aproach to disease managment Flashcards

1
Q

resourses for intoxication cases

A

Veterinary Poison Information Service (VPIS)
BSAVA/VPIS guide to common canine and feline poisons.
Ingredient lists/data sheets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Phone triage for toxcity case

A

Information to acquire:
Signalment- size??
Suspected toxicant, timing of ingestion/exposure, suspected dose.
Likely time of arrival.

Instructions for owner:
Prevent further exposure- dont let animal lick toxins off coat
Bring any packaging of the suspected toxicant.

Preparation by the team:
Set up necessary medication, supportive care etc.
Contact VPIS if required

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Decontamination for intoication

A

Topical-
Rinse eyes with tap water or sterile water
Wash skin/coat with a mild detergent

Emesis-
General rule: Sooner = better.
Solid toxins (grapes/raisins, chewing gum, chocolate) stay in the stomach longer than liquids (ethylene glycol) and powders (lily pollen).

Emesis contraindications:
Non-toxic/very low toxicity substance or dose.
Patients that have already vomited
Caustic/corrosive agent
Volatile agent e.g. petroleum products
High risk of aspiration - megaoesophagus, comatose ect
Respiratory distress
Severe acid-base or electrolyte derangements

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

agents for inducing emisis in toxicity cases

A

Inducing emesis:
Apomorphine – licensed for dogs
No licensed options for cats – xylazine preferred.
Soda crystals – care

Examine the vomitus to check the toxin has been expelled
Gastric lavage may be considered where emesis is contraindicated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

activated charcoal for decontamination

A

Adsorbant – bind to toxins to prevent absorption
Alcohol and xylitol do not bind to activated charcoal
Repeated doses recommended
Feed as a slurry with food if possible
May affect the efficacy of orally administered medications – give drugs parenterally while giving charcoal if possible.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

emergency stabalisation for toxicity

A

Primarily of the neurological, cardiovascular, and respiratory system.

See specific lectures for more details.

General advice:
Control seizures- rectal diaxopam
Provide oxygen
Get an IV line

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

baseline tests for toxicity

A

Haematology and biochemistry-
Often normal, especially in acute, asymptomatic cases.
Most useful for monitoring and symptomatic cases.

Urinalysis-
Especially useful for suspected ethylene glycol toxicity to look for calcium oxalate crystals.

Coagulation profiles-
Where anticoagulant rodenticide intoxication is suspected

Toxic metabolites:
It is possible to check stomach contents and blood/urine samples for a great number of toxins
Mostly used for forensic work (e.g. wildlife crime) and in zoos and other very valuable animals.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

supportive care for toxicity

A

Intravenous fluid therapy-
Replace fluid loses e.g. from vomiting
Maintain renal perfusion and diuresis

Analgesia-
Opioids preferred over NSAIDs in most cases

Antiemetics-
Maropitant and ondansetron preferred options

Gastroprotectants-
H2 blockers- ranitidine, famotidine
Proton pump inhibitors - omeprazole
Sucralfate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Common Intoxications

A

Alliums
Anti-parasiticides
Avocado
Chocolate
Ethylene glycol
Grapes/raisins
Herbicides and fertilisers
Lilies
Metaldehyde
NSAIDs
Rodenticides
Teflon
Xylitol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Alliums as intoxicants

A

The allium family includes onions, garlic, and leeks as well as ornamental varieties.

Cats more sensitive than dogs (5 g/kg for cats; 15 to 30 g/kg for dogs).

Toxicology: Contain organosulphoxides -> organic sulphur compounds -> oxidative damage to erythrocytes -> Heinz body anaemia.

Clinical effects: Inappetence, vomiting, diarrhoea, Heinz body anaemia, methaemoglobinaemia and/or jaundice.

Treatment:
Decontamination (if possible)
Fluid therapy
Symptomatic and supportive care.

Prognosis: Favourable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Anti-parasiticides for toxicities- Pyrethroids:

A

Cats and snakes
Toxicity: Prevents closure of voltage-dependent sodium channels in nerve membranes, -> repetitive membrane depolarization.

Cats: Vomiting, hypersalivation, ataxia, dilated pupils, tachycardia, hyperexcitability, hyperaesthesia, hyperthermia, tachypnoea, twitching, convulsions and respiratory distress.

Reptiles: Loss of coordination, loss of righting response, sensitivity to bright light, and muscle spasms and panic.

treatment-
Active cooling
Lipid infusion

Decontamination
Seizure control – (diazepam, midazolam, pentobarbital, phenobarbital, propofol, or levetiracetam).
Fluid and nutritional support

prognosis- gaurded to poor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Anti-parasiticides for toxicities- Fipronil

A

frontline

Rabbits
Toxicity: Blocks GABA receptors in the CNS -> prevention of chloride ion uptake -> excessive CNS stimulation.

Fipronil: Seizures, tremors,
anorexia, lethargy, and death

treatment-
Stasis treatment if needed
Decontamination
Seizure control – (diazepam, midazolam, pentobarbital, phenobarbital, propofol, or levetiracetam).
Fluid and nutritional support

prognosis- gaurded to poor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Anti-parasiticides for toxicities- Ivermectin

A

Chelonia- can use in low doses
Toxicology: Binds to GABA-gated chloride channels, -> increased chloride ion uptake -> hyperpolarization and flaccid paralysis

Flaccid paralysis and death

treatment-
respiritory support
Decontamination
Seizure control – (diazepam, midazolam, pentobarbital, phenobarbital, propofol, or levetiracetam).
Fluid and nutritional support

prognosis- gaurded to poor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Avocado as an intoxicant

A

Toxic compound = persin
Birds are the most commonly affected species in small animal practice.

Toxicology: Myocardial necrosis in birds and mammals; mammary necrosis and haemorrhage in mammals.

Clinical effects: GI signs (anorexia, vomiting, diarrhoea,), mastitis, cardiac insufficiency.

Treatment:
Decontamination (if possible)- gastric lavage necessary in birds and horse
Symptomatic and non-specific

Prognosis: Poor if cardiac signs have developed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Chocolate as intoxicant

A

Toxic compound = theobromine
Cocoa powder = highest concentration of theobromine; white chocolate contains negligible amounts.

Toxicology:
Antagonism of cellular adenosine receptors -> CNS stimulation
Inhibition of cellular calcium reuptake -> increased muscle contractility in cardiac and skeletal muscle.

Clinical effects: Vomiting

Treatment:
Decontamination
Fluid therapy
Anti-emetics e.g. maropitant
Sedation e.g benzodiazepines
Beta-blockers (e.g. atenolol, propranolol)

Prognosis: Good

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Ethylene glycol as an intoxicant

A

Antifreeze; used in screen wash, brake fluid, fountains over winter etc.
Cats more sensitive than dogs.
Toxicology: Converted by alcohol dehydrogenase to various toxic metabolites -> renal damage and hypocalcaemia.

Clinical effects:
cannot decontaminate once symptoms show
Stage 1: Non-specific signs (vomiting, ataxia, tachycardia, weakness, PU/PD) + CNS signs in cats (convulsions, rapidly progressing to coma)
Stage 2: Cardiopulmonary signs
Stage 3: Renal signs

Clinical pathology: Metabolic acidosis, oxaluria, hyperglycaemia, hyperkalaemia and hyperphosphataemia

Treatment:
Decontamination rarely useful
Ethanol = specific antidote- competes for metabolites in liver and stops toxins being metabolised from the ethalyene glycol
Fomepizole = a competitive inhibitor of alcohol dehydrogenase
Sodium bicarbonate
Intensive fluid therapy and monitor renal enzymes

Prognosis:
Good in dogs if presented at time of ingestion, guarded to poor in all cats, and dogs once signs of renal failure have developed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Grapes/raisins as an intoxicant

A

Dried fruit appears to be a greater risk than fresh fruit.
There is no apparent correlation between dose ingested and the incidence of toxicity.
Primarily canid species affected, cats tend to show GI rather than kidney signs.
Toxicology: Toxic mechanism unknown

Clinical effects: Vomiting and diarrhoea (both +/- blood), hypersalivation, ataxia, weakness, and lethargy, progressing to renal failure over 24-72 hours.

Treatment:
Decontamination (if possible)
Aggressive fluid therapy
Supportive care- very expensivve and possibly not needed! onwer needs to choose

Prognosis: Good to poor. much wosr once renal signs show

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Herbicides and fertilisers as intoxicants

A

Herbicides:
Phenoxyacetic acid derivative herbicide – very common lawn weed killers, very acidic and volatile.
Diquat/diquat dibromide
Glyphosate
Moss killer is often iron based – treat as for iron toxicity
Most clinical signs are associated with irritation caused by the products, but renal and hepatic toxicity may occur with some products.

Fertilisers:
Most very low toxicity; clinical effects due to irritation

Clinical effects: Variable, but many are related to irritation (hypersalivation, vomiting, diarrhoea, ulceration of mucous membranes)

Treatment:
Decontamination – NOT EMESIS- topical, fairy liquid
Supportive care – fluid therapy, analgesia, GI protectants.
Feeding tube in severe cases.
Prognosis: Favourable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Lilies as an intoxicant

A

True lilies (Lilium spp.) and day lilies (Hemerocallis spp.) are the toxic species.
All parts of the plant are toxic.
Even very small amounts e.g. grooming pollen from fur can -> toxicity
Toxicity: Mechanism unknown, causes necrosis of renal tubular epithelial cells

Clinical effects: Vomiting, anorexia, depression, PU/PD and renal failure.

Treatment:
Decontamination – topical, emesis and activated charcoal
Fluid therapy and close monitoring of renal function
Supportive care

Prognosis: Favourable if treatment is started before onset of renal damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Metaldehyde as an intoxicant

A

Outdoor use of metaldehyde slug baits has been banned in the UK from 31 March 2022.

Toxicology: Not fully understood; possibly due to decreased inhibitory GABA concentrations.

Clinical effects: CNS signs (hyperaesthesia, muscle spasm/rigidity, tremors, twitching, convulsions), hyperthermia, tachycardia, tachypnoea or respiratory depression, and cyanosis

Treatment:
Decontamination (gastric lavage)
Diazepam to control twitching/convulsions, with escalation to full GA if required.
Active cooling
Supportive care – fluid therapy, liver support if needed.

Prognosis: Favourable if mild signs, poor once covulsions develop.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

aspirin as an intoxicant

A

Stimulates the respiratory centre -> hyperventilation and respiratory alkalosis, ->metabolic acidosis over time.

Depression, vomiting, anorexia, hyperthermia, tachypnoea, haematemesis, melaena, abdominal tenderness and anorexia.

treatment-
Decontamination
Fluid therapy
Oxygen therapy (if required)
Antiemetics (if required)
Gastroprotectants e.g. sucralfate, ranitidine or famotidine, omeprazole
Monitor renal and hepatic enzymes, electrolytes, and acid-base changes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

paracetamol as an intoxicant

A

Toxic metabolite which induces cellular necrosis, methaemoglobin, and Heinz body formation.

three pathways it can be metabolised- third pathway is the toxic one, this kicks in once overdosed- cats hae limited ability to use first tow pathways so no safe dose like there is for dogs

Depression, vomiting, anorexia, hyperthermia, tachypnoea, haematemesis, melaena, abdominal tenderness and anorexia.
: Brown mucous membranes, hypothermia, and facial and paw oedema (mainly cats)

owners may be reluctant to tell about giving paracetamol- tell by clinical sigsn- face and paw oedema

treatment-

Specific antidote:
N-Acetylcysteine

Methaemoglobinaemia treatment:
Vitamin C
Methylene blue- very carcinogenic! be careful

Decontamination
Fluid therapy
Oxygen therapy (if required)
Antiemetics (if required)
Gastroprotectants e.g. sucralfate, ranitidine or famotidine, omeprazole
Monitor renal and hepatic enzymes, electrolytes, and acid-base changes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

ibupropen as an intoxicant

A

Non -selective COX inhibitor; toxicity due to COX-1 inhibition

Depression, vomiting, anorexia, hyperthermia, tachypnoea, haematemesis, melaena, abdominal tenderness and anorexia.

treatment-
Decontamination
Fluid therapy
Oxygen therapy (if required)
Antiemetics (if required)
Gastroprotectants e.g. sucralfate, ranitidine or famotidine, omeprazole
Monitor renal and hepatic enzymes, electrolytes, and acid-base changes.

