reproductive and endocrine Flashcards
mastitis
Inflammation of the mammary gland
Although most of the time when we refer to mastitis we are thinking of bacterial infections of the gland, technically it is simply inflammation of the mammary tissue. This has particular relevance when we think about treatments as although historically the mainstay of treatment has been antimicrobials, with growing consideration of antimicrobial resistance there is greater reflection on other causes of inflammation (eg trauma).
Whilst we most commonly talk about acute mastitis in dairy cows due its prevalence and economic significance, mastitis and its treatment is of significance in most farmed species. Although much of this lecture will centre on dairy cows the principles of treatment and control are relevant to all species even if specific products/options may vary
mastitis treatment
Antimicrobials-
Intramammary
Parenteral
Anti inflammatories-
NSAIDs
Steroids
Nursing
Supportive therapies- ketosis ect
Alternative treatments- not ususally effective but prevelant
NSAIDs for mastitis
NSAIDS have a number of important properties which are beneficial in the treatment of mastitis. First and foremost mastitis is widely acknowledged to be a painful condition. A number of studies have demonstrated physiological and behavioural changes associated with mastitis. Whilst the use of anti inflammatory medicines to control endotoxaemia in severe case of mastitis has been practiced for decades, in recent years there has been growing understanding of their important role in less severe cases. Even relatively mild cases of mastitis result in gait changes with cows increasing the distance between their hocks to avoid contact with the udder. Various pharmaceutical studies have shown the benefits of NSAIDs in reducing udder inflammation as part of the treatment of mastitis. As with other clinical conditions this kind of symptomatic relief is critical to support the animals general health leading to a reduction in the chance of culling
Corticosteroids for mastitis
QUESTIONABLE
Parenteral
Local
Whilst corticosteroids also provide potent anti inflammatory properties, they convey less analgesia than NSAIDs which may limit their benefits in promoting appetite. When administered systemically they also convey immunosuppressive properties which may be deleterious to the animal’s own abilities to fight the infection. As such they are best avoided as a treatment for mastitis.
Some intramammary mastitis treatments contain steroids for local administration. Whilst there is some evidence that these can have a positive effect, reducing udder inflammation and potentially promoting distribution of the medicine in the gland, there is a lack of evidence to suggest that this enhances cure rates. There is also the possibility that these impacts may mask signs leading to cessation of treatment before bacteria have been fully eliminated
antimicrobials for mastitis
Antimicrobials have formed the bedrock of mastitis therapy for over 60y years but as with all uses of antimicrobials this use is increasingly scrutinised in light of growing AMR concerns. Many studies over the years have demonstrated the benefit of antimicrobial on undifferentiated cases but there can be major differences between pathogens. Results from microbial cultures of mastitis cases frequently demonstrate a significant number of no growths some of which will be the result of infections that have already been eliminated by the cows immune system or other causes of inflammation (eg trauma). There is also a significant body of evidence that most gram negative infections, particularly E.coli, will self sure without the use of antimicrobials. As such there is a growing trend toward the use of rapid on farm diagnostics to identify gram +ve cases allowing a more targeted approach to therapy.
culling in mastitis cases
Despite treatment some infections will fail to cure and become chronic. These infections have a very poor chance of cure generally. Not only does treating these infections represent a poor return on investment and use of antimicrobials, these animals also act as a reservoir for infection for other animals in the herd. Culling is an important part of mastitis prevention and should not be ignored as a consideration when considering treatment options
classification of mastitis cases
Mild- changes in milk only- localised therapy
Moderate- inflamation of udder- non steriodals
Severe- systemic signs- pyrexia ect
Chronic/recurrent- intensive therapy or culling
When considering treatment options for a clinical mastitis case it’s important to consider what we are trying to achieve. This ay vary between species, and clinical scenarios, In some case (eg gangrenous mastits, summer mastitis) our principle focus may simply managing the health of the animal as the gland itself is too severely affected for a realistic chance of cure. It’s common to categorise mastitis cases with differing treatment strategies deployed for different severities
Parenteral antibiosis for mastitis
Whilst commonly antibiosis of mastitis cases is done through local intramammary formulations, on some occasions systemic antimicrobials may be considered. Historically there have been two rationales put forward for the use of injectable antimicrobials in the treatment of mastitis cases.
For many years arguments have been put forward that injectable antimicrobials may enhance deep tissue penetration leading to enhanced cure rates. Although some studies have shown small benefits from the sue of systemic antimicrobials, the evidence is equivocal with others failing to show an improvement. This may relate to differences in pathogens involved but given the prevailing concerns about the use of systemic antimicrobials from an AMR perspective this use is questionable
The other predominant use of systemic therapy is in the treatment of toxic mastitis cases. In this instance the animal is often suffering from bacteraemia due to changes in the blood gut membrane caused by the toxaemia. In these cases parenteral antimicrobials can be useful
practicalities of mastis treatment
Whilst all these principles are important to make the most effective use of the tools we have available to us, it is also important to consider practicalities. In most dairy situations regular repeat treatment and use of intramammary preparations is fairly easy but when dealing with more extensively managed livestock some compromises may need to be considered to ensure treatment compliance
Cascade
Withdrawal periods
Antimicrobial use
Nursing and support of mastitis
Nursing and support shouldn’t be underestimated in the treatment of mastitis. Regularly stripping of affected 1/4s to remove pathjogens and toxin can be highly effective in helping the cow to combat the infection. In more severe infections where cows become recumbent fluids and nutritional support may be vital in preventing the animal deteriorating while treatments take effect
prevention of mastitis
best strategy!
Treat & record clinical cases- Prevention strategies rely on identifying risk factors
Post milking teat disinfection
Dry cow therapy
Cull chronic cases
Milking machine maintenance
Lactating period prevention of mastitis
Whilst there are a number of important aspects to controlling mastitis during the lactating period, the physical act of infection almost always occurs through the teat sphincter around either milking or suckling. Infection is generally the result of an imbalance between exposure and protection so identifying the specific risk factors and either addressing or mitigating them is key. In some cases it may prove difficult to adequately decrease the risk of exposure and in these instances there are options to enhance the animals ability to fight the infection through the use of either vaccines or immunomodulators
Dry period prevention of mastitis
During the dry period the cows key defence mechanism against infection is the keratin tear plug. Unfortunately this teat plug fauils to form in1/4 of teats. There are a number of options available to combat this but the most effective is the use of internal teat sealants to replace the plug preventing pathogens gaining entry to the udder.
insulin tolerance test (ITT)
tests for tissue insulin resistance (factor of laminitis)
measures the ability of tissues to take up glucose (i.e. insulin sensitivity). The glucose concentration of a baseline blood sample is compared to the concentration in a blood sample taken 30 minutes after a dose of insulin is administered. The horse is insulin resistant if the second blood glucose concentration does not decrease to 50% or less of the baseline glucose value.
