CVNT 2 > Endocrine > Flashcards

Endocrine Flashcards

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1
Q

causes of diabetes mellitus

A
  • destruction of beta cells in pancreas
    (immune-mediated, pancreatitis, idiopathic)
  • insulin resistance leading to beta cell exhaustion
    (obesity, concurrent disease, dioestrus)
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2
Q

clinical signs of diabetes mellitus

A
  • concurrent disease
  • diabetic ketoacidosis
  • polyuria, polydipsia (secondary to glucosuria)
  • cataracts
  • polyphagia
  • weight loss
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3
Q

diagnosis of diabetes

A
  • glucosuria
  • persistent hyperglycaemia
  • fructosamine blood test (glycated proteins)
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4
Q

treatment of diabetes

A
  • insulin
  • diet
  • exercise
  • consistency
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5
Q

insulin treatment for diabetes

A
  • vary in time of onset, max effect and duration of action
  • ‘lente’ (intermediate acting) insulin is used most commonly
  • neutral (short acting) insulin is used for diabetic ketoacidosis
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6
Q

insulin handling

A
  • store in fridge
  • replace bottles after 4 weeks
  • invert to mix (allow foam to disperse)
    • don’t shake
  • vary injection site
  • use red syringe for caninsulin
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7
Q

intact females and diabetes

A
  • progesterone can be cause of insulin resistance
  • entire females should be spayed
  • consider algepristone if unable to spay
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8
Q

diabetes diet

A
  • avoid simple sugars
  • more complex carbohydrates and proteins
  • increased fibre
  • consistent timing, quantity and diet
  • ad libitum feeding for grazers
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9
Q

initial stabilisation of newly diagnosed diabetic dog

A
  • start at low insulin dose
  • check blood glucose several times a day (blood glucose curve)
  • monitor for hypoglycaemia
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10
Q

monitoring of newly diagnosed diabetic dog

A
  • first recheck= 7-10 days
  • next= 14 days
  • 1 month
  • continue every 3 months
  • monitor clinical signs and for hypoglycaemia
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11
Q

clinical signs of hypoglycaemia

A
  • lethargy
  • reluctance to exercise
  • collapse
  • seizure
  • BG <3mmol/L
  • feed small meal or give glucose
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12
Q

urinalysis of diabetes patient

A
  • usually mild amount of glucose before insulin admin
  • no glucose >24hrs may indicate insulin overdose
  • ketones may indicate poor glycaemic control
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13
Q

blood glucose curve

A
  • feed and give insulin
  • check BG levels every 2 hours until next feed and insulin injection
  • create graph
  • ensure BG is mainly below renal threshold (12mmol/L) and above 4mmol/L
  • shows duration of action\
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14
Q

somogyi overswing

A
  • rebound hyperglycaemia caused by physiologic response to hyperglycaemia
  • BG<3.6mmol/L or drops quickly following insulin
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15
Q

long term consequences of diabetes

A
  • cataract formation
  • hypertension
  • diabetes ketoacidosis
  • diabetic nephropathy
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16
Q

diabetes in cats

A
  • commonly non-insulin dependent
  • increased insulin resistance
  • plantigrade stance common
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17
Q

diagnosis of diabetes in cats

A
  • fructosamine test more common
  • stress hyperglycaemia is common so diagnosis is difficult
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18
Q

treatment of diabetes in cats

A
  • diet (high protein, low carbs)
  • weight loss in obese cats
  • insulin (unpredictable response in cats)
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19
Q

diabetes ketoacidosis

A
  • lack of insulin/insulin resistance prevents glucose from being transported into cells for respiration
  • body used fats as energy source
    • excessive fatty acid breakdown decreasing pH
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20
Q

clinical signs of diabetes in cats

A
  • lethargy, collapse
  • acetone odour on breath (pear drops)
  • severe dehydration and hypovolaemia
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21
Q

management of the sick DKA

A
  • restore water and electrolyte balance
  • rapid and short acting insulin (neutral)
  • correct acidosis
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22
Q

