obvious but…..  Bacitracin-Neomycin-Polymyxin [(BNP) without steroid]  Bachycephalics >>>> cats, dolichocephalics
 See in dogs >>> cats  Must evaluate patient’s stability for surgery AND prognosis ophthalmic ointment For globe salvage
 Other signs (depending on degree/type of trauma): for eye/vision  Sterile lubricant Good: minor to moderate proptosis, avulsion 1 extraocular
Fractures (skull, appendicular), neuro deficits (brain trauma),  Physical exam If vision or globe can be salvaged for cosmetic purposes muscle, +/- minimal hyphema
shock, respiratory distress, recumbent  Evaluate for hypovolemic or hemorrhagic shock  REPOSITION GLOBE IN ORBIT Guarded: moderate proptosis, moderate hyphema, avulsion
Classic case: Bug-eyed spaniel fell off sofa and his eye popped  Suspect pneumothorax, pulmonary contusions? thoracic Perform ASAP under general anesthesia as soon as patient 2+ extraocular muscles
out radiographs stable Grave: severe proptosis, extensive tissue damage, avulsion 3+
-orHit-by-car dog of any type  Suspect orbital or skull fracture? skull radiographs  Lateral canthotomy extraocular muscles, globe rupture,
 Ophthalmic Exam - Only 20% of proptosis cases regain some  1-2 cm incision at lateral canthus to widen the palpebral optic nerve avulsion
functional vision fissure Prevention:
Must assess eye damage & vision  Allows eyelid replacement over globe Avoid aggressive handling of exophthalmic dog breeds
 Menace Response  Replace globe into orbit (brachycephalic)
 Positive menace = GOOD prognostic indicator for vision  Lavage globe with sterile saline Prevent reoccurrence: Perform a permanent medial
 Pupillary light reflexes (PLR): direct and consensual  Apply copious amounts of BNP ophthalmic ointment on eye canthoplasty
 Resting pupil size does not correlate with prognosis for vision surface
 Positive PLR = GOOD prognostic indicator  Gently press globe into orbit w/ moist surgical sponge or flat
 Dilated, unresponsive pupil = POOR prognostic indicator of scalpel handle
 Optic nerve avulsion likely  Close lateral canthotomy
16.pancreatitis
Acute or chronic, may be subclinical
History of dietary indiscretion or high-fat diet
History of blunt abdominal trauma
Vomiting, anorexia, diarrhea, abdominal pain
Weakness, dehydration
+/- Medication history of KBr, azathioprine, Lasparaginase,
phenobarbital, thiazide diuretics
Miniature schnauzers are overrepresented
Pancreatitis flashnotes
Presentation:
Risk factors
• Miniature schnauzers (poster dog for pancreatitis)
• Middle-aged to older
• Overweight
• Dietary indiscretion (FATTY FOODS, got into garbage)
• Pancreatic hypoperfusion (shock, hypotension secondary to
general anesthesia)
• Blunt abdominal trauma
• Pharmaceuticals – KBr, phenobarb, TMS
• Severe hypertriglyceridemia
• Infections – viral, mycoplasma, parasitic (babesiosis)
Clinical signs
• Anorexia, vomiting, weakness
• Abdominal pain (prayer position), dehydration, fever
• +/- diarrhea, icterus, shock
Classifications
• Acute pancreatitis – MOST COMMON, reversible
• Chronic – long-standing inflammation, permanent damage
SNAP canine pancreatic lipase (cPL) patient-side test is very Aggressive fluid therapy with appropriate additives based on Prognosis depends on severity; worse with systemic
sensitive. If SNAP cPL positive, confirm with canine pancreatic. lab work +/- colloidal support or complications (multiple organ failure,
lipase immunoreactivity (Spec cPLI) test which is highly plasma acidosis, hypocalcemia, peritonitis, DIC)
sensitive and specific for acute and chronic pancreatitis Pain medications (opioid or lidocaine CRI) Corticosteroids are no longer considered to be a cause of
Abdominal ultrasonography: Enlarged hypoechoic pancreas. Anti-nausea medications (maropitant [Cerenia], ondansetron, pancreatitis and are not
Hyperechoic peripancreatic fat dolasetron) Contraindicated
Fluid around pancreas Enteral nutritional support (ultra-low-fat diet) unless
Abdominal radiographs not particularly useful for diagnosis, but intractable vomiting
aid in ruling out other Avoid antibiotics unless necessary
differentials
4-5X elevation of lipase and amylase are suggestive only (50%
sensitivity and specificity)
5yo overweight miniature schnauzer with anorexia, vomiting,
and weakness
DDX: Rx of choice: Prognosis:
GI obstruction, FB, gastroenteritis, ulcers, pyometra, ACUTE pancreatitis: IV fluids and supportive care Good: mild pancreatitis without pancreatic or systemic
pyelonephritis • Treat inciting cause if known complications
Test(s) of choice: ▪ Discontinue medications if known risk factor Poor to grave: severe pancreatitis with pancreatic +/- systemic
cPL (canine pancreatic lipase) • Aggressive fluid therapy complications
• SNAP test – patient side test ▪ Isotonic crystalloid fluids IV Prevention:
▪ Rule in or out pancreatitis • Monitor labwork Avoid high-fat foods and treats
▪ Must confirm positive test with Spec assay ▪ Monitor and treat for hypokalemia (2 to vomiting) Eliminate risk factors, especially in high risk dogs