Pituitary pars intermedia dysfunction (PPID)
(Equine Cushing’s Disease)
Age related degenerative condition
Loss of dopaminergic inhibition
Hypothalamus unable to regulate pars intermedia of pituitary gland
Hypertrophy / hyperplasia of PI
Increase production of many hormones from PI which have wide array of effects on body
high levels of acth (and cortisol but not so much in horses)
clinical signs-
pot belly
fluffy coat
pupd
skeletal muscle atrophy
abnomal sweating
regional adiposity
fertility issues
insuline disregulation in a third of all cases (lamanitis risk)
suseptability to infection
1/5 horses over 15
Condition of older horses (average age 19yo)
Rarely diagnosed in younger horses (<10yo)
No sex predilection
Ponies more likely to be affected than horses
must be differentaited in lami itis cases from EMS-
seen in older horses
test for by uing basal acth-
acth however has seasonal changes- higher in autumn
breed differences
stressed or ill orses also display higher levels- PAIN FROM LAMINITIS CAN CAUSE THIS
Differentiating PPID and EMS
Both PPID and EMS result in laminitis due to ID. PPID may only serve to exacerbate pre-existing ID
Regardless, PPID remains an important consideration/ rule out in horses with ID
For EMS, ID is the central feature of the condition and may be the only apparent abnormality apart from laminitis or may be present concurrently with obesity.
Differentiating between the two conditions involves ruling in or out PPID in cases of laminitis of suspected endocrine origin.
diagnosis of PPID
basal acth
trh stimulation test for borderline cases- not reliable between july and december- false positives
trh administered and so adh produced and can be measures- offlicence so must be selective
acth test also used to monitor progression/ recovery- allows for finite assesment of management practices as they are often very different for each horse
What are your first line tests for EMS?
risk factors- podgy innactive native pony?
basal insulin- non fasted sample, fasting cuses insulin to drop, feeding also causes artificail rise though
dynamic tests-
oral glucose test
oral sugar karo) test
basal adiponectin test-
cgit/ inaulin tolerance test
basal insulin test
hightly specific- if high, horse at risk for laminitis- had insulin disregulation
can be used a baseline for future tests
easy and convinient
not as sensitive as dynamic tests- imporves with fasting
not if grain fed in last 2-3 hours
good for monitoring isulin during treatment to asses managemtn practices- feeding ect
dynamic insulin test
better than basal for rested horses on box rest ready to go back out to see if ready
glucose or sugar (karo)
blood sample 2 hours or 60-90 mins later (karo) later
cgit/ inaulin tolerance test
rarley used test of insulin disregulation
when should you test for insulin diregulation
laminitis cases
for moitoring of at risk horses
9-year-old Shetland pony
Presents with suspected laminitis
Willing to walk but with a notably shortened stride.
Would you perform endocrine testing in this case and what would you test for and why?
Signalmet points to EMS so test for insulin disregulation- basal insulin
obvios that hteres insulin dysregulation without test but can be starting point for monitoring with dynamic tests
19-year-old Welsh cob X gelding
Presents with suspected laminitis in May
Normal HR, RR and temperature
Constantly shifting weight when stood on the yard and bounding digital pulse in both front feet.
The owner notes that the horse has been late to shed his winter coat this year
Would you perform endocrine testing in this case and what would you test for and why?
signalment points to PPID- basal acth
trh if acth inconclusive/ not maching signalment/ horse stressed
test basal insulin- allows baseline to be known for monitoring
20-year-old horse
Presented for a suspected foot abscess on the right fore
The mare is non weight bearing on the leg and there is a bounding digital pulse.
Her heart rate is 60 bpm and she is sweated up. You successfully pare the foot, and the abscess begins to drain
Whilst you are there the owner notes that the mare has lost her top line and has been drinking and urinating more than normal and would like the mare tested for PPID.
There are no other clinical abnormalities noted on clinical examination
How do you respond?
trh test as horse is stressed and otherwise unwell but more usefull to wait until systemically well and do basal acth
this allows better interpritation and less liklyhood for borderline results
ppid may be behind the abcess as it causes immunocompromised states
24-year-old TB mare
The owner has heard about “Cushing’s” disease (PPID) and thinks her horse may have some of the signs.
The mare has hair coat changes and patchy shedding. She has skeletal muscle atrophy and is more lethargic than in previous years.
The horse has no history of laminitis.
You agree with the owner and agree to test the horse for PPID using basal ACTH.
You mention the possibility of insulin dysregulation and so you decide to take a blood for basal resting insulin.
insulin is fine but ACTH high
How do you interpret her results?
What do you recommend?
What can you say about this horse’s insulin status?
PPID without insulin dysregulation likely
keep monitoring
managment to take precations against lamainitis incase insulin desensitivity developes
You have been managing a ten-year-old Dartmoor pony with chronic laminitis.
The pony has improved clinically through a combination of medical therapy, dietary restriction and management changes.
The pony has been on box rest and soaked hay and is now of an appropriate body condition score, off all medications and sound in walk and trot.
The owner wants to know if it is safe to put the horse back on grass?
How do you respond? How can you assess the risk?
try oral glucose test to see if insulin remains at acceptable level
if yes- put to grass
if no- continue to controle feed and manage
What Happens At Birthto the neonate?
Change from placental to lung oxygenation
Lungs have to inflate for first breath- Requires surfactant on lung surface
Stimulus for taking first breath is a build up of CO2- Respiratory acidosis in first few minutes of life
sulfactant availability in premies
Adaption to the external environment-
Takes 24-48hours
Cardiopulmonary
Gastrointestinal tract
Urinary
Thermoregulation
Neurological
Skeletal
Best Practice at Birth on farm
Make sure environment is as clean and dry as possible- Contaminated environments are a major risk factor for neonatal disease
Move neonate out of harms way and place in front of dam
Encourage animal to lie in sternal- lungs have equal opertunity to expand
recumbency for dam to clean off- ‘Frog legging’ an animal can help them to stay in this position and allows both lungs expand evenly
Do not ‘swing/hang’ an animal by its back legs to clear fluid- Rumen fluid
If animal is struggling for breath, percuss the chest and massage fluid out of nose and mouth
Dystocia
Most common cause is relative foetal oversize- Oedema, bruising and fractures can be common (esp, rib fractures)
Foetus becomes hypoxic due to reduced oxygen delivery:
Compression of umbilical cord
Premature placental separation
Metabolic acidosis then occurs due to lactic acid production and build up
Severe resp acidosis due to poor lung function
Net result: Acidaemia + Hypoxaemia in new born
Newborn then fails to suck (acidosis greatly reduces suck reflex)
Colostrum intakes affected, leading to failure of passive transfer
Ruminants are born essentially agammaglobulinaemic and therefore nearly entirely reliant on colostrum for immunity
How can we diagnose acidotic/hypoxic neonatal animlas on farm?