Prostaglandin analogue (misoprotol)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Rodenticides as an intoxicant

A

Usually anticoagulants, occasionally vitamin D is used.
1st generation anticoagulant rodenticides are less toxic than second generation.

Toxicology:
Anticoagulants: Competitively inhibit hepatic vitamin K1 epoxide reductase -> depletion of clotting factors (II, VII, IX and X); impairment of hepatic prothrombin synthesis.
Vitamin D: Hypercalcaemia -> tissue mineralisation and renal failure

Clinical effects:
Non-specific: Lethargy, weakness, depression
Other signs will depend on the site of bleeding – petechiation, abdominal distension, cough/respiratory distress etc

Prognosis:
Favourable in mild and asymptomatic cases; poor where uncontrolled haemorrhage is present.

Treatment:
Decontamination
Anticoagulant:
Chronic/symptomatic cases = start vit K immediately.
Acute/asymptomatic cases = wait and check PT after 48-72 hours.
Severe anaemia = Blood transfusion.
Vitamin D:
Promote diuresis - fluid therapy and diuretics (e.g. furosemide)
Promote calcium excretion - bisphosphonates or calcitonin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Polytetrafluoroethylene as an intoxicant

A

AKA Teflon; used in non-stick coatings, especially on cookware.

Primarily effects birds; humans can also be affected but symptoms tend to be self-resolving.

Toxicology: Overheated PTFE releases fumes which, when inhaled, -> alveolar congestion and pulmonary oedema.

Clinical effects: Respiratory distress, acute death.

Treatment:
Decontamination not possible
Supportive care only – oxygen supplementation, NSAIDs and diuretics, fluid therapy, and supplemental heat
Consider antibiosis

Prognosis: Guarded to poor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Xylitol as an intoxicant

A

Artificial sweetener, commonly found in chewing gum.

Toxicology: Stimulates insulin release in dogs -> severe, rapid-onset hypoglycaemia; hepatotoxic.

Clinical effects: vomiting, tachycardia, ataxia, depression, eventually coma, convulsions and collapse; signs of liver failure and coagulopathy less common.

Treatment:
Decontamination – emesis and activated charcoal
IV dextrose CRI where hypoglycaemia is present
Liver support (SAMe, silybin)

Prognosis:
Favourable if caught early, poor where liver failure has developed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

NEOPLASIA

A

–> the uncontrolled, abnormal growth of cells

Benign neoplastic masses do not spread (metastasize) - Examples include lipomas and sebaceous adenomas

Malignant neoplasia frequently invade locally and metastasize “cancer” – Examples include lymphoma and carcinomas

Both benign and malignant disease are commonly seen in practice

Cancer is the cause of death in approximately 47% of dogs >10 years of age

What type of neoplasia is it? -We cannot treat it effectively if we do not know what it is

Is it benign or malignant? -Benign disease may not always need treatment

If malignant, has it spread? “Staging” - Important for prognosis and treatment

Are there any paraneoplastic effects? -High calcium with anal sac adenocarcinoma

Does the patient have co-morbidities that could impact on treatment?

Consider whole patient welfare and what is appropriate for the pet and owner

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

cytology for neoplasia

A

FINE NEEDLE ASPIRATE – For solid tumours or enlarged lymph nodes – External and internal via ultrasound guided FNA

FLUID CYTOLOGY – Abdominal & thoracic effusions, prostatic wash etc. – Make a fresh smear and put some into EDTA
(care some neoplastic effusions may not have detectable neoplastic cells on cytology)

BONE MARROW ASPIRATE –
Indications – Cytopenia - especially when multiple cell lines are affected (anaemia, thrombocytopaenia) Unexplained big increase in cell lines – lymphocytosis, neutrophilia etc. Hyperglobulinaemia (multiple myeloma)

Slides are best sent to the lab in my opinion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

fine needle asprirate for neoplasia

A

Pros:
Simple, quick and non-invasive
Quick turnaround for results
Lower cost than surgical biopsy and histopathology
Performed awake in most cases unless:
-Fractious
-The mass in near a delicate structure
-Abdominal mass

Cons:
Smaller sample so may not be representative
Some masses such as sarcomas do not exfoliate well
Masses cannot always be graded

Contraindications:

Bleeding disorders- If no gross bleeding disordersexternal FNA is fine. For internal FNA’s check the PLT count first. (Clottingprofile if unsure)

Bladder tumours- Risk of seeding tumour cells

Immobilise the mass/or lymph node with your non dominant hand
Needleonly: -Introduce a 21 or 23g needle into the mass and move the needle back and forth several times

Suction:
-Useful for masses that do not exfoliate well
-Attach a syringe and apply suction whilst moving the needle back and forth. Release suction prior to needle removal

Attach an air-filled syringe and spray onto the slide
Make a smear

Costs: £120 FNA plus consult fee £50 (local Staffordshire practice 11/23)

Managing owner expectations -Important in all aspects of veterinary care:
Make owners aware of the cost and the benefits of the procedure

That samples may come back inconclusive or that further testing may be required

That their pet may yelp or have minor bleeding from the procedure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

histopathology for neoplasia

A

Various methods -Incisional, excisional, pinch, Tru-Cut….

Pros:
Larger sample so increased chance of diagnosis
Architecture can be assessed, and masses graded
Provides more prognostic info

Cons:
More invasive
GA or deep sedation required
Takes more time to get results
Increased cost

Risks:
Bleeding, seeding, compromising future surgery
Contraindications:
Bleeding disorders, co-morbidities increasing the risk of GA

In practice cytology and histopathology arecomplimentary:

FNA’s are often performed first todistinguishbetweeninflammatory/hyperplastic andneoplasticlesions

Biopsy and histopathology is used if the FNA is inconclusive

Otherwise,histopathology is performed after full mass excision toconfirm the diagnosis, allow full grading and to assess surgical margins

INCISIONAL WEDGE BIOPSY-
For solid tumours and LN
Choose an appropriate location
Avoid infected, haemorrhagic or necrotic regions
Inclusion of a normalarea of tissue can beuseful,as long asthe whole biopsysite can be fully removed at follow up surgery
Be aware of local anatomy – avoid important structures!

Surgery
If subcutaneous incise overlying skin and blunt dissect down to the mass or LN
Cut a wedge out of the mass – routine closure
Place in formalin
Do not includeformalin histo samples in the same package as slides

Excisional biopsy - removing the entire mass
FNA advised first ideally. Excisional biopsy can potentially be used without FNA in:
Mammary masses
Haemorrhaging splenic masses – emergency
Deep pulmonary tumours (FNA superficial ones – syringe on!)
In some cases, for dog masses wherefunds are limited
60% skin masses benign in dogs vs only 20% in cats

Not appropriate for:
Masses of an unknown diagnosis
Poorly defined masses
Inflamed or oedematous masses (e.g. MCT)
Rapidly growing masses (feature of malignancy)
Ulcerated masses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

HEAT DIFFUSING IMAGING for neoplasia

A

Cancer cells have different thermal properties than normal tissue. Heat waves (visible blue light) are sent into the mass and are read by a thermal sensor. This is thenassessed by AI and a numerical value is generated:

1 – 4 increased risk of malignancy, further testing recommended (FNA)

5 – 10 the mass appears to be benign (98% certainty)

It cannot diagnose the mass, only give an indication of benign vs malignant

Limitations:
Deep s/c masses
Large masses
Some cysts

False positives can occur in some of the above cases. Further testing would then be advised which would then identify that they areactually benign

Interesting novel, non-invasive technique. Likely further research is required

Cost:
£80/mass local Staffordshire corporate 11/23

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

TUMOUR STAGING – HAS IT SPREAD? TNM

A

T – Tumour – What is the primary tumour? - Grade?

N – Nodes – Has it spread to the local lymph node? – FNA, biopsy

M – Mets – Has it spread to distant sites? – Imaging – Thoracic radiographs and abdominal ultrasound vs CT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

pulmonary mets diagnostics

A

Nodular interstitial pattern

Always take 3 inflated views:
R lateral
L lateral
VD or DV

THORACIC RADIOGRAPHS:

Pulmonary METS under 3 – 5mm are not visible

CT
Preferred to radiographs where possible
Able to detect pulmonary masses as small as 1 – 2mm

Even CT has limitations:

Osteosarcoma -the chestCT may benormal, but around95% of dogs havemicrometastasesat thetime of presentation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Abdominal ultrasonography for METS

A

Can be limited by patient size and equipment/operator- Even specialist diagnostic imagers often CT abdomens of large dogs >30kg beforeultrasound

Ultrasound cannot distinguish between benign and malignant nodules just on appearance-
The exception are targetnodules - 81% predictor of malignancy wherethere are multiple in oneorgan

FNA’s of nodules. Benign regenerative liver nodules are common in olderdogs so a dog should notbe suspected of havingMETS (and then euthanised) just off ultrasound

A liver and spleen can also have MCT METSand look normal on scan!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

ONCOLOGICAL SURGERY

A

KNOW WHAT IT IS BEFORE YOU ATTEMPT TO REMOVE IT!-

With diagnosis and staging you can provide the owner with all the necessary information to make their decision
You do not need to know all the median survival times and treatments off the top of your head, this can be researched once a diagnosis is achieved

IS SURGERY EVEN APPROPRIATE?-

What is the prognosis with or without surgery?
What is the expected benefit?
Will surgery be curative?
What will the impact of surgery be? (to the patient and owner finances)

SURGICAL PREP-
Gentle surgical prep to reduce the risk of tumour seeding
Strict asepsis due to the higher risk of post op infections in cancer patients

SURGICAL MARGINS-
The amount of normal tissue around the tumour that is resected
Narrow surgical margins can be obtained in benign masseslimiting morbidity
If narrow margins are obtained in malignant disease, it is likely to result in treatment failure

The aim is to fully remove the tumour with appropriate margins on the first surgery to get the best chance of a cure-

Tumours are more active at their edges. Partial resection leaves the most aggressive cells behind

There will be less tissue available for closure second time round. A wider resection is also needed second time round which can compoundthe problem.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

SURGICAL MARGINS for neoplasia

A

Narrow margins – up to 1cm – Suitable for benign masses

Wide excision- 2cm+ depending on grade, plus a fascial plane-
-Low – intermediate grade MCT -2 cm and one fascial plane (1cm for low grade)
-High grade MCT – 3 – 4 cm and one fascial plane

Radical excision – The removal of the tumour with extensive margins (includes limb amputation)

CAN YOU GET THE REQUIRED MARGINS?

Tumour location may make it difficult or impossible to get appropriate margins (for example – distal limb)

Advanced surgical skills may also be required to close deficits created by these surgeries (surgical flaps etc.)

