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DC22 Flashcards

1
Q

What are some clinical effects of hyperkalaemia?

A
  1. depression/ obtudation
  2. Muscle weakness
  3. Slow conduction (bradycardia)
  4. ECG changes
  5. Reduced cardiac contractility
  6. Hypotension
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2
Q

What are some drug options for managing hyperkalaemia?

A
  1. Calcium gluconate
  2. Dextrose +/- insulin
  3. Sodium Bicarbonate (reduces EC H+)
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3
Q

What are some general causes of incontinence?

A
  • Neurologic
  • Storage dysfunction
  • Urethral disorders
  • Anatomic
  • Retention
  • Mix of all of these
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4
Q

What is the common signalment for urethral sphincter mechanism incontinence? What are some risk factors?

A

Female, middle age to older, medium-large breed
Risk factors: Neutering, conformational characteristics (eg. bladder neck position), obesity, large to medium breed, early tail docking

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5
Q

What are some possible side effects of administering sodium bicarbonate as a tx for high K?

A

Hypernatraemia
hyperosmolality
Acute CV collapse if given as a rapid bolus
Paradoxical intracellular and CSF acidosis

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6
Q

What are some possible causes of FLUTD?

A 
Idiopathic FLUTD**
Bladder stones (uroliths)
Urethral obstruction (M>F, stone, plug)
UTI
Congenital or acquired urinary abnormalities (rare, young)
Urinary tract trauma
Urinary cancer
Nerve/ spinal disorders
Combos of all of the above
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7
Q

What are potential causes of iFLUTD?

A 
Viral/ bacterial infections
Autoimmune
Leaky internal bladder lining
Urinary toxins
Stress
Mast cell mediated inflammation
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8
Q

What are common causative organisms of prostatitis?

A

E.coli, Staph and Strep

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9
Q

What medical treatments options are available for USMI?

A
  1. Alpha agonists (phenylpropanolamine)

2. Oestrogens (oestriol)

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10
Q

What are some risk factors for FLUTD?

A

Basically anything that causes stress (eg. indoor confinement, change in routine, litter tray changes); obesity, dry food diets

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11
Q

What are some typical urinalysis findings in a cat with FLUTD?

A

Well concentrated urine, red cells, acidic

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12
Q

What tx options are available for FLUTD?

A

Symptomatic treatment only. Usually self resolving.

  • Analgesia (eg. buprenorphine, tramadol, fentanyl)
  • Phenoxybenzamine (SM relaxant)
  • Dantrium/ prazosin (skeletal muscle relaxants)
  • Feliway
  • Anti-anxiety meds
  • good hydration
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13
Q

What are the tx options for benign prostatic hyperplasia?

A
  • Castration**
  • Delmadione acetate/ finasteride (blocks local test pdn)
  • progestins (suppress LH and test. pdn) 3-8 weeks
  • GnRH analogues
  • Manage constipation
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14
Q

What are some causes of complicated UTIs?

A

Resistant organisms, mixed infection, wrond drug/ dose/ duration/ absorption/ compliance

  • Immune deficiencies
  • urinary incontinence, incomplete voiding, obstruction, catheters
  • Glucosuria, high urine pH
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15
Q

What is subclinical bacteruria? In what animals is it most common?

A

Positive urine culture but no clinical urinary disease. Most often Enterococcus
Dogs: cushings, DM, obesity, immunosupp, spinal cord disease
Cats: CKD, HyperT, DM

*No Tx req’d

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16
Q

What is the most common cause of urinary incontinence in dogs?

A

Urethral sphincter mechanism incompetence

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17
Q

What are some treatment options for bladder neoplasia?

A 
Surgery (if no mets and if margins obtainable)
Urinary stents (or cystotomy tube)
Radiation
Piroxicam (or other NSAIDs)
Chemo (mitoxantrone)
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18
Q

What is the most common renal neoplasia in cats and dogs?

A

Cats: lymphoma
Dogs: adenocarcinoma
Young dogs: nephroblastoma

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19
Q

What are some treatment options for renal neoplasia?