hypothalamic-pituitary-thyroidal axis

A
  • hypothalamus secretes TRH
  • pituitary gland is stimulated to produce TSH
  • thyroid glands are stimulate to make T4, T3, rT3
  • this negatively feedbacks to pituitary gland to produce less TSH and to hypothalamus to secrete less TRH
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23
Q

feline hyperthyroidism aetiology

A
  • > 95% benign adenomatous hyperplasia/adenoma of thyroid tissues
    • spontaneous secretion of thyroid hormones
  • <5% adenocarcinoma
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24
Q

risk factors for feline hyperthyroidism

A
  • middle-aged to elderly cats
  • nutritional (iodine rich diet)
  • environmental (flea sprays)
  • genetic (siamese, himalayan cats)
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25
clinical signs of hyperthyroidism
increased: - metabolic rate, CO, HR, BP, GI motility, CNS activity decreased: - sleep, body weight - palpably enlarged thyroid glands - polyphagia, polyuria, polydipsia
26
handling the feline hyperthyroidism patient
- hands-off approach - consider gabapentin 2hrs before travel - quiet, dark room - give time to acclimatise in consult, nursing room
27
diagnosis of feline hyperthyroidism
- compatible clinical signs - screening tests - confirmatory tests
28
screening tests for feline hyperthyroidism
- haematology - biochemistry (elevated liver enzymes) - look for concurrent disease (chronic kidney disease) - urinalysis (look for concurrent disease) - BP measurement
29
confirmatory diagnostic test for feline hyperthyroidism
- serum total thyroxine (TT4) - false negatives are possible (can fluctuate over 24hr day, can be falsely low in patients with concurrent disease)
30
treatments for feline hyperthyroidism
- anti-thyroid drugs - iodine restricted diet - surgery - radioactive iodine
31
anti-thyroid drugs for hyperthyroidism
- block production of T3 and T4 - methimazole BID (tablet, gel, liquid) - carbimazole - must be given whole, once a day - converts to methimazole - care with handling if pregnant - regulates thyroid within 2-3 weeks
32
advantages of anti-thyroid drugs
- readily available - effective - inexpensive - practical (bioavailable) - no GA or hospitalisation
33
disadvantages of anti-thyroid drugs
- lifelong (expensive) - long-term resistance - compliance - side effects
34
side effects of anti-thyroid drugs
- vomiting, anorexia, lethargy (10-20%) - GI irritant, leukopenia, anaemia, dermatitis, hepatopathy, myasthenia gravis
35
iodine-restricted diet for feline hyperthyroidism
- starves the thyroid of iodine which is needed to make hormones - euthyroid within 3 weeks - less effective, not suitable for severely hyperthyroid cats - life long
36
thyroidectomy
- increased surgical risks due to systemic effects of hyperthyroidism (cardiac disease, hypertension) - stabilise medically prior to surgery - excision of thyroid adenoma - preservation of parathyroid tissue - euthyroidism in >90% patients
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advantages of thyroidectomy
- curative - rapidly effective - short hospitalisation period
38
disadvantages of thyroidectomy
- GA risks - cost - complications - depends of location of adenoma - recurrence
39
complications of thyroidectomy
- damage to parathyroid tissue (post-op hypoparathyroidism) - damage to recurrent laryngeal nerve - damage to sympathetic nerve (horner's syndrome) - possible recurrence
40
Iatrogenic hypoparathyroidism
- associated with bilateral thyroidectomy - removal of parathyroid glands prevents TTH production which causes hypocalcaemia
41
clinical signs of iatrogenic hypoparathyroidism
- inappetence - weakness, tremors - hypersalivation monitor serum calcium BID if bilateral thyroidectomy
42
Iatrogenic hypoparathyroidism treatment
- hospitalisation - IV 10% calcium gluconate - avoid bicarbonate, lactate, phosphate fluids as precipitates calcium - ECG to monitor for arrythmia and bradycardia
43
radioiodine treatment for feline hyperthyroidism
- only available in specialist centres - single injection of radioactive iodine IV - administered systemically but concentrated in thyroid as it rapidly takes up iodine to make thyroid hormones - beta particles can cause local cell death - cat needs to be isolated for 1-2 weeks - most ideal treatment