Referral may be required

Even in referral hands margins may be impossible to achieve due to tumour size and location

This is where adjunctive treatments play a role

Chemotherapy to shrink a tumour pre surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

General surgical principles for malignant neoplasia:

A

Be careful with tumour manipulation during surgery as this could seed cells – use atraumatic forceps rather than rat-tooth’s

Ligate vascular supply to the tumour as early as possible

If there are any adhesions to the tumour remove these with the mass as they could have tumour cell invasion

Remove local LN if staging has shown them to be affected or if they appear grossly abnormal during surgery. Biopsy normal appearing local LN

Lavage the op site post excision and change, drape, kit and gloves prior to closure

Adhere to normal surgical principles of closing dead space and reducing tension

Avoid chemotherapy 7 days prior to surgery and 7 days post-surgery – can affect wound healing

Approximate first opinion costs of GA, surgery, histology

£600 - 800 for an average size mass
£1000+ for more involved surgery

Cost could be reduced where needed, depending on the case,as long as the potential impacts are discussed:
No pre-GA blood – save £65
No IVFT – save £110
No histology – save £165

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

CHEMOTHERAPY

A

The use of cytotoxic drugs to kill tumour cells

Chemo drugs target rapidly dividing cells:

Tumours with a high growth rate (high grade and mitotic index)
GI tract and bone marrow- Diarrhoea and myelosuppression

The dose and frequency used aims to balance effective tumour kill whilst minimising side effects by allowing time for normal tissue to recover

Lower dosages are used in veterinary medicine compared to human oncology. We want to improve median survival times in our patients whilst limiting any negative side effects

As the main treatment for conditions such as lymphoma/leukaemia andmetastatic neoplasia

After the surgery of tumours with a high risk of metastasis- Intermediate grade MCT with a high mitotic index, high grade MCT, osteosarcoma,haemangiosarcoma

Neoadjuvant chemo to reduce a non-operable tumour into a smaller operable size

For in-operable chemo-sensitive tumours

There are published protocols for a variety of neoplasticconditions, but in an ever-evolving field it can be useful to contact an oncologist for advice

Chemopetis an oncologist led business that provides expert advice and pre prepared chemotherapeutics to first opinion practices

Cytotoxic drugs are carcinogenic, mutagenic, teratogenic, abortifacient and increase the risk of stillbirth.

At risk people should avoid administering chemotherapy and being around patients posttreatment

At risk groups:
Pregnant, lactating or people trying to conceive
Young children and elderly people
Immunocompromised people

Safe handling is essential to reduce the risk to staff and owners

Appropriate PPE:
Thicker nitrile gloves
Gown
Face shield/eye protection
Mask

Use PPE when handling patient urine, faeces, saliva or vomit.

Drug residues can be found in the urine and faeces for around 7 days
Double bag faeces
Pour water over the site of urination/defecation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

CHEMOTHERAPUTICS Safety considerations

A

Safe administration of injectable chemotherapeutics

PPE

Low risk staff

Safe handling using a needle free closed system to reduce the risk of spillage

Appropriate disposal of materials contaminated with cytotoxic residues

miroclave extentsion set
syringe with spyros attached

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

CHEMOTHERAPY – PATIENT CONSIDERATIONS

A

Chemotherapy drugs have a narrow therapeuticindex so accurate dosing is essential:- Use mg/m^2 rather than mg/kg for most dosages (table in the back of the formulary)

Save peripheral veins for chemotherapy – take bloods from the jugular

“One-stick” technique when placing IV catheters- Avoids multiple punctures of the vein that could lead to chemo drugs leaking perivascular
Draw back to demonstrate a “blood flash”

Vincristine, vinblastine and doxo/epirubicinare vesicants – local tissue necrosis can occur if the chemo leaks outside the vein
Early signs of extravasation:
Pain, swelling and redness at the catheter site

If extravasation is suspected:
Stop the chemo
Attach a new syringe and try to aspirate as much as possible
Cold and warm compresses – contact an oncologist for specific treatments where available

iv protocall-
Pre-procedure checks – Appropriate neutrophil count - >1.5 × 10^9/L - if less, delay treatment (2 – 7 days) & reduce dosage (10 – 20%)

Maropitant

First stick catheter

Attach extension set with the clave port

Saline flush and demonstrate “blood flash”

Put on PPE
Attach the chemo syringe Spirosto the clave port

Administer the chemo at an appropriate rate

Monitor for signs of extravasation

Flush 10 – 15ml saline through to clear drug residue from the catheter lockoff and do not disconnect

Remove the IV, extension set and syringe as one and put into cytotoxic bin

Apply dressing – remove PPE and wash hands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

CHEMOTHERAPY – PATIENT SIDE EFFECTS

A

GASTROINTESTINAL-
Diarrhoea, nausea/loss of appetite
Pre-treatment with maropitant – oral for home use
Delayed ileus with vincristine – metoclopramide and supportive treatment

MYELOSUPPRESSION-
Takes time for max suppression – monitor the neutrophilnadir(peak of suppressiom) – around 7 days (5-10)
Risk of sepsis if the neutrophil count drops <0.75 × 109/L- Prescribe prophylactic potentiated amoxicillin
Febrile neutropaeniais an emergency – isolation, IV broad spectrum AB including a fluroquinolone

STERILE HAEMORRHAGIC CYSTITIS-
Cyclophosphamide

RENAL TOXICITY-
Carboplatin and cisplatin

CARDIOTOXICITY-
Doxo/epirubicin

HEPATOTOXICITY-
Lomustine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

ELECTROCHEMOTHERAPY (ECT) for neoplasia

A

Electrical pulses are administered to a mass after an IV or local dose of chemotherapy

The electrical pulses make the tumour cells more permeable to the chemotherapy drug allowing greater uptake and increased sensitivity to the drug- may decrease dose needed

Side effects are generally low but can include local inflammation and myelosuppression

Whilst general chemotherapy for conditions such as lymphoma can be performed in general practice ECT typically requires referral

Treatment is administered under GA/sedation and often two treatments are used two weeks apart

Indications:
Tumours that are inoperable
As part of palliative care in advanced disease

Typical tumours treated:
Carcinomas such as nasal squamous cell carcinomas in cats
Mast cell tumours
Melanomas, sarcomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

radiotherapy for neoplasia

A

High energy x-rays from a linear accelerator can beused to killcancer cells

Indications:
Tumours of the nasal cavity (carcinoma, lymphoma)
Brain neoplasia – Meningioma
Palliative pain relief of bone tumours such as osteosarcomas
Palliative care of inoperable tumours e.g. oral malignant melanoma that is not amenable to surgery
After the surgical removal of invasive tumours (mast cells tumours, soft tissue sarcomas) to reduce the risk of regrowth

Acute:
Inflamed skin, hair loss etc.
Reversible

Late:
Damage to vascular and connective tissue
Cataracts, retinal issues,skin & joints etc.
Rarely neoplasia
Irreversible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

CANCER TREATMENT- PAIN

A

The control of pain is essential in all aspects of veterinary care to ensure patient welfare

Sources of pain in oncology patients:

The cancer itself – bone neoplasia is notoriously painful

The treatment – surgery etc.

Pre-empting pain and multi-modal analgesia is essential. Chronic pain is often underestimated

Multi-modal analgesia-
NSAIDs – Ensure no contraindications and do not give to patients having corticosteroids as part of their treatment

Paracetamol – Dogs only

Gabapentin – Good for neuropathic pain

Monoclonal antibodies targeting nerve growth factor (Librela/solensia)

Amantadine – Good for pain refractory to NSAIDs but could be restricted

Ketamine – Low dose subcutaneously – monthly to weekly

Antidepressants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

CANCER TREATMENT- EUTHANASIA

A

One of the options to alleviate pain and suffering in our patients

It must be approached with great care and empathy

In our patients it could be due to welfare of the patient and/orcost concerns

We need to be compassionate and ensure the process goes as smoothly as possible

lead with open questions. “Have you thought about euthanasia” is too direct and can be jarring

“How is Kevin getting on?”

“How are you feeling about his treatment?”

If open questions do not prompt the discussion and you are concerned about the patient’s quality of life a delicate more direct approach can be considered:

“We always have to be mindful of how happy our pets are. Are we having more bad days than good days?”

“I’m worried Kevin is not doing as well on treatment anymore. What do you think?”

Quiet private room and where possible ensure there is enough time

Ensure consent and understanding
“Put to sleep term”
Options for their pets afterwards
Signed consent form

Discuss the procedure and whether owners would like to stay
Most do but never assume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

SEBACEOUS ADENOMAS

A

Benign
Raised pink to pigmented lobulated masses – “wart like” – “brains”
Common in middle aged to older dogs – terriers, poodles, cocker spaniels

The appearance is fairly typical but ddx can include:
Viral papilloma  
Dermal MCT
Melanoma
Basal celltumour
Squamouscellcarcinoma
Melanoma

Diagnosis:
High suspicion on gross appearance – definitive by FNA/histo

Treatment:
Not required if not causing a problem – just cosmetic
Surgical excision if bothering the dog

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Common neoplastic conditions of the skin

A

SEBACEOUS ADENOMAS
BENIGN CUTANEOUS CYSTS
HISTIOCYTOMAS
LIPOMAS
CANINE MAST CELL TUMOURS (MCT)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

BENIGN CUTANEOUS CYSTS

A

Multiple types which can be considered under the umbrella term of cyst
Follicular cysts – Dermal raised masses filled with a thick keratinaceous material (cheese/paste like on gross FNA) – dilated hair follicles
Sebaceous cysts – look similar – develop in and around the sebaceous gland

Both can rupture generating an inflammatory response and secondary infection

Common in multiple breeds of dog including Shih Tzus, Hounds, Schnauzers and Boxers

Ddx – dermal MCT, deep pyoderma – can look similar to a ruptured cyst

Diagnosis:
Suspicion on appearance and paste like gross FNA material
Benign on heat imaging although false malignancies can occur
Definitive on FNA/histo

Treatment:
Monitor vs surgical excision
Excision recommended for cysts that are prone to rupture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

HISTIOCYTOMAS

A

Benign small pink-red domed cutaneous mass, often found on the limbs, ears or head/neck

Common in young dogs <2 years but can be seen in middle aged dogs too

They can ulcerate -> self-trauma

Ddx
Dermal MCT, Ulceratedmelanoma, Cutaneous lymphoma
Non neoplastic lesion – inflammation, FB, insect bite

Diagnosis:
Suspicion on appearance in a young dog on the limbs
Benign reading on heat imaging
Definitive on FNA (ideal)

Treatment:
May regress spontaneously in a month or so
If not and/or bothering the dog – surgical excision is curative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

LIPOMAS

A

LIPOMAS

Subcutaneous mass made up of fat cells, normally soft and mobile on palpation (occasionally can be found internally)

Very common in middle aged to senior dogs

Gross oily fat on slide after FNA

Ddx:
S/c MCT, soft tissue sarcoma, liposarcoma

Diagnosis:
“Targeted” FNA
Cytology will come back as “lipid”, but this could be just subcutaneous fat, so the clinician needs to ensure the FNA was directly from the mass

Treatment:
None required unless growing in an areas that could cause a problem – axillae - surgical excision

Is it appropriate to diagnose a lipoma based off the exam and demonstrating a fatty oil-like appearance on gross FNA?
No – some neoplasia such as MCT can appear fatty
Yes & no – Where funds are limited, or surgery would never be considered
As long as the limitations are discussed with the owners and documented in the clinical notes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

CANINE MAST CELL TUMOURS (MCT)

A

Mast cells have an important role in inflammatory, immune and allergic reactions

They are present in most tissues in the body and malignant transformation leads to MCTs