A
  1. Uteronephrectomy (when unilateral and not metastatic)
  2. Chemotherapy (for lymphoma)
  3. surgical excision (nephroblastoma)
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20
Q

What are some ddx for urinary incontinence?

separate into large and small bladder

A

Large bladder:
1. Neurological (LMN, UMN, detrusor urethral dyssynergia, dysautonomia)
2. Non-neuro (Geriatric, iatrogenic, PU/PD)
3. calculi, plugs, infl, urethral spasm, prostatic disease, neoplasia
Small Bladder:
1. USMI
2. Detrusor hyperreflexia/ instability
3. congenital abnormalities (ectopic ureters, vaginal strictures, pelvic bladder, pseudohermaphroditism)

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21
Q

Where do lesions occur that lead to a LMN or UMN bladder?

A

LMN= S1-S3/ sacral plexus lesion

UMN L4 or higher

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22
Q

In which animals is detrusor urethral dyssynergia most commonly seen?

A

Large breed male dogs

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23
Q

What is Detrusor hyperreflexia/ instability?

A

Involuntary bladder contractions resulting in the frequent voiding of small volumes of urine.
Unable to control urination due to strong urge to urinate due to inflammation of the bladder or urethra, and resultant pollakiuria, dysuria-stranguria,

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24
Q

What drugs can be used for the following:

a) increase bladder contraction
b) reduce bladder contraction
c) increase urethral tone
d) reduce urethral tone

A

a) increase bladder contraction= parasympathomometic (bethanechol); prokinetic (metaclopromide)
b) reduce bladder contraction= parasympatholytics (propantheline, oxybutynin)

c) increase urethral tone
alpha adrenergic (phenylpropanolamine); hormone replacement

d) reduce urethral tone= alpha-sympatholytics (phenoxybenzamine, prazosin); striated skeletal muscle relaxants (diazepam, dantrolene)

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25
Q

In which dog breeds are ectopic ureters most common? What are tx options?

A

newfoundlands, GRs, labs, and westies

  1. cystoscopic guided laser ablation (intramural)
  2. surgery (intramural -> neoureterostomy; extramural-> ureteroneocystotomy)
  3. tx secondary infections
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26
Q

What methods are available for a renal biopsy?

What area do you aim for?

A

Blind percutaneous needle bx
US guided needle
Laparoscopic guided needle bx
open needle biopsy

Glomeruli. Avoid medulla due to large vasculature

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27
Q

What are some indications for a ureteronephrectomy? How about for a ureteral surgery?

A
  1. Trauma to kidney, renal vessels or ureters
  2. Persistent pyelonephritis
  3. Persistent obstruction with hydronephrosis
  4. Renal- perirenal masses
  5. Organ harvest for transplantation
  6. Ureteroliths
  7. Ectopic ureters
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28
Q

What are some ways in which you can determine which cat is inappropriately eliminating in a multicat household?

A
  1. confinement
  2. video
  3. Flurescein caps (0.5ml of a 10% solt orally or 6 strips in a capsule
    Clue: problem cats don’t cover
  4. Compare characteristics (i.e for house soiling, large volume, horizontal surfaces, one or few area, sometimes faeces)
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29
Q

What are general litter preferences for cats?

A

Small particle size (sandy)
Unscented litter
Clumping
Carpet

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30
Q

How prevalent is urine spraying? What are some ddx?What are some broad tx options?

A

25% of cats in single cat households
close to 100% in households with 10 or more cats

House soiling, medical disease, separation anxiety

Tx: Surgery, behavioural mod, environmental mod, pheromones, pharmacological therapy

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31
Q

What are some behavioural/ environmental modifications that can be made to manage urine spraying?