▪ If negative look at other DDx ▪ Monitor BUN & Cr Pearls:
• Spec cPL Assay (link to IDEXX page on Spec cPL test) • Analgesia NPO no longer standard therapy for dogs w pancreatitis unless
▪ TEST OF CHOICE ▪ Treat pain even if clinical signs are not apparent vomiting is uncontrollable
▪ Highly specific and sensitive ▪ Buprenorphine or fentanyl CRI
▪ Does not assess severity • Antiemetic
▪ Monitor disease progression ▪ 5-HT3 serotonin receptor antagonist (Dolasetron,
• Abdominal ultrasound Highly specific for diagnosing Ondasetron)
pancreatitis ▪ NK1 receptor antagonist (Maropitant)
▪ Enlarged hypoechoic pancreas ▪ Metoclopramide is contraindicated – decreases pancreatic
▪ Peripancreatic fluid accumulation perfusion
▪ Pancreatic mass effect • Plasma transfusions
▪ Hyperechoic peripancreatic fat ▪ May be LIFE-SAVING in dogs with severe pancreatitis
▪ Dilated pancreatic duct ▪ Replaces macroglobulins, clotting factors
Chronic cases ▪ Maintains albumin concentration
▪ 18 hour serum triglyceride concentration test to rule out • Antibiotics
hyperlipidemia ▪ Not necessary unless concurrent infection
▪ Monitor serum Ca++ • Nutritional support
▪ Monitor cPL ▪ Enteral nutrition preferred over parenteral unless incessant
Acute cases vomiting
• Monitor CBC, chemistries, cPL, coagulation panel ▪ If incessant vomiting
▪ Total or partial parenteral nutrition
18.megaesophagus
Regurgitation (distinguish from vomiting - May be idiopathic or secondary to systemic disease
regurgitation contains undigested food or water) Thoracic radiographs: (may or may not need contrast
Coughing, drooling esophagram)
Weight loss Air-filled, dilated esophagus
Weakness (if due to myasthenia gravis, polyneuropathy, +/- Secondary aspiration pneumonia (best seen on
or polymyopathy) VD)
+/- Signs of pneumonia (fever, cough) Test for possible underlying conditions
Acetylcholine receptor antibody test for myasthenia gravis
ACTH stimulation test for Addison's disease
Free T4 level for hypothyroidism
Lead level
EMG/nerve conduction for polymyopathy or polyneuropathy
Treat underlying condition and/or aspiration pneumonia
Upright feeding using gruel or meatballs
GI motility medications do not affect esophageal motility, but
aid in gastric emptying to
reduce esophageal reflux (cisapride)
Gastric acid reducers to help decrease acid reflux (proton pump
inhibitors - pantoprazole,
omeprazole, or H2 receptor blockers - famotidine, ranitidine)
Congenital breed predilection: German shepherd, miniature
schnauzer, fox terrier - may see
spontaneous improvement
Rule out vascular ring anomaly in puppies
Some drugs can cause temporary megaesophagus (eg,
ketamine, xylazine)
Most eventually die secondary to aspiration pneumonia
19.cancer overview
Osteosarcoma: Osteosarcoma: Osteosarcoma: mostly palliative for pain Osteosarcoma:
Radiography: bony lysis (moth-eaten) and periosteal Amputation 75% are appendicular; common locations are proximal
bone formation Radiation humerus, distal radius, distal
Thoracic radiographs: 3 views to detect metastatic Chemotherapy for micrometastasis (doxorubricin, carboplatin) femur, and proximal tibia ("away from elbow, toward knee")
disease Mammary gland tumors:Numerous cystic calculi 90% of dogs will have clear thoracic radiographs at initial
CBC, chem profile, UA to stage Surgery depends on size and location (lumpectomy, diagnosis, but most will
Fine needle aspirate (FNA) or biopsy (best to confirm regional/simple mastectomy, radical develop mets later, even with amputation
diagnosis) mastectomy), but best if can excise with a minimum of 2-cm Survival is 4-12 months, elevated ALP associated with poorer
CT for axial tumors and to help plan surgery or margins in all planes prognosis
radiation therapy +/- Inguinal lymph node removal Mammary gland tumors:
Mammary gland tumors: Adjuvant chemotherapy for gross metastasis or advanced stage 50% benign, 50% malignant
Excisional biopsy and histopathology Mast cell tumors: Multiple tumors are common as are multiple tumor types
Surgical excision with 2 cm or greater lateral margins and 1 Poorer prognosis if > 3 cm, lymph node involvement, or distant
fascial plane deep metastasis
Histamine blockers (diphenhydramine, famotidine, ranitidine) Spaying after 2 yr does not decrease risk
Chemotherapy or radiation Mast cell tumors:
Lymphoma: chemotherapy with combination protocol is best More aggressive at mucocutaneous junctions, prepuce,
scrotum, muzzle, digit, pinna
Tumor grade determines prognosis
Lymphoma:
T cell lymphoma has poorer prognosis ("B is better")
Prednisone before chemotherapy will decrease response to
chemotherapy
Many dogs can achieve remission with chemotherapy
Simple carcinoma, subclassification of tubulopapillary
Large or giant breed, bimodal age incidence carcinoma. This tumor was graded I, well differentiated. Note
(1.5-2y then 7-9y) the tubule with clear lumen formation (stars)
Chronic, progressive lameness (acute if pathologic
fracture)
Cough if pulmonary metastases present
Mammary gland tumors:

Palpable mammary chain mass or ulceration

Intact or late spayed female
Simple carcinoma, subclassification of Solid Carcinoma with
Mast cell tumors:
grade III. Note to lack of tubule formation, large vesicular nuclei
with prominent nucleoli (Black arrows) and different mitotic
figures (White arrows) and high mitotic index

FNA of regional lymph nodes

3-view thoracic radiographs and abdominal ultrasonography to
Cutaneous or subcutaneous (+/- pruritic) mass that
screen for metastatic
may shrink and swell intermittently
disease
Breed disposition: Boxer, Boston terrier, Golden
Mast cell tumors:
retriever, Labrador, Pug
If degranulates: vomiting, diarrhea, melena
Lymphoma:

1.intervertebral disk disease IVDD
PAIN in neck or back – arched back or head held down
Ataxia, paraparesis/paraplegia, tetraparesis
Any breed, but chondrodystrophoid most common
2.epilepsy
1- to 5-year-old with history of seizure activity; normal
Presentation
Idiopathic epilepsy IE flashnotes
Presentation:
 Signalment
 Dogs 1-5 years old, slightly more common in males
 Any dog breed, but inherited in beagle, Belgian Tervuren,
keeshond, dachshund, Labrador retriever, golden retriever,
Shetland sheepdog, Irish wolfhound, Viszla, Bernese mountain
dog and probably more
 Cat, idiopathic epilepsy (IE) less common than dogs
 Horses
o Arabian foals
o Adult horses do not usually have seizures due to IE
 History - Need detailed, accurate Hx. IE has many, many rule
outs
 One or more seizures, usually about a month apart
 Generalized tonic-clonic – duration of 30 seconds to 3 minutes
o Loss of consciousness
o Sustained contraction of all muscles
o Paddling limb motions or rhythmic muscle contractions (esp
limbs, masticatory muscles)
o Usually urinary and fecal incontinence
 Generalized mild seizures affecting only the face and jaws
 Clinical presentation
 Patients are usually normal when presented in clinic
 May have temporary neurologic deficits if present w/in 24
hours of a seizure
o Ataxia, abnormal behavior, cortical blindness, hemiparesis
o If these sx continue more than 24 hours after a seizure –
consider differentials below
 Normal fundic examination – if abnormal, consider
differentials listed below
Canine Neurology
MRI is safe, fast, and best quality; CT is safe and faster If pain only (no neuro signs) – strict cage rest and
thanCentral
MRI, but lower quality; myelography is invasive and
Preganglionic analgesia with opiates or NSAIDs
Postganglionic
seizures may occur during recovery Nonambulatory or unresponsive to conservative
treatment
– surgical decompression by experienced surgeon or
neurologist
Hemilaminectory for thoracolumbar disks
Ventral slot for cervical disks
Steroids are increasingly unpopular for pain control
Falling out of favor with surgeons and neurologists
because of numerous adverse effects and poor
efficacy
Better results with NSAIDs
Rule out other causes of seizures using CBC, biochemistry Anticonvulsants (phenobarbital, levetiracetam,
profile, bile acids, cholinesterase, lead level, MRI, CSF analysis zonisamide, etc.)
to prevent/reduce seizures; spay females
3-year-old Beagle; History of two seizures in past month.
He is otherwise normal on exam.
DDX: VITTAMINN D acronym: Rx of choice:
Vascular (stroke, coagulopathy)  Acute treatment to halt seizure activity
Inflammatory (encephalitis)  Benzodiazepines: Intravenous diazepam, midazolam,
Toxic (lead, metaldehyde, organophosphate) lorazepam (if necessary, diazepam may
Trauma be given rectally and midazolam may be admistered
Anomalous (hydrocephalus, lissencephaly) intramuscularly or intranasally)
Metabolic (hepatic encephalopathy, hypocalcemia, hypoglycemia) o Very short half-life; will need concurrent
Idiopathic (epilepsy) maintenance anticonvulsant if seizures recur
Neoplasia o If not effective after 3 doses, give propofol IV to stop
Nutritional (thiamine deficiency) seizure then continuous infusion)
Degenerative (lysosomal storage disease)  Digital ocular pressure – vagal stimulation
Test(s) of choice: Diagnosis is based on exclusion of other causes of  If temporarily effective but seizures reoccur
seizures o Benzodiazepine continuous rate infusion (CRI)
 Basic work-up o Propofol or isoflurane anesthesia
 Bloodwork to rule out metabolic or toxic cause of seizures  After seizure stops
 Bile acids to rule out hepatic encephalopathy o Administer oxygen; Place IV catheter
 If normal physical and neurologic examination and typical signalment, o Check glucose, calcium, hematocrit, protein
o Presumptive diagnosis of epilepsy can be made at this point. o Maintain hydration & blood pressure w fluid therapy
o If deterioration or failure to respond to medication, pursue more o Monitor temperature and treat >104ºF (40ºC)
advanced testing o Turn at least every 4 hours
 Advanced testing o Express bladder if needed every 8 hours
 MRI or CT of brain to rule out structural brain disease (e.g., brain o Keep clean, warm dry
tumor) o May require 24-72 hours of heavy sedation
 Cerebrospinal fluid analysis to rule out encephalitis  If animal is not already on anticonvulsants
 ± Electroencephalography to confirm seizure activity o Give parenteral loading dose of Phenobarbital (IV) or
 Monitoring levetiracetam (Keppra) (IV or SQ)
 Monitor anticonvulsant blood levels (DO NOT USE SERUM SEPARATOR o Then continue with maintenance therapy
TUBES)  If animal is already on anticonvulsants
o 2-4 weeks after starting meds or changing dosage (3 months for o Draw blood for anticonvulsant levels
potassium bromide) o Continue anticonvulsants on schedule (give
o Every 6-12 months parenterally if necessary, potassium
o If there is poor seizure control bromide can be given rectally if necessary)
Hansen Type I occur in chondrodystrophoid breeds
and the nucleus pulposus extrudes through the annulus; Hansen
type II are usually
nonchondrodystrophoid breeds and there is hypertrophy or
bulging of the annulus; prognosis
guarded to excellent
Monitor anticonvulsant blood levels and bile acids if on
phenobarbital
Prognosis:
 Guarded to good
 Can have normal lifespan if well-controlled.
 Animals with repeated emergency episodes of status
epilepticus (continuous seizure >5 min)
or clusters (several seizures in a 24 hour period) tend to have a
shorter lifespan.
 Only 70-75% of dogs will be controlled with phenobarbital
and/or potassium bromide
 Larger breed dogs tend to have more difficult to control
seizures
Prevention:
 Spay females (estrogen can lower seizure threshold)
 Client education – give meds on time. A missed dose can
precipitate a cluster or status epilepticus.
 Do not breed affected dogs
Pearls:
 Goal of treatment is to reduce seizure frequency by 50%
 Less than two seizures every 2-3 months is considered
adequate control
 Its an emergency when:
 More than 3 seizures in 24 hours
or
 A single seizure lasting more than 5 minutes
 Have owner keep diary of seizure activity, meds, med levels,
unusual events
 Seizures happen most often at night or when patient is resting
or sleeping.
 Can be “provoked” by a visit to the veterinary hospital,
groomer, or loud noises.
 Have owner videotape episode if possible-helps ddx from
syncope,
Active substance

