ENDOCRINE DISEASES Flashcards
WHAT IS THE NORMAL WATER INTAKE?
60-100ml/Kg/24 hrs
what is the normal urine output?
20-45 ml/Kg/24hrs
what is diabetes insipidus?
insufficient ADH secretion/ action causing inadequate urine concentration.
define polyuria
> 50ml/Kg/ 24hrs
define polydipsia
> 100 ml/Kg/ 24hrs
A 5-year-old male neutered Domestic Short haired cat presents for ongoing evaluation of Diabetes Mellitus. The cat was diagnosed 6 months ago and has continued to be markedly polyuric, polydipsic, polyphagic and losing weight. The owner noted that the cat’s head seems to be larger than her other cats.
- State two concurrent diseases that can be causing insulin resistance in this case.
hyperadrenocorticism (Cushing’s disease) and acromegaly.
state the usual ranges for USG in fenine, canine and large animals
feline….. 1.035- 1.060 ….. (>1.040)
canine…….1.015- 1.045……(>1.030)
large……1.015-1.030………(>1.025)
LIST THREE THERAPIES THAT CAN BE USED FOR BOTH CENTRAL AND NEPHROGENIC DIABETES INSIPIDUS
- CHLOROTHIAZOLE……THIAZIDE DIURETIC
- DIETARY SODIUM RESTRICTION
- DESMOPRESSIN ACETATE…..SYNTHETIC ADH
LIST FIVE CLINICAL SIGNS TYPICALLY ASSOCIATED WITH DIABETES INSIPIDUS
- POLYURIA
- POLUDIPSIA
- WEIGHT LOSS
- NOCTURIA
- RECURRENT UTIs From diluted urine
OTHERS…….INSATIABLE THIRST, ANOREXIA, REZTLESSNESS, INCONTINENCE
STATE THE TWO MAIN TYPES OF DIABETES INSIPIDUS AND DESCRIBE THEIR PATHOGENESIS
- CENTRAL…….decreased ADH secretion
- NEPHROGENIC……DECREASED ADH ACTION DUE TO RENAL TUBULAR RESISTANCE
STATE THE CLINICAL SIGNS ASSOCIATED WITH PITUITARY OR HYPOTHALMIC TUMOURS ASSOCIATED WITH DIABETES INSIPIDUS AND STATE THE PROGNOSIS……WHICH FORM OF DIABETES INSIPIDUS IS THIS ASSOCIATED WITH?
- VISUAL DEFECITS
- SEIZURES
- INCOORDINATION
PROGNOSIS…….GRAVE….ESPECIALLY IF TUMOURS ARE GROWING
STATE THE PROGNOSIS FOR CENTRAL AND NEPHROGENIC DIABETES INSIPIDUS
GOOD WITH TREATMENT FOR CENTRAL
GUARDED WITH NEPHROGENIC
state five causes of secondary NEPHROGENIC diabetes insipidus
- pyelonephritis
- hyperadrenocorticism
- hyperthyroidism
- pyometra
- hypokalemia
state four methods of diagnosing diabetes INSIPIDUS and the parameters to look for in each test.
- biochem…….hyponatremia, hypokalemia
- urinalysis….isosthenuria, hyposthenuria
- modified water deprivation test…….USG is unchanged I. a clinically dehydrated animal
- DDVAP …DESMOPRESSIN ACETATE STI ULATION TEST…..INCREASED USG AND REDUCED WATER CONSUMPTION…..DIAGNOSTIC FOR CENTRAL DI.
STATE THE TYPICAL SIGNALMENT FOR CUSHINGS …….BE SPECIFIC
HYPERADRENOCORTICISM
…..SEEN IN DOGS MORE THAN CATS
….. CATS NORMALLY ALSO GET A DIABETES
….. SEEN MOSTLY IN MIDDLE AGE TO OLDER ANIMALS….MORE THAN SIX YEARS
WHAT ARE THE THREE MOST COMMON. AETIOLOGIES ASSOCIATED WITH CUSHING’S DISEASE…BE SPECIFIC, EXPLAIN THE PATHOPHYS
- PITUITARY DEPENDANT HYPERADRENOCORTICISM
MOSTLY A PITUITARY ADENOMA…BUT CAN ALSO BE A PITUITARY ADENOCARCINOMA OR A PITUITARY HYPERPLASIA.