A
  1. Eliminate outside cats (scarecrow, mothballs, prevent visual access to windows, indoor only cat)
  2. Ensure predictable environment/ consistent schedule
  3. Provide environmental enrichment (puzzle feeder, water fountain, owner interaction, interactive toys)
  4. Create core areas/ increase vertical living areas
  5. Address litter box factors
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32
Q

What are pharmacological treatment options available to manage urine spraying? Which are preferred?**

A
  1. Anxiolytics
    a) Benzodiazepines. eg. diazepam
    b) Azapirones. eg. buspirone
    c) TCAs. eg. clomipramine
    d) SSRIs. eg. Fluoxetine**
  2. Antiandrogenic
    a) Progestins (historically). eg. megestrol acetate, medroxyprogesterone
    b) Cyproheptadine
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33
Q

How does feline synthetic facial pheromone work?

A

Induces cheek gland marking preferably to urine spraying/marking. Is an anxiolytic, appetite stimulant and may lower aggression.

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34
Q

What are surgical options for the management of ureteroliths?

A
  1. Re-implantation***
  2. Ureterotomy
  3. Double pigtail catheter
  4. subcutaneous ureteral bypass systems
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35
Q

How does the muscle types differ in the urethra between males and females?

A

Males: Distal 2/3 are striated muscle (ext urethral sphincter)
Females: Striated muscle in distal 1/3 (OHE increases collagen and decreases muscle)

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36
Q

What are some principles of bladder closure?

A
  • Use absorbable monofilament
  • Try not to penetrate lumen
  • Engage submucosa
  • Simple continuous
  • Don’t need ABs unless infection present of >90 mins
  • Full thickness defects regain 100% strength in 2-3 weeks
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37
Q

On the urine pH scale, where do different urine crystals fall?

A

Acidic: urates, cystine
Acidic-Neutral: calcium oxalate, silicate
Alkaline: struvite (usually associated with UTI)

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38
Q

What are some surgical tx options for UMSI and how do they work?

A

Increase functional length
- colposuspension, urethrocystopexy/ Urethropexy

Advance bladder neck into abdo pressure zone (as above)

Increase static resistace via reduction in urethral diameter

  • submucosal injections
  • artifical urethral sphincters

Restoration of structural support (TVT-O?)

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39
Q

What are abnormal drinking values for dogs and cats?

A

Dogs > 90-100

Cats >10 if eating moist food (>50 if eating dry food)

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40
Q

What is the normal water intake for dogs and cats?

A

40-60ml/kg.day

(greyhounds drink 100-600mls. day)

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41
Q

In what age group in DM most often seen in dogs and cats?

A

Middle-aged to senior

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42
Q

What are some indicators for hyperadrenocorticism in dogs?

A
  • 6 years or older
  • Increased appetite
  • Loss of muscle
  • Potbelly
  • Thin hair coat
  • Prominent skin vessels
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43
Q

What are some indicators for hyperthyroidism in cats?

A
  • Older than 10 years old
  • Increased appetite
  • Weight loss
  • Increased activity, vocalisation or aggression
  • V+ and/ or D+
  • Tachycardia and/ or gallop rhythm
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44
Q

What is glucose toxicity?

A

Glucose toxicity is defined as a decrease in insulin secretion and increase in insulin resistance due to chronic hyperglycaemia. Over time, toxic effects of hyperglycaemia on beta-cells of the pancreas are irreversible.

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45
Q

What may cause insulin resistance?

A

Insulin resistance may be caused by a number of factors, including obesity, other endocrinopathies (e.g. acromegaly), drugs (e.g. steroids) or pancreatitis.

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46
Q

What is the renal threshold for glucose in dogs and cats?

A

Dogs, >10-12 mmol/L

Cats >15-16mmol/L

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47
Q

Why may cataracts develop with diabetes mellitus?

A

They occur secondary to the accumulation of sorbitol in the lens. Sorbitol= sugar that can’t diffuse from lens. It is osmotically active- draws water and splits lens fibres

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48
Q

What are some ddx for dogs and cats presenting with PU/PD and PP?

A 
Dogs:
-Drugs (phenobarb, pred)
-HyperA
-SARDS
-Acromegaly
-Hepatic encephalopathy
Cats:
-HyperT
-Acromegaly
-Drug induced
-Hepatopathy
-HyperA
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49
Q

What are some ddx for dogs and cats presenting with hyperglycaemia or glucosuria?