Blood Gases?-
Not practical in the field
Labile results
asses time to sternal recumbency-
Should be within 5 minutes
If >9mins risk of death is increased
Reduction/absence of suck reflex around the time of birth also sign
What is in colostrum?
ENERGY (high in protein, fats vitamins etc)
Immunoglobulins (IgA, IgG, IgM primary immunoglobulins present)
Growth factors (IGF-1, IGF-2, Insulin, prolactin, growth hormone, steroids etc)
Lots of leukocytes? (enhance lymphocyte response to nonspecific mitogens, increase phagocytosis and bacterial killing ability, and stimulate humoral immune responses (IgG formation) in the calf?? Godden 2008)
“Colostrum management is the single most important management factor in determining calf health and survival
Factors Affecting Quality + Quantity Of Colostrum
Timing!! I.e. When the colostrum was collected from the dam- Decrease in IgG quality with time
Breed (Dairy vs beef breeds)
Parity- heifers may give less but higher quality
Pre-partum nutrition - (adequate dry cow diet, length of diet, BCS of dam)
Length of dry period (<30d)
Abortion/induction- colostrogenisis may be absent
Mastitis
Colostrum Intake + Absorption
Intake-
Inadequate supply
Quantity
Quality – Dilution effect
Poor udder/teat conformation
Poor mothering by dam
Maternal disease
Poor calf/lamb vigour - Reduced sucking ability (acidotic?)
Time from birth to sucking-
<6 hour timeframe
<2hours is gold standard
Method of administration
Dam/teat/tube feeding
Acidosis in calves/lambs reduces the absorption capability
Induction of parturition
recomendation is 2 liters within first two hors of life then another 2 2hours later
faulure of passive tranfer of colostrum
MAJOR RISK FACTOR FOR ALL NEONATAL DISEASE IN RUMINANTS
30-50% calves affected
34% calves failed to suckle in first 6 hours
15% Holstein calves suffer fpt despite receiving 3 litres within first 6 hours
Case definition in herd: >20% of calves with TP <55g/L
How do we investigate Failure of Passive Transfer
Measure serum immunoglobulin
Refractometer – Total Proteins >55g/L- influenced with dehydration- neonatal diahorea
Zinc Sulphate Turbidity (ZST) - >20 Units
Sodium Sulphite Turbidity (SST) - Ig > 20g/L
Radial Immunodiffusion
Nasal Stick test – Measures IgG
Lateral flow testing to measure IgG ‘calf-side’?
Sample calves from 24hrs-7d old
If using TP beware affects of dehydration (false elevation of protein portion of blood)
Useful to get a snapshot of current effectiveness of colostrum management- Monitor improvements after giving corrective advice
Prevention of FPT
Adequate pre-partum nutrition
Avoid dystocia- Easy calving/lambing sires
Tube feed 10% of Bodyweight e.g. 40kg calf gets 4L colostrum ASAP (Within 6 hour window, can split in to 2 feeds)- All dairy calves
Beef cows should be closely supervised
Keep a store of frozen good quality (>22% Brix) colostrum available
Colostrum ‘substitutes’ - £££ and variable efficacy…
best practice management for neonatal dairy calves
Remove calf within 2 hours of birth
Collect colostrum ASAP- Check for quality (if poor, then used stored if possible)
10% Bodyweight (between 3-4l) colostrum ASAP (Within 6 hours but preferably within 2!)- Repeat again within 12 hours of birth
Feed colostrum for another 3-5 days if possible- Enhance local gut immunity ‘Teflon effect’
Store any excess colostrum
Must be of good quality (>22% Brix)
Dam must be Johnes negative!
Pasteurise?
Keep covered and refrigerated if not using straight away
best practice management for neonatal lambs
Lambs as for calves- Immunoglobulin from dam via colostrum
Zero or inadequate colostrum intake -> inadequate immunity + no energy -> death
50ml/kg in first 6 hours of birth (200ml)
250ml/kg in first 24 hours (1li1tre)
Check status in lambs under 7d of age using ZST
At risk lambs = triplets, orphans, from thin/hogg/gimmer dam, dystocia, weak lambs
Target lambs likely to have problems for supplementary feeding
If lamb is hypothermic, give intraperitoneal glucose (20% glucose 10ml/kg) + place in warming box/raise body temp before giving oral colostrum- Hypothermic lambs are prone to regurgitation and therefore inhalation pneumonia/asphyxia
managment of foalling- important history
Was the foaling observed or unobserved?
The length of the pregnancy and due date – to term?
History of the mare
Vaccination status of the mare- how? when? tetnus status very important
Behaviour of the foal since birth
Colostrum intake
Placenta passed?
Examination of the newborn foal
Every foal should be examined within 24 hours of birth
General clinical examination
Ensure normal behavioural milestones have been met
Identify any risk factors for onset of disease or problems that require addressing
Establish/administer preventative care where required
Behaviour- Normal hyperreactivity, bonding with mare, avoidance of humans
Head- Symmetry, signs of trauma
Signs of milk staining on forehead or around nose
Abnormal mucous membrane colour
Eyes- Scleral haemorrhage may be present, slow/sluggish PLR & menace
Look for signs of uveitis
Thorax- Look for normal respiratory rate and effort. Lung sounds audible
Check for Trauma/rib fractures - palpate
Holosystolic hear murmur (PDA) expected
Abdomen- Relaxed, non distended
Umbilicus- Heat pain or swelling
Limbs- Angular/flexural limb deformities/joints
Extremities- Warmth and peripheral pulses
managment of the umbilicus is foals
What to look for-
Evidence of hernia or excessive trauma
Inflammation
Should be pink, diameter <2cm
Management-
Dipping of the umbilcal stump in iodine (2%) or chlorhexidine (0.5%)
Any heat, swelling or abnormal thickening should be taken seriously and evaluated using US
important clinical observations for managemnt of the neonatal foal
Meconium-
Dark brown pellets or paste all passed within 24hrs
Urine-
Dilute and large volumes first passed by six hours (colts) or ten hours (fillies)
Prematurity
A foal born at a gestational age of < 320days that displays immature physical characteristics
Dysmaturity
Characteristics
low birth weight
Short, silky hair coat
Floppy ears
Domed head
Weakness, prolonged time to stand
Flexor tendon laxity
Incomplete ossification of tarsal and carpal bones
SEVERE CASES
Multi-organ dysfunction
GI
Neurological
renal
endocrine
Risk factors for prematurity/dysmaturity
Health of the dam during gestation
Gestational and foaling environment
Ease of delivery
Foal’s gestational age at birth
Placental abnormalities
Adequacy of placental transfer of maternal immunglobulin
colostrum managment in the foal
Foals are immunocompetant at birth – competent specific & non-specific immune system
But immunologically naïve
autogenous IgG adult levels by 4 months of age
Also some components of non-specific immune system may be compromised (neutrophils, complement, & macrophages)
Gap in immunoglobulin is filled by colostrum
IgG, IgG(T), (IgA, IgM)
Other factors: complement, cytokines, lactoferrin, lymphocytes
Half life of maternal IgG
20-23 days
Decline by 1-2months
More rapid if initially poor levels
Remember this from 1st year…
3 Qs
Quality
Quantity
Quickly
Colostrum specific gravity can be checked pre-suck
Brix optical refractometer
<45g/L foal should be considered for donor colostrum supplementation
Absorption of colostrum in foals
Specialist enterocytes absorb the immunoglobulins by pinocytosis
These cells have a lifespan of a maximum 24hours
Maximum absorption occurs within 8hours of life
Foal MUST ingest 1L colostrum within first 6hrs
Often owners will report they haven’t seen the foal suckling
Empty udder = fed!
