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Flashcards in Dogs and Cats 26 Deck (102)
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1
Q

Medical therapy for feline hyperthryoidism what are the pros - EXAM

A
○ Effective and rapid in most cases
○ Generally safe
○ Avoids hospitalisation
○ Readily available
○ Inexpensive in short term
○ Reversible, adjustable
○ Co-morbid disease setting (20% of cases)
○ Short term control setting (prior to definitive Rx)
○ Available, practical
2
Q

Medical therapy for feline hyperthryoidism what are the cons - EXAM

A
  • Not curative, ongoing Rx required - ONCE STOP WITH START AGAIN
  • Small % poor responders -> will need higher doses overtime
  • Does not halt the underlying disease
  • Less cost effective long term
  • Titration can be challenging
  • Need for good compliance, ongoing daily tableting
  • Drug side effects
3
Q

Drug side effects of medical therapy for feline hyperthryoidism what are they

A

○ GI – common, anorexia, V, D, usually mild and self-limiting, give with food, stop if persists OR transdermal
○ Facial pruritus & excoriation – Stop Rx
○ (Rare) BM suppression, IMHA, coagulopathy – Stop Rx
○ Liver (ddx other hepatopathy) – Stop Rx
○ Iatrogenic hypothyroidism (15-37%)
○ Other – lymphadenopathy, myasthenia gravis
○ Client contact allergies (gel, non-coated tablets) - WEAR GLOVES

4
Q

In terms of feline hyperthyroidism what are the 2 main options and how to adjusty

A

1) Carbimazole SR 10 mg SID PO (Vidalta, MSD) - most common
○ Don’t crush tablet
- Increase PO methimazole 2.5 mg/day until euthyroid
○ Reduce by 2.5mg/day if low TT4
○ May later be able to go to SID
○ If total dose > 10mg/day need to question compliance
○ Consider with food, or transdermal if GI side effects
○ Stop medical therapy if skin, BM or liver toxicity
2) Methimazole 2.5 mg BID PO (Felimazole, Dechra)
- From 10 days, no change > 5mg

5
Q

Feline hyperthyroidism medical therapy how to monitor and what looking for afterwards

A

How do I monitor therapy?
- 2-3 weeks after dose change or adjustment
- 3 months then as required
What to look for after any Rx
- Has the hyperthyroidism resolved
○ TT4
○ Weight, clinical signs
- Is there concurrent renal disease?
○ Urea, creat, alb, electrolytes, P, Ca, PCV, Urinalysis, +/- UPC, BP, SDMA
- Has iatrogenic hypothyroidism developed?
○ CBC, cholesterol, TT4, (+/- TSH, fT4, T3)
§ Anaemic?, TT4 low?

6
Q

Feline hyperparathyroidism how to judge adequacy of therapy, what else checking, which lives longer between that and other therapies

A

How do I judge the adequacy of therapy?
- The TT4 needs to be in the LOWER HALF of the reference range for adequate control
What else should I be checking?
- Monitor blood pressure at diagnosis and during/after treatment
○ 13% of 303 untreated hyperthyroid cats were found to be hypertensive at initial diagnosis
○ 23% of initially normotensive hyperthyroid cats BECAME hypertensive following medical and/or surgical therapy of hyperthyroidism
Who lives longer?
- Radioiodine MST 4 years
- Methimazole MST 2 years - medical therapy

7
Q

Thyroidectomy as a treatment for feline hyperthyroidism what needs to be done first, what effective against but negatives

A
  • Medical stabilise first
  • Effective / cure
    ○ Most bilateral
    ○ No requirement for radiation / facilities / isolation
    ○ Available
  • Negatives
    ○ GA, surgery (pain)
    ○ Requires experience
    ○ Ectopic thyroid tissue common and cannot remove
    ○ Medium up-front costs
    ○ High risk of post-operative complications
    § hypothyroidism / hypoparathyroidism) – failure in 1 in 3 cases, 4-(20%) complications
    § 2% mortality rate, 6% risk of hypoparathyroidism
    ○ Unilateral OR Bilateral? (can’t treat ectopic tissue)
    ○ Pre-treatment required
8
Q

Dietary therapy as a treatment for feline hyperthyroidism what need to feed, what does it have and how effective

A
  • Iodine Limited Diet
  • Must be fed exclusively
    ○ Variable efficacy
    ○ As effective in outdoor cats
  • Recently available
  • Low protein and low phosphate
    ○ Associated with lower serum [creatinine], possible option CKD cases - NOT CHRONIC
    ○ Palatability can be a factor, monitor BW, muscle mass
    ○ Not recommend for lean cats, DM, DM remission
  • Need greater numbers / long term research
9
Q

Dietary therapy for treatment of feline hyperthryoidism pros

A
  • No pilling!
  • No Sx, GA, special facilities/training or isolation
  • Available
  • No carbimazole / methimazole side effects
  • Reversible
  • Cat and client friendly
  • Low initial costs
    Potential diet for IRIS stage 1-3 CKD
10
Q

Dietary therapy for treatment of feline hyperthryoidism cons

A
  • Not a cure
  • Compliance - BIG ISSUE
  • Time to euthyroidism (stable renal state) - takes longer than radioiodine and medical therapy
  • Not for cats that eat other food sources
  • Iodine levels
11
Q

Dietary therapy for treatment of feline hyperthryoidism what are the unknowns and would you use it

A

the unknowns
- Long term effects?
○ On Hyperthyroid and Normal cats
○ Goitre?
○ Immune deficiency? Cancer? Infection?
○ Causing Hyperthyrodisism?
- Wash out times prior to scintigraphy? - at least a week, could be up to a month
- Long term survival times?
- Studies on transition from y/d to medical therapy?
- Long term effects on thyroid pathology?
- Malignant transformation?
would I use it?
- Maybe if I-131 or medical therapy not possible
- Maybe if need short term option needed before do more definitive therapy

12
Q

Does unmasking CKD by treating hyperthryoidism affect prognosis and what to do once diagnosed