A 
Hyperglycaemia:
-drugs (GCs, Progestagens, medetomidine)
Disorders associated with insulin antagonism (hyperA, dioestrus, acromegaly)
-stress/anxiety/shock
• pheochromocytoma
• sepsis
• pancreatitis
• diabetes mellitus
• DKA
• hyperosmolar hyperglycaemic syndrome
Glucosuria:
-Renal tubular disease
-Fanconi syndrome
-Laboratory interference
-Stress
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50
Q

DM Remission is less likely if the cat has peripheral neuropathy or has been treated for DM > 6 months. T or F?

A

True

51
Q

What factors make cats more likely to achieve DM remission?

A
  1. Medication that antagonises insulin was present in last 6 months and has been discontinued
  2. Excellent glycaemic control in achieved in< 6 months
  3. Required insulin dose to achieve tight control is low

Note: Approximately ¾ of cats that achieve remission continue to have an impaired glucose tolerance with approximately 19% having elevated fasting blood glucose

52
Q

What are some consequences of poor diabetic control in dogs and cats?

A

Dogs:

  1. Cataracts, blindness and anterior uveitis
  2. Chronic pancreatitis
  3. Recurrent infections
  4. Hypoglycaemia
  5. Ketoacidosis

Cats:

  1. Peripheral neuropathy
  2. Weight loss and poor grooming
  3. Hypoglycaemia
  4. Recurrent ketosis or DKA
  5. Hyperglycaemic hyperosmolar syndrome
53
Q

What is the Somogyi effect?

A

Rebound hyperglycaemia following a hypoglycaemic event or a rapid decrease in glucose

54
Q

What are some reasons for no obvious nadir?

A
  1. The patient is too stressed
  2. Insulin dose has been missed
  3. Marked underdosing of insulin
  4. Somogyi overswing
  5. Disease causing insulin resistance
  6. Anti-insulin antibodies
55
Q

What are some clinical signs of acromegaly?

A
  1. Respiratory stridor
  2. Dental spacing
  3. Prognathia inferior
  4. Broad facial features
  5. Lameness
  6. Clubbed feet
  7. Organomegaly
  8. Neurological signs (cats)
56
Q

What is phenoxybenzamine?

A

Treatment for phaechromocytoma

57
Q

What are the three ketones produced by the body?

A

acetone, acetoacetate and beta

hydroxybutyrate (β-HB)

58
Q

What is normal osmolality for dogs and cats?

A

Normal osmolality for dogs and cats is ~ 310 mOsm/kg

59
Q

How does hyperA affect other endocrine systems?

A
  1. reduces circulating T4/T3/fT4/TSH so dx of hypoT becomes difficult
  2. CSs result in increased calciuresis which causes increased release of PTH ->secondary hyperparathyroidism
  3. Reduces GH secretion (GCs stimulate somatostatin)
  4. Stress of DM can influence endocrine tests and make hyperA dx more difficult
60
Q

What are some tx options for a dog that has PDH hyperA and AT hyperA?

A 
PDH: 
-Trilostane
-(Mitotane)
- Hypophysectomy
AT:
-Adrenalectomy
-Trilostane
-(Mitotane)
61
Q

What is trilostane? What are some side effects? What are some CIs?

A

Competitive inhibitor of enzyme in cortisol production pathway. Treatment option for hyperA.

Side effects:

  • GI adverse side effects
  • Hyperkalaemia
  • Hypoadrenocorticism (adrenal necrosis)
  • Adrenal necrosis
  • Nelson’s phenomenon (neuro signs)

CIs:
Avoid if possible, in animals with hepatopathy or pre-existing renal disease.
Use with caution in patients also treated with ACE-inhibitors

62
Q

What is the prognosis for PDH and AT with trilostane and surgery?

A

PDH trilostane: 662-900d
AT trilostane: 353d
AT surgery 2-4 years

63
Q

What are some signs and causes of hypercalcaemia?

