Endocrine Diseases Flashcards
what is the most common endocrine condition in cats?
hyperthyroidism
where in the world is hyperthyroidism seen?
everywhere
why is feline hyperthyroidism being recognised much more commonly now?
awareness is better
older cats that are living longer
may be becoming more common
is there evidence that feline hyperthyroidism is auto-immune?
no, unlike in humans
what are 95% of feline hyperthyroidism cases caused by?
benign adenomatous hyperplasia
adenoma pf thyroid tissues
what does benign adenomatous hyperplasia / adenoma of thyroid tissues cause?
spontaneous secretion of thyroid hormones
escaping control of hypothalamus and pituitary gland
what are <5% of feline hyperthyroidism cases caused by?
adenocarcinoma (malignant)
is feline hyperthyroidism more commonly bilateral or unilateral?
2/3 bilateral
1/3 unilateral
where is ectopic thyroid tissue most commonly seen?
mediasteinum
how many cases of feline hyperthyroidism have ectopic thyroid tissue?
5%
what are the potential causes of feline hyperthyroidism?
nutritional factors
environmental factors
genetic factors
circulating factors
what are the nutritional factors which cause feline hyperthyroidism?
high levels of iodine in diet
presence of goitrogens
what cats are much less likely to have feline hyperthyroidism?
siamese or himalayan (10x less likely)
what circulating factors can increase the risk of feline hyperthyroidism?
thyroid growth stimulating immunoglobulins in the blood stream
what are the risk factors for feline hyperthyroidism?
regular use of flea sprays or powders
indoor cats
reported exposure to lawn herbicides, fertilisers and pesticides
cats fed mainly canned foods
what is the signalment of feline hyperthyroidism?
middle aged to elderly cats (10-13 years)
no sex predeliction
what does the severity of signs of feline hyperthyroidism depend on?
duration of disease
presence of concurrent diseases
what are the effects on the body of raised thyroid hormones?
increased: metabolic rate cardiac output HR BP GI motility CNS activity
decreased:
sleep
body weight
what does increased GI motility due to increased thyroid hormone mean for feline hyperthyroidism patients?
may have vomiting and diarrhoea
what are the major clinical signs of feline hyperthyroidism?
palpable enlarged lymph nodes weight loss polyphagia hyperactive for their age PUPD tachycardia
what are the minor clinical signs of feline hyperthyroidism?
lethargy intermittent anorexia voice changes muscle weakness / tremors CHF heat intolerance mild pyrexia dyspnoea / tachypnoea
what is apathetic feline hyperthyroidism?
type of hyperthyroidism seen in a small number of patients (<10%) who likely have underlying comorbidity
in how may patients is apathetic feline hyperthyroidism seen?
<10%%
what are the signs of apathetic feline hyperthyroidism?
lethargy
inappetance
weight loss
obtundation
what is apathetic feline hyperthyroidism likely reflecting?
underlying comorbidity
what abnormalities are often present in patients with apathetic feline hyperthyroidism?
cardiac
what effect can thyroid hormones have on cardiac disease?
often worsen
how should feline hyperthyroidism patients be handled?
cat friendly
hands off
should be allowed to acclimatise and settle
what parameters should be closely monitored in feline hyperthyroidism patients?
RR
what may be provided to feline hyperthyroidism patients on arrival to veterinary practice?
O2 therapy if tachypnoeic
why are feline hyperthyroidism patients often stressed?
high thyroid hormones cause agitation
what can feline hyperthyroidism patients be given before travel to calm them?
50mg Gabapentin 2 hours before travel
how is feline hyperthyroidism diagnosed?
compatible clinical signs
screening tests
confirmatory diagnostic tests
how can thyroid glands be palpated?
lift head with one hand and extend neck
use other hand thumb and index finger to feel all the way from the larynx to the thoracic inlet
what are screening tests used for when diagnosing feline hyperthyroidism?
baseline health
what screening tests are used during feline hyperthyroidism diagnosis?
haematology
biochemistry
urinalysis
BP
what is often seen on biochemistry in a cat with feline hyperthyroidism?
elevated liver enzymes (mild to moderate)
what can be shown by biochemistry when testing for feline hyperthyroidism?
CKD
what will urinalysis show in a feline hyperthyroidism patient?
if concurrent CKD
what sudden issue can severe feline hyperthyroidism patients get?
sudden blindness due to hypertension
what is the gold standard confirmatory diagnostic test for feline hyperthyroidism?
serum total thyroxine (T4) - TT4
how elevated is total T4 in most hyperthyroid cases?
> 50-60 nmol/L
what total T4 level may be seen in some feline hyperthyroidism patients?
fluctuating
high normal
why may high normal total T4 levels be seen in some feline hyperthyroidism patients?
early disease
presence of non-thyroidal illness that lowers T4 prodution
what are the 4 main treatment options for feline hyperthyroidism?
medical management with antithyroid drugs
iodine restricted diet
thyroidectomy
radioactive iodine treatment
which of the treatment options for feline hyperthyroidism are curative?
thyroidectomy
radioactive iodine treatment
what should be tried first to treat feline hyperthyroidism?
medical management
what should be assessed before undertaking any irreversible feline hyperthyroidism treatment?
renal function when patient is euthyroid
what must be done before any surgery/GA if the patient has feline hyperthyroidism?
patient should be stabilised
what is the purpose of anti-thyroid drugs?
block thyroid production
what is the main drug used to treat feline hyperthyroidism?
methimazole
how often should Methimazole be given?
BID
in what form can Methimazole be given?
tablets
transdermal gel
oral liquid
where is transdermal Methimazole applied?
pinna
what tablets are available to treat feline hyperthyroidism that can be given once a day?
slow-release carbimazole tablets
what is the role of slow release anti-thyroid tablets?
converted in the body to methimazole which is then utilised
who should be careful when handling anti-thyroid drugs?
pregnant women
when is a feline hyperthyroidism patient normally euthyroid after anti-thyroid drugs?
<2-3 weeks
when should total T4 be checked following anti-thyroid treatment?
2-3 weeks
what tests should be run in the first 1-3 months following anti-thyroid drugs?