7 – 21% of call canine skin tumours

Majority are dermal but they can be subcutaneous

Predisposition:
Any breed but particularlyBulldogs, Staffordshire bull terriers, Boston terriers, Boxers, Pugs, Beagles, Lab/Golden Retrievers, Dachshunds, Shar-peis, Rhodesian Ridgebacks, Weimeraner

Pugs are prone to getting multiple low grade MCT
Shar-peis tend to get high grade metastatic disease

Appearance - Variable – why FNA is so important

Approx 2/3rds of masses may show benign behaviour and present as a slow growing cutaneous lesion

Subcutaneous masses are often less aggressive and may appear like lipomas – FNA’s are very important

Masses can be inflamed from histamine release and can wax and wane in size (vomiting, diarrhoea/melaena)
Rapid growth and mass ulceration can be seen in high grade MCT

MCT diagnosis
FNA -fine basophilic cytoplasmic granules

The Camus grading system and 2022 Paes adaptation were developed to try and give an indication of grade based off cytology

The study showed a high correlation between cytological and histopath grade so it can give a good initial indication

Cytology can overestimate the grade compared to histo

MCT Grading from Histopathology:

Currently only apply to cutaneous MCT’s not s/c ones although dogs with s/c MCT’s tend to have a longer survival time

Various grading systems -Patnaik orKuipel

Grade correlates to prognosis

OTHER PROGNOSTIC INDICATORS-
Size and growth rate – High growth is a sign of malignancy, larger MCTs are harder to remove

Appearance – Inflammation, ulceration and pruritus = poorer prognosis

Systemic signs – vomiting and melaena = poorer prognosis

Breed- pug low grade, sharpei high grade

Location – In some but not all studies, preputial, muzzle, nail bed, perineal and those in mucocutaneous areas = a poorer prognosis

Grade is the most important prognostic indicator

The histology report will come back with the grade and the option of further testing - proliferation markers. These can provide more prognostic information

Ki67 – identifies the growth fraction (activelydividing cells)

AgNOR– identifies the generation time (speed ofcell cycle progression

They can cost an extra £300 odd to test
SHOULD WE TAKE AN INCISIONAL BIOPSY AFTER FNA OF EVERY MCT TO ALLOW FULL GRADING?

Historically yes – before the cytological grading system was developed this was the only way to establish the MCT grade to then know what surgical margins to take

Today with a good cytological grading system we often decide on appropriate staging and treatment based off the FNA grade and other prognostic indicators

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Patnaik Grading

A

CANINE MCT - GRADING

Grade 1 (low grade, well differentiated)– no mitotic figures

Grade 2 (Intermediate)
0 – 2 mitotic figures per hpf, some pleomorphic cells- variation in size
Areas of oedema and necrosis
Infiltration of lower dermis/subcutaneoustissue

Grade 3 (high grade, poorly differentiated)- multiple abnomal cells
3 – 6 mitotic figures per hpf, sheets of pleomorphic cells
Odema/necrosis/haemorrhage and ulceration is common,
Infiltration of lower dermis/subcutanous tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

KuipelGrading

A

Low grade

High grade-
7 or more mitotic figures

Generally low mitotic index and well differentiated = lower grade and better prognosis

High mitotic index (>5) and poorly differentiated = higher grade and worse prognosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Canine MCT – Proliferation markers

A

Ki67 from immunohistochemistry:
A high Ki67 expression = increasedrate oflocalrecurrence, metastasisand mortality

This can be useful for intermediate grade MCT as around 30% of these are found to be more aggressive when Ki67 tested(Van Erp, M et al)

HigherAgNORcounts are also associated with an increasedrate of localrecurrence, metastasisand mortality

55
Q

CANINE MCT – APPROACH TO STAGING AND TREATMENT when FNA suggests a low-intermediate grade + no other negative prognostic indicators

A

FNA the local LN

LN positive for METs-
Full staging
Abdominal ultrasound
FNA lesions
FNA liver and spleen even if they look normal
Lung METs are very rare
–>
LOW – INTERMEDIATE GRADE WITH METS
2cm margin, 1 facial plane excision

Remove the metastatic LN

Grade the mass and assess margins

Chemotherapy

OR

LN negative-
Surgical excision
2cm* margin & one facial plane
Biopsy the local LN if the FNA was inconclusive
Grade
Assess margins
–>
LOW – INTERMEDIATE GRADE CLEAN MARGINS (no METS)
No further treatment

Consider proliferation markers for intermediate grade

Monitor the site

For low grade reoccurrence risk is low

For intermediate grade this risk is slightly higher (up to 23%)

consider the implications of histamine release during surgery

Chlorphenamine is used pre-op alongside omeprazole which is continued post operatively

56
Q

CANINE MCT – HIGH GRADE

A

Referral where possible – they are very difficult to manage

Wide excision + post op radiotherapy + chemotherapy (regardless of margins achieved)

High grade MCT median survival time (MST) with surgery = 3.5 months

Surgery + radiotherapy = 20 months

Surgery + radiotherapy + chemotherapy = 65% of patients alive at 3 years

57
Q

CHEMOTHERAPY FOR CANINE MCT’S – WHAT AND WHEN?

A

INDICATED POST SURGERY FOR DOGS WITH POOR PROGNOSTIC INDICATORS:

High grade III MCT

High mitotic index

Intermediate grade with high prognostic indicators

METs

Other factors such as tumour location and malignant features

Chemo is often started around 2 weeks post op to allow time for wound healing

Typical first line protocol
IV vinblastine – 8 doses – weekly for the 1st 4 then every 2 weeks
Oral prednisolone

In cases wheregross disease is present this protocol may be continued weekly until full effect is seen then the frequency decreased. In some cases, lomustine is used
Contacting an oncologist is advised!

MCT location (such as on the distal limb) can make it impossible to achieve the desired surgical margins.

Options for these cases:
Referral
Pre op (neo-adjuvant) chemo can shrink some non-operable masses down to an operable size
1 – 2mg/kg prednisolone for 7 – 10 days prior to surgery +/- vinblastine
Pre op radiotherapy
Tigilanol Tiglate (Stelfonta®) intra-tumour injection

58
Q

TigilanolTiglate

A

(Stelfonta®) - A natural molecule extracted from the seed of an Australian plant. Injected intra-tumour

Itbreak down the tumour cell walls and blocks blood vessels to the mass –> inflammation, tumour necrosis & drop off –> wound healing

For non-resectable, non-metastatic mast cell tumours of the following types in dogs:

  • Cutaneous mast cell tumours (located anywhere on the dog)
  • Subcutaneous mast cell tumours located at or distal to the elbow or the hock.

Tumours must be less than or equal to 8 cm3in volume and be intact/non ulcerated to avoid product leakage

Local LN must be FNA’d or biopsied first

Prednisolone and H1/H2 receptor blocking agents are neededboth before and aftertreatment

Sedation can be required along with a 2nd injection in 4 weeks
Cost £400 per vial

59
Q

TYROSINE KINASE INHIBITORS

A

CANINE MCT
Anti-cancer and anti-angiogenic properties

Toceranib is licensed for use in recurrent, non-resectable intermediate or high-grade MCTs

Masitinib is licensed for use in non-resectable intermediate or high-grade MCTs with demonstrable c-KIT mutations.

Not first line therapy - reserved for masses where clean surgical excision is not possible, or where surgical excision to microscopic disease followed by radiation is also not possible

60
Q

Mammary neoplasia

A

In dogs – approximately 50% are benign, 50% are malignant

Malignant transformation of benign mammary masses can occur with time

Entire bitches and those neutered late are predisposed

Can present as a single mass or multiple along the chain

Smaller mobile masses <3cm are more likely to benign vs larger masses which can grow rapidly and ulcerate

In cats’ mammary masses are rarer but up to 95% are malignant

MAMMARY MASS DIFFERENTIALS-
Ductal and lobular hyperplasia – can be influenced by oestrus

Mastitis

Mammary enlargement related to oestrus

Pregnancy or pseudopregnancy

DIAGNOSIS-

FNA-
Not commonly performed as it normally cannot distinguish between benign vs malignant
Benign mammary masses should be removed anyway to avoid malignant transformation
Could be used to rule out other differentials such as ductal hyperplasia

EXCISIONAL BIOPSY-
Removing the entire mass and then sending for histo is performed most commonly

Cases with small solitary mobile lesions <3cm are more likely to be benign

These cases could be taken straight to surgery and the mass assessed on histo post excision

If benign – no further staging or treatment if needed

If it was malignant –> full staging

This approach can save client funds and reduce the length of GA

Full staging should be performed on all cases with larger or multiple mammary masses

This helps with prognosis and decision making
Is it fair to do two mammary strips in a dog with pulmonary METs?

The surgical approach depends on the case

Neutering has no effect on future malignant mammary tumour development, or on incidence of metastatic spread

It can be considered in entire bitches however to eliminate the future risk of pyometra

61
Q

Mammary neoplasia - Surgery

A

Single or regional (more than one gland) mastectomy is generally indicated
2cm margin and one facial plane

Mammary strips (radical mastectomy) +/- local LN are used when multiple masses are found along the mammary chain

Surgery is normally staged in bilateral disease

62
Q

Mammary neoplasia ->Further treatment

A

Repeat surgery for dirty margins or for very narrow margins in high grade disease

Chemotherapy is debatable but normally recommended for high grade tumours or if there is evidence of LN METs

Various protocols:
Single agent carboplatin
Single agent doxi/epirubicin
They are given once every 3 weeks for 4 – 6 treatment

If chemo is declined for personal or cost reasons ongoing NSAIDs (meloxicam) could be considered as they have some anti-neoplastic properties with carcinomas

Neutering before the first season drops the risk to 0.5%

Note - this must be balanced against the behavioural impact of early neutering and the increased risk of joint disease and bone neoplasia seen with neutering before the first season in some larger breeds of dog

For this reason, neutering is often advised to be performed around 3 months after the first season

Neutering after the first season, prior to the second – 8%
Neutering after the second season, prior to the third – 26%

63
Q

GENERALISED LYMPHADENOPATHY

A

Multicentric lymphoma
Reactive

Infectious-
Severe generalised pyoderma
Leishmania, Ehrlichia,Babesia (important in travelled dogs)
Brucellosis
Aspergillus

Inflammatory
Mineral associated lymphadenopathy
Leukaemia
Secondary to METs from other neoplasia

64
Q

Canine lymphoma

A

Neoplasia arising from lymphoid tissue

7 – 24% of all canine malignant neoplasia

Various forms
Cutaneous
Alimentary
Thymic
Hepatic etc

We will be focusing on the most common form
Multicentric lymphoma (around 70% of all lymphoma cases)

Any breed can be affected, higher incidences in:

Golden Retrievers
GSD
Boxers
Cocker spaniels
Basset Hounds
Scottish terriers
Rottweilers

Affected dogs are normally middle aged but younger patients can be affected too.

Most dogs are well on presentation with no clinical signs other than the generalised peripheral lymphadenopathy, normally affecting all peripheral LN.