THIS CAUSES EXCESSIVE ACTH SECRETION
THIS CAUSES BILATERAL ADREOCORTICAL HYPERPLASIA
THIS CAUSES EXCESSIVE CORTISOL - ADRENOCORTICAL DEPENDANT HYPERADRENOCORTICISM
USUALLY AN ADRENAL CARCINOMA OR ADENOMA
USUALLY UNILATERAL RESULTING IN THE CONTRALATERAL BEING ATROPHIED
ADRENAL TUMOUR RESULTS IN EXCESSIVE CORTISOL RELEASE. - IATROGENIC
EXCESSIVE OR PROLONGED CORTICOSTEROID USE THAT LEADS TO ATROPHY OF ADRENAL CORTICES
what are the 8 main clinical signs associated with CUSHINGS?
the 8 Ps:
1. polyuria …80% of cases
2. polydipsia…..80% of cases
3. panting…….mineralization of airways
4. pot belly/ pendulous abdomen
5. polyphagia…..90% of cases
6. hyperpigmentation /calcinosis cuti
7. pacing….neurological signs for macroadenoma in PITUITARY…..ataxia, incoordination
8. pyoderma/ poor wound healing due to immunosuppresion
list the 6 non-specific screening tests that can be used in a suspected cushing’s case, and state the specific parameters to look for.
- urinalysis……glucosuria; proteinuria; hyposthenuria/isosthenuria; recurrent UTI
- CBC…stress leukogram: leukocytosis, monocytosis, eosinopenia, neutrophilia, lymphopenia
- biochemistry……elevated ALP and ALT; hypercholesterolemia; low total T4
- abdominal ultrasound——-adrenal HYPERPLASIA/atrophy
- MRI……PITUITARY tumours
- CT scan…..PITUITARY tumours
explain how cushing’s affects the total T4 value
increased CORTISOL secretion suppresses the TSH secretion which is responsible for T4, therefore total T4 is low
why would a patient with cushings be mildly hyperglycemic and have glucosuria?
hyperglycemia due to increased gluconeogenesis in the liver due to excessive CORTISOL release
glucosuria is usually with a concurrent diabetes mellitus
how can an abdominal ultrasound differentiate between PDH and ATH cushing’s?
PDH - BILATERAL ADRENAL hyperplasia- cuz of PITUITARY tumor
ATH- UNILATERAL usually ADRENAL hyperplasia, with an ATROPHIED adrenal
list 3 screening tests and 3 distinguishing tests for ADRENAL function. include the sample needed and sample container
screening:
- ACTH stim test…..blood serum….red top tube
- urine cortisol:creatinine ratio ………urine…..urine sample cup
- low dose dexamethasone suppression test……..blood serum….red top
distinguishing:
- high dose dexamethasone suppression test……..blood serum…..red top
- endogenous ACTH concentration…….blood……purple top
- ultrasound/CT/MRI……..live body
describe 2 ADRENAL function tests most appropriate for a dog with mild clinical signs of cushing’s and a history of prolonged CORTICOSTEROID use
- ACTH stim test….measure CORTISOL levels b4 and after 1-2 hrs of administration of ACTH/ cortrosyn
- IATROGENIC …CORTISOL levels would remain at baseline…usually < 5ug/dL
- normal….CORTISOL levels usually 6- 17ug/dL
- spontaneous cushing’s……CORTISOL levels elevated…usually >30ug/dL - high dose dexamethasone suppression test (if its not IATROGENIC, and is spontaneous)
record CORTISOL levels b4 and after administration of dexamethasone
- PDH……CORTISOL levels suppressed >50% of baseline
- ATH….CORTISOL levels not suppressed
- normal CORTISOL levels suppressed
how can you use endogenous ACTH to differentiate between ATH and PDH cushing’s?
- PDH…..high levels of ACTH
- ATH….lower levels
A 7 year old toy poodle presented with severe PU/PD, polyphagia and panting. the two diagnostic tests done showed only a proteinuria and hypertension. what screening test for ADRENAL function is your best bet to diagnose this dog?
low dose dexamethasone suppression test
- PDH in >505 suppression of baseline CORTISOL concentration at 4 hrs but not 8 hrs
why is it better to do a LDDST than a HDDST?
a hddst will suppress a normal dog and a PDH dog
a lddst will suppress a normal dog, but not a cushing’s dog
list 3 treatment plans for cushings….be specific, state mechanism of action and dosages
- mitotane…..cytotoxic to zona fasicularis(produces glucocorticoids)
- induction 20-25mg/kg PO q 12hrs after meal
- ACTH stim test…to demonstrate adequate control of CORTISOL levels
- maintainance…….50mg/kg/week PO (2-4 treatments/week) - trilostane
inhibits CORTISOL synthesis
- induction 2-10mg/kg SID
- ACTH stim test 2-6 hrs post drug…determine if to increase dose or just monitor and maintain
- monitor/maintain…..every 3 months…then every 4-6 months repeat - adrenalectomy….still have to give mitotane and trilostane…and obv for ATH!!
