Top 20 Canine Flashcards
Canine
Diabetes mellitus
CS? Dx? Supportive? Tx/Management? Meds to avoid?
Classic CS
* PU/PD/PP + weight loss
Diagnosis
* persistent hyperglycemia (>300 mg/dL)
* glucosuria +/- ketonuria
* fructosamine - estimates BG over last 2 weeks, can help r/o stress hyperglycemia
Supportive
* Often have elevated liver enzymes and cholesterol too
Treatment
* BID insulin - intermediate or long-actin insulin (vetsulin, NPH, etc.) if stable - monitor with BG curve at first if you can
* Dietary management - high fiber, low calorie
* +/- Oral hypoglycemics - may decrease insulin requirements & resistance – Glipizide (glucotrol) - efficacy controversial although the MC used
Avoid corticosteroids - can contribute to insulin resistance
– Even though diabetes can have an immune component - don’t give immunosuppressants
canine
why use high fiber, low calorie diet in diabetics? Diet to avoid?
High fiber: delays glucose absorption in GI, can increase sensitivity to insulin
Low calorie/exercise: increase insulin sensitivity
Avoid high fat - pancreatitis can be underlying cause of diabetes
Diabetic ketoacidosis
CS? Dx? Tx?
CS
* Anorexia, vomiting, weakness
Dx
* Severe metabolic acidosis, BG >500 mg/dL, ketonuria
Tx
* Short-acting insulin (regular) q6-8 or CRI until ketosis resolves
Frequent BG monitoring - want it to decline gradually
* Aggressive IV fluids with K and P supplementation as needed
* Correct acidosis (bicarb if low and fluids not working for acidosis)
Canine
HypERadrenocorticism
CS? Types? Dx? Rule out/screening? Supportive? Tx?
aka Cushings, HypERcortisolism
CS
* PU/PD/PP/Panting
* Pendulous abdomen, truncal alopecia
* Pyoderma
* Thin skin
* Hyper pigmentation
* Seborrhea
* Calcinosis cutis
Types
* MC Pituitary-dependant (PDH) - tumor in pituitary secretes ACTH
* Adrenal tumors (AT) that secrete cortisol
* Iatrogenic steroids w/o adequate weaning period
Dx
* LDDST - highest sensitivity, MC used
* ACTH stim - best for iatrogenic an used for monitoring therapeutic response (prevent iatrogenic Addisons)
* HDDST - rarely used, can DDx between PDH and ADH in hard cases
Screening/Supportive/Rule-outs
* normal ALP = unlikely to have Cushings
* supportive = elevated ALP, hypERcholesterolemia, stress leukogram, USG hyposthenuric (<1.010) +/- proteinuria
* rule OUT = normal urine cortsiol:creatinine
Tx
* PDH - trilostane, mitotane, Sx (risky), or radiation
* ADH - trilostane, mitotane, Sx (risky)
* Iatrogenic - slow taper with ACTH stim monitoring
what is trilostane? mitotane?
Trilostane - inhibits enzymes needed for cortisol production
Mitotane (Lysodren) - adrenocortical lysis
LDDST test for Cushings
Measure baseline cortisol
Give IV dexamethasone (0.01 mg/kg)
8 hour cortisol level >1.4 ug/dL = likely Cushings
4 hour cortisol level <50% baseline or <1.4 = likely PDH
Canine
Collapsing trachea
predisposed? types? causes? CS? Tx?
Predisposed
* older small breed dogs, especially obese
Types
* Intrathoracic - collapse on expiration
* Extrathoracic (neck) - collapse on inspiration
Can be primary or secondary due to cardiopulmonary disorders
Clinical signs
* Expiratory distress, honking cough on palpation/excitement +/- a retch at the end of cough
* exercise intolerance, cyanosis if severe
Diagnosis
* eliciting a coughing spasm on tracheal palpation
* rads (hard for dynamic collapse sometimes) - ENd expiratory for INtrathoracic collapse
* Fluoroscopy
* endoscopy
Treatment
* May need sedation to break cough cycle in acute episodes
* Medical - 70% respond = Weight loss, Anxiolytics, Bronchodilators (theophylline, terbutaline), Cough suppressants (hydrocodone), Short course corticosteroids
* Surgical - if medical doesn’t work enough, not all that successful = Dorsal tracheal membrane plication, Intratracheal stent, External tracheal support
canine
IMHA
predisposed? path? CS? Dx? Tx?