Owners typically noticed the enlarged submandibular LN

20 – 40% of cases present with additional clinical signs:

Lethargy
Anorexia
Weight loss
Vomiting

Dogs that present with these clinical signs typically have shorter survival times

Diagnosis is normally straightforward and involves FNA of the enlarged LN – sample multiple nodes - The

Once diagnosed we need to discuss with the owner the implications of this diagnosis

Rapid progression to death without treatment 4 - 6 weeks
Most patients however do well on treatment and whilst it cannot be cured, remission with a good quality of life can be achieved

65
Q

Canine multicentric lymphomaImmunophenotyping & staging

A

We also need to discuss the costs and benefits of finding out the specific type of lymphoma (immunophenotyping) and disease staging

The form of lymphoma (B vs T cell) and whether it is low or high grade,has a big impact on prognosis and treatment

Most are intermediate to high grade and B-cell phenotype

High grades can be identifiedon cytology, but low grades may need LN biopsy and histopathology to identify- They are often resistant to doxorubicin (commonly used in lymphoma) so a different protocol should be used

B-cell lymphoma - the most common form (70% of cases)

High grade T-cell lymphoma – Aggressive and have a poorer prognosis

Low grade T-cell lymphoma (Indolent)
Better prognosis of around 2 years
Chemo does not affect prognosis and so may not be needed, only if the disease if progressing

NK-cell lymphoma – Like high grade T cell is associated with a shorter remissionand survival times

PARR CLONALITY-
You can ask the lab to run this PCR test on the FNA slide you already submitted
It identifies whether the lymphoma is T-cell or B-cell
Useful if the owner declines further sampling

FLOW CYTOMETRY-
Uses a liquid suspension of a fresh fine needle aspirate
More accurate than PARR

IMMUNOHISTOCHEMISTRY – On LN biopsy

BLOODWORK -Haematology, Biochemistry &Urinalysis

Needed to assess co-morbidities that could affect treatment, for screening of paraneoplastic disease (hypercalcaemia) and for staging

Further staging (ideal for unwell patients) involves imaging the thorax and abdomen +/- sampling (aspirating liver and spleen for example)

Always be mindful of costs and ensure this does not impact on treatment

66
Q

Canine multicentric lymphoma-Treatment - chemotherapy

A

As a systemic disease chemotherapy is the treatment of choice

As a rough guide multidrug chemotherapy will induce remission (happy dog with no detectable disease) in 60 – 90% of patients

80% of patients live for a year, 20% of these up to 2 years

This does depend however on grade and phenotype

Treatment choices will be impacted by owner views, the individual dog (co-morbidities, bad at the vets etc.) and finances

Oral prednisolone only-

Remission achieved in 45 – 50% of cases

Remission lasts 60 – 90 days

Fairly common low-cost palliative option

Note – cannot start treatment with prednisolone alone and then decide to use a full chemotherapy at a later date as the efficacy will then be reduced

67
Q

Canine multicentric lymphomaTreatment – B-cell lymphoma

A

CHOP PROTOCOL-
The most effective protocol currently for B-cell lymphoma (8K)

Vincristine (IV), Cyclophosphamide (PO), Epirubicin/doxorubicin (IV), Prednisolone (PO)

Weekly induction protocol, moving to every 2 weeks. 25-week duration – then stops

90% of dogs (with uncomplicated B-cell lymphoma) go into remission with this protocol
Duration of first remission is 10 – 12 months on average

There is no maintenance phase after this protocol.

When most patients come out of remission a rescue protocol can be considered

COP PROTOCOL INDUCTION
Shorter 8-week induction with Cyclophosphamide (PO), Vincristine (IV),Prednisolone (PO)

Then ongoing maintenance protocol – IV & oral protocols vs less expensiveoral only protocols

70% remission with B-cell lymphoma

Average first remission time of 5 – 6 months

68
Q

Canine multicentric lymphomaTreatment – High grade T-cell

A

High grade T-cell lymphoma carries a worse prognosis

Shorter remission times are seen with “standard” lymphoma protocols, so the LOPP protocol is favoured

Includes alkylating agents such as lomustine and procarbazine alongside prednisolone and vincristine

Use for 6 months and then followed by a maintenance protocol

6 – 11 months median survival time

In cats and some dogs, sedation is used to facilitate the first stick catheter

This does require a lot of sedations depending on the protocol so this may not be appropriate in every case

Oral only palliative protocols could be used (which are also lower cost) such as prednisolone only or prednisolone in combination with other oral chemotherapy agents

69
Q

Canine multicentric lymphomaTreatment – Low grade T cell

A

Low grade T-cell lymphoma is the least aggressive form

Median survival time of around 2 years

Treatment is not always needed unless there are clinical signs in which case prednisolone and chlorambucil tablets are the treatment of choice

Prednisolone every 48 hours and chlorambucil every 2 weeks

70
Q

FELINE ALIMENTARY LYMPHOMA

A

Lymphoma is the most common neoplasia in the cat

Like the dog there are various types but, in the cat,alimentary lymphoma is the most common anatomical form

The median age of affected cats is 10 – 13 years

Cats may present with vomiting, diarrhoea, and weight loss

Low grade lymphoma leads to diffuse thickening of theintestinal tract, and it can be tricky to distinguish from inflammatory IBD​

Intermediate to high grade lymphomas generally presentwith a palpable abdominal mass and often present moreacutely and severely than the low-grade form​

Patients are more likely to present with GI obstructionwith the intermediate-high grade as the mass can block the bowel

71
Q

FELINE ALIMENTARY LYMPHOMA (AL)Low grade AL (LGAL)

A

Cases present similarly to IBD with chronic gastrointestinal signs andweight loss. Appetite can be normal, reduced, or increased

Intestinal thickening and enlarged mesenteric lymph nodes may be palpable

differentails
Routine bloodwork, urinalysis and TT4
In limited finance cases biochemistry plus T4
If super limited just biochemistry (ALT is up in most hyperthyroid cats and there is often other clinical signs)- Other hyperthyroid clin sig:
Normal to PP appetite
Palpable goitre
Tachycardia/gallop/murmur
Dry, unkempt coat
Spicey

FPLi for pancreatitis where appropriate, FeLV/FIV

If all normal – imaging and cobalamin testing (B12)
Then diet trials, faecal testing, intestinal biopsy etc.

Rule out non-GI disease with bloodwork

Cobalamin (B12) bloods
Hypocobalaminemia can be present in up to 78% of cases

Abdominal ultrasonography
Could be normal!
Often seeintestinal thickening, especially of the muscularis layer+/- mesenteric lymphadenopathy
You also see this in IBD!

As the u/s appearance is not specific further testing is required

Fine needle aspiration of enlarged mesenteric LN and PARR clonality can be used to try and achieve a diagnosis of LGAL over IBD but this is not always possible

Gut biopsy

FOR DIFFUSE ALIMENTARY NEOPLASIA -Such as feline alimentary small cell lymphoma

Endoscopic pinch biopsy vs full thickness surgical

Endoscopic:
Less invasive – especially important in hypoproteinaemia – poor healing
Further equipment and expertise required
Smaller sample – less chance of diagnosis

Surgical:
Larger sample including all layers – increased chance of diagnosis
Multiple areas of the GI tract can be sampled
More accessible in first opinion practice
Ideal for ileal biopsy in low B12 cases as upper GI endoscopy cannot get to the ileum
Higher risk of complications which can be very serious – peritonitis
Dehiscence risk of 1.9% (Swinbourne et al. 2017 vs older report of 12%

72
Q

FELINE IBD TREATMENT

A

Diet-
Hydrolysed/hypoallergenic (Purina HA),or novel
Pre and probiotics can play a role

Supplement B12

Faecal sample/fenbendazole trial

Prednisolone anti-inflammatory to immunosuppressive dosages

Chlorambucil if signs persist

73
Q

FELINE ALIMENTARY LYMPHOMALGAL TREATMENT

A

B12

Prednisolone 2mg/kg then taper based on response and chlorambucil 20mg/m^2 every 2 weeks

Diet
Pre and probiotics
Supportive treatment
Mirtazapine appetite stimulation etc.

Prognosis – 70% chance of remission (95% partial response), 26 – 29-month median duration of remission

74
Q

FELINE INTERMEDIATE-HIGH GRADE ALIMENTARY LYMPHOMA (I/HGAL)

A

Clinical signs are normally more acute, and cats are often unwell

Cats present with GI signs and a palpable abdominal mass in the majority of cases

GI obstruction or intussusception can occur in some cases

Ultrasound-
Identify the mass

FNA-
May require PARR testing ifinconclusive cases

Treatment-
Chemotherapy (e.g. COP)
MST 1 – 3.5 months
7 – 10 months in 33% of cases that fully respond
Palliative prednisolone
B12 supplementation if needed

IF THE CAT IS VOMITING AND HAS GI OBSTRUCTION:

Stabilisation and surgery is required – end to end anastomosis

75
Q

CANINE OSTEOSARCOMA

A

The most common primary bone cancer in dogs

They are seen more often in larger breeds and cause significant pain, lameness and occasionally, pathological fractures

Microscopic METs are present in around 95% of cases at the time of diagnosis

Often larger breeds:

Dobermans
Greyhounds
Rottweilers
German Shepherd dogs
Golden Retrievers

Great Danes​
Irish Setters​
Irish Wolfhounds​
Deerhounds​
Saint Bernard​

It can occur insmaller breeds, butit is rarer.

Progressive lameness-
Can become non weight bearing
Initially maybe partially analgesic responsive

Limb swelling/mass-
More obvious when the distal radius/tibia is affected

Pathological fracture-
Not as common a presentation but it is still seen
Any large breed dog presenting with a fracture should have the radiographs scrutinised closely for any traces of possible bone neoplasia

76
Q

CANINE OSTEOSARCOMA - DIAGNOSIS

A

Radiographs-

Typical appearance on radiographs:

Single, aggressive bone lesion
Forelimb – Proximal humorous and distal radius
Hindlimb – Distal femur, proximal and distal tibia
(“away from the elbow and near to the knee”)

Areas of lysis

Periosteal reaction “sun-burst”

Radiographs are typical but full diagnosis requires cytology or histopath

FNA-
It is relatively non-invasive, quick and can be performed under sedation
A full osteosarcoma diagnosis is not always obtained but a diagnosis of a malignant mesenchymal neoplasia (that is most likely an osteosarcoma) is

Jamshidi needle

77
Q

CANINE OSTEOSARCOMA - STAGING

A

Thoracic radiographs-
3 inflated views

CT is the preferred modality for a MET check-
Note - >40% of METS seen on CT are missed with radiographs
95% of cases have micro-METs at the time of diagnosis that will be missed by imaging

FNA local lymph nodes

78
Q

CANINE OSTEOSARCOMA - Treatment

A

This depends on several factors including patient suitability, the presence of gross METS and owner opinion/finances. Euthanasia will be required in all cases at some point.