what part of the ADRENAL glands is responsible for glucocorticoid production? be specific
cortex
- zona reticularis
- zona fasicularis
state 3 metabolic effects of glucocorticoids
- gluconeogenesis
- fat mobilization
3.liver protein synthesis
list 4 typical signs associated with diabetes mellitus
- PU/PD
- polyphagia
- weightloss
- UTI
list 4 clinical signs associated with ketoacidosis (DM)
- coma
- dehydration
- vomiting/diarrhea
- acetone breath
state the two types of diabetes mellitus, specific to their PATHOGENESIS.
type 1- insulin DEPENDANT - destruction/decreased beta pancreatic cells (due to pancreatitis, amyloidosis in cats, immune mediated) which results in decreased insulin production/ secretion.
type 2- non-insulin dependent- the pancreas secretes insulin, but their is peripheral resistance to it, due to: obesity (increased down regulation of insulin receptors); acromegaly (increased growth hormone); excess CORTISOL (cushing’s, decreased thyroid hormone, stress, increased epinephrine)
which type of diabetes mellitus is more common in cats?
type 2
- non-insulin dependant
describe the PATHOGENESIS of cataracts in a diabetic patient. (DM)
diabetes mellitus= hyperglycemic animal which causes excess glucose to be diffused into the lens, because it’s too much to be phosphorylated by hexokinase. the glucose in the lens is converted to sorbitol by the aldose reductase, and then broken down to fructose by sorbitol dehydrogenase.
- because fructose nor sorbitol can cannot diffuse out of the lens they remain in the lens and cause an increase in osmotic pressure which causes increased water to enter the lens to balance off the gradient, and degenerates the lens fibres
- leading to sugar cataracts seen
state 3 metabolic reactions of insulin
- decreases blood glucose
- promotes glycogen synthesis
- inhibits gluconeogenesis
how does diabetes mellitus lead to put/PD?
DM causes an overall insulin deficiency
- decreased cellular glucose uptake and increased hepatic gluconeogenesis
- leads to hyperglycemia which rises above the renal threshold causing a spill over into the urine…..glucosuria and an osmotic diuresis causing the PU/PD
what is the blood glucose value for a DM patient? be specific to cats and dogs
cats: 280-290 mg/dL
dogs: 180-200 mg/dL
state the 3 specific scenarios that require a blood glucose curve
- change dose of insulin
- change type of insulin
- start of insulin
state 2 insulin therapies that can be used in dogs dand cats….be specific
dogs:
- regular….IM/IV/SQ……..4-10 hr duration……0.25-0.5 U/Kg BID….. after meal
- ultralente…….SQ……8-24 hrs duration…….0.25-0.5 U/Kg BID….after meal
cats:
- humulin R…….4- 10 hrs…….1-2 U/cat BID…..after meal
- glargline…….6-12hrs……1-2U/cat BID…after meal……remission is common in type 2 cases
describe the somogyi effect
when too much insulin is given and you get an acute hypoglycemia (<65 mg/dL) followed by a rebound hyperglycemia (>300mg/dL)
describe the ideal glucose curve
- NADIR- 250 mg/dl at 6hrs
- duration - 12hrs (blood glucose 100-250)
describe the typical signalment for hypoadrenocorticism
- dogs>cats
- female dogs >males
- young to middle aged
state the 2 types of addison’s disease and explain the PATHOGENESIS of the AETIOLOGIES of addison’s
type: atypical and typical
- typical: more common and involves BOTH glucocorticoid and mineralocorticoid deficiency
- atypical: less common and involves ONLY glucocorticoid deficiency
aetiology:
- primary addisons: linked to ADRENAL failure (destruction of cortex) and can be immune mediated or idiopathic
- secondary addisons : linked to decreased secretion of ACTH and can be IATROGENIC or spontaneous (destructive lesions in PITUITARY/congenital malformations in PITUITARY of hypothalamus leading to decreased ACTH)
state the typical clinical signs associated with a patient with addison’s and state the signs associated with a patient in a crisis.
typical clinical signs: vomiting, diarrhea in dogs only, weightloss, anorexia, lethargy, PU/PD is less than with cushings
crisis: dehydration, hypovolemic shock, bradycardia
state three main diagnostic tests and the expected parameters to diagnose a patient with addisons
- biochemistry:hyponatremia, hyperkalemia, hypocholesterolemia, hypoglycemia
- CBC: no stress leukogram; normocytic, normochromic non-regenerative anemia in chronic cases
- ATH stim test - <2ug/dL cortisol
state the shock rate and maintainance rate in dogs and cats
shock:
- dog : 80-90 mls/kg
- cat: 45-60 mls/kg
maintainance: 2-4mls/kg/hr
state the 3 different doses for prednisolone
- immunosuppressive
- dog - 2mg/kg/day
cat- up to 4mg/kg/day - anti-inflammatory
- dog- 0.5-1 mg/kg/day
- cat- 1-2 mg/kg/day - physiological-0.2mg/kg/day
state the four main therapies required for an addison’s patient, be specific…give examples
- fluid therapy….normal saline/LRS
- glucocorticoid therapy……dexamethasone (2-4mg/kg IV SID)
- mineralocorticoid therapy……….fludrocortisone (0.02mg/kg PO BID….shared BID)
- GI protectant/ blood transfusion……????