Cocker spaniels predisposed
CS
* Lethargy
* pallor
* fever
* icterus, bilirubin/hemoglobinuria
Dx
* saline slide agglutination test (blood clumps)
* Coombs test - looks for antibodies against RBCs
* Blood smear - spherocytosis
* CBC - normocytic normochromic regenerative anemia
* Rads - screen for neoplasia
Tx
* immunosuppression (corticosteroids or immunomodulators like cyclosporine or azathioprine), blood products as needed
* Prevent thromboembolism - aspirin, LMW heparin, clopidogrel
canine
IVDD
CS? MC location? Types? Dx? Tx? Prognosis?
MC location
* Usually T3-L3 = UMN hindlimbs
CS
* Pain in neck/back (arched back or head down
* paraparesis
* paraplegia
* ataxia
- Hansen’s Type I Disc herniation chondrodystrophic breeds such as Dachshunds, corgis, Shi-tzu
- Acute, painful, emergency
- Nucleus pulposus extrudes through the annulus
Hansen’s Type 2 disc herniation
* non-chondrodystrophic breeds
* usually Chronic, nonpainful, nonemergency
* Annulus hypertrophies or bulges
Dx
* CT(safest, best quality)
* MRI (fastest)
* Myelogram (invasive, chance of seizures during recovery)
Tx
* Conservative = NSAIDs, strict cage rest 8 weeks (50% will improve) - only use if NO neurologic signs (ie, pain only)
* Surgical = decompression via hemilaminectomy (thoracic) or ventral slot (cervical) - used in nonresponsive to medical or has true neuro signs or if the owner wants
Prognosis
* Ambulatory = excellent
* Nonambulatory = guarded w/o Sx, excellent w/ Sx
* Nonambulatory + deep pain negative = 50% chance of regaining function only ig Sx done within 24h
canine
heart failure
CS? Dx? Acute tx? Chronic tx?
CS
* Exercise intolerance
* Cough
* Abdominal distension
* +/- heart murmur, arrhythmia
* Harsh lung sounds/crackles
* If LHF → pulmonary edema
* If RHF → ascites, pleural effusion
Dx
* Rads = cardiomegaly (>3.5 intercostal spaces, dorsal tracheal deviation) enlarged pulmonary veins, alveolar-interstitial lung pattern in caudodorsal lung field
* Echo = LA +/- LV enlargement, +/- poor contractility, valvular insufficiency, RA/RV dilation
Acute tx
* Oxygen
* furosemide (loop diuretic)
* nitrates - (nitroprusside, nitroglycerin for venodilation (both do this) + arteriodilation (prusside only)
* Mild sedation if needed
Chronic management
* Na-restricted diets - Decreases preload
* ACE inhibitors (enalapril) - Decreases preload, reduces afterload by prevention AT2 (a vasoconstrictor)
* Diuretics (furosemide) - Decreases preload
* Pimobendan - Positive inotrope, improves systolic function
canine
Heartworm disease
Life cycle, CS, pathology, Dx, Tx, Prognosis, Prevention, DDx
**Dirofilaria immitis life cycle and pathology
**
* Depend on mosquitoes for life cycle
* Transmitted as L3 larvae through mosquito bites → take 6 months for microfilariae to release into blood and thus diagnosis
* Might carry Wolbachia bacT which is intracellular and used for HW survival
* Adults live in pulmonary artery and RV - can stay for 3-5y
* RVH → pulmonary hypertension
Clinical signs
* Exercise intolerance
* cough
* abdominal distension
* weight loss
* poor body condition
Diagnosis
Antigen SNAP test
* detects female adult worms starting @5 months post-infection
* False negatives possible (complex formation, no females, light load)
Microfilaria tests - always do this due to potential for false negatives on snap
* ID on smear
* Modified Knotts
* Filter test
TXR
* RV hypertrophy (reverse D)
* prominent/dilated pulmonary Aa
* +/- pulmonary parenchymal dz
Echo
* pulmonary A dilation
* RH dilation
* visible worms in pulmonary A
* caval syndrome - HW in RA/RV
Supportive
* Proteinuria
* Eosinophilia
Treatment
Macrocyclic lactones (preventatives = ivermectin, milbemycin)
* give for 2 months (2 doses) prior to adulticide
* Pre-tx with diphenhydramine and corticosteroids if microfilaria positive
* Prevents new infections + eliminates susceptible larvae and microfilaria
Doxycycline
* give for 30d prior adulticide
* Treats Wolbachia → makes worms more susceptible to adulticide
Corticosteroids
* for 1-2 months prior to adulticide if symptomatic or are microfiliaria positive to control CS of pulmonary thromboembolism
* tapering anti-inflammatory dose
Immiticide/adulticide = Melarsomine (IM)
* kills 98% adult worms
* 1st injection → wait 4-6 weeks → 2nd injection → wait 24 hours → 3rd injection
* Risk of thromboembolic dz = strict rest during this tx and 6-8 weeks after
Sx for caval syndrome
Prognosis
* Good-guarded
* Poor-grave if caval syndrome
Prevention
* monthly low dose PO ivermectin or milbemycin, topical selamectin or moxidectin/imidacloprid
DDx
* Acanthocheilonema reconditum - not pathogenic - looks similar on smear
canine
pyometra
MC etiology/Pathology? CS? Dx? Tx? Prognosis?