A

NO - hyperthyroid state is DAMAGING THE KIDNEYS
- Unmasking CKD by obtaining euthyroidism does not worsen prognosis! - It is better as can now treat the kidney disease
- As long as you avoid iatrogenic hypothyroidism
I have just diagnosed CKD and hyperthyroidism
- Expect with treatment of hyperthyroidism, patient to progress one IRIS stage within 1 month, but then not very progressive if maintain euthyroidism - generally quite stable
○ (and avoid hypothyroidism!)
- Mild stable renal disease should not affect the advice to clients - STAY WITH THE SAME DOSE OF HYPERTHRYOID TREATMENT
- Can still treat with I-131 once stable - radioiodine
○ Scintigraphy, low dose I-131, start L-thyroxine at discharge
§ Associated with minimal worsening azotemia (due unmasking hyperthyroidism effect on kidney) and not due to hypothyroidism when managed this way

13
Q

Do you need to do a treatment trial for hyperthyroidism before a definitive therapy

A

NO unless
- To establish underlying renal status?
○ Only if you have advanced renal disease (IRIS stage 3-4)
- Perhaps if you suspect other concurrent disease
Tendency is do to I-131 earlier now

14
Q

When treating feline hyperthyroidism do you need to worry about iatrogenic hypothryoidism

A
  • Iatrogenic hypothyroidism can develop after medical, surgical or radioiodine therapy
    ○ Diagnosed by low TT4 and high cTSH
  • 5 – 30% of cases
  • Transient or permanent
  • Clinical signs are uncommon
  • Usually transient and generally not a problem in non-azotaemic cats
  • Iatrogenic hypothyroidism and CKD have shorter surival (MST 456 days vs MST 905 days
15
Q

When to suspect carcinoma causes feline hypothyroidism - IMPORTANT

A
  • Large of multiple thyroid mass - more than 2 cm in size
  • High TT4 > 250 nmol/L, 5x10 fold increase
  • No response to medical therapy
  • Only respond with very high doses
  • Long term medication > 2 years
  • No response to bilateral thyroidectomy
  • No response to standard radio-iodine
  • Find metastasis
16
Q

Cachexia what is it, diagnosis and treatment

A
  • Cachexia ≠ Starvation
    ○ Inflammation is a consistent feature
    » ↑ Acute phase proteins, ↑ excessive production of pro-inflammatory cytokines
    ○ Rise in resting energy expenditure
    » Altered protein, fat and carbohydrate metabolism
    » Insulin resistant state may develop
  • Diagnosis : PE + chronic inflammatory disease
  • Not a specific diagnosis. State of disordered metabolism
  • Rx: Underlying disorder
    ○ Hypercaloric feeding
17
Q

Cancer cachexia how common, most common cancer, what occurs and treatment

A
  • More common people & cats > dogs
    ○ Most common to cause is lymphoma
  • Negative impact on survival
  • Host vs. tumour competition - tumour generally winning
    ○ Favours anaerobic metabolism
    ○ Altered cytokine profiles
    ○ ↑[lactate]
    ○ Altered insulin responsiveness - intake reduces and don’t get energy needed out of food
  • Treat underlying tumour, consider iatrogenic contributors (drugs), appetite stimulants, control nausea / vomiting,
  • Diet: high fat (n-3 fatty acids) (hills N/D), low carbohydrates
18
Q

Hypoadrenocorticism what also called and signalment

A
(addisons disease) 
Signalment
- Female > Male Dogs
○ Poodles, westies 
- Young – middle aged (4-5 years)
- Rare in cats
19
Q

Hypoadrenocorticism what are the 4 main causes, what is deficient and what occurs

A

1) Primary (most common)
○ Usually glucocorticoid and mineralocorticoid deficient
○ Immune mediated adrenal cortex destruction
○ Occasionally glucocorticoid only deficient early = atypical, only zon fasciculata and reticularis affected, may later progress to typical
2) Secondary (rare)
○ Inadequate ACTH production due to abnormality within the brain (adrenal gland normal)
§ EG - sudden cessation of long term glucocorticoids (rare takes a while to produce as cells atrophy), brain tumours, brain trauma, congenital pituitary defects
§ Only glucocorticoid deficient
3) Atypical
○ Only glucocorticoid deficient
4) Iatrogenic
○ Some cases of HAC (cushings) treated with mitotane/trilostane
○ May be reversible

20
Q

Hypoadrenocortcism history and physical exam what seen with glucocorticoid deficiency

A
History
- Acute, gradual, wax and wane, chronic intermittent progressive signs
- Signs often triggered by stressful event / illness
- Vague
Physical Exam
Glucocorticoid deficiency
- Anorexia
- Vomiting
- Regurgitation (megaoesophagus) 
- Lethargy / depression
- Weakness
- Weight loss
- Diarrhoea, Tremor
- Pu / Pd
- Abdominal pain
- (Melena)
- (Hypoglycaemia / seizures) - rare
21
Q

Hypoadrenocorticism what seen with mineralcorticoid deficiency

A
  • More severe
    • Pu / Pd
    • Shock : Hypotensive / hypovolaemia
    • Weak pulses
    • Prolonged CRT
    • Collapse
    • Dehydration
    • Bradycardia
    • Hypothermia
22
Q

Hypoadrenocorticism clinical pathology findings

A

on-regenerative normocytic normochromic anaemia - DUE TO CHRONIC DISEASE
○ Or dehydration and polycythaemia
- Normal to increase WCC (INAPPROPRAITE RESPONSE)
○ Eosinophilia (20-30% cases) - BIG CLUE
- Lack of stress leukogram (INAPPROPRIATE AS VERY SICK)
- decrease Na, decrease Cl, decrease Alb, decrease Cholesterol, decrease Glucose
- increase K, increase Ca, increase P, increase ALT, increase ALKP
- Na:K < 27:1 (but not if atypical)
- Prerenal azotaemia
- Metabolic acidosis
- USG < 1.030

23
Q

Hypoadrenocorticism imaging findings

A
  • Generally done due to regurgitation and thinking maybe aspiration pneumonia
  • Microcardia
    ○ Small pulmonary arteries
    ○ Small vena cava
  • Microhepatica
  • +/- Megaoesophagus (oesophageal dysfunction)
  • Small / absent adrenal (supportive, not diagnostic) - if normal could also be that as well
24
Q