how to asses colostrum intake of the foal
Often owners will report they haven’t seen the foal suckling
Empty udder = fed!
Blood sample should ideally be collected for:
Assessment of serum IgG concentration
Why?
Assessment of colostral transfer of immunity to the newborn foal
Screening for failure of passive transfer
When?
18-24 hours old – limitations?
IgG blood test in foals
to monitor passive tranfer of immunoglobulins
Options:
Foal side snap tests
Immunoturbidimetric method
Results:
Ideal - >8g/l
<4g/l suggest failure
4-8g/l suggest partial failure
Incidence of failure of passive transfer 2.9-35%
Depends on definition
Depends on foal management
Predisposing factors of Failure of Passive Transfer in the foal
Loss of colostrum via premature lactation-
May be associated with twinning, placentitis or premature placental separation
Inadequate colostrum-
Severe illness, premature foaling with disruption of normal maturation (colostrum produced last 2-4weeks of pregnancy)
Failure to ingest an adequate volume of colostrum-
e.g. neonatal weakness, rejection of the foal
Failure to absorb colostrum-
esp. premature foals and/or foals with concurrent illnesses, endogenous or exogenous glucocorticoids may hasten maturation or the specialised enterocytes
treatment of failure of passive transfer of colostrum in the foal
Depends on timing-
>12-24 hours need plasma
Plasma source?-
Mare, geldings, commercial
Colostrum source-
Mare, banks, commercial
Consequences of FPT in foals
Immediate – septicaemia
Risk is highly dependent on other factors:
Stress, management and hygiene
Later risk-
before full IgG production
rapid waning of ingested IgG
1-4 months of age
e.g. Rotaviral infections
respiratory disease
Complete haematology and biochemistry
Point of care tests
Lactate Increased – sepsis, shock, hypovolaemia, ischamia
Glucose Decreased – hypoglycaemia = <5mmol/L
USG Hydration status
When to refer in managment of the neonatal foal
Foals are more likely to survive if:
Owners/vets have recognised problems and acted quickly
Transportation to an appropriate hospital with appropriate supportive care before and during transport
Response by 24 hours into treatment is often a good indicator
Referral should be strongly considered in the following scenarios:
suspicion of sepsis;
significant prematurity (less than 320 days gestation) or dysmaturity;
HIE or other conditions where the foal is unable to nurse by four hours of age;
moderate to severe dehydration;
severe colic or colic signs that fail to respond to initial medical treatment;
suspicion of bladder rupture;
excessive posturing, straining or lack of normal urination by 18 hours of age
*hypoxic ischaemic encephalopathy *
tests for cushings
stim acth test- higher sensitivity for pituitary dependant, less so for adrenal dependant. Good specificity- best test to rule IN cushings
Low does dex- high sensitivity, ok specificity
Urine cortisol to creatinie ratio- sensitive but not specific (can 100% rule it out)
Basal cortisol less usefull as produced in stressed animals- more usefull in addisons
urine cortisol to creatine ratio-
The UCCR is a useful screening test for canine hyperadrenocorticism as a low (normal) result makes Cushing’s unlikely, with approximately 90% sensitivity. It is useful in those cases where hyperadrenocorticism is unlikely but needs to be definitely excluded
sample must be taken first thing in the morning to minimise stress
ACTH stimulation test
if the dog is overproducing cortisol by testing the response of the adrenal glands to stimulation by the hormone ACTH. As is discussed in the ‘What is Cushing’s page’, ACTH is the hormone produced by the pituitary gland, which then stimulates dogs to produce cortisol.
Your vet will undertake this test by first measuring the ‘normal’ level of cortisol in your dog’s blood. They will then inject a synthetic version of ACTH and take a further blood sample after 1 hour.
As ACTH naturally stimulates the production of cortisol, the cortisol levels after injection will increase beyond ‘normal’ levels in dogs without Cushing’s. However, this response is normally mild – with most healthy dogs producing a 1 hour cortisol of between 300-400 nmol/l .
In most dogs with Cushing’s, cortisol production after injection of synthetic ACTH is much increased, and for the majority of cases a 1 hour cortisol value of greater than 550 - 600 nmol/l will be seen. theres no negative feedback loop in cushings dogs, hence this result
sensitivity for this test is low- higher incidence of fase negatives- esspecially with adrenal dependant cases
there is also overlap between cushings and non cushings dogs in cortisol levels and so can result in false negs
iatrogenic cushings cases will not respond to this case and will stay at base line because drugs have overloaded neg feedback loop
low dose dexmethasone test
the dog will be injected with a drug called dexamethasone. In dogs that do not have Cushing’s, this injection will completely suppress the production of cortisol.
Your vet will determine this by first measuring the ‘normal’ level of cortisol in your dog’s blood. They will then take two further blood samples at 3-4 hours post injection of dexamethasone, and 8 hours after injection.
In dogs without Cushing’s, the cortisol levels after injection of dexamethasone will be low when compared to ‘normal’ levels – as the injection of dexamethasone has stopped the dog’s adrenal glands from producing any cortisol.