Etiology & Pathology
* MC etiology = E. coli
* MC occurs from hormonal imbalance during diestrus 3-4 weeks post-estrus - P4 dominance promotes endometrial growth, myometrial activity, and inhibits leukocyte infection response
* In dogs >8y, Cystic endometrial hyperplasia MC cause, which is due to repeat exposure to P4 in intact females → thickening of the endometrium and hypertrophy of glands
Clinical signs
* Mucopurulent or hemorrhagic vaginal discharge
* enlarged teats
* PU/PD
* V/d
* Abdominal pain
* Large, palpable uterus
Diagnosis
* AXR - fluid-filled loops in caudal abdomen
* Vaginal cytology - degenerate neutrophils +/- phagocytized bacteria
* AUS - enlarged fluid-filled uterus
Treatment
* Stabilize - IVF, abx, analgesics
* SURGERY (OHE)
* If owner refuses → prostaglandins to increase myometrial contractions, breed next cycle - recommend referral
Prognosis
* good to guarded
canine
flea allergy dermatitis
MC age/season? CS? Dx? Tx?
MC in warm seasons and >6mo old
CS
* acute onset pruritis
* caudodorsal alopecia
Dx
* Finding fleas or flea dirt
* Up to 15% do not have evidence of fleas → 3 month flea tx trial
Tx
* Acute - tapering corticosteroids + flea adulticide
* Chronic - monthly adulticide, oral month development inhibitors (lufenuron), environmental control
canine
Hip dysplasia
Pathology? CS? Dx? Tx? Prevention?
Path
* instability of 1 or more hip joints
* Hip joint instability often → DJD/OA, coxofemoral luxation (MC in craniodorsal direction)
Clinical signs
* Bunny-hopping gait, difficulty rising
* Juvenile - positive ortolani sign (indicates joint laxity = feel a clunk when manipulating the femur = coxofemoral subluxation)
Diagnosis
* Rads = shallow acetabulum, flattened femoral head, <50% femoral head coverage by acetabular rim, thickened femoral neck
* special rads include OFA (must be 2yo, more subjective) and Penn Hip (based on distraction index, more accurate at younger age, ideally done at 1yo). DI <0.3 is best
Treatment
* Medical/conservative: NSAIDs, weight management, neutraceuticals, light low-impact exercise - up to 80% improvement
* Juveline Pelvic symphysiodesis - encourages acetabular coverage/growth. Can only be done 14-20w old
* Triple pelvic osteotomy - gives more acetbular coverage, only done in <1yo with minimal changes/laxity and with already good acetabulums
* Femoral head and neck ostectomy - best used when <30lbs, well muscled, and good BW. Often results in mechanical (but non-painful) lameness
Prevention
* good BW
* breed based on PennHIP/OFA
canine
Osteochondritis dissecans
predisposed? path? CS? Dx? Tx? Prevention?
Pathology
* Abnormal cartilage development → separation from underlying bone
Clinical signs
* Acute lameness, joint effusion, decreased ROM
Diagnosis
* Rads or CT- effusion, widened joint space on one side, flattening of subchondral bone, joint mice
Treatment
* Medical - NSAIDs, nutraceuticals
* Surgical debridement
Prevention
* good dog food for breed, avoid excess Ca and vitamin D
MC young large breeds
canine
panosteitis
predisposed? CS? Dx? Tx? Prognosis?