Hypoadrenocorticism ECG findings

A
  • Hyperkalaemia - LIFE THREATENING - bradycardia
    ○ Peaked T waves
    ○ Flattened P waves
    ○ Increased QRS and P-R interval
    ○ P waves absent
    ○ Decreased R waves
    ○ Bradycardia, ventricular fibrillation / asystole
25
Q

Hypoadrenocorticism what gives high suspicion

A
  • Sick patient has no stress leukogram
  • Sick patient has slightly low- low normal BG (especially with low cholesterol +/- albumin)
  • Azotaemic patients with other suggestive changes
  • Inappropriate relative/absolute bradycardia
  • Patients with clinical hypoglycaemia
  • Patients with mild hypercalcaemia
  • Eosinophilia in a sick patient
26
Q

Hypoadrenocorticism diagnostic testing what are the 2 main ones, what do they do and how to perform

A

1) Basal cortisol ($66) – rule out if > 55nmol/L - MOST COMMON first option
○ RULE OUT ADDISONS but cannot confirm
2) ACTH stimulation test ($450) - to confirm
○ Basal cortisol sample
○ IV or IM ACTH (synacthen) (250 ug/dog, 5-10 ug/kg)
○ Post cortisol 1 hour later
○ (Note if use Depot, 0.25-0.5mg IM and post 2 hrs)
○ Dogs with addisions - flatline cortisol after an hour or 2 (should be increased) - ALL TYPES

27
Q

Atypical Hypoadrenocorticism what need to differentiate and how

A
  • Atypical (just glucocorticoid deficient) - is it primary (brain) or secondary (adrenal) - ONLY IF WORRIED ABOUT CNS (already need to diagnose addisions disease)
    ○ ↑ [ACTH] (endogenous ACTH assay - how much can dog produce itself) - Primary
    ○ Normal / ↓ [ACTH] Secondary
28
Q

Hypoadrenocorticism emergency therapy what are the 5 things you need to correct

A

Emergency therapy - REFERAL - generally in hospital for 2-3 days
1. Correct hypotension / hypovolemia
○ IV catheter, shock rate fluids, +/- colloids, blood products, dextrose
2. Correct electrolyte imbalances – treat high K - IVFT will dilute and resolve on its own
○ IVFT, +/- IV glucose (if hypoglycaemic), insulin (once hypoglycaemic corrected), IV Ca gluconate
○ Only correct Na by 10-12 mEq/24 hrs! - SLOWLY
3. Provided glucocorticoids
○ IV hydrocortisone 0.2-0.5mg/kg/day CRI - dose adjust based on response
4. Correct acidosis, hypoglycaemia & hypercalcaemia
5. Mineralocorticoid
○ Desoxycorticosterone pivalate IM (never IV) better than fludrocortisone

29
Q

Hypoadrenocorticism maintenance therapy what are the options for mineralocorticoid and glucocorticoid deficit and prognosis

A

Maintenance therapy - LIFELONG THERAPY
1) Mineralocorticoid - 2 options
a. DOCP IM q 25 days, start 2.2 mg/kg - preferred
§ Electrolytes at 12 and 25 day
§ May be able to reduce dose / extend interval
§ Require glucocorticoid - JUST A MINERALICORTICOID
§ Monitoring - electrolytes and adjust dose based on response (want K to decrease and Na to increase)
b. Fludrocortisone acetate 0.02mg/kg divided BID PO
§ Electrolytes every 1-2 weeks (increase PRN) then q 6 months
§ Can result in bad side effects - PU/PD, polyphagia, poor coat
§ May required glucocorticoids
- Glucocorticoid – Percortate ideally > prednisolone (common side effects)
Excellent prognosis with treatment

30
Q

Feline hypoadrenocorticism how common, type, main signs, diagnosis and treatment

A
  • Rare in cats
  • Primary (immune mediated)
    ○ (Bilateral adrenal disease, trauma, iatrogenic, LSA)
    ○ Not atypical
  • No age / sex / breed predilection
  • Diarrhoea / bradycardia
  • 125 mcg synacthen/ cat IM (for ACTH stim test)
  • Post ACTH cortisol samples should be obtained 30 min & 1 hour post (cf. 1 hour in dogs) with synacthen use
  • Response to acute therapy is slower
31
Q

Greyhounds which sex more advanced, what is the general racing life and there aerobic capacity

A
  • Socialisation starts from when they are puppies
  • Females are usually more advanced than males
    ○ The racing life of most greyhounds is from 18 (females), 24 (males)-48months of age
  • Canines are essentially anaerobic sprinters for 10-15seconds
    ○ After this point use aerobic energy pathways
  • Some greyhounds have difficulty competing after 350m (15 seconds)
32
Q

What are the 4 main greyhound idiosyncrasies

A

1) PU/PD and catabolism with cortisone
2) PU/PD, poor form and catabolism with progestogens (for oestrus control)
3) Slow recovery from barbiturate anaesthesia
○ Use alfaxalone or propofol for induction
4) Morphine may cause restlessness distress and vocalisation

33
Q

How do dogs lose heat and control body temperature

A
  • Dogs lose heat through their pads and head via panting
  • Dogs will control their body heat production by slowing down
  • If dogs cannot adequately cool down they do progress to heat stress and may die
34
Q

Haemotology and performance in greyhounds

A
  • Low red blood cell parameters (anaemia) will cause poor performance
    ○ It is uncommon to find low red cell levels as a cause of poor performance in any breed of dog
    ○ Red blood cell levels below normal parameters indicates a major problem and needs to be worked up
  • Can race successfully with haematocrits as low as 50%
    ○ These dogs are best suited to shorter distances up to 450m
  • Dogs which compete successfully over 500-700 m usually have high red cell parameters
35
Q