In dogs with Cushing’s, the cortisol levels after injection of dexamethasone will remain elevated– as the dexamethasone is unable to suppress the increased amount of cortisol produced by dogs with the condition.
quite sensitive in pituitary dependant cases- dexmethasone negativly feedbacks on hypothalamus and pituitary and so DOES reduce production in these cases
100% sensitive in adrenal dependant cases- there will be no chnge at all in cortisol
fairly specific but this reduces markedly with concurrent disease
does not work at all in iatrogenic cases
also not usefull in stressed patients
need to tay in the practice for a while
can distinguish between pituitary and adrenal cases
Hyperadrenocorticism can be adrenal dependent or pituitary dependent.
Describe what is happening in the pituitary and adrenal glands at a cellular level and why this causes excessive cortisol release.
tumour cells produce excessive cortisol regardless of the amount of srenocortitropic hormones in adrenal dependant- large breeds are more likley to get adrenal dependant cushings
tumour cells produce excessive adrenocorticotropic hormone regardless of feedback, resulting in increased cortisol from the adrenals in pituitary dependant- small breeds are more likley to get pituitary dependant cushings
how can we differentaite between adrenal and pituitary cushings
measure endoginous adth for pituitary
ultrasound adrenals for adrenal
Hyperthyroidism
Brief overview:
Overproduction of thyroid hormone -> increased sympathetic stimulation and associated signs
Common in cats, very rare in dogs.
Usually due to hyperplasia or functional thyroid adenoma, rarely adenocarcinoma.
Co-morbidities common-
Congestive heart failure
Renal disease
Diabetes mellitus
(both due to hyperthyroidism and becuse its common in older cats)
Hyperthyroidism – Co-mobidities-Congestive heart failure
Due to prolonged excessive sympathetic stimulations
Increases GA risk for surgery and hospitalisation risk for I131, so medication or diet more appropriate.
Hyperthyroidism – Co-mobidities- Renal disease
Often masked due to increased blood pressure -> increased renal blood flow which prevents azotemia developing.
Warn owners that renal disease may be unmasked before starting treatment.
Increases GA and hospitalisation risks as per cardiac disease.
Hyperthyroidism – Co-mobidities- Diabetes mellitus
Hyperthyroidism increases peripheral insulin resistance so could -> development of DM, but this has not been empirically proven.
Hyperthyroidism does make DM more difficult to manage.
Hyperthyroidism - Treatment
Treatment options:
Thiamazole
(methimazole)
Carbimazole
Diet
Surgery
Radioactive iodine
Thiamazole (methimazole) for hyperthyroidism
Mechanism of action: inhibits the enzyme thyroperoxidase, thereby reducing synthesis of T3 and T4
“Felimazole” - twice daily oral tablet
“Thyronorm” - twice daily liquid
Methimazole gel - compounded gel medication administered on the pinna
Used to stabilise thyroid prior to surgery or for long term management.
Pro’s -
Lower risk cf surgery/radioactive iodine, safer in cats with concurrent problems
Multiple formulations available
Con’s -
Oral meds can be difficult for owners
Gel formulation can be unreliable, plus risk to owner.
Costs can mount up over time.
Carbimazole for hyperthyroidismd
Mechanism of action: Pro-drug which is converted to thiamazole either in the GIT or immediately following absorption. Thiamazole inhibits the enzyme thyroperoxidase, thereby reducing synthesis of T3 and T4
“Vidalta” - once daily oral tablet
As thiamazole, used to stabilise thyroid prior to surgery or for long term management.
Pro’s-
Lower risk cf surgery/radioactive iodine, safer in cats with concurrent problems
Once daily dosing only
Con’s-
Oral meds can be difficult for owners.
Costs can mount up over time.
diet as a treatment for hyperthyroidism
Diet:
Hills y/d – iodine restricted diet
Pro’s -
Easy for owners
No risk of side effects
Con’s -
Very variably effective.
House cats only – complete control of diet needed.
Not suitable for multicat households (unless all have hyperthyroidism or dietary separation can be guaranteed)
May also need to give bottled water only in some areas (e.g. coastal)
surgery as a treatmet for hyperthyroidism
Surgery (thyroidectomy):
Four techniques are described; Extracapsular, intracapsular, modified extracapsular, modified intracapsular.
Main difference is to what extent the parathyroid glands are preserved or sacrificed.
Intracapsular technique maintains the most tissue and therefore has the highest risk of leaving abnormal tissue behind.
Extracapsular technique removes the most tissue and therefore has the highest risk of iatrogenic hypothyroidism and hypoparathyroidism- commonly done despite side effects
Pro’s -
Curative - removes the problem tissue so no further treatment should be required.
Useful for cats which will not tolerate medication.
Relatively cost effective and does not require specialist facilities.
Con’s -
Recurrence can occur with ectopic thyroid tissue (5% cases), or residual tissue (unilateral or intracapsular technique).
Iatrogenic hypothyroidism and hypoparathyroidism can occur.
Requires GA (increased risk in cats with comorbidities).
Radioactive iodine therapy to treat hyperthyroidism
Mechanism of action:
Radioactive iodine (I131) is injected subcutaneously and concentrates in the thyroid gland.
I131 produces both beta and gamma radiation; Beta radiation penetrates tissue to a depth of no more than 2 mm (average depth is 0.4 mm) and causes the most damage, gamma radiation causes less local damage as it passes through tissues almost unaltered.
Normal thyroid follicles are suppressed in the hyperthyroid cat, so do not take up the I131, are not damaged and will gradually recover function once the overproduction of thyroid hormone ceases.
Practicalities:
Need to assess for concurrent conditions before considering treatment e.g. renal disease, heart disease.
Use anti-thyroid medication while assessing if radioactive iodine treatment is appropriate; withdraw 1-2 weeks before treatment (centre specific).
One off treatment, but hospitalisation required until radiation levels have dropped to below safe limits (~12 days).
Cats remain slightly radioactive for several weeks, so pregnant people and children should avoid getting too close to the cat after treatment for ~1 month.
Pro’s -
Curative - removes the problem tissue so no further treatment should be required.
Useful for cats which will not tolerate medication.
Recurrence very rare
Parathyroid glands are not affected.
Con’s -
Iatrogenic hypothyroidism (10-30% cases) can occur.
Requires hospital stay with very limited contact (increased risk in cats with comorbidities).
Can only be performed in a specialist center, therefore relatively higher cost.
Hyperthyroidism - Monitoring
Depends on therapy:
Oral medication
Diet
Surgery
Radioactive iodine
Hyperthyroidism - Monitoring- Oral medication
Serum T4: 2-3 weeks after starting treatment.
Upper end or above reference range = increase dose
Below reference range = decrease dose
Euthyroid (in the lower half of the reference range) = recheck as below.
Serum T4, biochemistry and hematology recommended at week 4, 8 and 12 after euthyroid state achieved, then every 3-6 months thereafter.