CBC and biochem
what is the purpose of CBC and biochem tests in the first 3 months after beginning treatment for feline hyperthyroidism?
monitor for side effects
what may anti-thyroid drugs be used for in the short term?
stabilisation prior to more curative therapy
what are the advantages of anti-thyroid drugs?
readily available rapidly effective inexpensive practical no GA or hospitalisation
what are the disadvantages of anti-thyroid drugs?
lifelong
long term resistance
compliance is crucial
side-effects
what are the minor, common, transient side effects of anti-thyroid drugs?
vomiting
anorexia
lethargy
what are the major, rare and persistent side effects of anti-thyroid drugs?
persistent GI signs blood dyscrasias (leukopenia, anaemia and thrombocytopenia) dermatitis hepatopathy lymphadenomegaly myasthenia gravis
what sort of dermatitis is commonly seen as a major side effect of anti-thyroid drugs?
facial excoriation
what is lymphadenomegaly?
enlarged lymph nodes
what should happen if major side effects of anti-thyroid drugs are seen?
stop treatment
how can diet be used to control feline hyperthyroidism?
iodine restricted diet fed to reduce T4 production
what iodine restricted food is available?
Hills y/d
what can be fed alongside and iodine restricted diet?
must be fed as sole food - no treats
how quickly can feline hyperthyroidism patients be euthyroid when fed an iodine restricted diet?
within 3 weeks
how long must be feline hyperthyroidism patient be on the iodine restricted diet for?
lifelong
when is an iodine restricted diet less effective / unsuitable?
for severe hyperthyroid cats
what are the main pre-surgical considerations for treatment of feline hyperthyroidism?
systemic effects of feline hyperthyroidism
cardiac disease
hypertension
other diseases
what should happen to a feline hyperthyroidism patient prior to surgery?
stabilisation
what is removed during thyroidectomy?
one or both of the thyroid glands
what must be preserved during a thyroidectomy?
parathyroid tissue
why must the parathyroid tissue be preserved in thyroidectomy?
to avoid post op complications such as hypocalcaemia
why could hypocalcaemia occur following thyroidectomy?
PTH is essential for calcium homeostasis
in what % of patients does thyroidectomy achieve euthyroidism?
> 90%
when is euthyroidism achieved following thyroidectomy?
24-48 hours
what structures must you be careful of when performing thyroidectomy?
parathyroid
vagus nerves
is is possible to save the parathyroid gland if feline hyperthyroidism is advanced?
not usually due to enlargement of glands
what are the advantages of thyroidectomy?
curative
rapidly effective
short hospitalisation period
what are the disadvantages of thyroidectomy?
GA skill required to save parathyroid location recurrance cost complications
what are the complications associated with thyroidectomy?
damage or removal of parathyroid tissue leading to post op hypoparathyroidism
damage to recurrent laryngeal nerve
damage to sympathetic trunk
possible recurrence of feline hyperthyroidism if only unilateral thyroidectomy
is laryngeal paralysis a common complication of thyroidectomy?
no
what is a condition that can be caused by damage to the sympathetic trunk during thyroidectomy?
Horner’s syndrome - nictating membrane prolapse and myosis
when does iatrogenic hypoparathyroidism occur?
usually after bilateral thyroidectomy
how long does iatrogenic hypoparathyroidism last for?
usually transient
when does iatrogenic hypoparathyroidism resolve?
recovery of glands/restored function of ectopic tissues
how long does it take to recover from iatrogenic hypoparathyroidism?
weks to months
when are clinical signs of iatrogenic hypoparathyroidism seen?
withi 2-3 days
what are the signs of iatrogenic hypoparathyroidism?
due to hypocalcaemia inappetance weakness tremors ptyalism pawing at face progression to tetany seizures coma death
what should be monitored if concerned about iatrogenic hypoparathyroidism or there has been bilateral thyroidectomy?
serum calcium twice a day
how should iatrogenic hypoparathyroidism be treated?
IV 10% calcium gluconate slowly (10-20 mins)
what is the initial bolus of calcium gluconate to treat iatrogenic hypoparathyroidism followed by?
CRI
what fluids should be avoided when giving calcium gluconate?
bicarbonate, lactate or phosphate containing fluids as will precipitate calcium
not Hartmann’s
can calcium gluconate be given SC?
no
why can calcium gluconate not be given SC?
skin sloughs
what should patients receiving calcium gluconate be monitored for?
ECG for arrhythmia and bradycardia
what should happen once the patient with iatrogenic hypoparathyroidism is stabilised on IV calcium gluconate?
oral therapy ASAP of calcium and vitamin D
how is the patient switched from IV calcium gluconate to oral therapy?
elemental calcium in divided doses to wean off IV
how are iatrogenic hypoparathyroidism cats managed orally once IV calcium gluconate has stopped?
oral vitamin D only
can iatrogenic hypoparathyroidism patients be weaned off all treatment?
yes - eventually
how long does oral therapy for iatrogenic hypoparathyroidism take to work?
1-3 days
what is the gold standard treatment for feline hyperthyroidism?
radioiodine treatment
how is radioiodine treatment administered?
systemically
where does radioiodine therapy target?
excessive T4 producing cells in the thyroid
what do beta particles of radioiodine cause?
cell death
how long must the cat be isolated for following radioiodine treatment?
1-2 weeks post injection
why does the cat need to be isolated for 1-2 weeks following radioiodine injection?
gamma rays they emit are dangerous
how many centres are available for radioiodine treatment in the UK?
15 (including Bris)
what are he advantages of radioactive iodine treatment for feline hyperthyroidism?
gold standard curative simple procedure higher dose to treat adrenocarcinoma no GA cost
what are the disadvantages of radioactive iodine treatment?
limited availability isolation period irreversible may take some time to achieve euthyroid very rarely iatrogenic hypothyroidism cost
what is the risk associated with feline hyperthyroidism and CKD?
hyperthyroidism may mask CKD and so treatment may unmask it
how much can treatment of feline hyperthyroidism change CKD level?
maximum of one IRIS stage
what must be considered about feline hyperthyroidism and CKD?
medical management of feline hyperthyroidism before curative treatment to see effect on kidneys
reassess once euthyroid
what may not prevent definitive feline hyperthyroidism treatment relating to CKD?
unmasking of mild azotemia through thyroid medical management
when should feline hyperthyroidism patients be monitored irrespective of treatment regime?
6 monthly check ups if stable
soone if not
what are you monitoring for when having feline hyperthyroidism check ups?
recurrence
hypertension
CKD (urea, creatinine, BP, urinalysis)
what is the prognosis of feline hyperthyroidism dependent on?
severity / presence of concurrent disease (especially heart disease)
what cats have excellent feline hyperthyroidism prognosis?
uncomplicated with curative treatment
what are the main types of canine thyroid neoplasia?
carcinomas more common
adenomas usually incidental
what sort of masses are canine thyroid neoplasia?
large, solid, palapabel
what type of tumor is canine thyroid neoplasia?
locally invasive
some metastatic
what are most canine thyroid neoplasia patients thyroid levels like?
most euthyroid or hypothyroid
what percentage of canine thyroid neoplasia patients are hyperthyroid?