MC in GSDs 5-18mo
CS
* Pain in long bones, lameness for weeks-months at a time
Dx
* Rads = patchy increased opacity (trabecular pattern) and periosteal new bone
Tx
* Pain control, rest
Prognosis
* Likely to recur many times until 2yo but, prognosis excellent and likely to self-resolve after that
canine
Hypertrophic osteodystrophy (HOD)
Predisposed? CS? Dx? Tx? Prognosis? Causes?
Weimaraners predisposed, often littermates, but large rapidly growing dogs in general are common
CS
* MC affects distal metaphysis of the forelimbs but can be all long bones
* swelling/pain in distal limb, metaphyseal pain + fever +/- recent hx of vaccination
Dx
* Rads = metaphyseal flaring, “double physeal line” in areas of bony proliferation, abnormal radiolucent lines within metaphysis
Tx
* rest, pain medication, time, +/- steroids
Prognosis
* Usually self limiting but often recurs while growing
Exact cause unknown
* Vaccine?
* Ca/P imbalance?
* Vitamin C deficiency?
* Distemper?
canine
Legg-Calve-Perthes disease
predisposed? CS? Path? Dx? Tx? Prognosis
= avascular necrosis of the femoral head
Predisposed = Young, small-breed dogs prior to closure of capital femoral physis 3mo-1y
CS = hindlimb lameness
Path = Disruption of bloodflow → collapse or fragmentation of femoral epiphysis
Dx
* Rads = shortened femoral neck, osteochondrosis, muscle atrophy, loss of bone opacity at femoral epiphysis, moth-eaten appearance of femoral head/neck
Tx = FHO (femoral head/neck ostectomy) or total hip replacement, analgesia
Prognosis = good-excellent with Sx
canine
ethylene glycol toxicity
Path? CS? Dx? Tx? Prognosis?
antifreeze - tastes sweet to dogs
Pathology and CS
metabolized into alcohol dehydrogenase, glycolic acid, and oxalic acid
Stage 1 = neurologic phase - 30min-12h
* ataxia, acting drunk, stupor? Coma?, anorexia, vomiting, PU/PD
Stage 2 = cardiovascular phase - 12-24h
* Hard to recognize alone
* CS: tachypnea, tachycardia
Stage 3 = 12-72h
* Oliguric renal failure!
Diagnosis
Urinalysis
* Calcium oxalate monohydrate crystalluria as early as 6h
* isosthenuria as renal failure develops
Blood gas
* high AG metabolic acidosis
* elevated osmolar gap (>20)
Chemistry
* HypOcalcemia, HypERphosphatemia
* hypERglycemia
* azotemia
EG test can dected 30min-12h - false positives possible
Treament
In general, tx most effective if done in <8-12h
Decontamination
* emesis, activate charcoal id within 2h
Fomepizole - prevents toxic metabolic conversion (must give early)
4-MP - inhibits alcohol dehydrogenase
20% ethanol - inhibits alcohol dehydrogenase
Symptomatic - GI protectants, IV fluids, diuretics if oliguric
If 8+h → consider hemodialysis, peritoneal dialysis
Prognosis
* good to fair if therapy started within 4-8h
* guarded if azotemic, grave if oliguria/anuria
* If 8-12+h → guarded-grace prognosis - consider dialysis
canine
parvovirus
etiology? transmission? path? CS? Dx? Tx?
Etiology
* CPV-2 = nonenveloped, single-stranded DNA virus
Transmission: fecal-oral, fomites
Path
* Destroys cells in intestinal crypts (villous atrophy/blunting), lymphopoietic tissue, bone marrow
CS = fever, lethargy, anorexia, vomiting, diarrhea
Dx
* CBC: leukopenia, neutropenia
* Confirm with fecal ELISA; False positives 5-15d post-vaccine; false negatives if too early
* Chem = hypOalbuminemia, hypOglycemia, hypOkalemia, prerenal azotemia
Tx = Supportive care
* IVF +/- KCl, dextrose, colloids
* Broad spectrum IV antibiotics
* Antiemetics
* Gastroprotectants
* Slow enteral or parenteral feeding as tolerated
predisposed to intussussceptions too
canine
GDV
Predisposed? CS? Path? Dx? Tx? Prognosis?