Urinalysis and blood pressure every 3-6 months
Hyperthyroidism - Monitoring- Diet
Serum T4 four weeks after starting diet to demonstrate decreasing levels.
May take up to six months for thyroid levels to stabilize – check monthly until euthyroid then q3-6 months ongoing
Monitor biochemistry, haematology, urinalysis and blood pressure q3-6 months ongoing.
Hyperthyroidism - Monitoring- Surgery
Unilateral:
Serum T4, biochemistry and haematology 2 weeks post surgery to demonstrate euthyroidism.
Ongoing monitoring at one, three, six and twelve months post-treatment.
Bilateral thyroidectomy:
Serum ionised calcium for 3 days post surgery.
Ongoing monitoring (T4, B&H) at one, three, six and twelve months post-treatment.
TSH if symptoms of hypothyroidism develop or T4 is persistently low (>6m).
Hyperthyroidism - Monitoring-Radioactive iodine
Serum T4, biochemistry and haematology at one, three, six and twelve months post treatment.
TSH if symptoms of hypothyroidism develop or T4 is persistently low (>6m).
Hyperthyroidism - Overview
Treatment overview:
Management: oral medication or diet.
Curative: surgery or radioactive iodine therapy
Co-morbidities of note:
Congestive heart failure
Renal disease
Diabetes mellitus
Potential treatment complications:
Iatrogenic hypoparathyroidism (surgery only)
Iatrogenic hypothyroidism (surgery and radioactive iodine therapy)
Medication side effects
Hypothyroidism
Underproduction of thyroid hormone -> decreased basal metabolism and associated signs.
Common in dogs, very rare in cats- can be induced by treating hyperthyroidism
Primary, acquired disease most common (>95%)
The most common causes of acquired primary hypothyroidism are lymphocytic thyroiditis and idiopathic thyroid atrophy.
Primary congenital, secondary and tertiary hypothyroidism all very rare.
Treatment overview:
Oral medication (levothyroxine)
Co-morbidities of note:
Cardiac disease
Diabetes mellitus
Hypoadrenocorticism
Potential treatment complications:
Thyrotoxicosis
Hamsters-
Most commonly due to adrenocortical adenoma or adenocarcinoma.
Usually diagnosed on clinical signs due to difficulty in collecting sufficient samples and lack of established reference ranges for hamsters.
Medical treatment with metyrapone and adrenalectomy have been reported
Horses-
Different pathophysiology to small animals – increase in circulating POMC-derived peptides rather than glucocorticoids.
More in the second block!
Hypothyroidism – Co-mobidities
Cardiac disease
Diabetes mellitus
Hypoadrenocorticism
Myxoedema coma
Hypothyroidism – Co-mobidities- Cardiac disease
Thyroid hormone deficiency can impair cardiac function -. bradycardia, weak apex beat, arrhythmias
Unlikely to directly cause cardiac disease but pre-existing cardiac disease likely to be impacted by concurrent hypothyroidism.
Thyroid hormones = positive chronotropic and inotropic effects on the heart, stimulate myocardial hypertrophy, and indirectly affect the cardiovascular system by increasing responsiveness to adrenergic stimulation. Thyroid hormone deficiency can therefore impair cardiac function (bradycardia, weak apex beat, arrhythmias). Unlikely to directly cause cardiac disease but pre-existing cardiac disease likely to be impacted by concurrent hypothyroidism.
Hypothyroidism – Co-mobidities- Diabetes mellitus
Immune mediated endocrinopathy; associative rather than causative link.
Hypothyroidism -> significant increases in circulating leptin and insulin -> insulin resistance.
May make DM treatment more difficult.
Hypothyroidism – Co-mobidities- Hypoadrenocorticism
Levothyroxine therapy may -> adrenal crisis (associated with increased steroid hormone clearance), so hypoadrenocorticism must be controlled prior to starting treatment for hypothyroidism.
Dose rates should be started at the low end of the range and titrated up.
Hypothyroidism – Co-mobidities-
Rare but serious.
Stuporous or comatose dog with hypothermia, bradycardia, hypotension and hypoventilation.
Precipitating disease (e.g. cardiac failure, overwhelming sepsis) common, may or may not be related to the thyroid disease.
Treatment = thyroid hormone supplementation + supportive care (respiratory support, fluids, warmth)
Prognosis guarded
Hypothyroidism - Treatment
Levothyroxine
Synthetic form of thyroid hormone, works exactly like T4 in the body.
Tablet and liquid forms available.
Avoid concurrent feeding- decreases absorbtion. also dont give oher meds at same time
Hypothyroidism - Monitoring
Serum total T4 concentrations measured at peak (4-6 hours after meds)- (do in morning)
T4 >90 nmol/l: decrease dose or consider once daily dosage if twice daily therapy is being used.
T4 = 35-90 nmol/l: no change necessary.
T4 <35 nmol/l: increase dose.
Monitor for clinical signs of thyrotoxicosis
.
If T4 is normal but clinical signs persist:
Inadequate time for an effect to be seen (takes months).
Intermittent poor owner compliance (measure cTSH – should be high in these cases).
Comorbidity e.g. cardiac disease, skin disease etc.
Cushing’s disease
Overproduction of glucocorticoids from the adrenal glands.
Common in dogs, very rare in cats.
In dogs pituitary dependant = ~85% cases, majority of the rest are adrenal dependant.
Pituitary dependant = micro- or macroadenomas- big tumour so can cause other signs
Adrenal dependant = hyperplasia, adenoma or carcinoma.
Treatment overview:
Trilostane
Surgery (rarely performed in dogs, more commonly in cats)
Radiotherapy (rarely performed)
Hypophysectoy (rarely performed)
Potential complications:
Macroadenoma induced neurological signs (dogs)
Diabetes mellitus
Cardiac disease (more common in cats than dogs)
Cushing’s disease in cats
75% Pituitary dependant, 25% adrenal gland dependant.
Usually presents as DM which may be insulin resistant, or acutely with cardiomyopathy and/or thromboembolism.
Treatment options are generally less successful in cats than in dogs.
Adrenalectomy appears to be the treatment of choice, but many considerations:
Morbidity and mortality not uncommon
Technically difficult, specialist facilities required.
Ongoing corticosteroid supplementation highly likely to be needed long term.
Radiotherapy, hypophysectomy, and medical treatment also reported.
Cushing’s disease – Co-morbidities
Less common in dogs cf cats
Diabetes mellitus-
Doesn’t tend to be causative in dogs, but makes treatment more difficult where concurrent.
Causative in cats; two pathways:
Peripheral insulin resistance -> increased insulin production initially -> subsequent beta-cell exhaustion and cell death -> diabetes mellitus.