10%
what is the signalment of canine thyroid neoplasia?
10 years
what are the signs of canine thyroid neoplasia?
mass in ventral neck
may have cough or dyspnoea due to pressure on trachea
how is canine thyroid neoplasia diagnosed?
histopathology of mass
FNA
surgery usually needed to confirm
why must care be taken when gaining histopathology of a mass to diagnose canine thyroid neoplasia?
very vasular area
what is the issue with FNA of canine thyroid neoplasia?
often blood contaminated sample
how is canine thyroid neoplasia treated?
surgical removal
chemotherapy or radiation to follow
why is radioactive iodine treatment for canine thyroid neoplasia not often performed?
high doses required
what does the prognosis of canine thyroid neoplasia depend on?
size
local invasion
functional status
histological diagnosis of carcinoma or adenoma
what is the prognosis for dogs with large, invasive canine thyroid neoplasia masses?
guarded to poor
6-24 months if aggressive treatment
when is the prognosis for canine thyroid neoplasia excellent?
surgical removal of adenomas
when is the prognosis for canine thyroid neoplasia good?
removal of small, well circumcised carcinomas
what is the most common endocrine disorder in dogs?
canine hypothyroidism
why is canine hypothyroidism likely to be over-diagnosed?
due to tests used
where are the thyroid glands located?
lateral to the proximal tracheal rings
what hormones are produced by the thyroid?
thyroxine - T4
triiodythyronine - T3
what are thyroid hormones produced from?
tyrosine amino acids
what enzyme causes the oxidation of iodine?
thyroid peroxidase
what is the main thyroid hormone that is secreted?
T4
where is 99% of T4 found in circulation?
bound to proteins
what is the role of unbound T4 (fT4)?
biologically active and exerts a negative feedback on TSH production
what happens to fT4 within the cell?
diodinated to form either T3 or reverse T3
what does T3 bind to in the cell?
nuclear receptor
how does the HPA control T4 and T3 release?
hypothalamus releases TRH
causes pituitary gland to release TSH
this stimulates the thyroid glands to release T4, T3 and rT3
how is T4, T3 release controlled?
T4 and T3 negatively feedback on hypothalamus and pituitary to stop TRH and TSH release
where does primary hypothyroidism occur?
at the level of the thyroid gland
what is the most common type of canine hypothyroidism?
primary
what are the 2 causes of primary canine hypothyroidism?
lymphocytic thyroiditis
thyroid atrophy
what is lymphocytic thyroiditis caused by?
immune mediated destructive process
infiltration of lymphocytes and other WBC
thyroid tissue is replaced by fibrous connective tissue
when do clinical signs of lymphocytic thyroiditis occur?
when 75% of gland is destroyed
what causes thyroid atrophy?
degenerative process
progressive replacement of thyroid tissue with adipose and connective tissue
possibly due to end stage lymphocytic thyroiditis
what are the causes of secondary hypothyroidism?
pituitary hypoplasia - congenital (disproportionate dwarfism) or dysfunction (neoplasia)
is secondary canine hypothyroidism common?
rare
what is the most common cause of secondary hypothyroidism?
suppression of TSH secretion by exogenous glucocorticoid administration (steroids) and hyperadrenocorticism (cushings)
what is the mean age of diagnosis of canine hypothyroidism?
7 years
what animals tend to develop canine hypothyroidism sooner?
those breeds predisposed to lymphocytic thyroiditis
what breeds are predisposed to lymphocytic thyroiditis?
english setter
golden retriever
cocker spaniel
boxer
what are the areas of the body which may exhibit signs of canine hypothyroidism?
decreased metabolic rate dermatologic repro cardiac neuromuscular occular GI
what are the clinical signs of canine hypothyroidism linked to decreased metabolic rate?
weight gain
lethargy
inactivity
what are the clinical signs of canine hypothyroidism linked to dermatologic signs?
endocrine alopecia
rat tail
tragic facial expression hair in telogen phase
mixoedema
what is endocrine alopecia?
symmetrical hair loss
non puretic
what is mixodema?
thickened skin
what are the clinical signs of canine hypothyroidism linked to the reproductive system?
persistent anoestrus weak/silent oestrus prolonged oestral bleeding inappropriate lactation no effect on males
what are the clinical signs of canine hypothyroidism linked to the CVS?
bradycardia
association with atrial fibrilation
some reports of atrial thromboembolysm
what cardiac condition may canine hypothyroidism be linked to?
DCM
what is the mechanism of neuromuscular disease linked to canine hypothyroidism?
accumulation of mucopolysaccharides leading to impaired transport along axons and arthrosclerosis
what are the clinical signs of canine hypothyroidism linked to neuromuscular diseases?
megaoesophagus
laryngeal paralysis
peripheral vestibular syndrome (head tilt)
facial nerve paralysis
are neuromuscular diseases usually linked to canine hypothyroidism?
more likely concurrent disorders than causal effect of hypothyroidism
what is myxoedema coma?
life threatening potential consequence of hypothyroidism
what are the signs of myxoedema coma?
profound mental dullness weakness hypothermia bradycardia hypotension
what usually leads to a hypothyroid patient developing myxoedema coma?
precipitating factor e.g. surgery, heart failure or sepsis
what are the clinical signs of canine hypothyroidism linked to the eyes?
corneal lipid deposits due do hyperlipidaemia
ulcreation
uveitis
what are the clinical signs of canine hypothyroidism linked to the GI tract?
diarrhoea due to bacterial overgrowth
constipation due to reduced peristalsis
how is canine hypothyroidism diagnosed?
appropriate history and clinical signs
haematology and biochemistry
specific thyroid testing
what signs are typically seen on the biochemistry and haematology of a canine hypothyroidism patient?
mild non-regenerative anaemia (normocytic and normochromic)
hypercholesterolaemia
hypertriglycerideaemia
what effect do thyroid hormones have on lipids?
stimulate synthesis, mobilisation and degradation (no T4 no degradation of lipids)
what thyroid abnormalities do you expect in a canine hypothyroidism patient?
low T4 high TSH (no inhibition)
what is total T4 useful for in canine hypothyroidism?
initial screeing test
why is total T4 not used as a definitive canine hypothyroidism diagnosis?
thyroglobulin antibodies can falsely increase TT4
TT4 decreases with age, breed, non thyroidal illnesses and drug therapy (steroids)
when are thyroglobulin antibodies produced?
in lymphocytic thyroiditis
what other tests apart from TT4 can be used to diagnose canine hypothyroidism?
canine TSH
anti-thyroglobulin antibodies
why is TSH increased in canine hypothyroidism cases?
lack of negative feedback
why does the canine TSH test have moderate sensitivity?
low TSH in central hypothyroidism (pituitary cause)
low TSH if there is corticosteroid therapy
what is canine TSH level not affected by?
largely unaffected by non-thyroidial illness or drugs
when may TSH be elevated in euthyroid dogs?
if recovering from NTI
what is a positive anti-thyroglobulin antibody test indicative of?
lymphocytic thyroiditis
what does anti-thyroglobulin antibodies give no information about?
thyroid function
when can anti-thyroglobulin antibodies be present?
long before hypothyroidism
how us canine hypothyroidism treated?
synthetic T4 - prohormone for active T3
what is the main drug given for canine hypothyroidism?
sodium levothyroxine
how often is sodium levothyroxine given?