A

Signs:

  • PUPD
  • Muscle weakness
  • GIT signs
  • Cardiac arrhythmias
  • Seizures
Causes (HARDIONS):
Hyperparathyroidism
Addisons
Renal disease
Vitamin D excess
Infectious/ idiopathic
Osteolysis
Neoplasia
Spurious
64
Q

How is calcium divided in the body?

A

Ionised (50%)
Protein-bound (40%)
Chelated (10%)

65
Q

What is desmopressin?

A

=a synthetic vasopressin (AVP, ADH) analogue with antidiuretic properties
(but without the vasoconstrictive properties of vasopressin)

66
Q

What is the most common signalment for primary hyperparathyroidism?

How to diagnose it?

A

Middle aged to older dogs and cats

Keeshonds predisposed (often singular adenoma)

Marked hypercalcaemia, hypophosphateaemia, parathyroid nodule found on US, PTH elevation

67
Q

What are the most common causes of hypercalcaemia of malignancy?

A

Dogs:

  • Lymphoma
  • Apocrine gland adenocarcinoma

Cats:

  • Squamous cell carcinoma
  • Lymphoma
68
Q

What is the tx for hypercalcaemia of malignancy?

A
  1. tx underlying cause
  2. Fluid (w/o Ca)
  3. Diuretics
  4. Pred (promote excretion)
  5. Sodium bicarb (treats acidosis and shifts calcium to chelated)

If chronic, treat with bisphosphonates (impedes osteoclasts)

69
Q

What are Bence Jones proteins?

A

Abnormal proteins which are seen in (canine) multiple myeloma or
possibly globulins associated with FIP in cats.

70
Q

What are some factors affecting urolith formation?

A
  1. Supersat if urine
  2. +/- presence of an organic nidus
  3. Reduced solubility (urine pH)
  4. Presence of crystalization inhibitors or promoters
  5. Retention of crystals within urinary tract
71
Q

What are the 5 different forms of dysphagia?

A

1) Oral dysphagia: difficult prehension and bolus formation. May chew on one side, excessive head movement etc.
2) Pharyngeal dysphagia: Normal prehension, repeated swallow attempts with flexion / extension of neck.
3) Cricopharyngeal dysphagia: inadequate relaxation of the cricopharyngeal muscle (achalasia), or failure of synchronization between pharyngeal contraction and cricopharyngeal relaxation (asynchrony) during swallowing. Repeated / exaggerated attempts to swallow, gagging, cough, immediate regurgitation with swallowing
4) Oesophageal dysphagia: difficulty passing a bolus through the oesophageal body. Regurgitation.
5) Gastroesophageal dysphagia: difficulty passing a bolus through the caudal oesophageal sphincter

72
Q

What are some common causes of dysphagia?

A

1) Obstructive lesions (eg. FB, neoplasia, abscess, criciopharyngeal achlasia)
2) Pain (eg. tooth root abscess, stomatitis, FIV)
3) Neuro disorders (eg. rabies, CNS disease)
4) Neuromuscular disorders (eg. myasthenia gravis, polyradiculitis)
5) Endocrine (eg. hypoT)

73
Q

What are some primary signs of orbital disease? What are some ddx?

A

Exopthalmos, enopthalmos, strabismus

Ddx:
If acute, painful and unilateral: FB, orbital abscess/ cellulitis/ necrotic tumour
If acute, painful and bilateral: masticatory myositis
If chronic: neoplasia or zygomatic salivary mucocoele

74
Q

What is masticatory muscle myositis? In which animals is it found? What are the CSs and how may it be treated?

A

=focal autoimmune myositis. Type II M myofibers of mastication

Young large dog breeds

Acutely-> swelling, pain, limited opening and increased [Cr]. Chronically-> atrophy and limited opening

To diagnose look for Abs against type II M myofibers. Treat with immunosuppressives (pred +/- cyclosporin/ azathioprine)

75
Q

What is thyrotoxic cardiomyopathy?

A

HyperT-> increased cardiac output, HT, and ventriculr eccentric hypertrophy. Tachycardia, systolic murmur and gallop result= reversible with treatment

76
Q

When treating hyperthyroid cats with radioactive iodine, how long do they stay in hospital?