Alternatively, glucose toxicity -> decreased insulin secretion -> diabetes mellitus.
Cardiomyopathy-
More common in cats
Excess circulating glucocorticoid -> cardiomyopathy and thromboembolism
Cushing’s disease - Treatment
Treatment options:
Trilostane
Other oral medications (mitotane and selegilene) are not licensed for use in the UK.
Adrenalectomy (adrenal dependant only)
Radiotherapy (macroadenomas only)
Hypophysectomy (pituitary dependant only)
Cushing’s disease - Treatment- Trilostane
Mechanism of action: Reversibly inhibits 3-beta hydroxysteroid dehydrogenase enzyme system, thereby decreasing synthesis of cortisol and aldosterone.
Used for both pituitary and adrenal dependant disease
Once daily dosing.
Capsules may not be split – compounded formulation can be ordered from specialist pharmacies- EXPENSIVE!
Cushing’s disease - Monitoring- Trilostane
ACTH stimulation test pre-treatment and then at 10 days, 4 weeks, 12 weeks, and thereafter every 3 months.
ACTH stim needs to be performed 4-6 hours post-dosing.
Dose can be adjusted after 10 days if cortisol is too low, or after 4 weeks – Idexx flow chart helpful:
give meds in morning to facilitate easy testing
Cushing’s disease - Treatment- Adrenalectomy
Technically difficult procedure with procedure-related mortality estimated at 30-60% even in referral settings.
Pre-operative stabilisation recommended
Need to establish full extent of tumour prior to surgery (ultrasound, CT or MRI)
Unilateral for adrenal tumour.
Bilateral adrenalectomy for PDH is not recommended in the dog and carries risk of post-operative Addisonian crisis.
Cushing’s disease - Treatment- Radiotherapy
Used for pituitary macroadenomas which are causing neurological symptoms.
Rarely performed referral procedure.
Treats neurological signs due to physical decrease in tumour size, but effect of ACTH release is less predictable; medical therapy likely to still be necessary
Cushing’s disease - Treatment-
Hypophysectomy
Surgical removal of the pituitary gland.
Rarely performed referral procedure.
50% of treated dogs will develop (possibly transient) diabetes insipidus post-surgery so intensive care facilities required.
Hypoadrenocorticism
(Addison’s disease)
Underproduction of glucocorticoids and mineralocorticoids from the adrenal gland.
Uncommon in dogs, very rare in cats.
Atypical form with only glucocorticoid deficiency reported but much rarer.
Immune mediated destruction of the adrenal gland thought to be the most common cause.
Iatrogenic (rapid glucocortisoid withdrawal) also occurs
Treatment overview:
Glucocorticoid therapy
Mineralocorticoid therapy (Zycortal)
Potential complications:
Hypothyroidism
Addisonian crisis
Addison’s disease – Co-mobidities
Hypothyroidism-
Poorly defined link, but can be seen as a polyendocrinopathy.
Treatment for hypothyroidism can predispose to Addisonian crisis.
Addisonian crisis-
Acute presentation of Addison’s disease
Addisonian Crisis
Chronic disease: Vague, waxing-waning signs. Weight loss, PU/PD, vomiting and lethargy often reported. Electrolyte changes often, but not always present on bloods. Easy to miss.
Addisonian crisis:
Hypovolemic shock (weak pulses, prolonged capillary refill time)
Bradycardia or tachycardia
Collapse
Depression
Hypothermia
Rapidly progressive and life threatening.
Addisonian Crisis - Treatment
Hypovolaemic shock:
Rapid infusion of 0.9% saline using shock rates, then decrease once BP stablised.
Continue IV fluids until electrolytes stabilized and animal eating again
Intravenous glucocorticoids (IV bolus or CRI); move to oral once eating and stable.- dexamethasone often of choice
Hypoglycaemia:
Glucose CRI
Hyperkalemia:
Dilution with fluid therapy usually sufficient.
If symptomatic e.g. ECG changes, insulin/glucose CRI or calcium gluconate.
Addison’s disease - Treatment
Glucocorticoid treatment:
Prednisolone most common.
Daily administration, titrated to lowest effective dose.
Increase at times of stress (risk of Addisonian crisis)
Mineralocorticoid treatment:
Desoxycortone pivalate (zycortal)
Very complicated!
Addison’s disease - Monitoring- Zycortal
Electrolytes and clinical signs are checked at day 10 and day 25 after the initial zycortal dose.
These are used to make dose adjustments to glucocorticoid and/or zycortal according to the flow chart.
Electrolytes are checked at day 10 and day 25 after each dose change.
If the dose is staying the same, the electrolytes can just be checked at day 25 (provided clinically stable)
Once the dog is controlled, routine monitoring of electrolytes is recommended every 3-6 months at day 25 (or the day zycortal is administered if different dosing intervals are being used)
Diabetes
Brief overview:
Type 1: destruction of beta cells -> complete and permanent loss of insulin secretory ability. Most common in dogs.
Type 2: Peripheral resistance to insulin -> hyperglycaemia. Most common type in cats.
Other types exist but are rarer e.g. induced DM due to concurrent endocrinopathy.
Type 2 and induced DM can progress to type 1 over time if not controlled.
Treatment overview:
Diet
Oral hypoglycaemics
Insulin therapy
Ovariohysterectomy (bitches)
Co-morbidities of note:
Obesity
Acromegaly
Hyperadrenocorticism
Hyperthyroidism
Hypothyroidism
Pancreatitis
Complications-
Diabetic neuropathy
Ocular disease
Urinary tract infection
Diabetic ketoacidosis
Diabetes – Co-mobidities
Hypothyroidism
Associative rather than causative link
Can increase insulin resistance and make DM more difficult to manage
Conditions which can induce peripheral insulin resistance -> DM:
Obesity
Acromegaly – see block 2
Hyperadrenocorticism
Hyperthyroidism?
Pancreatitis – chronic inflammation of the pancreas -> destruction of pancreatic tissue including beta cells.
Other inflammatory disorders e.g. gingivitis, stomatitis, etc.
Diabetes – Complications
Diabetic neuropathy
Ocular disease
Urinary tract infection
Diabetic ketoacidosis
Diabetes – Complications- Diabetic neuropathy
Due to glucose build up in nerves (which do not require insulin to take up glucose) -> toxicity and nerve damage.
Presenting signs include hindlimb weakness and muscle wasting.
Signs can improve with better control of DM.
Diabetes – Complications- Ocular disease
Cataracts (dogs) – due to osmotic disruption of the lens due to an accumulation of sorbitol (a metabolic product of excess glucose)- looks like cataract split into three sections
Retinal neuropathy (cats and dogs) – pathophysiology unclear.