Cocaine 6% Slight mydriasis No dilation No dilation

Phenylephrine 10% No dilation No dilation Normal mydriasis

Normal
Hydroxyamphetamine 1% Normal mydriasis No or incomplete mydriasis
mydriasis
 Small animal cardiology
1.dilated cardiomyopathy DCM
Large and giant breeds: Doberman pinscher, Radiography: Prior to onset of CHF: Prognosis:
boxer, great Dane, Irish wolfhound, standard Angiotensin-converting-enzyme (ACE) inhibitors Dogs with occult disease can live several years
poodle (but also cocker spaniels) Pimobendan (positive inotrope and vasodilator) if heart Sudden death due to arrhythmias can occur even
Middle-aged dilation present before echocardiographic changes of DCM are seen!
Early signs: Anti-arrhythmics (e.g., sotalol, mexiletine) for Pimobendan:
Heart murmur ventricular arrhythmias If started prior to onset of CHF will delay
Middle-aged After onset of CHF: development of CHF
Weak peripheral pulses Acute therapy: Can extend life during CHF, but prognosis after 1 yr
Exercise intolerance OxygenEchocardiogram of a dog with DCM is poor
Congestive heart failure (CHF) showing marked left atrial (LA) and Other causes of DCM
Cough Generalized cardiomegaly ventricular dilation (LV), long-axis view Taurine deficiency-linked in American cocker spaniels,
Tachypnea and dyspnea Variable venous dilation M-mode ultrasonography of DCM, golden retrievers, boxers, and Dalmatians
Tachycardia Pulmonary edema/perihilar infiltrate if decompensated right parasternal short-axis view Carnitine-responsive in boxers
Weakness Electrocardiography (ECG)/Holter monitor: ECG showing electrical alternans in a Chagas myocarditis caused by the protozoan
Ventricular ectopic beats are common human with PE Trypanosoma cruzi
May see significant ventricular arrhythmias early in Stress reduction Parvovirus due to in utero exposure, rare now
Dobermans Parenteral furosemide Doxorubicin-induced caused by cumulative doses
Atrial fibrillation in advanced disease Pimobendan greater than 180 mg/m2
Holter monitoring to determine: Chronic therapy: Feline DCM
Severity of arrhythmia Oral furosemide Breed predilections: Siamese, Burmese, Abyssinian
If therapy indicated ACE inhibitors Prognosis is poor because most present in CHF
Echocardiography: Pimobendan Dx and Rx similar to canine DCM
Left atrial and ventricular dilation Taurine-deficiency (commonly seen prior to 1987; now rare
Mitral +/- tricuspid valve regurgitation because of increased dietary
+/- Right atrial and ventricular dilation taurine in most cat foods)
Evidence of poor contractility:
Prolonged end-point septal separation (EPSS)
Decreased fractional shortening (FS
DCM extended 7 year old male Doberman Pinscher with tachypnea, dyspnea,
and cough
Presentation: DDX: Rx of choice: Prognosis:
History and Signalment Primary respiratory disease, non-cardiogenic pulmonary Acute CHF Fair to Good: Taurine deficiency responsive DCM, Irish
 Dogs, 4-10 yr, Males >> Females, LARGE breeds edema, pneumothorax, non-cardiogenic  Minimize stress, supplemental O2, IV fluids contraindicated wolfhounds
 Doberman Pinscher, Great Dane, Boxer, Irish effusions, heartworm disease, myxomatous valvular heart  Treat arrhythmias Poor to Grave: Death usually occurs 3 mos - 2 yrs post Dx
Wolfhound, Newfoundland, Spaniels, Afghan, Old disease, endocarditis, myocarditis,  Diuretics Worst prognosis: Cats w/out taurine deficiency; Dobermans w/
English Sheep dog, Scottish Deerhound, Dalmatian cardiac tumors, pericardial effusion, diaphragmatic hernia,  Reduce edema, effusion atrial fibrillation, ventricular
 Juvenile onset pulmonary hemorrhage, laryngeal  Furosemide (Lasix) – inhibits Na+ and H2O reabsorption in arrhythmia; Portuguese Water dogs: presented young (weeks to
 Portuguese Water Dog, Toy Manchester Terrier paralysis, collapsing trachea, congenital heart disease Loop of Henle mos old), usually die quickly
 RARE in CATS: Abyssinian, Burmese, Siamese Test(s) of choice:  Therapeutic thoracocentesis and paracentesis Prevention:
Clinical signs Thoracic auscultation  2% Nitroglycerin (topical vasodilator) Genetic testing – NC State College of Veterinary Cardiac
 Compensated early disease with no clinical signs  Tachycardia, I-III/VI systolic apical murmur (mitral  Sodium nitroprusside (dogs only) Genetics Lab
 Congestive heart failure (CHF) regurgitation),  Vasodilator to treat severe cardiopulmonary edema Pearls:
 Cough, tachypnea, dyspnea, exercise intolerance  Gallop sound (S3), Premature beats  Dobutamine  Treatment for compensated DCM is controversial
 Restlessness, abdominal distension, lethargy  Arrhythmias  Positive inotrope, ß1 adrenergic agonist  DCM is autosomal dominant in Irish Wolfhounds,
 Inappetence, weight loss (cachexia)  Abnormal lung sounds  Use to treat severe heart failure, cardiogenic shock Newfoundlands, Doberman Pinschers, Boxers
 Weakness, syncope, collapse  Dull ventral lung sounds (pleural effusion) Chronic CHF  DCM may be autosomal recessive in Portuguese Water Dogs
 Cyanosis, weak pulse quality, jugular pulse, distension  Increased bronchovesicular sounds   Several etiologies for DCM
 Pulse deficits (pulmonary edema)  Dobermans, Great Danes are usually NOT taurine responsive  Idiopathic, familial, genetic
Doberman Pinscher, poster dog for dilated  Crackles  L-carnitine supplementation – Boxers, American Cocker  Taurine deficiency – reversible, cats
cardiomyopathy (DCM). Urinalysis – important to perform prior to starting Rx spaniels  Carnitine deficiency
Photo courtesy of pato garza Taurine analysis  Omega-3 fatty acids  Infectious
 ANY dog or cat with DCM  Permanent exercise restriction  Trypanosoma cruzi – Southern USA – Chaga’s disease
 Cocker Spaniel, Newfoundland, Golden Retriever  Therapeutic thoracocentesis and paracentesis  Parvovirus – rare
Carnitine plasma analysis  Diuretics  Toxic – Adriamycin
11.endocarditis
Dogs over 4 yr; rare in cats Etiology: Several bacteria are possible, but most Antibiotics (at least 2-3 mos): Prognosis:
Breed predilections: German shepherds, commonly ... IV then oral Mitral valve more favorable than aortic
Labrador retrievers, boxers, Doberman Streptococcus spp Ideally based on culture or Bartonella testing Reported 20% survival rate
pinschers Staphylococcus spp Empirical therapy: No treatment specific for valve damage and secondary valvular
May have concurrent congenital heart disease (e.g., Klebsiella spp Broad-spectrum: Ampicillin/amoxicillin, insufficiency
subaortic stenosis, mitral dysplasia) Escherichia coli cephalosporin combined with a fluorinated New murmur (especially diastolic) in systemically ill dog should
Signs of systemic illness (lethargy, anorexia, weakness) Bartonella quinolone prompt evaluation for endocarditis
Intermittent lameness Echocardiography: Cidal drugs are best
Fever Thickened, hyperechoic valve For Bartonella : Combination of fluorinated quinolone and
Signs of CHF: Pedunculated mass on valve leaflet doxycycline (best therapy
Cough Valvular regurgitation not known)
Tachypnea, dyspnea +/- Secondary chamber dilation Therapy for CHF:
Approx 26% do NOT have a murmur CBC: Leukocytosis, anemia, thrombocytopenia Oxygen therapy
Serum chemistries: Azotemia Furosemide
Urinalysis: Proteinuria Pimobendan
Blood and urine cultures: Angiotensin-converting enzyme (ACE)-inhibitor
Collect blood from multiple sites Prevention of bartonellosis: Flea control
Not sensitive or specific
Can help guide antibiotic therapy
Bartonella serology and PCR