A

Until radiation reduces to less than 20uSv/hr

77
Q

What are some side effects to medical therapy for feline hyperT?

A
  1. GI- anorexia, V+, D+
  2. Facial pruritus and excoriation
  3. BM suppression, IMHA, coag
  4. Liver
  5. Hypothyroidism (iatrogenic)
  6. Other (eg. mG)
78
Q

When might you suspect a thyroid carcinoma?

A

Large or multiple thyroid mass
TT4>250 nmol/L
No response to medical or other txtherapy (or only at high doses
Find mets

79
Q

At what age does training start in greyhounds? At what age does racing start and finish?

A

12-14 months

18-48 months of age

80
Q

What are some odd drug idiosyncrasies in greyhounds?

A
  1. Cortisone-> PU/PD and catabolism
  2. Progestogens-> PU/PD, poor form and catabolism
  3. Slow recovery from barbiturate anaesthesia
  4. Morphine-> restlessness, distress and vocalisation
81
Q

What are some options for oestrus postponement in racing greyhounds?

A
  1. Hard training (-> neg feedback-> GNRH pdn decreases)
  2. Androgenic hormones (testosterone proprionate, ethyloestrenol)
  3. Progestogens
  4. GNRH agonists (deslorelin. Needs to be given when prog> 15nmol/L)
  5. GnRH anatgonists (acyine. Compete with endogenous GnRH)
82
Q

What is cancer cachexia?

A

Loss of weight due to host vs tumour competition which favours anaerobic metabolism and causes altered insulin responsiveness. More common in cats

83
Q

In what cases should you suspect hypoA?

A
  1. Sick patient has no stress leukogram
  2. Sick adult with high normal lymphocyte count
  3. Sick patient with low or low normal glucose
  4. Azotaemic patients with other suggestive changes
  5. Inapproppriate bradycardia
  6. Eosinphilia in a sick patient
  7. Vague illness
84
Q

In what age/ sex GH is post racing dysuria most common? What are the different stages? How do you treat?

A

Young nervous excitable male dogs. Related to stressful situations due to high cortisone levels increases bladder symp tone. Tx= alpha adrenergic blockers, diazepam, Hyoscine butylbromide, reduce stress, ABs, +/- catheterise

Stage 1= 2-48hrs post race. Delayed 10-30 secs
Stage 2= delayed >30 secs. Very thin stream
Stage 3: unable to urinate. Bladder distended

85
Q

Where is pain most prominent in canine exertional rhabdomyolysis? What is the aetiology of the condition? How is it treated?

A

TL muscles, quads and triceps

Tissue hypoxia due to dehydration and muscle cramping

Tx: IVF, sedation, analgesia, ABs (?), Oxygen and rest

86
Q

How can you manage muscle cramping in GHs?

A

Modify training regime and diet. Can give quinine bisulphate 4 hours before exercise (not before a race though)

87
Q

What are some broad ddx for FUO?

A 
Infectious
Immune-mediated
Inflammatory non-infectious
Neoplasia
Tissue trauma
Miscellaneous
88
Q

Lymphocytosis is a relatively common (~33%) finding with hypoA. What are other potential causes?

A
  • Reactive lymphocytosis (<18months old)

- Chronic lymphocytic leukaemia

89
Q

What treatment is available for hypoT?

A

Levothyroxine (monitor TT4 4-6 hrs after am dose 3-4 weeks into therapy)

90
Q

The crossed extensor reflex is indicative of lesions at what level?

A

T3-L3

91
Q

What is chondroid metaplasia?

A

A type of intervertebral disk disease in which there is dehydration of the nucleus pulposus-> hard/ calcification-> pushes dorsally-> disk extrusion

92
Q

What is fibroid metaplasia? in which dogs is it seen?

A

A type of intervertebral disk disease in which there is thickening and hardening of nucleus and annulus-> disk protrusion. NP is changed into fibrocartilage. Seen in older large breed dogs

93
Q

What disc spaces are most commonly affected by disk extrusion?

A

T11 to S1 (75% bw T12 and L2)

**C2 to T1 in Beagles

94
Q

How do you treat tetanus toxicity in dogs?