what should be changed in the therapy of an addison’s patient for maintainance treatment?
for maintainance, use prednisolone instead of dexamethasone
prednisolone2.5-10mg/dog PO SID or every other day
- ALSO check every 3 months to ensure the dose is working……..ACTH stim test
what is the typical SIGNALMENT for hyperthyroidism?
- older cats >8 yrs
- cats>dogs
- DSH cats
list the 4 AETIOLOGIES commonly associated with hyperthyroidism and state for each who is more prone to get it…dog/cat
- thyroid CARCINOMA……dogs
- thyroid ADENOMA….cats
- thyroid adenomatous hyperplasia….cats
- apathetic hyperthyroidism…..cats
state the 7 common clinical signs associated with hyperthyroidism
- PU/PD
- polyphagia…unless apathetic
- weightloss
- diarrhea
- vomitting
- patchy alopecia
- unkempt haircoat
list the 5 common signs to look for o the physical exam of a hyperthyroid patient
- hyperactivity- unless apathetic- depression
- tachycardia….gallop rhythm, sometimes murmurs
- palpable thyroid
- thin
- systemic hypertension….retinal haemorrhage….retinal detachment
a 10 year old cat presented for PU/PD, anorexia and weightloss. on physical exam the cat was extremely dull and depressed and had a bcs of 1/5. you palpate a swollen mass on both sides of the mid-ventral cervical vertebrae. what is your top differential? be specific. what tests would you do to confirm?
- hyperthyroidism
- apathetic hyperthyroidism
tests: biochem, total T4
list 4 therapies that can be used in the hyperthyroid patient
- prescription diet
- thyroidectomy
- methimazole/carbimazole…antithyroid drugs
- I-131
which biochemistry parameter is essential in a recheck hyperthyroid dog?
calcium
T4
what diagnostic should be done prior to a thyroidectomy?
nuclear scintigraphy
what is a common adverse effect of the drug methimazole? what is the drug used for?
- used in hyperthyroid patients
- causes head and neck pruritus
for hypothyroidism, list 2 clinical signs associated with each of the following:
1. cellular metabolism
2. dermatological signs
3. cardiac signs
4. neuromuscular signs
5. ocular signs
6. reproductive signs
- cellular metabolism: weight gain; lethargy
- dermatological signs: BILATERAL symmetrical alopecia; myxedema, rat tail
- cardiac signs: bradycardia; decreased contractility
- neuromuscular signs: SEIZURES; facial nerve paralysis
- ocular signs: corneal dystrophy; KCS
- reproductive signs: persistent anaestrous; decreased libido
what are the 2 main tests that should be done to rule out euthyroid sick syndrome from a hypothyroid case?
- TSH AND T4
euthyroid sick……both low
hypothyroidism: TSH high; T4 low
what diagnostic tests can help diagnose hypothyroidism?
- total T4
- free T4
- biochemistry- hypercholesterolemia
- CBC- normocytic, normochromic anemia
what treatment would you recommend for a hypothyroid patient?
describe how you would monitor the progression of the condition under treatment.
sodium levothyroxine- synthetic T4
monitor: at 4 weeks….measure total T4 4-6 hrs after levothyroxine
for the 1st 6-8 months measure TT4 every 6-8 weeks
lastly measure every 6-12 months for life
list the 4 AETIOLOGIES of hypothyroidism and give 1 example of each
- congenital - cretinism
- iatrogenic- methimazole
- primary- lymphocytic thyroiditis
- secondary- PITUITARY neoplasia
who/ what is the main component in TSH concentration?
T3
should an anaesthetist be made aware of a patient with hypothyroidism?
why doh?
yes
they are prone to hypothermia, and because of decreased cellular metabolism, the typical drug doses would remain for a long while and be more potent.
list three compounds that can inhibit TSH secretion
- dopamine
- serotonin
- glucocorticoids
list two compounds that would increase TSH secretion
- thyrotropin releasing hormone
- prostaglandin
what is the typical SIGNALMENT for a hypothyroid patient?
- large breed dogs> cats
- middle aged to older animals
what is the most common aetiology of hypothyroidism?
primary
thyroid gland disease
what three conditions can be found in polyglandular syndrome?
- diabetes mellitus
- hypothyroidism
- hypoadrenocorticism