Analgesia-
Bone neoplasia’s are very painful
Multi-modal analgesia is required
Most cases are euthanised within the first few weeks - months due to uncontrolled pain or occasionally from pathological fracture
Can be combined with bisphosphonates
Osteoclast inhibitors

Palliative radiotherapy-
Four treatments (fractions) given once a week under GA

Useful in patients that are not good surgical candidates

80 – 90% get a good analgesic response which can last up to 6 months

Unfortunately, pathological fracture or metastatic disease can affect them sooner, leading to a 3 – 4-month MST

AMPUTATION-
Fastest way to a pain free patient, if appropriate

Where gross METS are present the median survival time is 3- 4 months
Surgery where there are gross METS can be considered as part of palliative analgesia but should be carefully discussed with the owner before pursuing

Without gross METS the median survival time is:
6 months with limb amputation alone
Approximately 1 year if combined with chemotherapy, with 20% of patients living for 2 years

LIMB SPARING-
Aim to remove the bone neoplasia and preserve the limb

Higher risk of complications than limb amputation

Survival times are similar to limb amputation
As a highly aggressive malignant cancer chemotherapy following limb amputation is indicated

Various protocols

4 – 6 treatments of intravenous carboplatin every 21 days is used most often

Myelosuppression and GI side effects
The drug also reduces the glomerular filtration rate – watch the kidneys

79
Q

canine transitional cell carcinoma

A

surgery not normally possible due to location-> urethral obstruction

chemotherapy main treatment- treat secondary utis: check sediement, bloods not reliable

80
Q

Canine splenic masses

A

2/3 malignat
80% of cases presenting with haemoabdoent have mailgnant splenic tumour

acutr bleeds-
collapse, lethargy
pale mm
hypovolemia

pu/pd
gi dingd
mass may not be palpable in large dogs
enlarged abdomen

histeopath post splenectomy
non heamoabdomen cases- FNA and cytology

staging- abdo ultrasound
chest radiographs
chech right atrium if possible

individal factors effect treatment

treat hypovolemic shock-
fluid bolus

postop chemo if hsa

chemo- doxyrubicin

81
Q

Main causes of foot pathology in adult sheep in UK/Ireland

A

Interdigital dermatitis (scald)

Footrot

Contagious ovine digital dermatitis (CODD)

Toe granuloma

Toe abscess

Shelly hoof (white line disease) – usually not lame

82
Q

Non-infectious sheep lameness

A

Shelly hoof (white line disease)
Toe granulomas (‘strawberries’)
Foreign body penetration – thorns, sharp stones
Soil balling – mud stuck in the interdigital space causing inflamation
Hoof cracks – exposed corium
Overgrown, damaged or misshapen claws
Injuries to the limb

83
Q

Dichelobacter nodosus

A

primary pathoges for scald and footrot

Primary aetiological agent of interdigital dermatitis (scald) and footrot
Gram negative rod – terminal swellings giving ‘dumbbell’ appearance; anaerobes
Can survive in a wet environment (soil) - reservoir for infection of other sheep – spreads in sheep in wetter conditions – esp. Spring and Autumn in UK
Persists long time on disease interdigital skin and in lesions within the hoof – need to isolate clinical cases – but can eliminate if remove these sheep as environmental reservoir will die out if not seeded repeatedly

Multiple strains – wide range of virulence – some extremely virulent, others benign
Theory: moist, softened or traumatised interdigital skin > inflammation and necrosis facilitates subsequent infections with D. nodosus > footrot develops as scald and can progress to full-blown footrot if not treated
Often also associated with presence of Fusobacterium necrophorum – regarded now to be a secondary pathogen in footrot (excreted in faeces by some sheep)

The microbiome on diseased feet also appears to play some role – some kind of bacterial dysbiosis = footrot

84
Q

primary pathoges for scald and footrot

A

Dichelobacter nodosus
Often also associated with presence of Fusobacterium necrophorum – regarded now to be a secondary pathogen in footrot (excreted in faeces by some sheep)

85
Q

Footrot – treatment

A

The research evidence base shows that:

Aiming to treat within 3 days of onset has the best outcome – inspect flock regularly and pick out anything lame

Treat with antibiotic injection (oxytet. LA) and spray i/d space and foot – don’t trim. Analgesic for pain.

Focus on individuals to reduce flock spread – aim to avoid whole flock treatment

Flocks where feet are never trimmed have the lowest prevalence of lameness

Sheep footrot vaccine – Footvax (MSD Animal Health)- Can be used for prevention or in the face of an outbreak

86
Q

Sheep footrot vaccine – Footvax (MSD Animal Health)

A

‘For the active immunisation of sheep as an aid to the prevention of footrot and reduction of lesions of footrot caused by serotypes of Dichelobacter nodosus.’

Can be used for prevention or in the face of an outbreak

Thick, viscous vaccine (oil adjuvant) so hard to inject in cold weather, and can provoke skin reactions

87
Q

footbaths for sheep

A

10% zinc sulphate solution (or copper sulphate) (frowned upon for heavy metal environmental contamination)

3% formalin solution (carcinogenic chemical for humans, granulomas)

Others: e.g. Digicur Advanced 2% - combination of glutaraldehyde, copper and zinc

Others: e.g. Hoofsure Endurance - organic acids, tea-tree oil and wetting agents

[Antibiotic footbath solutions] - (soluble antibiotics (e.g. lincomycin) licensed for chickens/pigs) - imprudent use and lacking evidence of efficacy!

Lot of vets will support their use, esp. for scald outbreaks in lambs

Evidence for the efficacy of footbaths? Limited actual scientific trial evidence, but very commonly used over the years

results suggest 2% Digicur is ineffective at reducing the load of D. nodosus when applied as a one off or weekly footbath, however sheep may act as a reservoir for multi-drug resistant bacteria creating opportunities to spread antimicrobial resistance to other sheep and their environment.’

88
Q

Contagious ovine digital dermatitis (CODD)

A

First recorded in UK in 1997
Not quite as common as footrot, but still common in the UK (up to 58% flocks in UK)
Severe lameness and significant welfare issue on affected farms
Lesion at the coronary band and then extending under the horn down the toe – end up with avulsion of horn – exposes hoof laminae and affects pedal bone
Staton et al. (2021) found in an experimental study that 84% of lesions arose from existing scald/footrot lesions
Multiple bacteria present in CODD lesions – Treponema spp., D. nodosus, F. necrophorum
The treponemes: Treponema medium, Treponema phagedenis and Treponema pedis found
Can respond clinically to treatment with injectable LA amoxicillin (Betamox LA, Norbrook) or LA oxytetracycline; analgesics

Oxytetracycline injectables: licensed in sheep- Zoetis, Norbrook, MSD, Bimeda

Other antibiotic injectables: licensed in sheep- Norbrook (amoxicillin (not authorised for use in sheep producing milk for human consumption)
), Zoetis (– tulathromycin (macrolide)) , Boehringer Ingelheim (gamithromycin (macrolide))

89
Q

Analgesia in sheep lameness

A

No licensed analgesics in sheep in UK

Use of NSAIDs under the cascade

Some farmers are seeing the benefits of analgesic use – persuaded by vets

Meloxicam most purchased NSAID in this sample of 52 N. Irish farms

More work for vets to do with sheep farmers to educate regarding the benefits for sheep welfare

90
Q

Shelly hoof (white line disease)

A

Detachment of hoof horn wall from the underlying epidermis (often the abaxial wall)

The separation itself does not usually cause lameness, unless horn breaks off to expose sensitive laminae – very painful

Separation leaves a cavity – space for dirt to become impacted

Foreign body penetration easier into sensitive tissues - abscess formation and then severe lameness

risk facotors-
Reeves et al. (2019) found more likely in flocks that were footbathed in formalin compared with not footbathing (OR = 1.65; 95% CI 1.19–2.30)

It was less common in flocks that stocked ewes at higher stocking densities more than eight vs. four per acre (OR = 0.34; 95% CI 0.17–0.68) – why?

Found weak associations between shelly hoof and foot trimming

Reeves et al. (2019) proposed that flocks with shelly hoof would decrease incidence if farmers stopped footbathing (esp. with formalin), and avoided foot trimming whether as a therapeutic or routine practice

91
Q

Toe granuloma (‘Stawberries’) in sheep

A

Granulation tissue in response to injury/untreated footrot
Usually caused by excessive trimming
Bleed profusely and painful
hard to fix- Regrow if removed
Nursing care, analgesia, cull
Footbathing in formalin appears to predispose

92
Q

Toe abscess in sheep

A

Occurs when infection gets into the white line – e.g. stone or thorn penetration – abscess develops under the wall or sole horn
Pus from the coronary band once bursts
Smelly
Hoof likely to be hot to the touch and painful before pus becomes visible
Very painful = acutely lame
Can often see the penetration on white line on sole – gentle paring may reveal

93
Q

Post-dipping lameness in sheep

A

Caused by Erysipelothrix rhusiopathiae (also causes dimond marks in pigs)

Typically, in sheep that have been dipped in a dip that was used the day before and allowed to stand overnight

E. rhusiopathiae contamination from soil the previous day multiplies overnight and enters small skin abrasions – bacterial soup!

Dull, lame and pyrexic within next few days

Can have sizeable proportions of the flock affected, esp. lambs

Treat with injectable penicillin; avoid keeping dip too long

94
Q

Joint ill in lambs (infectious arthritis, polyarthritis)

A

Mainly Streptococcus dysgalactiae subsp. dysgalactiae
Lambs usually < 4 weeks old – clinical signs often at 10-14 days
Swollen, hot joints – lameness, recumbency – outbreaks possible
Thought to be acquired in first few hours of life – ewes, unsanitary conditions, lack of colostrum, untreated navel – umbilical entry, ear tag, tail dock, mouth
Procaine penicillin drug of choice, NSAIDs for pain
Joint pathology can be permanent if does not respond to treatment

95
Q

Preventing infectious sheep lameness

A

Culling policy – breeding for genetic resilience (less susceptible ewes)

Biosecurity - closed flock (rams), quarantine and examine all incomers, prevent straying, transport vehicles, recognize contaminated pastures, move feed troughs, isolate infected sheep if possible

Vaccination – only one vaccine on the market – Footvax (MSD)

Treat individuals promptly and effectively for the benefit of the whole flock

The five-point plaN-
- Treat, quarantine and avoid contaminated pastures to reduce challenge

  • Cull to build resilience
  • Vaccinate to establish protection

Lameness treatment drives most of the antibiotic use in sheep

Emphasis must also be placed on the importance of long-term commitment to lameness control strategies, as there is no one, short-term panacea for controlling lameness

96
Q

Cognitive Dysfunction Syndrome (CDS)

A

Known as well as Canine Cognitive dysfunction (CCD) in dogs, also affects cats (limited data).
Progressive neurodegenerative, linked to aging in dogs and cats and characterised by decline in cognitive performance and behaviour changes.
Risk factors identified in dogs – further research needed (MacQuiddy et al., 2022, Dewey et al., 2019)
Age
Anecdotally mentioned :
Female, neutered, Low BCS,
Diet? One study - high quality, controlled diet are 2.8 times less likely compared to uncontrolled low-quality diet.
Concomitant disease? One study on IE, more likely to develop at young age.

28% for dogs between 11–12 years old and 68% in dogs 15–16 years old. (Neilson et al., 2001)
8.1% in ages 8 to <11 years, 18.8% in ages 11 to <13 years, 45.3% in ages 13 to <15 years, 67.3% in ages 15 to <17 years, and 80% in ages >17 years (MacQuiddy et al., 2022)
14.2% for dogs between 8-19 years old, only 1.9% were diagnosed by a vet. (Salvin et al., 2010)
Cats: 36% 11-21y, 50% at 15+ and 28% 11-14y. (Moffat et al., 2003)

Pathophysiology - Pathologic features:
Perivascular and parenchymal neurotoxic amyloid beta (Aβ) protein accumulation into plaques that affect exchange at level of BBB.
Cerebrovascular diseases: decreased oxygenation to affected part of the brain.
Oxidative brain damage, due to decrease in endogenous antioxidants, leading to neuronal death and increase in free radicals. Reminder: brain tissues has high level of polyunsaturated FA, very sensitive to oxidative damage from free radicals.
Neuronal mitochondrial dysfunction
Decreased neuronal glucose metabolism
Glutamate-mediated excitotoxic neuronal damage
Decrease in catecholamine (Norepinephrine, dopamine), serotonin and GABA neurotransmitters and cholinergic system dysfunction, increase in monoamine oxidase B activity (MAOB)

Structural features:
Cerebrovascular disease: hemorrhages or infarcts
Meningeal calcification,
Reduction of overall brain mass (frontal and temporal lobes, hippocampus) with degeneration of white matter, demyelination,.
Increased in ventricular size

Generalised gliosis:
Microglial dysfunction: pro-inflammatory
Astrocyte dysfunction: increased neuroaxonal degeneration, decreased glutamate uptake, increase in free radicals.