SID or divided BID
what effect does food have on bioavailability of sodium levothyroxine?
halves bioavailability
what is crucial when giving sodium levothyroxine to treat hypothyroidism?
consistency with dosing times and monitoring times
how should dogs with cardiac disease, DM or hypoadrenocorticism be dosed with sodium levothyroxine?
start with 25% of dose and titrate up
when should sodium levothyroxine effect on hypothyroidism be evaluated?
6-8 weeks after first administration
when is peak sodium levothyroxine concentration?
3-5 hours post pill
what is the half life of sodium levothyroxine?
9-15 hours
why does dose and timing need to be tailored to the dog when giving sodium levothyroxine?
absorption and metabolism vary between dogs
what are the formulations of sodium levothyroxine available?
Soloxine - tablets
Thyroforon - flavored tablets
Leventa - liquid
what should be observed when monitoring the canine hypothyroid patient?
clinical response
TT4
fT4
cTSH
when should monitoring blood tests for canine hypothyroidism be carried out
6-8 weeks after starting treatment
2-4 weeks after dose altered
when should TT4 be measured when monitoring canine hypothyroidism that is being treated?
6 hours post pill SID
4-6 hours BID
when should fT4 be measured during canine hypothyroidism monitoring?
if chronic prednisolone admin
what is the aim for T4 and TSH values in canine hypothyroidism patients when receiving treatment
TT4 upper half of reference
TSH normal
does hyperthyroidism often occur after treatment for canine hypothyroidism?
rare
what are the complications of canine hypothyroidism treatment?
thyrotoxicosis
myxoedema coma
what is thyrotoxicosis secondary to?
drug overdose
what are the clinical signs of thyrotoxicosis?
panting anxiety/aggression PUPD weight loss polyphagia (signs of hyperthyroidism)
how is myxoedema coma treated?
supportive care of other conditions IV levothyroxine (hard to get hold of)
what is the prognosis for canine hypothyroidism?
good - adult dogs with primary
guarded if seocndary
what are the 3 areas of the adrenal cortex?
zona glomerulosa
zone fasiculata
zona reticularis
what is produced in the zona glomerulosa?
mineralocorticoids
what is produced in the zona fasiculata and zone reticularis?
glucocorticoids and sex hormones
what is produced in the adrenal medulla?
catecholamines
what is the main mineralocorticoid produced?
aldosterone
where is the major site of aldosterone action?
cells in distal convoluted tubule and collecting duct (renal tubules)
what is the action of aldosterone?
resorption of H2O and NaCl
secretion of K+ and H+
what electrolyte is aldosterone more important for regulating?
K+ more than Na+
what is the most important stimuli of aldosterone production?
hyperkalaemia
increased angiotensin II
how does the HPA axis stimulate secretion of cortisol and aldosterone?
hypothalamus produces CRH
pituitary gland is then stimulated to produce ACTH
stimulates adrenal glands to produce cortisol and aldosterone
what organ is affected by primary hypoadrenocorticism?
adrenal glands
what is caused by primary hypoadrenocorticism?
addison’s disease
lack of cortisol and aldosterone
what is caused by secondary hypoadrenocorticism?
lack of cortisol
what organ is affected by secondary hypoadrenocorticism?
pituitary gland
what is the most common type of hypoadrenocorticism?
primary
what happens as a result of primary hypoadrenocorticism?
lack of glucocorticoids and minuralocorticoids
what happens in atypical hypoadrenocorticism?
lack of glucocorticoids but normal mineralocorticoids
what is the suspected cause of primary hypoadrenocorticism?
immune mediated destruction of the adrenal cortex
what is the cause of secondary hypoadrenocorticism?
pituitary gland is cause
neoplasia, inflammation, infection, infarct, iatrogenic (hypophysectomy)
what deficiency does secondary hypoadrenocorticism cause?
glucocorticoid as aldosterone is regulated by RAAS as well
why may there be neurological signs with secondary hypoadrenocorticism?
brain lesion present
what are the typical dogs that get hypoadrenocorticism?
young/middle aged
female
what breeds are predisposed to hypoadrenocorticism?
standard poodles
bearded collie
novia scotia duck toller
great dane
what are the clinical signs of hypoadrenocorticism?
vague waxing and waning history
what are the signs caused by lack of cortisol?
weakness
vomiting
diarrhoea
anorexia
when are signs of lack of cortisol due to hypoadrenocorticism exacerbated?
at times of stress
what are the signs of lack of aldosterone?
PUPD to to low Na
not in atypical hypoadrenocorticism
what is a severe complication of hypoadrenocorticism?
Addisonian crisis - emergancy
what are the signs of Addisonian crisis?
collapse severe dehydration hypovolaemia (low sodium) pre-renal azotemia (dehydration) cardiac arrhythmias (hyperkalaemia - bradycardia)
how is hypoadrenocorticism diagnosed?
compatible history and clinical signs haematology biochemistry urinalysis basal cortisol
what is found on the haematology results of a patient with hypoadrenocorticism?
non-regenerative anaemia
absence of stress leukogram (which should be seen in a sick patient)
what will the leukogram of a hypoadrenocorticism patient show?
decreased neutrophils
increased lymphocytes
increased eosinophils
what is seen on the biochemistry results of hypoadrenocorticism patients?
hyperkalaemia and hypernatraemia hypercalcaemia pre-renal azotemia acidaemia (vomiting) hypoglycaemia increased liver enzymes decreased albumin and cholesterol
what sodium / potassium ratio indicates hypoadrenocorticism?
<27 - due to lack of mineralocorticoids
what is pre-renal azotemia in hypoadrenocorticism due to?
hypovolaemia and dehydration
what is hypoglycaemia in hypoadrenocorticism due to?
lack of glucocorticoids
why does hypoadrenocorticism lead to increased liver enzymes?
poor perfusion
why is decreased albumin and cholesterol seen in hypoadrenocorticism?