Hyperfibrinolysis in greyhounds what occurs, how common and pathophysiology

A
  • Greyhounds may develop delayed postoperative bleeding after routine surgery and trauma
  • NOT COMMON - will resolve, just take precautions next time undergo surgery
  • Pathophysiology NOT CLEAR
    ○ Platelets, coagulation and von Willebrand’s disease excluded
    ○ Thought be due to excessive fibrinolysis
    § Reduce incidence of post-operative bleeding following pre-emptive treatment with epsilom aminocaproic acid (EACA)
36
Q

Urinalysis what is normal specific gravity and urinary tract disease and performance

A
  • Specific gravity should be >1.025
    Urinary tract disease and performance
  • Greyhounds may suffer from low grade UTI
    ○ PU.PD, dysuria, pollakiuria
  • UTI will impact negatively on performance
  • Many dogs will show a transient post exertional myoglobinuria - will show up as blood
    ○ Differentiate - Serum from these dogs is clear coloured and the urine sediment is negative for RBCs
    § The post run myoglobinuria should clear within 6-12 hours
37
Q

Serum enzymes in greyhounds which important, what levels

A

○ ALT -> often slight elevation up to double upper normal but is of NO CLINICAL SIGNIFICANCE
○ AST -> often slight elevation post running indicating muscle injury
○ CPK -> should be <200IU 48 hours post run - if not muscle damage
○ Glucose -> rarely significant

38
Q

In terms of greyhounds how important is thyroid hormone and the role of progesterone

A

Thyroid
○ NO DEFINITIVE STUDY DEFINING THYOID LEVELS IN RELATION TO PERFORMANCE
○ Bald thigh syndrome in greyhounds may involve low T4 levels
§ Giving thyroid doesn’t help
○ Show dog coats may improve with T4 supplementation (as with high levels of fatty acids)
- Progesterone
○ High levels are important in dioestrus (false pregnancy)
○ Levels above 6nmol/l indicate that a bitch has had a recent oestrus period

39
Q

Define anoestrus, proestrus, oestrus and dioestrus

A
○ Anoestrus 
§ The period when a bitch has minimal hormonal events happening 
§ Progesterone levels are <6nmol/L
□ Differentiate with progesterone for dioestrus (NOT CYTOLOGY)
○ Proestrus 
§ Initial period of coming into season 
§ Progesterone levels are <6nmol/L
○ Oestrus 
§ In season 
§ Progesterone levels rise from 6nmol/L
○ Dioestrus 
§ Period after oestrus 
Progesterone increases for 5 weeks then fall away
40
Q

Oestrus cycle and performance

A

○ Greyhound NOT permitted to race whilst oestrus
○ Show dogs may be shown when oestrus
○ Bitches in oestrus can SEVERLY affect the behaviour of male dogs
§ Anorexia
§ Weight loss
§ Anxious behaviour
§ Prostate disease
Dieostrus - a decreased performance possibly due to increase tendency to injure soft tissue (usually 9 weeks - can go longer and effect performance)

41
Q

How to stop bitches from coming into heat - 4 main ways

A

a. Hard training: the stress of training provides a -ve feedback on the hypothalamus reducing GnRH production
b. Androgenic hormones
§ Testosterone propionate, Ethyloestrenol
c. Progestogens
§ Types
□ Norethisterone
□ Proligesterone
□ Nordiol
§ Use of progestogens may result in poor performance and may induce lactation
§ May also induce weight loss while in other breeds they may cause weight gain
d. GnRH agonists
§ Deslorelin has been shown to postpone oestrus if given in dioestrus when the progesterone level is > 15nmol/L
§ Given in anoestrus it will induce a fertile oestrus period and then the bitch will remain in anoestrus for 9-12months
§ Can also be used with males to stimulate castration

42
Q

What are the 4 main ways to suppress false pregnancy

A

○ Want to result in luteolysis of corpus luteum

1) Dopamine agonist: inhibit prolactin secretion (luteotropic)
i. Cromocriptine (parlodel) -
ii. Cabergoline (dostinex) -
2) Seritonin inhibitors - Metergolin (Contralac) -
3) Anabolic steroids: give a poor response
4) Prostaglandins to induce luteolysis

43
Q

How does diet effect greyhound performance and the suggest diet

A
  • Fats
    ○ Dog use fats as main source of energy, not carbohydrates
    ○ Fat deficient dogs will lose weight and not perform well
    ○ Overweight dogs
    § Are more susceptible to arthritis and soft tissue injury during athletic activity
    § Overweight dogs do not work or compete as well as lean dogs
    -> give R/D, fresh air and water
  • Racing dog diet
    ○ Moderate protein level (24% of energy) compared to high protein 36% of energy
    ○ High fat levels - provides 40-50% energy
44
Q

What are the 2 main types of stress on greyhounds and the 2 main responses

A
  • Types of stress
    ○ Physical stress
    § Heat, cold, over training, nutrition, parasites, infection, injury
    ○ Psychological stress
    § Kennel mates, owner, race track, car, show ring, crowds, overcrowding
  • Response to stress
    a. An increased secretion of cortisone which predisposes to
    § PU/PD weight loss and dehydration
    § Low grade infection - UTI, tonsillitis
    § Ill thrift
    b. Increased response of the autonomic nervous system
    § Sympathetic: dysuria, barking, panting and dilated pupils
    Parasympathetic: diarrhoea, salivation and coughing
45
Q

Water diabetes syndrome in greyhounds what are the 2 forms

A

a. Acute and subacute WSD - is a vasopressin responsive state of PU/PD
b. Chronic WDS - non vasopressin responsive state of PU/PD

46
Q

Acute water diabetes syndrome in greyhound clinical signs and cause

A
○ Clinical signs 
§ PU.PD, weight loss and dehydration 
§ Panting and distress
○ Cause - combination of below 
§ Stress 
§ Weather conditions - heat and cold 
§ Running over long distances
§ Pituitary exhaustion 
§ Hypothyroidism 
§ Dehydration 
§ Hypokalaemia
§ Urinary tract infection 
§ Exogenous cortisone
47
Q

Treatment for acute water diabetes syndrome in greyhounds

A

§ IV fluids - replacement and maintenance
§ ADH replacement
□ Vasopressin 10 units i.m then 5 units 12 hourly
□ Desmopressin acetate (minirin) 4 ug i.m then 2 ug 12 hourly or as needed
§ Allow access to water with electrolytes at 1 L per hour for 24 hours
□ Slowly reduce by 20% per day
§ Antibiotics, rest, minimise stress
§ Full history to determine the aetiology