deep-chested large breeds predisposed
Clinical signs
* Non-productive vomiting/retching
* abdominal distension
* Restlessness, nervous pacing
* painful, Increased respiratory rate
* +/- Signs of shock/cardiovascular collapse - tachycardia, weak pulses, pale mucous membranes, prolonged CRT, depression/coma
* Death if do not decompress quickly
Pathology
* Stomach rotates counterclockwise (when viewing cranial-caudal in dorsal recumbency)
* Stomach volvulus → venous compression, congestion, poor perfusion → necrosis
* May also tear short gastric vessels that connect the stomach and spleen
* Air accumulation in stomach → impedes on venous return through vena cava and heart → hypovolemic shock
* May result in global tissue ischemia and SIRS
* Inflammatory mediators and myocardial ischemia may lead to arrhythmias
Diagnosis
* stabilize 1st if you suspect (can be pinged!)
* right lateral abdominal radiograph - smurf hat/popeye arm/double bubble - displaced, gas-filled pylorus
* ECG - arrhythmias common, especially VPCs after surgery
* Blood gas - metabolic lactic acidosis +/- respiratory compensation +/- hypercapnia (gastric distension may impair ventilation)
* Often hemoconcentrated +/- DIC changes
Treatment
Most patients are shocky on presentation and need aggressive resuscitation, supportive care, and monitoring
* Place cephalic catheter(s) - large bore (saphenous has poor caudal venous return)
* Shock dose crystalloid fluids (80-90 mL/kg) - deliver in quarter doses until resuscitated
Decompress the stomach
* Orogastric tube: more effective emptying but requires heavy sedation, tube might be hard to pass, and may cause esophageal trauma/rupture
* Trocarization: more rapid intervention, no sedation required, but limiting decompression is achieved, risk of lacerating gastric wall or puncturing spleen – Do it at the maximum point of tympany – you don’t know if the spleen is on the left or right
Surgical emergency after stabilization
* Need decompression and de-rotation w/ gastropexy + Resect any necrotic tissue – Will see omentum covering the stomach when you enter the abdomen
* +/- splenectomy
Prognosis
* 15-30% mortality
* 75-85% live with Sx and appropriate post-op care
Negative prognosticators
* lactate > 6 mmol/L
* need for resection or splenectomy
* 5+ hours since onset of CS
* recumbent on presentation
Recurrence <4% with pexy, and 50% without
Prevention
* prophylactic gastropexy
canine
HypOthyroidism
Sig? CS? Dx? Tx? Prognosis?
MC in older, large breed dogs
CS
* Weight gain
* dermatopathies
* lethargy, bradycardia
* decreased appetite
* possible neuromuscular signs
* cold intolerance
* myxedema
Dx
* Free T4 by equilibrium dialysis - confirmatory and rules out euthyroid sick
* Total T4 low-normal
* TSH - low-normal
* TSH stimulation test, trial therapy
Supportive Dx
* CBC - mild nonregenerative anemia
* Chem - hypERcholesterolemia, hypERtriglyceridemia, lipemia
Tx
* lifelong oral levothyroxine (synthetic T4) w/ periodic monitoring of thyroid levels
* IV T4 for myxedema coma
Prognosis = good with continued management and therapies
Beware false diagnosis - euthyroid sick syndrome
canine
cataracts
CS? Dx/Types? Tx?
CS = Cloudy white pupil, decreased vision
Dx/types
* Incomplete = partially opacified, lens defect, can see tapetal reflection through it, animal can still see some through it
* Complete = completely opacified lens defect, cannot see tapetal reflection through it, animal cannot see through it
* Incipient cataract = focal cataract
* Resorbing cataract = lens protein degradation
* Also do a BG and UA (diabetes), ERG
Tx
* Phacoemulsification or other
* Potential to develop secondary uveitis = refer early for best results
canine
cherry eye
What is it? Predisposed? CS? Tx?
Prolapse of the 3rd eyelid - congenital
English bulldogs, beagles, Shih tzu, cocker spaniels predisposed
CS/Dx = Smooth, moist pink-red mass at medial canthus
Tx = Morgan pocket or Kaswan anchoring (replace the 3rd eyelid gland)
* If remove gland instead → high risk of KCS = not recommended
Consider not breeding these animals!
canine
uveitis
causes? Path? CS? Dx? Tx? Sequelae?