GI insult from lack of glucocorticoids affecting vascular flow to tract
what are the urinalysis findings of a patient with hypoadrenocorticism?
variable USG due to low Na and high Ca2+
could be dilute due to low Na or concentrated due to dehydration
what is basal cortisol used to test?
exclusion of hypoadrenocorticism
what basal cortisol level indicates hypoadrenocorticism is unlikely?
> 55 nmol/L - cortisol is being stored
what basal cortisol level indicates an ACTH stim is necessary?
<55 nmol/L
what is used to confirm the hypoadrenocorticism diagnosis?
ACTH stim
what are the levels of pre and post ACTH cortisol in hypoadrenocorticism patients?
both below 20 nmol/L
what can affect the results of ACTH stim?
exogenous glucocorticoid will cross react and be measured
previous glucocorticoid treatment will suppress adrenal cortisol production
how is an ACTH stim performed?
cortisol level tested before and 1hr after ACTH administration
collect serum for basal cortisol level
inject 5 mg/kg of ACTH IV
collect second sample 1 hr later
when is cortisol measured in an ACTH stim?
before and 1 hour after ACTH admin
what will the results of an ACTH stim be in a hypoadrenocorticism patient?
pre and post ACTH cortisol will be the same rather than increasing
how is an Addisonian crisis treated?
IV 0.9% NaCl at shock dose (60-90ml/kg)
hydrocortisone or dexmathasone IV (or CRI)
correction of hypernatraemia
treatment of hypoglycaemia and hyperkalaemia as needed
what si the shock does of 0.9% NaCl required for Addisonian crisis?
60-90 ml/kg
what are hydrocortisone and dexmathasone used for?
replacement glucocorticoids and mineralocorticoids
why must hypernatraemia be treated?
can cause brain oedema
how should hyponatraemia be treated?
slowly
how can hypoglycaemia and hyperkalaemia be treated?
glucose and/or insulin
calcium gluconate to protect myocytes
what is the most commonly used long term glucocorticoid therapy for hypoadrenocorticism?
prednisolone
what is the dose of prednisolone required to treat hypoadrenocorticism?
0.5 mg/kg PO q12hrs initially
then 0.1 or 0.2 mg/kg PO q12-24hr
what must the dose of prednisolone be tailored to do?
limit clinical signs of polyphagia, PUPD and weight gain
when should glucocorticoid dose be increased?
if signs of lethargy, vomiting and diarrhoea
double dose if stressful event expected
what drug is used as mineralocorticoid long term therapy?
desoxycortone pivalate
what is the benefit of Zycortal mineralocorticoid therapy?
able to manage GC need separately from MC
what is the starting dose for Zycortal (MC)?
1.5 mg/kg SQ
how can glucocorticoid levels be monitored?
ask for evidence of lethargy, vomiting, diarrhoea which would prompt increase in dose as indicate low levels
how are mineralocorticoid levels tested?
blood test to measure Na/K ration 10-14 days after DOCP admin to see peak effect
then measure Na/K 25/30 days after DOCP admin to see duration of
DOCP
what will the measurement of peak DOCP effect determine?
next mg/kg dose
what Na/K ratio will lead to dose increase of mineralocorticoids?
> 32 or K below reference range = 10% dose increase
what should happen if Na/K ratio is below 32 or K is in the lower half of the reference ranges 25-30 days after DOCP administration?
delay injection by 5 days and repeat the same process
what was the drug used preciously to treat hypoadrenocorticism?
fludrocortisone
why is fludrocortisone less commonly used?
required check of Na/K weekly initially
dose requirements would often increase
what is the prognosis of hypoadrenocorticism?
good if well managed on lifelong medication
what should dogs with atypical Addison’s be monitored for?
development of mineralocorticoid deficiency which may develop in the future
what is canine hyperadrenocorticism also known as?
Cushing’s disease
what does hyperadrenocorticism occur due to?
excessive production of cortisol as a consequence of pituitary or adrenal tumors
how is cortisol produced?
hypothalamus releases CRH
pituitary releases ACTH
adrenal glands release cortisol
cortisol provides negative feedback to hypothalamus and pituitary
what are the 3 types of hyperadrenocorticism?
pituitary dependent
adrenal dependent
iatrogenic- admin of glucocorticoids
what is the most common type of hyperadrenocorticism?
pituitary dependant
what is caused by pituitary dependent hyperadrenocorticism (PDH)?
overproduction of ACTH due to adenoma of pars distalis
loss of negative feedback from cortisol leading to bilateral adrenal hyperplasia
macroadenoma in some leading to CNS signs
what animals are predisposed to hyperadrenocorticism?
daschunds, poodles, small terriers
no sex predisposition
middle/old aged dogs
what is adrenal dependent hyperadrenocorticism caused by?
adenomas / carcinomas leading to the production of excess cortisol which suppresses ACTH production
leads to atrophy of other gland
in what breed / type is adrenal dependent hyperadrenocorticism more common?
female
large breeds
what is iatrogenic hyperadrenocorticism caused by?
suppression of CRH and ACTH production due to excessive glucocorticoids
bilateral adrenal atrophy
what are the major clinical signs of hyperadrenocorticism?
abdominal distension hepatomegaly lethargy and exercise intolerance panting PUPD (nocturia and incontinence as a result) polyphagia skin changes (thinning and erythema) alopecia (symmetrical and non-pruretic)
how is polydipsia defined in dogs?
> 100ml/kg/day
how is polyuria defined in dogs?
> 50 ml/kg/day
what are the complications associated with hyperadrenocorticism?
progression of major signs
DM from insulin resistance due to excess cortisol
pulmonary thromboembolism
neurologic signs - obtunded, blindness and seizure
pancreatitis due to poor fat management
secondary infections as immune system suppressed
hypertension
glomerulopathy and proteinuria - direct effect of cortisol in kidney
what are the main initial general screening tests used for hyperadrenocorticism?
haematology
biochemistry
urinalysis
what are the screening tests used for the HPA axis?