48
Q

Chronic water diabetes syndrome in greyhounds clinical signs and treatment

A
○ Clinical signs 
§ Low grade dehydration, slight skin tenting, daily fluid intake of 1-2L
§ Reduced track performance 
§ Mild illthrift 
○ Treatment 
§ Eliminate stress 
§ Antibiotics if indicated - UTI 
§ Diet - increase fat content - MOST WILL BE DEFICIENT 
§ Electrolytes 
§ T4 level monitoring 
§ Physical examination for musculoskeletal injuries 
§ Monitor USH until it is >1.025
49
Q

Post racing dysuria in greyhounds incidence, clinical signs and pathphysiology

A

○ Incidence
§ Young nervous excitable dogs
§ Related to stressful situations
○ Clinical signs - delayed onset of urination
§ Stage 1: 2-48 hours post run - delayed 10-30 seconds - thin stream
§ Stage 2: longer than 30 seconds, very thing stream or completely blocked
§ Stage 3: unable to urinate, bladder becomes distended
○ Pathophysiology
§ High level of cortical stimulation increase bladder sympathetic tone, and reduces parasympathetic tone

50
Q

Post racing dysuria in greyhounds treatment

A

§ Alpha adrenergic blockers - phenoxybenzamine 10-15mg tid - help with bladder
§ Valium and buscopan
§ Reduce stress
§ Antibiotics - if have concurrent UTI (status predisposes to this)
§ Stage 3 - catherization may need GA - medical emergency

51
Q

Canine exertional rhabdomyolysis “acidosis” clinical signs and cause

A

○ Clinical signs
§ Vary from mild cramping to severe rhabdomyolysis
§ Pain along thoraco-lumbar muscles, quadriceps femoris, and triceps
§ Distress and panting
§ Dehydration and weight loss
§ Death
○ Cause
§ Tissue hypoxia due to dehydration and muscle cramping
§ Subsequent myoglobinaemia may block the glomerulus

52
Q

Canine exertional rhabdomyolysis “acidosis treatment

A

§ Intravenous fluids, monitor haemogram and biochemistry
§ Sedation and anaglesia
□ Diazepam, tramadol, mu agonists morphine, methadone
§ NSAIDS - however there is concern about renal perfusion
§ Antibiotics intravenously
§ Oxygen
§ Long-term - rest, graded exercise, eliminate stress, diet (fat)

53
Q

Cramping in greyhounds what dogs, cause, where occur and treatment

A

○ Nervous excitable dogs, unfit dogs
○ Rare in non-greyhounds
○ Cause - hypoxia and electrolyte imbalance
○ Cramp - along lumbar spine, triceps, quadriceps, hamstring (rarely)
○ Treatment
§ Calcium, magnesium, potassium, phosphorus, selenium
§ Quinine bisulphate 300mg
§ 4 hours pre-trail - vary training regime

54
Q

Canine cough how spread, what caused by, clinical signs and treatment

A

§ Spread by droplets
§ Cause
□ Para influenza, canine adenovirus 2, canine respiratory coronavirus, canine herpes, reocirus, bordatella bronchiseptica, staph and strep and mycoplasma
§ Clinical signs
□ Husking cough, cough on tracheal palpation, variable fever
§ Treatment
□ Antibiotics - amoxicillin, clavulanic acid, cephalosporins, tetracyclines, enrofloxacin
□ Bronchodilators
□ Humidification/nebulise
□ Rest and avoid cold air

55
Q

Canine haemorrhage pneumonia in greyhounds cause, clinical signs, prognosis, predisposing factors and treatment

A

§ Cause - streptococcus zooepidemicus primary isolate, Pasteurella and E.coli may be isolated
§ Clinical signs
□ Acute onset of lethargy, fever, respiratory distress, cough, mucopurulent or haemorrhagic nasal discharge and sudden death
® Cellulitis may occur
§ Can be acutely fatal - prognosis is not good
§ Predisposing factors: stress, viral URTI, poor housing
§ Treatment
□ Antibiotics - IV - cephalosporins, amoxicillin clavulanic acid, enrofloxacin
□ Intravenous fluid therapy: affected dogs are hypotensive induced by bacterial exotoxins
□ Oxygen
□ All animals at risk - PROPHLYATIC ANITBIOTICS to all involved

56
Q

Chronic respiratory disease bronchitis how common, caused by, clinical signs adn treatment

A

§ A common condition in all breeds
§ Caused by chronic damage to respiratory tract mucous membranes, and mucus accumulation in the end bronchioles
§ Bronchoconstriction occurs
§ Clinical signs
□ Cough easily elicited on tracheal palpation
□ Commonly occurs post exercise
§ Treatment
□ Bronchodilators - NOT AN INFECTIOUS DISEASE - bronchospasm
® Clenbuterol, Humidification/nebulise
® Rest and avoid cold air
□ Prednisolone orally - if inflammation occurring
□ Inhalant bronchodilators and cortisone available

57
Q

Excercise induced asthma in greyhounds cause, clinical signs and treatment

A

§ Cause
□ Over stimulation of parasympathetic NS
§ Clinical signs
□ Post run cough
□ Affected dogs may not run as strongly as they used to
§ Treatment
□ Bronchodilators - clenbuterol, aminophyline, terbutoline, nebulise

58
Q

corns in greyhounds what does it cause, how occur, diagnosis and treatment

A

ANY LAMENESS ON GREYHOUNDS - CHECK ALL PADS
○ Causes lameness in greyhounds and whippets
○ Usually starts at puncture wound in the pad
○ Hard fibrous tissue develops
○ Radiography to check for Grit
○ Treatment
§ Remove with an elliptical incision
§ Close with interrupted sutures
§ Leave sutures 2-3 weeks (pads take a-while to heal)
§ Keep the wound clean and dry
§ Can try to shave corn down
§ Keep the wound and dry
§ Can try to shave the corn down