Causes
* bacterial, fungal, viral, rickettsial, immune-mediates, neoplasia, hypertension, trauma
* 50% idiopathic
Path/sequelae
* if Chronic - inflammatory mediators in anterior chamber → destroy cornea and lens proteins → corneal scarring, cataracts, glaucoma if debri plugs iridocorneal angle
CS
* Conjunctival hyperemia
* photophobia
* blepharospasm
* aqueous flare
* iris color change
* +/- miotic pupils
Dx
* Tonometry - IOP <10 mmHg
* Possibly greater if secondary to glaucoma
* Systemic workup for underlying cause
Tx
* Topical steroids or NSAIDs - reduce inflammation - but NOT if secondary to ulcer or infection
* Topical atropine - relieve ciliary spasm, reduce posterior synechiae development
* May worsen secondary glaucoma if they have it
* Tx underlying cause
canine
glaucoma
Path? CS? Dx? Tx?
Path
* Primary = inherited, often iridocorneal angle breakdown
* decreased outflow of aqueous humor → increased IOP
* Glaucoma in 1 eye → other likely to develop in 6-12 months (often inherited)
CS
* Buphthalmos, blue eye
* visual impairment
* tortuous episcleral vessels
Dx
* Tonometry - IOP >30
* Gonioscopy - visualize iridocorneal angle
* Ocular U/S
Tx
Goal = increase outflow, decrease aqueous production
Carbonic anhydrase inhibitors - decrease aqueous production
* oral methazolamide
* topical dorzolamide/ acetazolamide)
Prostaglandin analogues
* topical latanoprost
Acute = CAIs, B-antagonists or blockers, steroids
Chronic: prostaglandins, enucleation
Treat both eyes in predisposed breeds
canine
pancreatitis
risk factors? predilections? CS? Dx? Tx? Prognosis?
Risk factors
* obesity
* fatty meals
* systemic inflammation, trauma, ischemia
* endocrine dz (cushings, diabetes)
* drugs (azathioprine, l-asparaginase, tetracycline)
Mini schnauzers over-represented
Clinical signs
MC acute GI signs
* v/d, anorexia
* cranial abdominal pain
* “praying position”
If severe, necrotizing
* hypovolemia
* fever
* tachycardia
* jaundice
* SIRS
Diagnosis
cPLI (pancreatic lipase immunoreactivity) SNAP
U/S
* hypOechoic pancreas (edema)
* +/- mottling, enlargement with hypERechoic mesentery (focal peritonitis)
Chem - hyperlipemia (4-5x)
Treatment
* Acute
Fasting, post-duodenal feeding, ultra low-fat diet
Hospitalization, IV fluids
Analgesia
H2 blockers, antiemetics
+/- Abx
+/- plasma, heparin
Chronic
* Low fat, highly digestible diet
* Prognosis depends on presence of complications - acidosis, MOF, DIC, acidosis, peritonitis, etc.
canine
Kennel cough
Et? CS? Dx? Tx? Prognosis?
Canine infectious respiratory disease complex (CIRD)
Multiple etiologies
Viruses
* Canine parainfluenza (CPIV)
* canine influenza
* canine adenovirus 2 (CAV-2)
* +/- canine distemper (CDV)
Bacteria
* Bordetella bronchiseptica
* Mycoplasma
Clinical signs
* Exposure to other animals followed by acute onset non-productive cough that may end with a retch
Diagnosis
* B. bronchiseptica - PCR or culture from nasal or oropharyngeal swabs, TTW, or BAL
* TXR - may see pneumonia
Treatment
Cough suppressants - hydrocodone, butorphanol
For bronchopneumonia
* Antibiotics
* Nebulization with saline +/- abx (gentamicin)
* Fluid therapy
* +/- O2 therapy
Vaccination may reduce infection rate and severity
* Modified live CPIV/CAV-2/CDV combo
* Bordetella/CPIV combo
Prognosis - likely to resolve in 7-10 days if no secondary bronchopneumonia
canine
megaesophagus
causes? predisposed? CS? Dx? Tx? Prognosis?