ACTH stim
low-dose dexamethasone suppression test
urine cortisol:creatinine ratio
is there a single test for hyperadrenocorticism that is 100% accurate?
no
define test sensitivity
probability of positive result if patient is affected (if high sensitivity and negative result it can be ruled out)
define test specificity
probability of a negative result if the patient is not affected (high specificity, positive result, rule in)
what is seen on the haematology of a patient with hyperadrenocorticism?
mid erthyrocytosis and thrombocytosis - effect of cortisol on bone marrow
stress/steroid leukogram (increased neutrophils and/or monocytes, decreased eosinophils and/or lymphocytes) - opposite of Addison’s
what is seen on the biochemistry screening tests of a patient with hyperadrenocorticism?
increased ALKP (5-40x upper end of reference)
increased ALT
hypercholesterolaemia and hypertriglyceraemia due to lipolysis
hyperglycaemia due to insulin antagonism (resistance)
increased bile acids
what urine specific gravity is seen in patients with hyperadrenocorticism?
variable - <1.015
what is found on urinalysis of patients with hyperadrenocorticism?
dilute urine \+/- proteinuria \+/- glycosuria possible UTI calcium oxalate crystals due to over excretion of calcium
what is essential before pursuing diagnosis of hyperadrenocorticism?
some historical and clinical signs are apparent
no recent steroid administration
what will the ACTH stimulation test of a patient with PDH show?
excessive response to administration of ACTH
what will the ACTH stimulation show in a normal dog?
small cortisol increase
what is shown post ACTH stimulation in a patient with iatrogenic hyperadrenocorticism?
cortisol remains at pre-admin levels as they are unable to stimulate cortisol release
what are the advantages of ACTH stimulation tests to diagnose hyperadrenocorticism?
more specific than LDDST and less affected by non-adrenal illness
good first line test (if positive can be confident of illness)
useful for iatrogenic disease
used to monitor treatment response
what are the disadvantages of ACTH stimulation tests to diagnose hyperadrenocorticism?
less sensitive than LDDST
doesn’t distinguish PDH from ADH
how is low dose dexamathasone suppression test (LDDST) performed?
collect serum for basal cortisol
inject low dose (may need to dilute for small patients) IV dexamathasone
collect serum sample 4 and 8 hours after injection
what is the LDDST result of a patient with ADH and 40% of those with PDH?
flat line - no response and cortisol remains high
what is the LDDST result in 30% of PDH patients?
escape V pattern - cortisol drops at 4 hours but has climbed again by 8
what is the response of a normal dog to LDDST?
smooth drop in cortisol - lowest at 8 hours
what is the advantage of LDDST to test for hyperadrenocorticism?
more sensitive that ACTH (excellent sensitivity)
can distinguish PDH from ADH (escape V)
what is the disadvantage of LDDST for diagnosis of hyperadrenocorticism?
care with false positives
affected by non-adrenal illnesses
should not be used as sole diagnostic test
not useful for iatrogenic disease
how is urine cortisol:creatinine ratio test for hyperadrenocorticism performed?
urine sample collected at home
2 pooled morning samples
several days following a stressful event
what are the advantages of urine cortisol:creatinine ratio to diagnose hyperadrenocorticism?
high sensitivity
useful to exclude hyperadrenocorticism (if normal Cushing’s is very unlikely)
what is the disadvantage of urine cortisol:creatinine ratio to diagnose hyperadrenocorticism?
not very specific - false positives common
what tests can be used to differentiate PDH from ADH (adrenal tumors)?
LDDST
high dose dexamethasone suppression test (HDDST)
imaging
endogenous ACTH conc
what dose of dexamethasone is given for HDDST?
0.1mg
what will HDDST results look like for a patient with PDH?
escape V
what will the HDDST results look like for a patient with ADH and 15% with PDH?
no suppression of cortisol (flat line)
what will HDDST look like in a normal dog?
drop smoothly - lowest 8hrs after dex injection
what can an abdominal ultrasound be used for in hyperadrenocorticism diagnosis?
looking st symmetry and enlargement of adrenal glands
what will be seen on abdominal ultrasound of a patient with PDH?
symmetrical adrenal glands
enlarged or normal
what will be seen on abdominal ultrasound of ADH / AT?
asymmetrical adrenal glands
what is MRI used for in hyperadrenocorticism diagnosis?
evaluation of pituitary gland and adrenal glands
what is found in 90% of PD patients?
brain mass
what types of adenoma can be seen with PDH?
microadenoma
macroadenoma
what are endogenous ACTH levels like in PDH patients?
high (>45 pm/ml)
what is endogenous ACTH like in ADH patients?
undetectable / low
what is the issue with using endogenous ACTH to diagnose whether hyperadrenocorticism is PDH or ADH?
concentrations of ACTH between 10-45 pg/ml are unhelpful
lab may not be able to manage sample
what are the considerations for treatment of hyperadrenocorticism?
difficult to diagnose in some cases
progressive disease so could wait and retest if uncertain
treatment is expensive
when should hyperadrenocorticism only be treated?
if there is a high index of suspicion from history and clinical signs, haematology and biochem and specific tests
how is PDH treated?
medically with trilostane (Vetoryl)
surgically - hypophesectomy or bilateral adrenalectomy
radiation therapy
what does trilostane do?
blocks adrenal cortisol production
how is trilostane administered?
PO with food
SID or dose split to BID
lower dose than formulary suggests given first
how is response of patient to trilostane treatment for hyperadrenocorticism monitored?
clinical signs and ACTH stim or pre-pill cortisol
what are the side effects of trilostane?
uncommon but life threatening
GI signs
hypoadrenocorticism
bilateral adrenal necrosis
what is involved with hypophysectomy?
complete surgical removal of the pituitary gland accessed via the soft palate
what is the only potential curative (~75%) option for dogs with PDH?
hypophysectomy
what is the long term outcome of successful hypophysectomy?
3 year survival in 70%
what is needed after hypophysectomy?
lifelong hormonal supplementation
- glucocoticoids
- thyroxine
transient diabetes may insipidus may be seen post op but DDAVP treatment for this can usually be discontinued
where is radiation therapy for PDH available?
refurral only
what is the benefit of radiation therapy for PDH treatment?
linear accellerator photon irradiation may be effective in reducing the size of macroadenomas or eliminating neurological signs
what concurrent treatment is often required with radiation to treat PDH?
trilostane as reduction in ACTH secretion is variable and often not marked
what is radiation treatment of PDH particularly useful for?
large pituitary macroadenomas where surgery would be contraindicated
what is the mean survival time for dogs with PDH treated with radiation therapy?
25 months
how is ADH treated?
adrenalectomy - gold standard
medical therapy
what is required before adrenalectomy to treat ADH?
work up before operation (assess location/size/infiltration of tumor)
what are complications associated with adrenalectomy to treat hyperadrenocorticism?
haemorrhage hypertension acute hypocortisolaemia hypoaldosteronism wound breakdown (needs refurral treatment)
how effective is trilostane for treatment of ADH?