59
Q

Symmetrical lupoid onchodystrophy what is it, presentation and treatment

A

○ An autoimmune disease which commonly affects all the toes
○ Toe nails tend to slough off leaving raw surfaces
○ Responds poorly to therapy, and has a poor prognosis for racing
Prednisolone systemically and tropically provide some relief

60
Q

Musculoskeletal injury in greyhounds what 4 common injuries

A
1) Joint injury 
§ Sprains, fractures 
2) Bone fractures 
§ Fracture of the 3rd or 4th metatarsal - weight bearing digits 
§ Fracture of left 5 and right 2 metacarpal - weight bearing digits 
3) Periostitis "shin soreness" 
§ Metacarpals/metatarsals 
4) Soft tissue injuries 
§ Muscles and tendons
61
Q

Musculoskeletal injury in greyhounds soft tissue injuries treatment

A
○ Apply compression 
○ Apply heat or cold 
○ Physiotherapy devices 
○ Laser (class 3B and 4) 
○ Massage
○ Anti-inflammatory drugs 
§ Corticosteroids 
§ NSAIDS 
○ Nutraceuticals and joint disease 
○ Graded exercise 
○ Surgery 
○ Rest and diet  
○ Stem cells
62
Q

Back pain clinical signs

A

○ Reluctance to jump up
○ Crying when jumping up or down
○ Holding one leg up after jumping
○ Reduced suppleness of the paravertebral muscles
○ Pain on palpation of the paravertebral muscles

63
Q

Chronic muscle injuries what dogs seen in, what does and doesn’t it respond to, common muscles and treatment options

A

§ Seen in active working dogs
§ Lameness which is non-responsive to anti-inflammatory medications
§ It is responsive to rest
§ There is palpable tenseness in the affected muscle
§ Deltoid/infraspinatus, quadriceps femoris and psoas muscle are commonly affected
§ Concept of myofascial pain or “trigger points”
§ Treatment
○ Massage
○ Direct injection
○ TENS (transcutaneous electrical nerve stimulation)
○ Laser (Class 3B or 4) - photobiomodulation

64
Q

What are the 3 main roles of veterinarians in the greyhound industry

A
  1. Official track veterinarians
  2. Private practice
    ○ Musculoskeletal cases
    ○ Reproduction, neonatal and puppy care
    ○ Care of retired and aging greyhounds
    ○ General husbandry
  3. Industry/administration
    ○ State and national bodies
    ○ Private laboratories
65
Q

What is hyperthermia and pyrexia (define)

A

Hyperthermia
- Any elevation in core temperature above ‘normal’.
- Heat produced or stored in excess to loss
○ physiologic, pathologic or pharmacologic.
Fever/pyrexia
- Hypothalamic set point ‘reset’ to a higher T° by exogenous and endogenous pyrogens.

66
Q

Fever what are the good and bads parts

A

The good
- Direct inhibition of organism proliferation
- Increased leukocyte function
TRUE FEVER REDUCES DURATION AND MORTALITY OF MANY INFECTIOUS DISORDERS - normal response
The bad
- Increase metabolism (typically 1.3 x) - need more energy
- Suppressed appetite
Ø 41.6 degrees = cell and tissue damage - rare for true fever to get this high

67
Q

Fever of unknown origin what generally occurs and what looking for

A
  • No localising history or PE
  • No dx after MDB evaluation
    ○ Haematology, biochemistry and urinalysis - all normal
    So what are we looking for?
  • Deep, severe, persistent infections:
    ○ Bacterial
    ○ Systemic fungal (not sinonasal!)
    ○ Viral (cats) FIV, FeLV, FIP
    ○ Rickettsial
    Protozoal
    Normal bacteria in a deep site
    OR
    Evasion of the host immune response
68
Q

In terms of bacteria causing fever of unknown origin how to treat

A
- Surgical
○ Curative
○ Drain + lavage
○ Remove cause + lavage
- Medical
○ LONG course Abs (2-4 weeks +)
§ Risk of relapse 
○ Likely organisms?
○ Penetration of site?
○ Monitoring
69
Q

List some common viral, fungal, protozoal and vector born causes of fever of unknown origin

A
- Viral: - generally not unknown 
○ FIP C
○ FIV C, FeLV C
○ Parvovirus D
- Fungal 
○Aspergillus (rare) D>C
○ German shepherd dog predisposed (commonly in spine) 
○ Localised in nose or systemic 
○ Cryptococcosis C>D
- Protozoal:
○ Toxoplasmosis C
○ Neosporosis D (rare)
○ Babesiosis (pit bulls)
- Vector born
○ Babesia gibsoni, B vogeli D
○ Haemotropic mycoplasmas C
70
Q

Fever of unknown origin what are some non-infectious causes, treatment and what need to be careful of

A
  • Pancreatitis
  • Nodular panniculitis
  • Pansteatitis
  • Lymphadenitis
  • Panosteitis
  • Granulomatosis
  • Eosinophilic diseases
    Treatment
  • May need to use steroids - NEED TO EXCLUDE INFECTION
71
Q

Fever of unknown origin what are some immune-mediated, neoplastic and other causes

A
Immune-mediated
- Polyarthritis
- haemolytic anaemia
- Vasculitis
- Systemic Lupus Erythematosus
Neoplastic - OLDER ANIMAL 
- Leukaemia
- Lymphoma
Miscellaneous
- Metabolic bone disorders D
- Drug induced (tetracyclines, TMS, penicillins) C
- Toxins
NO CASE IN 10-15% OF CASES 
- Important for client information 
- Referral will be needed
72
Q

In terms of approach to fever of unknown origin what are important history and physical examinations considerations

A
History 
- Consider geographic area and season
- Activity/lifestyle
- Any travel history? Where and when?
- Previous injuries or infections
- Exposure to other animals
- Health of those other animals
- Any current or previous drug therapy. Response?
- Vaccine hx/FIV/FeLV status (cats)
Physical examination 
- Injuries, Tracts
- Masses, Infections
- Inflammation
- Localising signs ?
- Behaviour - true fever or not?
- Posture - stiff - polyarthritis, not jumping - neck issue
73
Q