Causes
* myasthenia gravis
* vascular ring anomaly
* endocrinopathies - Addisons, hypOthyroidism
* esophagitis
* lead toxicity
* myopathies
* neuropathies
* idiopathic
* Ketamine and xylazine can cause temporary
Congenitally predisposed - may see spontaaneous resolvement!
* GSDs
* mini schnauzers
* fox terriers
Clinical signs
* Regurgitation
* coughing, drooling
* weight loss, weakness
* +/- signs of pneumonia (fever, cough)
Diagnosis
Rads (ventral tracheal deviation), swallow study - air-dilated esophagus, +/- aspiration pneumonia (cranial alveolar)
Dx underlying conditions
* AChR antibody test for myasthenia gravis
* ACTH stim for Addisons
* FT4 for hypothyroid
* Lead level
* EMG/nerve conduction for polymyopathy/ polyneuropathy
Treatment
Diet: high calorie, soft
* fed in upright position and stay there 10-15 minutes after eating
* small, frequent meals are best
Prokinetics to aid gastric emptying and reduce reflux
* cisapride
Acid reducers to decrease acid reflux
* PPIs (pantoprazole, omeprazole)
* H2 blockers (famotidine, ranitidine)
Tx underlying condition
Tx aspiration pneumonia
Prognosis: Most will eventually die of aspiration pneumonia :(
canine
osteosarcoma
predeliction? sites? behavior? CS? Dx? Tx? Prognosis?
MC primary bone tumor in dogs
MC in large dogs overall
Bimodal age distribution, <2y and >7y
Location
MC appendicular, but sometimes axial in small dogs
* Mandible, maxilla, scapula, ribs, spine, pelvis
* Mandible better prognosis (70% survive 1y with sx)
* Other locations similar prognosis to appendicular
Appendicular MC
* MC in metaphyseal region of appendicular skeleton
* “Away from the elbow towards the knee” = distal radius, proximal humerus, distal femur, proximal tibia
Behavior
Locally aggressive and highly metastatic
* Metastasis MC to lungs, but also lnn
Clinical signs
Chronic or acute lameness
Diagnosis
Biopsy of bony lesion = gold standard (risk pathologic fx)
Rads
* Lytic (“moth eaten”) lesion in metaphyseal area that does not cross joints, periosteal new bone formation
* If in diaphysis → think its metastatic from another cancer
* TXR - very poor prognosis if metastasis present
FNA - warn about pathologic fracture
Bone Scan or NS - to look for bone metastasis
CT for axial, Sx planning, radiation planning
Chem - elevated ALP = worse prognosis
Treatment
Limb amputation (stage 1st!)
* Considered palliative - 90% of dogs will still develop metastasis
Limb-sparing surgery
* Ostectomy + prosthetic
* High complication rate
Chemotherapy
* can extend MST to 10-12 months
* Cisplatin or carboplatin +/- doxorubicin (adriamycin)
Radiation - palliative only
* Can improve pain for 2-3 months in 75% of cases
* Makes pathologic fractures more likely
Osteoclast inhibitors (bisphosphonates) can improve pain if Sx not an option
Prognosis
* Overall survival 4-12 months
* Amputation alone = 4-6mo
* Sx + chemo = 10-12mo
* If metastasis present = 1-3mo
* Most develop mets despite tx later
* ALP elevation = worse prognosis
canine
mast cell tumor
predisposed? Path/CS/Behavior? Dx? Tx? Prognosis?
Predisposed: boxers, pugs, boston terriers, other brachycephalics (Often develop many over their lifetime, but usually are low or intermediate grade with little metastasis)
Pathology/CS/Behavior
Mast cell granules release histamine and heparin (also proteases, cytokines) when they degranulate
* May cause v/d/melena
Can cause GI ulcers, bleeding, poor wound healing, anaphylactoid rxns (hypotension, vasodilation, collapse, etc.)