Canine genetic
1.von Willebrand disease
Doberman pinscher, German shepherd, golden Measure low vWF concentration Cryoprecipitate, fresh plasma, or fresh whole blood vWF is a factor VIII-related antigen which assists in the first step
retreiver, standard poodle, Pembroke Welsh Genetic testing Desmopressin: Mobilizes high-molecular-weight hemostatic in clot formation by
corgi, miniature schnauzer, Shetland sheepdog, Platelet numbers, APTT, and PT are normal multimers from endothelial facilitating platelet adhesion
Basset hound, Scottish terrier granules (Weibel-Palade bodies) Autosomal dominant with incomplete penetrance most
Excessive bleeding or bruising after venipuncture or Levothyroxine may worsen the disease common, autosomal recessive rare
surgery, epistaxis, gingival bleeding, hematuria
There are 3 types of von Willebrand disease:
Type I:
Most common mutation
Produces a truncated form of von Willebrand factor
(vWF)
Mild to moderate signs
Type II:
Intermediate form
Low vWF
German shorthaired and wirehaired pointers
Type III:
Rarest and most severe
Total abscense of vWF
Shetland sheepdogs and Scottish terriers
Click here to see images of an affected Shetland
sheepdog with severe bruising after
ovariohysterectomy

2.ivermectin toxicity (MDR1 mutation)