A

Supportive care (analgesia, diazepam/midazolam, minimise external stimuli)
Metronidazole
Anti-toxin
Debride wound

95
Q

What are three types of ataxia?

A
  1. Cerebellar ataxia: fairly recognisable. Consequence of a cerebellar
    (or cerebellar peduncles) lesion
  2. vestibular ataxia which is also easy to recognise and is a consequence of a lesion
    anywhere in the vestibular system;
  3. Spinal ataxia also called proprioceptive ataxia which is the consequence of a lesion
    anywhere along the course of the proprioceptive pathways; in the spinal cord, in the brainstem and in the forebrain.
96
Q

What is Schiff-Sherrington syndrome?

A

Hyperextension of thoracic limbs. It occurs in cases of

severe T3‐L3 spinal cord compression or intramedullary lesions

97
Q

How do you grade disk extrusion?

A

Grade 1= back pain
Grade 2= ambulatory ataxia and/or paresis
Grade 3= non-ambulatory ataxia and/or paresis
Grade 4= paralysis (loss of voluntary motor function)
Grade 5= loss of pain sensation

98
Q

What surgical management techniques are available for intervertebral disk disease?

A
  1. Hemilaminectomy (best for type 1, TL disks)
    Mini-hemilaminectomy
    Pediculectomy
  2. Ventral slot (for cervical disks)
  3. Fenestration
  4. Dorsal laminectomy (good for spinal cord tumours)
  5. Lateral corpectomy (best for type 2 disks)
99
Q

What is caudal cervical malformation syndrome and how can it be diagnosed? What are some clinical signs? How may it be treated?

A

= Wobbler syndrome
Dx via MRI*, CT or myelo using traction views
CSs: Suprascapular muscle atrophy, “two engine gait”
Tx: Medical (poor), surgical (distraction fusion/ ventral slot)-> domino effect

100
Q

What is the time frame for neurogenic vs disuse atrophy?

A

Neurogenic happens with 4-8 days, disuse happens within 4-8 weeks

101
Q

What are some general signs of forebrain syndrome?

A
  • Seizures
  • Central blindness
  • Decreased mental state
  • Gait (circling; pacing; head pressing; minimal PC deficits though)
  • (Abnormal behaviour)
102
Q

What is the Cushing’s reflex? What is the Cushing’s triad?

A

Brain lesion-> increased intracranial pressure-> increased systemic BP (to increase cerebral blood flow)-> if baroreflex works, decrease HR

  1. Brain signs (shallow breathing)
  2. High BP
  3. Low HR
103
Q

What is iohexol? What is gadolinium?

A

=iodinated contrast agent used for CT (absorbs more x-rays and appears white)

=paramagnetic contrast agent used for MRI (alters local magnetic field)

104
Q

What are the three main causes of seizures?

A

Brain lesions
Idiopathic/ familial
Metabolic

105
Q

What is the therapeutic range for phenobarbitone?

A

60-180 umol/L (test at 4 weeks)

106
Q

What proprioceptive, spinal and cranial nerve changes might you see with a severe forebrain lesion?

A
  • postural reactions may be decreased or absent contralateral to the lesion
  • spinal reflexes are not altered
  • may see uni or bilateral anosmia, absent/ decreased menace response, absent/decreased dazzle reflex
  • decreased/ absent sensation contralaterally
107
Q

What are some examples of intra-axial and extra-axial brain lesions?

A

Intra-axial:

  • glioma
  • lymphoma
  • neurocytoma
  • neuroepithelial tumour
  • abscess/ granuloma/ necrosis/ haematoma

Extra-axial:

  • meningioma
  • pituitary tumour
  • choroid plexus tumour
  • ependymoma
  • bone tumour
  • abscess
  • subdural haematoma
108
Q

What is the difference between the three different types of cerebral oedema?