A great pretender – can look and feel like almost anything
* Cutaneous or subcutaneous mass
* +/- pruritus
* May shrink/swell intermittently
More aggressive at mucocutaneous junctions, prepuce, scrotum, muzzle, digits, pinna
Diagnosis
FNA: single round nucleus (may stain light due to granules taking up so much stain) w/ dark purple cytoplasmic granules
* number of mitotic figures per hpf correlates with how aggressive the tumor behaves
Cannot determine grade via cytology - need biopsy
- Biopsy: if FNA is nondiagnostic and for grading - Patnaik system
- Required to determine grade - technically can only grade cutaneous canine MCTs
- Higher grade = more metastatic
FNA or biopsy of regional draining lnn
AUS and TXR
* If aggressive with high risk of metastasis Eval abdominal lnn, liver, spleen, and thoracic lnn
Buffy coat analysis or bone marrow aspirate – rarely indicated, often have a low yield
Stage the tumor
* Local lnn aspirates
* Abdominal and thoracic imaging
* Bloodwork
* Higher stage = worse prognosis
Treatment
surgical excision with wide margins (2-3cm lateral margins and one fascial plane deep)
* TOC if metastasis not already present
Radiation tx as adjuvant if adequate margins cannot be obtained
Chemotherapy
* vinblastine, lomustine, CCNU, other alkylating agents
* Tyrosine kinase inhibitors = Toceranib (Palladia) - only FDA approved chemo drug for vets
Supportive care
* H1 blockers - diphenhydramine
* H2 blockers - famotidine, cimetidine, ranitidine
* H blockers help reduce histamine release by mast cells (would cause increased gastric acid secretion predisposing to GI ulcers and GI bleeding)
* Glucocorticoids (prednisone) - Cytotoxic to mast cells, stabilizes mast cell membranes, and reduces inflammation associated w/ the tumor
Prognosis
* mostly depends on grade; only MCTs arising from the skin are graded
#1 MC dermal malignancy in dogs
canine
lymphoma
CS? Dx? Tx? Prognosis?
Clinical signs
* Generalized lymphadenopathy
* v/d/weight loss
* Dyspnea
Treatment
* Cytology - mostly large lymphocytes/lymphoblasts (much bigger than neutrophils)
* Biopsy for grading and definitive dx
* Staging - txr, aus
* CBC - pancytopenias + lymphocytosis
* Chem - hypERcalcemia
* Bone marrow aspirate
* Flow cytometry or IHC for B vs T cell
Treatment
Prednisone - can decrease response to future chemo
Chemotherapy (CHOP)- doxorubicin, cyclophosphamide, vincristine, L-asparaginase, lomustine
* Many achieve remission
Prognosis for B cell»_space; T cell
canine
Predisposed? Et? Tx?
struvite
Usually induced by a UTI/cystitis with urease positive microbes such as Staph or Proteus
Treatment
* abx for UTI using C/S
* +/- cystotomy
Dietary dissolution can work - reduce crystal components
* low Mg, low P, low protein diet (Hills s/d or w/d)
canine
Predisposed? Path? Tx?
calcium oxalate dihydrate
Predisposed - Schnauzers, Lhasa apso, yorkies, bichon frise, shih tzu, and mini poodles are predisposed
Pathology
* Most likely to occur in acidic urine
* May occur due to hypERcalcemia (check Ca levels!)
Treatment
* Most difficult and least likely to dissolve
* MC need Sx, voiding hydropulsion, or lithotripsy
* alkalinize the urine w/ diet & low protein to prevent recurrence (Hills u/d or RC Urinary SO)
canine
Predisposed? Dx? Tx?
Cystine
Predisposed: Bulldogs, newfoundland, dachshunds, basset hounds, chihuahuas, yorkies predisposed - may have genetic defect
Dx: UA - Cannot be seed on rads
Treatment
Dietary management
* Hills u/d - Reduced protein (methionine),Reduced Na
Alkalinize the diet
* Potassium citrate > sodium bicarbonate
* Thiola (2 -mercaptopropionyl-glycine aka 2-MPG): binds cystine and forms a more soluble compound
Keep on this diet for 1mo → then switch to low purine to prevent recurrence
canine
predisposed/causes? Tx?
Urate
Dalmations are predisposed to urate uroliths due to a metabolic defect – they cannot convert uric acid to allantoin
If other breeds make urate stones → think about a portosystemic shunt
Diagnosis - UA only, cannot be seen on radiographs
Treatment
Dietary management
* Reduce protein (low purine), no soy - low purines can cause cardiomyopathy over time?
* Alkalizing diet - potassium citrate or sodium bicarbonate
Allopurinol: decreases uric acid by inhibiting hypoxanthine → xanthine → uric acid
* must reduce protein in the diet or can lead to xanthine stone formation