Collie, border collie, longhaired whippet, German shepherd,
Shetland sheepdog
Treatment with greater than 120 mcg/kg ivermectin
Mydriasis, ataxia, tremors, coma
History of ivermectin administration in susceptible breed
Genetic testing
Supportive care Mutations of the MDR1 gene are associated
with the ability of drugs to cross into the CNS causing
toxicity
Susceptibility to other drugs as well: Loperamide,
vincristine, doxorubicin, milbemycin, and others
 Canine endocrine
1.hypothyroidism**
Middle-aged (4-10 y) dog with insidious clinical signs Initial screening: Oral synthetic T4 (levothyroxine) Px: Excellent
Weight gain, lethargy, exercise intolerance, hypothermia CBC: Possible mild normocytic, normochromic nonregenerative GI absorption is poor Congenital is rare: See disproportionate dwarØsm at birth
Bilaterally symmetric nonpruritic alopecia with rat tail, dry coat anemia Give q 12-24 h for life Euthyroid sick syndrome can make Dx challenging
Rare: myxedema with “tragic” facial expression, stupor, Serum chemistries: Possible hypercholesterolemia, See SLOW improvement over weeks to months Hyperthyroidism is rare in dogs (but common in cats!): In dogs
hypotension, bradycardia, neuropathies hypertriglyceridemia Monitor post-pill total T4 4-6 wks after starting Tx & then q 3-6 due to thyroid carcinoma (or over-supplementation)
Etiology: Lymphocytic thyroiditis or thyroid atrophy Serum total T4: Low = true hypothyroidism or sick euthyroid months Prognosis:
Classic case: Lethargic Golden Retriever with weight gain, state Iatrogenic thyrotoxicosis: PU/PD, polyphagia, hyperactivity, Good to Excellent for primary hypothyroidism
bilateral nonpruritic alopecia, “tragic” face REMEMBER: Sick euthyroid syndrome tachycardia Usually Guarded for secondary hypothyroidism – pituitary
Presentation: Very common endocrine disease of DOGS (https://www.merckvetmanual.com/endocrinesystem/the- If myxedema coma: T4 must be given IV neoplasia most common
• History and Signalment thyroid-gland/hypothyroidism-in-animals#v3270959) with non- Rx of choice: Prevention:
▪ ANY dog 2-9 yo, no gender thyroidal illness • Levothyroxine sodium (synthetic T4) Monitor T4 levels periodically after diagnosis to prevent
predilection ▪ Predisposed breeds can cause low total T4 and confuse testing ▪ Use brand name as bioavailability varies in generics recurrence of clinical signs
▪ Mixed breeds, Boxers, Doberman Further screening (https://zukureview.com/node/20642) only IF Obesity is more common than Pearls:
Pinschers, Dachshunds, Golden total T4 is low: hypothyroidism. • Obesity far more prevalent than hypothyroidism
Retrievers, Irish Setters, Miniature Serum free T4 (fT4): Low = true hypothyroidism, normal = sick • If concurrent disease, treat other disease first
Schnauzers euthyroid syndrome • 2 most common causes of adult onset primary hypothyroidism
▪ Cats – iatrogenic hypothyroidism Occasionally fT4low-normal with hypothyroidism; if suspicious ▪ Lymphocytic thyroiditis
due to hyperthyroid treatment pursue further testing (below) ▪ Idiopathic atrophy of thyroid gland
- Thyroid stimulating hormone (TSH): High = true hypothyroidism;
▪ Congenital normal or low = most likely sick euthyroid syndrome
▪ Foals – Other assays: total T3, thyroglobulin autoantibody
• Pregnant mares grazing on plants containing goitrogens or DDX:
dietary iodine • Obesity, weight gain, alopecia, seborrhea from other causes.
imbalance (too much or too little) Hyperadrenocorticism, hyperestrogenism, ectoparasites,
• Thyroid gland hyperplasia and multiple congenital neoplasia
musculoskeletal anomalies Test(s) of choice:
▪ Dogs – • Serum concentrations of total T4, free T4,
• Disproportionate dwarfism and TSH
• Impaired mental development (cretinism) ▪ Total T4
• Clinical signs (adult onset) stem from ▪ About 90% sensitive
decreased basal metabolic rate ▪ Could also be low due to sick euthyroid
▪ Gradual onset syndrome
▪ Weight gain without increased appetite ▪ Free T4 – by dialysis
▪ Dullness, lethargy, exercise intolerance ▪ More useful in distinguishing euthyroid from
▪ Heat seeking hypothyroid dogs
▪ Tragic facial expression ▪ T3 – may be low, normal, or high in
▪ Droopy eyes hypothyroidism
▪ Myxedema – thickening of skin, mostly on forehead and face ▪ TSH – must be species specific assay
▪ Bilateral nonpruritic truncal alopecia ▪ Flaky skin, ▪ Normal or increased TSH
seborrhea, pyoderma • Evaluate in light of T4, cholesterol, etc
▪ Failure to cycle, decreased libido, infertility • Hypothyroid ▪ Normal or low TSH
▪ Neuropathy – weakness, facial paralysis, ataxia, bark change • Sick euthyroid, early hypothyroid, or pituitary (rare) ▪ High TSH
▪ Myxedema coma – rare syndrome with
▪ Lethargy, stupor, coma normal T4
▪ Hypoventilation • Early hypothyroid, recovery from sick euthyroid illness,
▪ Hypotension antibody interference
▪ Bradycardia ▪ Thyroid levels may be decreased by other factors
▪ Profound hypothermia ▪ Certain breeds: Greyhounds, Scottish Deerhounds, Alaskan
sled dogs
▪ Phenobarbital, KBr, prednisone, clomipramine, propranolol,
some NSAIDs and other
medications
• Fasting hypercholesterolemia (80% of cases) – excellent
screening test

1.external parasites
Fleas: Pruritus, Crusts, scabbing, and hair loss over hips
and base of tail, +/- Anemia
Mites: Sarcoptic mange (scabies): Intense pruritus
Small bumps, excoriations, crusts, and seborrhea
on abdomen, chest, ears, elbows, and legs
Cheyletiellosis (walking dandruff):
Intense pruritus (but sometimes no itching), Scaling on the back
"Dandruff" that moves around on the animal's fur
Ticks: Tick attached to skin +/- redness around bite
+/- Tick-borne diseases (e.g., Rocky mountain spotted
fever, ehrlichiosis, Lyme disease): Fever, Anorexia,
Lymphadenopathy, Splenomegaly, Polyarthritis, Petechiae,
Coughing
Vomiting, diarrhea
+/- Lower motor neuron paralysis
Canine shelter
Fleas: Insects Always check for more ticks in ears, head, neck, perineal region, Fleas:
Etiology: Usually Ctenocephalides felis (cat flea), between toes, and under tail Dog are usually infested with cat fleas, not dog fleas
sometimes C. canis (dog flea) Fleas: There are several products available, but many are too Fleas are intermediate hosts of tapeworms and can transmit
See fleas and flea feces (crumbly red-brown debris) expensive to use in a shelter environment certain rickettsial diseases
Mites: Arachnids Fipronil (Frontline® spray) is safe for puppies older than 8 wks Fleas may not be seen on dogs with flea allergy dermatitis due
Sarcoptic mange: and kills adult fleas within 12 h to excessive selfgrooming
Selamectin (Revolution®) is safe for puppies older than 6 wks Mites:
and kills adult fleas within 12 h (prepackaged doses for large Sarcoptic mange can infest humans, however is self-limiting
dogs can be divided between smaller animals based Cheyletiellosis is contagious to humans
on their weight) Ticks:
Lufenuron (Program® flavor tabs) is safe for puppies older than Most common causes of tick paralysis: D. andersoni (Rocky
6 wks and kills immature fleas Mountain wood tick) and D.
Mites: Treatments are similar for both sarcoptic mange and variabilis (American dog tick)
cheyletiellosis, Lime-sulfur dips, Selamectin Lyme disease is transmitted by Ixodes spp. (I. scapularis and I.
Single dose of fluralaner (Bravecto®) is very effective, albeit not pacificus )
labeled for sarcoptic mange
Ivermectin is effective, however is toxic in breeds that have the
MDR1 mutation (e.g., collies)
Etiology: Sarcoptes scabiei canis Ticks: Removal with forceps or hemostats close to skin and
Skin scrapings slightly twist, Fipronil, Fluralaner
Cheyletiellosis:

Etiology: Cheyletiella yasguri

Direct observation and microscopy

Ticks: Arachnids
Etiologies:
Ixodidae family: Hard ticks
commonly Amblyomma spp.,
Core Vaccinations: Recommended for all dogs
 Core vaccines (except rabies) are given as early as 6 weeks of age
then every 3-4 weeks until 14-16 weeks of age
 Maternally-derived antibodies will cause vaccine inactivation
 Maternally-derived antibodies are generally lost by 9-12 weeks,
but some are lost as early as 6 weeks
 Rabies is given as early as 12 weeks (depending on type), one year
later, then every year (or 3 years depending on vaccine and state law)

Preferred
Antigen Disease Comments
type
Canine distemper – mild to
severe
systemic illness with high
morbidity and Very vulnerable to modified-live or
CDV variable mortality characterized inactivation after recombinant
by upper reconstitution – use w/in 1 hr CDV (rCDV)
respiratory and gastrointestinal
signs.
Sometimes neurologic signs.
Canine parvovirus – destruction
of crypt
cells of the villous epithelium of
small All current vaccines provide
intestine, lymphocyte depletion, immunity from disease by any
CPV-2 modified-live
neutropenia. Clinical signs are field variant (CPV-2a, -2b, and
severe –2c)
enteritis with hemorrhagic
diarrhea,
vomiting, shock
 CAV-2 intranasal is non
core for at risk dogs – can
Canine adenovirus – highly be given earlier, but does
CAV-2
contagious not protect against CAV-1 modified-live
(parenteral)
respiratory disease (hepatitis virus)
 Parenteral form protects
against CAV-1
Fatal polioencephalitis of warm-
blooded See product literature for route
Rabies killed
mammals (including humans); of administration
hydrophobia
Combination vaccine: DA2PP

Definitions

 Efficacy – ability to stimulate a protective immune response

 Purity – pure culture of starting materials ie: attenuated strain, virulent strain to be inactivated later

 Potency – quantity of antigen in a vaccine

 Safety – reversion to virulence, local or systemic reactions, shedding of live vaccine organisms

 …prevents infection with… – product is able to prevent all colonization or replication of the challenge

microorganism in vaccinated and challenged animals

 …indicated for the prevention of disease… – product provides complete or partial protection from

severe clinical signs of disease in most animals.

 …indicated as an aid in the prevention of disease… – product efficacy is significantly different

between vaccines and controls, but not at the level as the statements above

Optional: p = parenteral form, IN = intranasal form

Antigen Disease Comments Preferred type
 Do not give to puppies < 6
weeks or female breeders
Measles virus – cross-protective
MV after 12 weeks Modified-live
against CDV in young puppies
 Follow-up with CDV vaccine
 Must be given IM
 Only available in combination
Canine parainfluenza virus -
with core vaccines Modified-live (p),
CPiV highly
 IN is only given once, then modified-live (IN)
contagious respiratory disease
annually if at risk
Bordetellosis is a bacterial  Erroneous SQ injection of
infection intranasal vax can cause
Bordetella Inactivated (p) OR
that results in fever, severe acute hepatic injury
bronchiseptica live (IN)
lymphadenopathy, sneezing,  Intranasal is “core” for
oculonasal discharge shelter dogs
Uncommon but highly contagious
Canine respiratory pathogen, mutation of A single initial dose will not
Killed
influenza equine influenza A subtype H3N8 immunize a seronegative dog
virus
Lyme disease – bacterial disease
that infects humans, mammals,
and
Controversial vaccine because
birds. Less than 5% of Killed whole cell
Borrelia severe nephropathy of canine
seropositive bacterin or
burgdorferi Lyme disease is
dogs show clinical signs of recombinant
immune-mediated
arthritis,
fever, lymphadenopathy,
nephropathy
Bacterial disease affecting humans
and animals. Most infections are 4-way killed whole
asymptomatic. Symptoms include cell or subunit
lethargy, anorexia, shivering, bacterin – contains
Leptospira Lepto 2-way killed bacterin is
vomiting, serovars canicola +
interrogans NOT recommended.
lumbar pain, icterus, hemorrhage icterohemorrhagiae
due + grippotyphosa +
to endothelial damage and pomona
vasculitis
Only used in melanoma
Canine oral treatment.
Oral melanoma
melanoma Not used for melanoma
prevention.
 May have some cross
Western diamondback
protecion against Eastern
rattlesnake
diamondback venom but not
Crotalus atrox vaccine – envenomation causes Toxoid
Mohave rattlesnake venom
swelling, local tissue damage,
 Dog still requires treatment
systemic bleeding and coagulation
if envenomation occurs
Infectious intestinal disease that Killed & modified
CCoV NOT recommended
causes mild diarrhea in dogs live
Giardia Protozoal disease that causes mild May reduce shedding of cysts but Not recommended
 to
ineffective in preventing infection
severe diarrhea

Typical Schedules: p = parenteral form, IN = intranasal form

Puppies DA2PP Rabies Non-core (if at risk)
< 16 weeks
 MV (single dose at 6-12 weeks)
 CPiV (p, IN)
6 weeks +  B bronchiseptica (IN)
 Influenza
 CPiV (p)
9 weeks +  B bronchiseptica (p)
 Influenza
 CPiV (p)
 B bronchiseptica (p)
12 weeks + +  B burgdorferi
 Lepto
 CPiV (p)
 B burgdorferi
15 weeks +  Lepto
 Crotalus atrox (16 weeks)
20 weeks  Crotalus atrox
12 months + +  CPiV (p)
 CPiV (p, IN)
+ (depending on vaccine and  B bronchiseptica (p, IN)
Annually Every 3 or so years state law – may be every 3  Influenza
years)  B burgdorferi
 Lepto (only if high risk)