97
Q

Clinical signs of Cognitive Dysfunction Syndrome

A

Often unreported and missed by owners as thought to be part of the normal aging process, especially with mild signs (socialization and sleep changes in dogs, vocalization and house soiling in cats).
No apparent early clinical signs to owners, but cerebral changes will already be occurring.
Dogs (> 8yo), Cats (>10y approximately)

DISHAA (L)-
Disorientation
Alterations in social Interactions
Changes in Sleep-wake cycle
House soiling (part of it linked to memory)
Alterations in activity levels
Anxiety level changes
Learning and memory

Diagnostic approach:
Based on history, signalment and exclusion of other pathologies
Identification of stress factors (acute or chronic) that may impact wellbeing
Examination: general, neurological, orthopedic, pain assessment.

Use of scale / scoring tools:
Canine Cognitive Dysfunction Rating scale (CCDR) (Salvin et al., 2011)
CAnine DEmentia Scale (CADES) (Madari et al., 2015) - better at differentiating stages of CCD, identify earlier stages and follow progression

98
Q

Cognitive Dysfunction Syndrome Management

A

Delay onset and progression – Uncurable currently
Early recognition and intervention is likely to lead to positive outcome.
Client education is paramount.
Preventative approach even in subclinical cases as patients no behavioral changes may still have pathological changes
Consistency at home is important to prevent increasing stress levels

diet and nurtritional suppiments
pharmcologic intervention
cognative and enviromental enrichmet
adjunctive therapies

CARE - Lack of clinical evidence in cats and many drugs are off licence.

cognative dysfuntion-
Increase and provide varied training, play and exercise time
Introduce new stimuli: toys, smells, sounds and touch.
Introduce hand or voice cues to palliate for sensory changes
Ensure positive and varied interactions (people and pets).
Ensure opportunities to explore new areas.
Cats: provide 3D environment and favours hunt-and-chase game.

soiling-
Increase frequency and safe proof access to outdoors
Add an indoor toilet area
Cats: provide low sides litter tray and add-in ramps

mobility-
Ramps
Ramps
Physical support devices: slings, cart, pram.
Facilitate access to ALL resources (outdoor, toileting area, sleep area, feeding area, toys)

sleep-
Provide a consistent day-night cycle: reduce exposure to artificial light during nighttime, increasing outdoor time
Reduce night disturbances
Provide a safe space for rest
Allow a final interactive and physical session before sleep

nutrition an ideat supliments–
Combination with behavioural enrichment would lead to a better cognitive performance compared to without (Milgram et al, 2004).
Provide antioxidants (AO, including vit B, C, E ), mitochondrial co-factors, phosphatidylserine and Omega-3 Fatty-acids to reduce the effects of free radicals and reduce Aβ deposits.
MCT (medium-chain Triglycerides, C8 and C10) - Provide alternative source of energy to palliate for deficient glucose metabolism.
Phosphatidylserine - neuronal membrane component and participating in synaptic processes.

Hill’s Prescription Diet b/d Canine - AO, omega-3
Purina One Vibrant Maturity 7+ Senior Formula (US) - MCT
Purina ProPlan Veterinary Diet NC NeuroCare - MCT

No current specific diets for Cats but Hill’s Prescription Diet Feline j/d – AO and omega-3

Coconut oil
Senilife®, Ceva - dogs/cat. Phosphatidylserine and AO
Aktivait®, Vet Plus – dogs/cats. Phosphatidylserine, AO and co-factors.
SAMe – increase AO production, improve catecholamine system performance. Care when use alongside serotonergic drugs.
Silymarin (milk thistle) – AO and anti-inflammatory properties.

99
Q

medication for cognative dysfuntion syndrome

A

Selegiline-
Selective inhibitor of monoamine oxidase B (MAOI).
Enhance brain catecholamine activity and decrease free-radicals production and increase clearance.
Dogs– 0.5-1mg/kg SID in the morning. Improvement > 2 weeks.
Cats (off licence, anecdotal) - 0.5-1mg/kg SID
Should not be use alongside other serotonergic drugs (MAOIs, TCA and SSRIs - clomipramine, trazadone, fluoxetine and sertraline - tramadol)

Propentofylline-
Phosphodiesterase inhibitor.
Increase blood flow to CNS, muscle and heart. Inhibition of platelet aggregation and thrombus formation. Decreases free radical production.
Dogs – 2.5-5mg/kg PO BID 30min before food.
Cats (off licence, anecdotal) – 12.5mg SID
Bronchodilator, positive inotropic and chronotropic effects. Care in patient with cardiac disease and contraindicated in pregnant animals

Anxiolytic and behaviour modification drugs-
Memantine (POM off licence) – block activity of glutamate. Used in compulsive disorders in dogs – 0.3-1.0 mg/kg BID
Sertraline (POM) – SSRI. Used in compulsive disorders in dogs – 3mg/kg SID.
Fluoxetine (POM-V) – SSRI. Used in separation anxiety ad compulsive disorders. Dogs 1-2mg/kg SID, Cats 0.5-mg/kg SID
Clomipramine (POM-V) – TCA. Used in separation anxiety and inappropriate elimination, compulsive disorders. Dogs 1-2mg/kg BID, Cats (of Licences) 0.25-1mg/kg SID
Trazodone (POM) – antidepressant, sedative. Chronic anxiety. Dogs 2-5mg/kg up to TID
Gabapentin (POM) – GABA analogue. 10-30mg/kg TID to BID and Cats 5-10mg/kg TID to BID

Adjunctive therapies-
Sleep and stress -
Melatonin
Alpha-casozepine (Zylkene®, Vetoquinol) – dog and cat
Pheromones (Adaptil®,Feliway®, Ceva)- dog and cat
Anti-anxiety/compressive gear (Thundershirt®)
Situational use of sedative: inducer – phenobarbital, trazodone, benzodiazepine (clonazepam, lorazepam))

mobility-
Physiotherapy, hydrotherapy
Osteoarthritis treatment and management: NSAIDs, Paracetamol, Solensia®, Librella®, Tramadol, joint supplements

100
Q

Selegiline

A

used for cognative dysdfunyion syndrome

Selective inhibitor of monoamine oxidase B (MAOI).
Dogs– 0.5-1mg/kg SID in the morning. Improvement > 2 weeks.
Cats (off licence, anecdotal) - 0.5-1mg/kg SID
Should not be use alongside other serotonergic drugs (MAOIs, TCA and SSRIs - clomipramine, trazadone, fluoxetine and sertraline - tramadol)

101
Q

Propentofylline

A

used for cognative dysdfunyion syndrom

Phosphodiesterase inhibitor

Increase blood flow to CNS, muscle and heart. Inhibition of platelet aggregation and thrombus formation. Decreases free radical production.

Dogs – 2.5-5mg/kg PO BID 30min before food.
Cats (off licence, anecdotal) – 12.5mg SID

Bronchodilator, positive inotropic and chronotropic effects. Care in patient with cardiac disease and contraindicated in pregnant animals.

102
Q

anatomial reasons for incontinence

A

Structural abnormalities -
Urethral length
Urethral diameter

Storage capacity-
Innervation
Detrusor atony

Urethral tone-
Bladder neck positioning
Neutering
Innervation

transitional cell carcinoma in th etrigone

103
Q

Approaching Urinary Incontinence

A

Patient factors: Age, breed, sex, reproductive status (neutered or entire, age of neutering)

Description of the leaking: is it continuous or intermittent? Normal micturition in between episode? Episode information- time of day, progression over time & onset (acute, chronic, progressive, improving), association with stress, conscious or unconscious.

Other useful information: defecation patterns, back pain/history of neurological problems, PU/PD, abnormalities in normal urination (eg: stranguria, pollakiuria, haamaturia)

clinical exam-
Physical exam- full clinical examination. Specific areas of focus on:
Bladder size- normal/small or distended- obstruction? faulty innervation?

Neuro exam- proprioception, sensation and movement of the tail, perineal reflex, lumbar-sacral pain.

Genital exam- exteriorise penis, check for vulval dermatitis

Rectal examination- palpate urethra (stones or masses), check prostate in males, lymph nodes

Other indicators of conditions that maybe be associated with PU/PD for example: muscle wastage, alopecia in patient with hyperadrenocorticism

104
Q

Diagnostics for urinary incontinance in the geriatric patient

A

Hematology, biochemistry and urinalysis

Radiographs – plain or contrast
Plain- abdominal radiograph without any contrast medium.
Retrograde urethrocystogram- contrast is administered via a urinary catheter and a series of radiographs are taken.
Aids identification of structural abnormalities in the bladder or urethral.

IV urethrography- contrast medium is administered IV and filtered out by the kidneys. Series or radiographs are taken. Helpful to identify pathologies associated with the ureters and kidneys.

Cystoscopy – endoscopic examination of the urethra and bladder.
Ultrasound

CT

105
Q

Urethral Sphincter Mechanism Incontinence (USMI)

A

Reduction in the tone of the smooth and striated muscle comprising the internal and external sphincter respectively resulting involuntary urine leakage.

Why does it occur?
Anatomical abnormalities eg: short urethra and intra pelvic bladder position.
Hormonal changes associated with neutering eg: reduced circulating oestrogen.
Degenerative processes eg: loss of collagen
Other risk factors include breed and obesity- larger breeds

106
Q

medical treatment of incontinance

A

Focus of treatment is to increase urethral sphincter tone.

Phenylpropanolamine (Propalin)
Mechanism of action: Adrenergic agonist that increases the contractility of the smooth muscle therefore resulting in a stronger close of the urethral sphincter.
1st line medical treatment in female and male dogs.

Estriol (Incurin)
Oestrogen replacement
Mechanism of action: increases the number of receptors responding to phenylpropanolamine.
2nd line medical treatment to be used in conjunction with phenylpropanolamine.
Contraindicated in male dogs as it is a oestrogen derivative.

107
Q

surgical treatment of incontinance

A

You do not need to know how to perform each of the procedures just the principles of how they reduce incontinence by alternating urethral tone.