Diabetes – Complications- Urinary tract infection
Presence of glucose in the urine predisposes to the development of infections.
Can ascend and cause pyelonephritis if left untreated.
Diabetes – Complications-Diabetic ketoacidosis
Life threatening metabolic crisis; occurs with uncontrolled DM
Presentation: Signs of PU/PD, vomiting, lethargy and anorexia likely to have been present, may have decompensated by time of presentation to severe depression or even coma.
Clinical exam: Tachypnea or slow deep breathing (Kussmaul respiration) + acetone smell on breath, profound dehydration, hypothermia, slow CRT.
Investigations:
Urinalysis – glucosuria +/- ketonuria
Increased serum ketones + hyperglycaemia
Metabolic acidosis (pH <7.3)
Diabetic ketoacidosis - Treatment
Correct dehydration:
If hypovolaemic shock is present, give a bolus (20ml/kg for dogs or 15ml/kg for cats, over 15 minutes)
Otherwise, calculate fluid deficit and replace over 12 hours.
Maintenance fluid requirements may be high due to polyuria 2o to hyperglycaemia
Address electrolyte and acid/base disorders:
Hypokalaemia – address by adding potassium into IV fluids. Must be done prior to insulin therapy- insulin drives potassium into cells so will make any deficit worse
Phosphate – will decrease 12-24hr after starting therapy so supplement proactively.
Calcium and magnesium – only tx if symptomatic.
Acidosis – bicarbonate correction only required in severe cases (pH <7.1 or bicarbonate concentration <10 mmol/l) provided renal function is normal
Halt ketosis and address hyperglycemia:
IV or IM rapid acting regular (soluble) insulin given initially.
CRI preferred - BG must be checked every 2 hours for at least the first 36 hours and adjust CRI and/or provide supplemental dextrose as necessary.
Continue regular insulin until animal clinically stable and eating.
Identify and address underlying or precipitating factor:
>70% cases in dogs and the majority of cases in cats involve a concurrent disorder
Pancreatitis, UTI, Cushing’s disease, CKD and infection = most common concurrent conditions in dogs.
Hepatic lipidosis, cholangiohepatitis, pancreatitis, CKD and infection = most common concurrent conditions in cats.
Diabetes - Treatment options
Diet
Oral hypoglycaemics
Insulin therapy
Ovariohysterectomy (bitches)
Diabetes - Treatment- diet
Aims of a diabetic diet:
Weight loss (obese animals)/maintain ideal body condition.
Minimise post-prandial blood glucose increases (calorie content from protein and fat rather than carbohydrate; high fibre content).
Be palatable to encourage regular, predictable intake
Useful in all uncomplicated diabetic patients to help control disease.
Cats can go into diabetic remission with diet alone in some cases.
Not suitable for patients with concurrent renal disease (high protein content) or pancreatitis (relatively high fat content).
Diabetes - Treatment- Oral hypoglycaemics
Not used in dogs.
In cats, used in cases where owners feel unable to give injections.
Glipizide
Velagliflozin – brand new!
Glipizide:
Previously the only drug suitable for use as a sole agent in cats.
Mechanism of action: Stimulates insulin secretion from the pancreas.
Effective in approx. 40% patients; may stop working over time.
Velagliflozin:
Released last week
Mechanism of action: Sodium glucose co-transporter 2 inhibitor; stops reuptake of glucose from the urine after it has been filtered out.
Diarrhoea = common side effect
Risk of UTI due to glucosuria
Risk of euglycaemic ketoacidosis as no mechanism to move glucose into cells.
Velagliflozin
diatbetes treatment
Released last week
Mechanism of action: Sodium glucose co-transporter 2 inhibitor; stops reuptake of glucose from the urine after it has been filtered out.- controlls hypoglycemia and hence controlles clinical signs
Diarrhoea = common side effect
Risk of UTI due to glucosuria
Risk of euglycaemic ketoacidosis as no mechanism to move glucose into cells.- drug just pushes glucose out of bosy
Only for use in newly diagnosed diabetics (no previous insulin therapy)
Do not use in dehydrated animals
Screen and monitor for ketonuria
Any patient receiving velaglifozin who becomes unwell should have ketones checked using a ketometer (urine sticks = poor sensitivity)
Diabetes - Treatment- Insulin therapy- Caninsulin
Caninsulin (porcine insulin)
Intermediate duration of action
Can be given via u-40 syringes or using vetpen with cartridges.
Once daily dosing suitable for most dogs, cats require at least twice daily dosing.
Given via s/c injection
Diabetes - Treatment- Prozinc
Prozinc (protamine zinc insulin human)
Longer acting form of insulin, more suitable for cats.
Once daily dosing suitable for most dogs, twice daily for cats.
Given via s/c injection
Care with vial – prozinc insulin is delicate and can become inactivated with shaking.
very sensitive to temp change- store IN fridge, not in fridge door
Diabetes - Treatment- Ovariohysterectomy
Adjunct to insulin therapy.
High concentrations of progesterone and growth hormone in diestrus antagonize insulin.
Once DM is stabilised, entire bitches should be sterilised to aid long term management.
Diabetes - Monitoring
Owner should keep a diary containing the following:
Insulin dose, and time of administration.
Daily food intake (time offered, amount offered, amount consumed)
Daily water intake (amount offered, amount consumed)
Demeanor
Weekly weight and body condition
Presence of urine glucose and/or ketones (daily if possible)
Blood glucose curves
Best performed at home if possible as reduces the effect of stress on blood glucose levels
Values are then sent to the vet to be interpreted.
Other monitoring options:
Continuous glucose monitoring is now starting to be offered for veterinary patients.
Fructosamine-
Serial measurements to evaluate trends in glycaemic control most useful.
May be useful for Velagliflozin
HBA1C-
Monitoring test of choice in humans. Further studies needed in veterinary species.
Diabetes - Monitoring- Blood glucose curves
First curve is done 2-3 weeks after starting insulin therapy.
Must use a veterinary glucometer e.g. AlphaTrak
Method:
Capillary blood samples collect from the pinna.
1st blood sample in the morning before the animal has had food or insulin.
Then sample every 2 hours for 12 hours.
Interpretation: maximum ideally below 14mmol/L, nadir ideally between 5-8mmol/L
accounts for somogyi overswing-
aka rebound hyperglycaemia
Response to an overdose of insulin
As hypoglycaemia begins to develop, release of glucose from hepatic glycogen stores is triggered -> rebound hyperglycaemia +/- glucosuria
CARE: risk this could be interpreted as a need for increased insulin if single glucose measurements are used, when a dose decrease is actually required.
if signle blood glucose taken wrong interpritation more likley
Bacteraemia
the presence of viable bacteria in the bloodstream