What is the most common cause of pyrexia of unknown origin

A
DOGS
- Bacterial most common
- Systemic fungal or vector-borne dz most common some locations
CATS
- Bacterial (cat fight abscess)
- Viral may be more common
74
Q

When not to give empiric therapy with fever of unknown origin

A
  • SICK animal
  • Chronic/relapsing
  • Exam gives you clues
    ○ Neck pain
    ○ Shifting lameness
    ○ Back pain
    ○ New heart murmur
    ○ Abnormal lung sounds
75
Q

Antibiotic trial for fever of unknown origin when give and how to perform

A
- For relatively happy patients 
○ Mild lethargy, depression, hyporexia
○ Drinking, hydrated 
- How to perform 
○ 5-7 days 
○ Oral, broad spectrum
○ Good soft tissue penetration
§ TMS - prostatis
76
Q

Antipyretics in fever of unknown origin what is the issue and when give

A
  • True fever is beneficial and rarely dangerous
  • TOTAL body cooling is COUNTERPRODUCTIVE
  • If > 41 degrees
    ○ Consider NSAIDS
    § Inhibit PG synthesis, reset thermoregulation, avoid if dehydrated
    ○ +/- phenothiazones
    § Hypotension risk
77
Q

Prednisolone in treatment of fever of unknown origin

A
  • Blocks the acute phase response and fever
  • Only consider when
    ○ You KNOW there is no infection
    ○ Effect will be beneficial
    ○ AFTER diagnostics that may be affected
  • If unsure pred vs. NSAID
    ○ IV fluids
    ○ +/- paracetamol (dogs) IV or PO
    ○ Opiate analgesia if required
78
Q

Further investigation in fever of unknown origin when do and the 4 main rounds

A
  • All cases that don’t respond to ONE round of empiric therapy
    ○ DO NOT DO FOR THESE CASES
    § Trial corticosteroids
    § Switch antibiotics in case of resistance
    § Give multiple antibiotic or anti-inflammatory courses without diagnosis
    1. Round 1
    ○ Least invasive tests
    § PE, MDB (minimum database - haem, bio, urin), +/- imaging
    2. Requires sedation/more costly/more risk
    ○ Imaging, aspirates, cultures, serology or PCR
    3. More advanced/invasive
    ○ Advanced imaging, biopsy - more disease specific - CT, MRI, bone marrow samples
    4. Most invasive
    ○ Exploratory surgery, if indicated
79
Q

What is important around client communication with fever of unknown origin

A
  • Always warn you may not reach a diagnosis
  • Justify chasing a specific diagnosis
  • Suspected immune-mediated disease
    ○ may be due to other infectious, inflammatory or neoplastic foci you have missed.
    ○ These diseases may emerge with time
80
Q

What is teh treatment approach with 10% of cases that cannot diagnose with fever of unknown origin

A
  • Wait
  • Specific antibiotic (mycobacteria) or antifungal therapy (rare)
  • Immunosuppressive glucocorticoids - SHOULD WE?
    ○ Start with low dose
    ○ IF
    § Immune mediated - improve 24-48h, long term response
    § Infectious - initial improvement, disseminate, relapse, DEATH
    § Neoplastic - initial improvement, relapse refractory
81
Q
CASE 
- 12 year old, spayed 
- Presents with a history of weight loss 
- Eating normally and losing weight 
- No vomiting or diarrhoea 
- No other cats, indoor/outdoor
- Senior diet 
- Normal activity, no other signs 
List some possible differentials and what do next
A
  • Hyperthyroidism
  • Diabetes
  • Small Intestinal lymphoma, IBD
  • Protein losing enteropathy - no evidence so unlikely
  • Food allergy -> Can occur even when
  • Chronic liver or renal insufficiency
  • Exocrine pancreatic insufficiency - GENERALLY large volumes of diarrhoea in cats
    NEXT - haemotology and biochemistry
82
Q

Before using antibiotics what are the 6 things to ask yourself

A
  1. Are bacteria present?
  2. Are bacteria likely to cause disease?
    ○ Which ones will cause problems?
  3. Where antibiotics used in the last month?
  4. Can the disease be controlled without antibiotics?
  5. Can the disease be controlled with topical antibiotics?
  6. Did signs improve last time I treated?
83
Q

Empirical use of antibiotics what is it based on, what use and why

A
  • Use is based on PREVIOUS experience and observation
  • Likelihood of right decision increases with experience
  • Definite organism of THIS CASE is not known
  • There is ALWAYS a possibility that THIS CASE is different
  • Use the antibiotic with the narrowest spectrum that is effective against all bacteria suspected to cause a problem.
84
Q

What are the steps in using empirical antibiotics

A

1) ideally use the most effective FIRST LINE antibiotic
- good compliance (animal and owner)
- >90% of suspected bacteria are susceptible
- good pharmacokinetics
- little drug interaction
2) Appropriate dose, frequency and treatment length with follow up

85
Q

Culturing fr use of antibiotics when considered and when may avoid

A
  • Culture and sensitivity testing should always be considered!
  • One may avoid culture if:
    ○ First apparent “infection” in >3-6 months
    ○ Non-complicated
    § No antibiotic use (for this or other problem) in > 1 month prior
    § Typical disease
    § Signs typical
    § Patient is otherwise healthy
    ○ Risk of procedure to obtain sample is too great
86
Q

Culture and sensitivity when strongly recommend

A

○ Prolonged antibiotic course is needed (>7 days)
○ Previous treatment failure, including no improvement
○ Gram-negative organisms expected
○ Complicated infection
§ Recurrence
§ Patient suffers from significant underlying disease
§ Previous antibiotic resistance documented
§ Unusual disease
○ If in doubt, samples can be taken and stored adequately

87
Q

De-escalation of antibiotic therapy what does it do and how performed

A
  • Helps to preserve effectiveness of antibiotics
    1. inital suspicion of infection
    2. empirical wide spectrum antibiotics
    3. test results
    4. narrow spectrum targeted therapy
88
Q
Case 1 - SURGERY
Mammary tumour (5cm diameter) of a 6 year F German shepherd, scheduled for removal - are you planning to use antimicrobials?
A
  • No clean and elective surgery, short surgery time - NOT NEEDED
89
Q