Reduce urethral diameter by injection agents such as collagen, vet foam into the urethra. Minimally invasive procedure performed by endoscopy- will need to be repeated every 6 to 18 minths

Increase urethral tone through surgical placement of a urethral cuff resulting in permanent narrowing of the proximal urethra- complex abdominal surgery, more invasive

In patients with anatomical abnormalities eg: short urethra and intra pelvic bladder position a surgical procedure to move the bladder neck and urethra cranially. This will reduce incontinence as the urethra will be subject to intra abdominal pressures.
Procedure name: colposuspension.

no garentied fix, may be used in combo with medical managemnt

108
Q

primary hyperaldosteronism in cats

A

may present with-
tetraparesis
cervial ventroflexion
bilateral misdriasis

adrenal mass present on ultrasound

the zona glumerolosa in the cortex of the ad=lrenal gland produces aldosterone- mainains systemic blood pressure- RAAS

in this condition too much aldosterone is produced- more than 5 times normal range, ususlally due to functional mass

assosited with low circulating rnin concentration- RAAS neg feedback

causes hypocalemia which results in neuromuscular junction adn possible organ damage

retinal detachmet ot intraocular haemorages can also be present

can mimic other geriatric diorders- CKD, DM
palpable abdominal mass
systemic hypertension- coiuld presipitate renal disease

can mimic renal signs- azotemia, isosethenuria

109
Q

diagnstics for primary hyperaldosteronism in cats

A

urinary aldosterone to creatanie ratio often used

dynamic testing with flufrocortisone- has no effect in cats with htis disease so diagnostic

abdominal ultrasound- not as specific, adrenals can be enlarged for other reasons

110
Q

treatment for primary hyperaldosteronism in cats

A

unilateral adrenaectomy treatment of choice- contraindications?- bilateral presentation, other diseases

medical options-
ARB- spirolactone
potassium suplimentation
calcium blocker for hypertension-Amlodipine

111
Q

hypersomatotropism in cats

A

causes acromegally

hepatomegally
uncontrolled diabetes- high dose of insulin >1.5, plantigrade stance from diabetic neuropathy
arythmia
broad facial fetures

Imaging- functional adenoma
imaging not diagnostic

overproduction og groth hormone-
organomegally

males more effected than females- domestic short hair

polyphagia may be increased
respiritory stridor - hyperglosia
mild cardiomegally
neuro signs form mass in later disease

diagnosed by testing for inusline like growth factor- can get false neg
repeat 6-8 weeks
short term fasting can lead to false neg

can test for growth hormone in a lab setting

112
Q

hypersomatotropism treatment

A

durgical- transsphenoidal hypohyectomy

medical-
somatostatin analougs- pasireotide

radiation therapy- widley used

conservative options- high doses of insulin to control diabetes

113
Q

primary hypoprathyroidism in dogs acute managment

A

slow bolus of Ca gluconate- 1ml/kg calium gluconate over 15-20 mins
administer IV through IV catheter
ECG attached
submit blood to regional laboratory for a PTH

114
Q

diagnostic for hypoparathyroidism

A

decreased ionised calcium and parathyroid hormone

and absense of any other markers

115
Q

primary hypoprathyroidism in dogs

A

results in electorlite imabalence
low ca high p
hyperexitability of cns and pns
idiopathic

116
Q

primary hypoprathyroidism in dogs management

A

acute- iv calcium

chronic-
vitamin d- needs to be activated

calcitrol- activated vit d 3 gold standard
downside is short time to max effect
no vet formulations
cant split human capsuals

alfacidol- one alpha
best current option- not much literature
check tCa/iCa daily and adjust dose incramentally

117
Q

Calcium distribution

A

99% of body calcium resides in the skeleton and is stored as hydroxyapatite
Most skeletal calcium is poorly exchangeable, and less than 1% is readily available
0.1%of total body calcium is in the extracellular fluid
The rest of the calcium is in the cells and its organelles

50% ionised calcium (diffusible)
E.g. Ca carbonate, Ca phosphate
Physiologically active

40% protein-bound (non-diffusable)
10% chelated calcium

Calcium pool-
Gains from:
GI absorption – 35% of ingested calcium is absorbed
Bone resorption

Loses to:
Endogenous faecal excretion ~ 90%
Urinary excretion ~ 10%
Milk
Bone formation

118
Q

Calcium homeostasis

A

3 key components
Parathyroid hormone (PTH)
Calcitonin
Vitamin D (Calcitriol)
(also PTHrP)

important for-
Nerve Conduction
Neuromuscular transmission
Muscle contraction
Smooth muscle tone
Membrane stability
Membrane transport
Enzymatic reactions
Hormone secretion
Blood coagulation
Bone formation
Control of hepatic glycogen metabolism
Cell growth and division

119
Q

Hypercalcaemia

A

Total Calcium >3mmol/L or iCa >1.5 mmol/L
Reference ranges vary between machines
Mild increases may not be relevant in juvenile dogs
High total calcium should prompt ionised calcium evaluation before further investigation

Clinical signs proportionate to:
Rate of increase
Magnitude of increase
Cause of hypercalcaemia

Increased calcium ions is toxic to cells:
affects membrane functionandmetabolism
ultimatelyends in cell death

HARD IONS

H – Hyperparathyroidism (primary vs secondary)
A – Addison’s
R – Renal disease (acute and chronic)
D – Vitamin D Toxicosis
I – Idiopathic (cats)
O – Osteolytic
N – Neoplastic (e.g., lymphoma, multiple myeloma, anal sac adenocarcinoma)
S – Spurious
G – Granulomatous disease (infectious)

Common Signs-
PU/PD
Anorexia
Dehydration
Lethargy
Weakness
Vomiting
Chronic renal failure

Uncommon Signs-
Constipation
Cardiac arrhythmia
Seizures
Twitching
Acute intrinsic renal failure
Calcium urolithiasis
Death

120
Q

Hyperparathyroidism as a differential for hyper calcemia

A

Increased PTH increases calcium absorption-
Increased osteoclast activity –> increased calcium concentration in ECF
Increased calcium reabsorption from the renal tubules (less excretion)
Increased absorption of calcium from the GIT

Primary Hyperparathyroidism-
Parathyroid tumour – usually single parathyroid adenoma
Loss of normal negative feedback control
Uncommon in dogs, rare in cats
High calcium, low phosphate

121
Q

Addison’s as a differential for hyper calcemia

A

30% of Addisonian dogs are hypercalcaemic
Rare in cats
Middle-aged dogs with Standard Poodles and PortugeseWater dogs being over-represented
Unknown mechanism

122
Q

Vitamin D toxicosis as a differential for hyper calcemia

A

Relatively uncommon
Common examples:
Psoriasis cream (licking cream off the owner)
Vitamin D tablets
Nutraceuticals
Rodenticide
Plant ingestion e.g., nightshade, oatgrass, jasmine

123
Q

Renal disease as a differential for hyper calcemia

A

CKD-
Azotaemia, hyperphosphataemia, normocalcaemia/hypocalcaemia, isosthenuria
Occasionally hypercalcaemia
31% of azotaemic cats, 10% of azotaemic dogs
Feeding early CKD cats severely-phosphate-restricted diets can cause them to develop hypercalcaemia
Renal disease due to other causes can also lead to hypercalcaemia

124
Q

Idiopathic hyper calcemia

A

Cats not dogs
Most common cause of hyperCa in cats
Diagnosis of exclusion
50% don’t have clinical signs at time of diagnosis
10-15% have calcium oxalate uroliths

125
Q

Osteolysis as a differential for hyper calcemia

A

Rare cause of hypercalcaemia
Usually secondary to other disease e.g., multiple myeloma, primary bone tumours

126
Q

Neoplasia as a differential for hyper calcemia

A

Hypercalcaemia of malignancy
Typically driven by tumour PTHrP production-
Total calcium and ionised calcium increased
Phosphate normal/low
Low PTH, high PTHrP
Also, with tumour metastasis to the bone

Most common-
Lymphoma – especially T-cell lymphoma
AGASACA – rare in cats
Multiple myeloma

Less common-
Osteosarcoma
Metastatic bone tumours
Mammary carcinoma

Also reported in-
Thymoma, pulmonary carcinoma, nasal carcinoma, malignant melanoma

127
Q

Spurious hypercalcemia

A

Acidosis
Lipaemia
Haemolysis
Young animal! (not spurious but also may be normal for them if mild)

128
Q

Granulomatous disease (infectious) as a differential for hyper calcemia

A

Increased macrophages
Macrophages can synthesise calcitriol from calcidiol without negative feedback regulation
Macrophages may also synthesis PTH-rP which may activate PTH receptors

Granulomatous diseases-
Fungal (uncommon in the UK)
Schistosomiasis
Angiostrongylos vasorum
Nocardia
Mycobacteria
FIP in cats

129
Q

approch to hypercalcemia- clinical exam

A

HARD IONS

Cat versus dog
Age of dog – is physiological likely?
Breed-
Large breed dogs <1 years old may have a mild hypercalcaemia
Keeshonds over-represented for primary hyperparathyroidism

Clinical signs-
Anorexia
Polydipsia/polyuria
Vomiting
Muscle weakness or twitching

Diet-
Raw diet
Toxin ingestion e.g., Vitamin D tablets, creams, rodenticide exposure
Supplements

Travel?

Palpate lymph nodes-
Submandibular, prescapular, axillae, inguinal, popliteal
FNA – can often reach diagnosis if lymphoma

Rectal Examination-
AGASACA – can be diagnostic with FNA
Sublumbar lymph node enlargement or urethral stones may be palpable
If not amenable, ensure do when asleep

Orthopaedic examination-
Bony swellings, pain

130
Q

approch to hypercalcemia- diagnostics

A

initial blood tests-
Ionised calcium measurement-
Is hypercalcaemia true, repeatable especially if no clinical signs associated with this

CBC-
Lymphocyte count

Biochemistry-
Renal disease
Addison’s (Hyperkalaemia, hyponatraemia)
Phosphate

Basal Cortisol in dogs

PTH and PTHrP-
When to perform?

Is hypercalcaemia parathyroid dependent or independent?
Dependent – PTH is high normal or increased
Independent – PTH production is suppressed in response to the hypercalcaemia

Vitamin D analogues
Basal cortisol +/- ACTH stimulation if suspect Addison’s
FIV/FeLV in cats
Angiodetect

urinalysis-
Increased excretion of calcium in the urine of cats that are hypercalcaemic can predispose them to calcium oxalate urolith formation
Uroliths identified in 15% of hypercalcaemic cats – 73% calcium oxalate
Evaluation for underlying renal disease-
Protein

imaging-
Thoracic and abdominal radiographs-
Include bones!
Look at the spine

Abdominal ultrasound-
Kidneys
Lymph nodes
Neoplasia

Ultrasound of parathyroid glands

Soft tissue calcification-
Kidneys and gastric mucosa are the predominant organs to be affected
Uroliths, nephroliths, ureteroliths

Other-
Bone biopsy
FNA/biopsy masses

131
Q

Dietary management – idiopathic hypercalcaemia in cats

A

Increased concentrations of fibre, sodium, water
Fibre binds to intestinal calcium thus reducing reabsorption
Decreased concentrations of calcium, vitamin D3, vitamin A (or a combination)
Diet options:
Hills Prescription diet w/d, or gastrointestinal biome
Psyllium husk
Chia seeds (controversial, but harmless?)

132
Q

Treatment of hypercalcemia

A

Underlying disease dependent!
Treatment of underlying disease often can resolve hypercalcaemia

Depends on the aim-
Anaesthesia safety
Supportive treatment? e.g., seizures, arrhythmias,urolithiasis

Timing-
Will it influence diagnostics?
Steroids very effective but risks
How acute is the hypercalcaemia?
How unwell is the pet?

Saline 0.9%-
Increase calciuria
Na competes with Ca reabsorption so more Ca is excreted
Furosemide-
Increases diuresis because of increased lumen electronegativity
NaK2Cl transporter in the thick ascending loop of Henle aims to maintain electroneutrality
Ensure patient well hydrated before therapy
Glucocorticoid-
Reduce bone turnover and GI absorption
Also possibly increased renal excretion
Cytotoxic to lymphocytes so reducedPTHrP
Avoid use until definitive diagnosis reached

Bisphosphonates-
Inhibit osteoclast-mediated calcium mobilisation from bone
Risks include oesophagitis and mandibular necrosis(especially in cats)
e.g., Alendronate (give after fasting)

133
Q

Emergency management of hypercalcaemia

A

Intravenous fluid therapy (0.9% NaCl) - for fluid deficits and promoting diuresis

Furosemide when well hydrated – promotes diuresis and rapid onset of action

Calcitonin – may be helpful in short-term
Oral bisphosphonates and oral
glucocorticoid therapy have a slower onset of action (1-2 days after administration) so are often not helpful in the acute setting