A
  1. Vasogenic=most common. Tracts along white matter. Occurs with tumours/ necrosis. Increased permeability of the vascular endothelium (diffuse vasc injury)
  2. Cytotoxic= ischaemia-> failure of ATP Na pumps-> Na accumulation and water accumulation in cells. Hypoxic injury and hepatic encephalopathy.
  3. Periventricular: increased ventricular pressure-> CSF seeps through ependyma into adjacent brain parenchyma. occurs with obstructive hydrocephalus
109
Q

What are the four phases of a seizure?

A
  1. Pre-ictal (prodromal)= anxiety
  2. Aura= first electrical activity
  3. Ictus= the seizure
  4. Post ictal= cerebral exhaustion
110
Q

What is the difference between a cluster of seizures and status epilepticus?

A 
Cluster= 2 seizures or more/ day
SE= 2 seizure w/i 30 mins w/o recovery OR 1 seizure >5 mins duration

(isolated= one seizure or less/day)

111
Q

What is the best option to treat atrial fibrillation?

A

Digoxin combined with diltiazem (aim to reduce vent rate to <150 in dogs)

112
Q

What are some causes of excess vagal tone?

A
  • chronic resp disease
  • GI disease
  • HypoT
  • ocular or retrobulbar disease
  • CNS disease (incr. inra-cranial pressure)
113
Q

What are some metabolic disorders which may cause syncope? How about some cardiac disorders?

A

Met: hypoG, Addisons, acute hypoxaemia, toxins/ drugs
Cardiac: heartworm, cardiomyopathy, neoplasia, pulmonary HT…

114
Q

With regards to arrhythmias, what are some disorders of impulse formation? Provide examples. Which is most common?

What are some disorders of impulse conduction?

A
  1. Enhanced normal automaticity (SVT)
  2. Depressed normal automaticity (high vagal tone, hyperK, sick sinus syndrome)
  3. Abnormal automaticity** (premature ectopic beats)
  4. Block/ delays in conduction system (AV blocks)
  5. Re-entry (A-fib)
115
Q

How do you treat dogs and cats with acute VT?

A

Cats: First rule out hypoK, then esmolol or propanolol

Dogs: lignocaine. If refractory, procainamide, magnesium, B-blocker

Aim for >85% reduction in VPCs

116
Q

What is vasovagal syncope?

A

=neurally mediated syncope in Boxers-> arterial vasodilation in face or relative or absolute bradycardia. Usually outgrown

117
Q

How do you interpret an atropine response test?

A

Give atropine. ECG 10-15 mins later. if HR increases by 100% or>140= vagal. If p increases but not QRS= not vagal. If no change in P= atrial standstill

118
Q

What are some sequelae of aortic stenosis? How do you diagnose it?

A

Coronary arteriosclerosis
Myocardial ischaemia/ fibrosis
Malignant arrhythmias

Dx: CSs (exertional syncope and sudden death), Radiography (LV enlargement and post stenotic dilation), echo, angiography

119
Q

What are the four components of a tetralogy of Fallot?

A
  1. High VSD
  2. Pulmonic stenosis
  3. Overriding aorta
  4. RV hypertrophy
120
Q

What are some common clinical signs of separation anxiety in dogs?

A
  1. destructive
  2. house soiling
  3. anorexia
  4. salivation/ vomiting
  5. vocalisation
121
Q

What are some behaviour modification techniques for dealing with separation anxiety?

A

a) have a routine
b) short departures may be tolerated
c) calm behaviour/ resilience- always reward quietly
d) “Look-sit-stay” relaxation program training
e) redirect knowledge seeking behaviour
f) counter conditioning= change emotional response of dog to a particular stimulus

(decoupling departure cues does not work)

122
Q

What are some negative consequences of using punishment as a behaviour mod technique?

A
  1. increases anxiety
  2. impedes learning
  3. damages human bond
  4. does not teach the desired behaviour
  5. welfare concerns
  6. difficult to perform properly
  7. must be effective after 2-3 attempts (if not= abuse)
123
Q

What is the difference between fear and a phobia?

A 
fear= normal response to threatening stimulus. Protective
Phobia= a maladaptive fear response that is out of proportion (and context) to the stimulus/ threat

DVM3 (13 decks)

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