Adults and
puppies > 16 DA2PP Rabies Non-core (if at risk)
weeks
 CPiV (p, IN)
 B bronchiseptica (p, IN)
 Influenza
Initial + +  B burgdorferi
 Lepto
 Crotalus atrox
 B bronchiseptica (p)
 Influenza
3 weeks later  B burgdorferi
 Lepto
 Crotalus atrox
 12 mos later +
 CPiV (p, IN)
+ (depending on vaccine and  B bronchiseptica (p, IN)
Annually Every 3 or so years state law – may be every 3  Influenza
years)  B burgdorferi
 Lepto (only if high risk)

Killed (inactivated) agent vaccines

 Adjuvant

 Frequently used in killed agent vaccines to enhance immune response

 Associated with local inflammatory reaction at injection site

 Slower response

 Predominantly systemic antibodies – little to no secretory IgA on mucosal surfaces

 Poor protection at mucosal surfaces of respiratory and gastrointestinal tract

 Only cell-mediated immunity - type 1 T-helper

 More stable than live or attenuated

 More likely to have hypersensitivity reaction

 Usually requires at least 2 initial doses 2-6 weeks apart (rabies is exception)

 First dose primes the immune system and second dose immunizes

Attenuated-live vaccines

 May revert to virulence

 Normal host immune response is required

Serologic Testing

 Useful for monitoring immunity to CDV, CPV-2, CAV-1, and RV

 Can be used after 16 weeks to ensure immunity

 Ensures protection in cases of previous adverse reactions to vaccine

o Is sometimes used in lieu of CDV and CPV-2 revaccination

 Cannot be used in place of rabies vaccination by law

 Virus neutralization is gold standard for CDV

 Virus neutralization and hemagglutination inhibition are gold standards for CPV

Adverse Events
 Appetite loss, pain at injection site, lethargy, reluctance to walk/run, mild fever

 May be expected for 2-3 days after vaccination – if longer, contact veterinarian

 Does not predict future risk to vaccination

 Vomiting, diarrhea, seizures, facial swelling, collapse, difficulty breathing

 Contact veterinarian immediately

 These should be reported to the Technical Services section of vaccine manufacturer(s)

 Report to the APHIS’s Center for Veterinary Biologics (CVB)

 Examples

 Injection-site reactions

o Abscess, granuloma, seroma, pain, swelling, hair loss assoc. with ischemic vasculitis

 Transient post vaccinal nonspecific illness

o lethargy, anorexia, fever, regional lymphadenopathy, soreness, abortion, encephalitis,

polyneuritis, arthritis, seizures, behavioral changes, hair loss or color change at injection

site, respiratory disease

Adverse Events (continued)

 Allergic and immune-mediated reactions

o Type 1 – acute anaphylaxis –

 Does not predict future risk to vaccination because it is usually due to

constituent proteins of the manufacturing process

 Angioedema (especially head), hives, anaphylaxis, death

o Type 2 – cytolytic – Avoid future vaccination if possible

 Immune-mediated hemolytic anemia, possibly immune-mediated

thrombocytopenia

o Type 3 – immune-complex – Avoid future vaccination if possible

 Cutaneous ischemic vasculopathy (rabies vaccine), corneal edema (‘blue-eye’)

associated with CAV-1 vaccine, immune-mediated disease

 Failure to immunize

o Puppy has enough maternally derived antibodies to block the vaccine (most common)
o Inactivation of vaccine

 Improper storage and handling

 Reusing syringes

 Cleansing skin with alcohol before injection can also inactivate vaccines

o The dog is a poor or nonresponder (immune system doesn’t recognized as an antigen)

 Tumorigenesis - Vaccine-associated sarcoma or other tumors

 Multisystemic infectious/inflammatory disorder of young Weimaraner dogs

o May be genetically linked to immunodeficiency and autoimmune disorders

o Ie: Hypothyroidism, Hypertrophic osteodystrophy

 Vaccine-induced immunosuppression

o Assoc. w/ 1st or 2nd dose of combo MLV vaccines containing CDV and CAV-1 or CAV-2

o Begins 3 days after vaccination and persists for 7-10 days

 Reactions caused by incorrect administration of vaccine

o Fatalities reported after SQ administration of avirulent-live B bronchiseptica bacterin

(intended for intranasal administration)

o Intravenous vaccine administration

 Reactions associated with residual virulence of attenuated vaccine

o Postvaccinal sneezing associated with intranasal attenuated vaccine

o Such as B bronchiseptica and parainfluenza virus

 Vaccine-induced interference with diagnostic tests

o False-positive PCR test results for parvovirus antigen in feces

o Not an adverse reaction

 Reversion of vaccine virus to a virulent pathogen

o Generally rare when used as licensed

o More of a problem when used unlicensed with wild or exotic animals

Pearls: Vaccines are intended for healthy, non-pregnant dogs

 Avoid vaccination of pregnant dogs to avoid potential injury to the fetus.

 Avoid vaccination of dogs receiving immunosuppressive or cytotoxic therapy.

 Glucocorticoid treatment – short-term should not have a significant suppressive effect on antibody
production, but it is a good idea to revaccinate 2-3 weeks after long-term therapy has ended.

 Do not give vaccinations more often than every 2 weeks, even if different vaccines.

 Do not vaccinate colostrum-derived puppies earlier than 4 weeks – may cause heart and CNS damage.

 Artificial colostrum can be given if puppy is less than 3 days old

 Serum (3-10 ml) from a well-immunized adult dog can be given SQ or intraperitoneally

to a puppy twice daily for 3 days