ADH generally more resistant
used pre-surgery to stabilise
what are the general considerations when treating any hyperadrenocorticism?
may unmask other underlying diseases that have been hidden by high cortisol
reduced cortisol can make pituitary lesions expand leading to CNS signs
what is the prognosis of PDH?
depends on age, overall health and owner commitment
~30 months survival post diagnosis
what is the prognosis of ADH?
following successful surgery mean survival is 36 months
metastatic disease leads to death/euthanasia within 12 months
is hyperadrenocorticism common in cats?
less os
what concurrent disease is seen in 80% of cats with hyperadrenocorticism?
insulin resistant DM
what signs are seen in cats with hyperadrenocorticism?
insulin resistant DM
cachexia
fragile skin syndrome (skin may slough off during routine handling so care needed)
alopecia (ventral, symmetrical)
what biochemistry signs seen in dogs with hyperadrenocorticism is not seen in cats?
increase in ALP
how is hyperadrenocorticism in cats diagnosed?
HDDST
ACTH stim with post sample at 60 and 90 mins
how is hyperadrenocorticism in cats treated?
difficult
adrenalectomy if adrenal mass
no reliable medication for PDH - can use trilostane and hypophysectomy is possible
what is the prognosis of hyperadrenocorticism in cats?
guarded to poor
worse than dogs
what type of diabetes mellitus is seen more commonly in dogs?
insulin dependent (type 1)
what are the possible causes of diabetes mellitus in dogs?
destruction of pancreatic beta cells
insulin resistance leading to beta cell exhaustion
what causes destruction of pancreatic beta cells?
genetics
immune mediate pancreatic damage
pancreatitis
idiopathic
what causes insulin resistance leading to beta cell exhaustion?
obesity
concurrent disease (e.g. pancreatitis or endocrinopathy)
dioestrus
drugs
what is the signalment for canine diabetes mellitus?
middle aged/older dogs
female more than male
breed predisposition
what are the top 3 dog breeds predisposed to diabetes mellitus?
Australian terrier
schnauzer
bichon
what are the clinical findings in a dog with diabetes mellitus?
PUPD polyphagia weight loss cataracts DK concurrent disease
what causes PUPD in diabetes mellitus patients?
kidney is unable to process the excess glucose so glycosuria occurs
due to the osmotic pressure of the glucose in the urine more water is drawn out
why are polyphagia and weight loss seen in diabetes mellitus?
decreased glucose utilisation due to lack of insulin there is a negative calorie balance
what are cataracts caused by in diabetes mellitus?
altered osmotic relationship in the lens
accumulation of sugars in the lens causing swelling and rupture of lens fibres
what are the main signs of diabetic ketoacidosis?
vomiting
collapse
dehydration
what is necessary to confirm a diabetes mellitus diagnosis?
glycosuria
persistent hyperglycaemia
what is shown by fructosamine?
average of glycaemia over the past 2-3 weeks so give an impression of blood sugar levels over time
how does fructosamine measure glycaemia over weeks?
glucose binds to proteins (glycated proteins) in an irreversible reaction between glucose and plasma proteins
what should fructosamine results be interpreted alongside?
clinical signs
how is diabetes mellitus treated in dogs?
insulin (in almost all cases) diet exercise consistency owner commitment
what varies between types of insulin?
time of onset
time of maximum effect
duration of action
what is the most commonly used insulin for dogs?
Lente (Caninsulin) - intermediate acting
what insulin type is needed to treat DKA?
neutral / short acting insulin
are oral hypoglycaemic drugs of any use in dogs?
no
what are the 2 types of long acting insulin?
PZI
glargine
what is a Caninsulin VetPen used for?
small doses
makes administration easy for owners
what syringe colour is used for Caninsulin (canine product)?
red syringe
how many insulin units are within Caninsulin?
40 IU/mL
how should insulin be handled?
store in fridge / avoid extremes of temperature replace bottles after 4 weeks invert to mix gently use appropriate syringe vary site of injection
how should intact females with diabetes mellitus be managed?
spayed 1-3 days after starting insulin especially in dioestrus
why do intact females with diabetes mellitus need to be spayed?
progesterone is a cause of insulin resistance so makes DM harder to treat as insulin is needed in larger volumes
what should be used if it is not possible to spay intact females who have diabetes mellitus?
aglepristone
what diet should diabetes mellitus patients be fed?
diabetic specific food
no simple sugars (reduce glucose spike)
in a diabetic diet what should the calories be supplied by?
complex carbohydrates and proteins
increased fibre content for overweight dogs
what should thin diabetic dogs be fed?
calorie dense, low fibre maintenance diet
what should picky diabetic dogs be fed?
whatever they are used to
what is important about the feeding schedule of a diabetes mellitus patient?
consistent timing, quantity and type of diet
how should patients receiving BID insulin be fed?
half daily requirement at time of each injection
how should patients receiving SID insulin be fed?
1/3-1/2 at time of injection and remainder 8 hours later
how long can stabilisation of diabetic patient take?
weeks to months
how should the first day of insulin administration be managed?
start with low dose
avoid hypoglycaemia
check BG several times (q2-3 hours) in the day in practice
what are the most important clinical signs to monitor for in the healthy newly diagnosed diabetes dog?
PUPD
polyphagia
weight loss
what should be checked for if the diabetes patient on insulin no longer has diabetes signs?
are there signs of hypoglycaemia
what are the signs of hypoglycaemia?
lethargy
reluctant to exercise
collapse
seizure
when should diabetic dogs on insulin have their first recheck?
7-10 days after first dose
when should follow up appointments be scheduled for the newly diagnosed diabetic dog?
7-10 days post first insulin
14 days later
1 month
then every 3 months if well controlled
when is a blood glucose curve important?
if there is poor glycaemic control so adjustments can be made to insulin therapy
what should a glucose curve be used in conjunction with to make management / insulin changes?
clinical signs
how is a blood glucose curve performed?
serial blood glucose with a glucometer
continuous glucose monitoring
how is serial blood glucose taken?
in the ear every 2 hours and then every hour close to the nadir
how is continuous glucose monitoring performed?
measured interstitial blood glucose - device placed on scruff and glucose levels monitored constantly
what is the nadir?
lowest blood glucose value
what parameters should be assessed when doing a blood glucose curve?
nadir
duration of action of insulin
what is the renal threshold for glucose?
point at which glucose will be secreted in the urine as kidneys are no longer able to prevent glucose spilling into urine so PUPD is caused
how much glucose will be seen in the urine of a patient with insulin controlled diabetes melitus?
mild amount in urine especially before glucose administration
what may no glucose in the urine of a patient with insulin controlled diabetes melitus for more than 24 hours indicate?
insulin overdose
what would ketones in the urine of insulin controlled diabetes melitus patients indicate?
poor glycaemic control - not enough insulin
what can one off blood glucose monitoring show?
good glycaemic control if prior to insulin administration but curve is more useful
what are the complications of insulin therapy?
hypoglycaemia
somogyi overswing
what are the clinical signs of hypoglycaemia?
lethargy
weakness
collapse
seizure
what blood glucose level indicates hypoglycaemia?