What are the 3 steps in choosing antibiotics for surgery

A
  1. Hygiene - antibiotics DO NOT REPLACE PROPER HYGIENE
  2. Categorize surgery
    a. Check for complicating factors
  3. Antibiotic choice and duration
90
Q

In terms of dentals when give antibiotics

A

Routine dentals - generally no antimicrobials
Extractions - bacteraemia 20 mins so give to patients that cannot handle this
- Immunosuppressed
- Older patients
- Patient with heart disease or systemic illness
If needed give amoxicillin 30mins prior to surgery

91
Q

Perioperative antibiotic use what doesn’t it do, when need to be given and how often

A
  • Does not replace proper aseptic technique
  • Does not prevent infection if started during surgery
    ○ If given IV give 30-60 min prior to surgery (e.g. at the start of anaesthesia); longer if SC - IMPORTANT
  • Perioperative repeat dosing interval = 2 x elimination half-life of the drug
    ○ E.g. cefazolin: 4 hours
92
Q

Postoperative antibiotic use what doesn’t it do, what does it do and length of treatment

A
  • Does not replace aseptic technique
  • Does not replace perioperative antibiotics - has a different purpose
  • Used to help resolve existing infection
  • Antibiotics used and length of treatment depend on
    ○ Suspected organism
    ○ Infected organ
    ○ Patient factors
    ○ Client factors
93
Q

skin infections in dogs and cats, how common, how many bacterial (what most common type) and what need to do first before treatment

A
  • 20% of dogs and cats presenting to vets present with a skin infection
  • Only up to 25% of infections are bacteria
    ○ Majority is staph pseudintermedius
  • Differentiate between:
    a. Surface infection
    § Often in folds (intertrigo) or associated with pyotraumatic events (“hot spots”)
    b. Superficial pyoderma
    § Infection is contained within the superficial skin layers; most common is folliculitis
    c. Deep pyoderma
    § Infection has spread into the deep dermis, for example with furunculosis or granulomas
94
Q

Surface pyoderma work up, and types and treatment with examples

A
  • Work up: Perform cytology to check whether cocci or bacilli +neutrophils
  • Topical treatment
    ○ Shampoos or wipes with e.g. chlorhexidine
    ○ Topical antimicrobials if needed e.g. Mupirocin (Bactroban) or Fusidicacid (Fusiderm) - get staph
  • Systemic treatment is only needed if no response
    ○ Culture and sensitivity before
    ○ Also possible skin biopsy - underlying skin disease could be leading to this
95
Q

Superficial pyoderma work up, and types of treatment needed

A
  • Look for and treat underlying disease, e.g. atopy, demodicosis
  • Work up as for surface pyoderma
  • Prioritise on topical treatment
  • If systemic antimicrobials are needed:
    ○ Clindamycin empirical first-line
    ○ Culture and sensitivity if no response or gram-negatives seen on cytology
96
Q

Deep pyoderma work up and treatment involved

A
  • Look for and treat underlying disease
  • Work up:
    ○ -as for surface pyoderma
    ○ +-histopathology
    ○ +-culture and sensitivity
  • Add systemic antibiotics if disease is wide-spread
    ○ Cephalexin, Amoxicillin/clavulanate or Clindamycin
    ○ Treat until 2 weeks after resolution of signs
97
Q

How to treat cat bite abscesses

A
- Which bugs?
○ Anaerobs (Bacteroidesspp., Fusobacteriumspp.)
○ Pasteurellaspp.
○ Streptococcus spp.
- Attend to wound
- If antibiotics necessary
○ Amoxicillin, ampicillin
○ clindamycin
○ 5-10 days
98
Q

What are the 2 ways to treat otitis and the steps within

A
  • Otitis externa may be treated topically
  • Otitis media or interna requires systemic treatment
    Steps
  • Ear cytology
    ○ Basis for drug choice
    ○ C&S if no resolution
    ○ Work up for underlying disease if recurrent or persistent
  • Check whether tympanic membrane intact
  • Thorough clean before each AB administration
99
Q

Urinary tract infections what must first identify and what need to do if so

A
  • Must first identify whether there is:
    ○ Subclinical bacteriuria (SBU) - presence of bacteria in urine in an animal that isn’t showing clinical signs
    ○ Uncomplicated UTI
    ○ Complicated UTI
  • If UTI is complicated, ensure to control underlying disease
    ○ Urolith and urinary tract infection - NEED TO REMOVE UROLITH
    ○ Diabetes mellitus - glucose nutrient for the bacteria - need to bring glucose level down
100
Q

In terms of urinary tract infections what is special about cats and what is the most common organism causing in both species and antibiotic used

A

What is special about cats?
- Remember UTI is rare in young cats
- Check for uroliths if there are LUTD signs
- Culture of urine always recommended
- Avoid enrofloxacin(adverse effect: blindness)
What is the most common organism causing UTI in dogs and cats, and which antibiotics can be used first-line to treat it?
- E.coli and amoxicillin

101
Q

Neutropenia and prophylactic antibiotics when given and what given

A
  • Antibiotics may be considered in cases of neutropenia even if there is no sign of infection (yet)
  • Neutropenia may be due to sepsis, immune deficiency or chemotherapy
    Give first-line antibiotics (TMS, amoxicillin) if:
  • Grade 2-4 neutropenia +-fever
  • Fever and any grade neutropenia (1-4)
  • Significant GIT signs after chemotherapy (grade 3-4 toxicity) and any neutropenia
102
Q

what are 5 main factors why antibiotics treatment may fail

A
1. Vet related 
○ Wrong - diagnosis, drug, route and dose/dosing frequency, dismissed drug interactions 
2. Owner related 
○ Poor compliance, wrong administration 
3. Patient related 
○ Immunocompromise 
○ Pus or foreign body 
○ Side effects
4. Bug related 
○ Antibiotic resistance 
○ Biofilm formation 
5. Drug related 
○ Drug absorption 
○ Drug metabolism 
○ Drug interactions