<3 mmol/L
how should hypoglycaemia be treated?
small meal
glucose / sugar solution PO or IV
what is somogyi overswing?
rebound hyperglycaemia response from other hormones in the body due to physiologic response to hypoglycaemia
when may somogyi overswing occur?
when blood glucose is <3.6 mmol/L
or quick drop in glucose following insulin
how long does lente (caninsulin) work for?
8-12 hours
how are issues with insulin therapy diagnosed?
glucose curve
when may short duration of inslin occur?
using Lente if duration of action is less than 8 hours
how can you tell if patients insulin is too short acting?
PUPD between injections
how can short duration of insulin be managed?
switch to long acting insulin BID
when does prolonged duration of insulin occur?
when nadir is >10 hours post injection
what is the risk of prolonged action of insulin?
risk of hypoglycaemia and Somogyi overswing
how can prolonged duration of action of insulin be managed?
if long acting give SID or switch to short acting
what should you do if insulin is having inadequate action?
make sure owner is administering the insulin correctly
what are the long term complications of diabetes?
hypoglycaemia cataract formation (inevitable in dogs) diabetic neuropathy (uncommon in dogs) diabetic nephropathy (uncommon in dogs) hypertension DKA
what causes diabetic neuropathy?
distal neuropathy due to segmental demylination and axonal degredation
what is the prognosis of dogs with diabetes melitus?
good if well managed with committed owners (MST - 3 to 5 years)
what type of diabetes melitus do cats most often get?
non-insulin dependent - type 2
what are the risk factors for diabetes melitus in cats?
old age
obesity
male
indoor
what cat breeds are predisposed to diabetes melitus?
burmese
main coon
russian blue
siamese
what are the 2 main causes of diabetes melitus in cats?
insulin resistance
reduced insulin secretion
what can cause insulin resistance in cats?
genetically determined
obsetity (antagonises effect of insulin)
what element of diabetes can further damage the pancreas in cats?
hyperglycaemia
how is reduced insulin secretion caused in cats?
chronically increased glucose and free fatty acids
amylin is co-secreted with insulin by beta cells
toxic amyloid polypeptide deposition leads to inflammation and cell death
beta cell damage (some function remains)
what can cause insulin resistance?
obesity
inflammatory / infectious diseases
endocrinopathies
what inflammatory / infectious diseases can cause insulin resistance in cats?
pancreatitis UTI CKD dental disease enteropathy
what endocrinopathies can cause insulin resistance in cats?
hyperthyroidism
acromegaly
hypercorticism (iatrogenic steroid use)
what are the signs of pre-diabetes melitus in cats?
impaired fasting glucose (rarely seen due to stress hyperglycaemia)
BG constantly above >6.5 mmol/L (elevated but not in diabetic range)
what is the blood glucose level in subclinical DM in cats?
> 10mmol/L and <16mmol/L (renal threshold) persitantly
what can be done to manage cats with subclinical DM?
low carbohydrate diet
weight loss
insulin sensitisers (glipizide)
try to avoid overt DM
what is the BG of a patient with overt DM?
> 16 mmol/L
renal threshold is exceeded
what are the signs on biochemistry and urinalysis of overt DM cat?
hyperglycaemia
increases fructosamine (unaffected by stress hyperglycaemia)
glycosuria
what are the clinical signs of DM in cats?
as for dogs - weight loss, polyphagia, DKA
peripheral neuropathy
cataracts (rare)
how is DM diagnosed in cats?
hyperglycaemia and glycosuria
what should you be aware of when screening cats for DM?
stress hyperglycaemia altering results
what does fructosamine show in cats?
mean BG in the last week
what can be used to differentiate between stress hyperglycaemia and DM?
combine fructosamine with history and clinical signs
how is DM in cats treated?
insulin diet exercise commitment from owner consistantcy
what insulin is used in cats?
longer acting
what is the first insulin type that will be tried in cats with DM?
Prozinc
can Caninsulin be used in cats?
yes but response is very unpredictable
what is the other insulin type that can be used if prozinc and caninsulin have not worked?
Glargine - on cascade as not licenced
what do oral hypoglycaemic drugs do?
increase insulin secretion to decrease IR
when are oral hypoglycaemic drugs useful in cats?
if owner declines insulin
with diabetic diet and weight loss
as long as no comorbidities
what is a key benefit for management and prevention of DM in cats?
diet
what should the composition of feline diabetic diets be?
wet high protein low carbohydrate reliable intake fibre less key than in dogs
what can be the result of dietary management and associated weight loss in cats?
resolution of DM in 30% of cats
reduction in insulin dose for 50% of cats
what is a serious complication of DM?
DKA
what often caused DKA?
DM with serious concurrent disease (e.g. heart failure, pancreatitis or sepsis)
how is DKA caused?
increased production of glucoregulatory hormones (glucagon, adrenaline, cortisol)
lack of insulin in DM allows the glucogenic effects of the stress hormones to be unopposed in liver, muscle and adipose tissue
leads to excessive breakdown of fatty acids, excessive ketone formation (e.g. acetone) leading to a build up in the body
what are the clinical signs of DKA?
PUPD
polyphagia
weight loss
systemic signs such as lethargy, anorexia and vomiting which worsen
additional signs of concurrent disease
strong odour of pear drops on breath (acetone) - not everyone can smell it
severe dehydration and hypovolaemia
what is the aim of treatment of DKA?
restore water and electrolyte balance
provide adequate insulin to ‘switch off’ ketone production
correct acidosis
identify any underlying disease
what electrolytes may be altered by DKA?
sodium
potassium
phosphorus
what insulin is needed to treat DKA?
neutral - CRI or IM every hour
what supportive therapy is needed for the DKA patient?
analgesia (if pancreatitis etc)
feeding to avoid hypoglycaemia (appetite stimulants, mariopitant, feeding tube)
careful monitoring
how long does it take for hypoglycaemia to improve?
12-24 hours
how long does it take for ketosis to improve?
48-72 hours
what is the prognosis of DKA?
challenging to treat
often underlying disease
25% will die or be euthanised
what can happen to cats after DKA?
DM remission in some cases