44
advantages of radioactive iodine therapy
- curative - simple procedure - no GA, minimally invasive - can treat carcinoma
45
disadvantages of radioactive iodine therapy
- limited availability - isolation treatment - irreversible - may take time to achieve euthyroid - high initial cost (cheaper long term)
46
monitoring of feline hyperthyroid patient
- 6 monthly check-ups once stabilised - recurrence (history, clinical signs, blood test) - hypertension - chronic kidney disease (urinalysis, urea- creatinine)
47
hyperthyroidism and chronic kidney disease
- hyperthyroidism may mask underlying CKD, treatment will uncover CKD - consider medical management before curative treatment
48
canine thyroid neoplasia
- carcinomas are far more common - large, solid, palpable mass on neck - only 10% hyperthyroid (most euthyroid) - surgical removal and chemotherapy - prognosis is poor (6-24 months with aggressive treatment)
49
canine hypothyroidism clinical signs
- most commonly caused by atrophy or immune mediated destruction of thyroid - decreased metabolic rate (weight gain, lethargy, inactivity) - alopecia, rat-tail and 'tragic' facial expression - neuro, repro, cardiac signs are less common
50
diagnosis of canine hypothyroidism
- compatible clinical signs - haematology and biochemistry - confirmatory tests - low T4, high TSH - anti-thyroglobulin antibodies
51
total T4 (TT4) test
- useful initial screening test, excellent sensitivity - thyroglobulin antibodies can falsely increase TT4 - TT4 decreases with age, breed, non-thyroidal illness and drug therapy - not recommended as single diagnostic test
52
Canine TSH (cTSH)
- increased in hypothyroidism due to lack of negative feedback - good specificity: largely non-affected by non-thyroidal illness or drugs
53
Anti-thyroglobulin antibodies
- if positive, consistent with immune mediated destruction of thyroid gland - only recognises one path of development of hypothyroidism - can be present long before hypothyroidism - provides no information about thyroid function
54
treatment of canine hypothyroidism
- synthetic T4 - available in tablet and liquid forms - bioavailability is halved with food - try give on empty stomach
55
monitoring of hypothyroidism patient
- clinical response (weight loss, higher activity levels, less dermatological symptoms) - check up 6-8 weeks after treatment start - measure TT4 6hrs post pill (SID) or 4-6hrs post pill (BID) - measure cTSH
56
canine hypoadrenocorticism (addison's disease)
- suspected to be due to immune mediated destruction of adrenal cortex - results in loss of production of cortisol and aldosterone lack of cortisol: weakness, vomiting, diarrhoea, anorexia (esp when stressed) lack of aldosterone:
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aldosterone
- acts on cells in the late distal tubule and collecting tubule - stimuli of aldosterone production: hyperkalaemia, increased angiostensin II - action of aldosterone: reabsorption of NaCl and H2O - secretes K+ and H+
58
clinical signs of canine hypoadrenocorticism
- polydipsia and polyuria - addisonian crisis: - collapse, severe dehydration, hypovolaemia, pre-renal azotaemia, cardiac arrhythmias due to hyperkalaemia
59
screening tests for hypoadrenocorticism
- haematology (absence of leukogram) - biochemistry (hyperkalaemia, hyponatraemia, hypercalcaemia, hypoglycaemia - urinalysis (variably concentrated) - basal cortisol (test to exclude disease) - >55nmol/L (addison's is unlikely) - <55nmol/L ACTH stimulation test indicated
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confirmation tests of hypoadrenocorticism
ACTH stimulation test 1. collect serum for baseline cortisol measurement 2. inject 5mcg/kg of ACTH IV (synacthen) 3. collect serum 1hr post ACTH admin diagnosis= pre and post ACTH cortisol concentrations below 20nmol/l
61
treatment of canine hypoadrenocorticism (addisonis crisis)
- manage hypovolaemia (fluid boluses) - hydrocortisone or dexamethasone IV - sudden correction of hyponatraemia can cause brain oedema - treat hypoglycaemia, hyperkalaemia if necessary - long term treatment
62
long-term therapy of canine hypoadrenocorticism
glucocorticoid (prednisolone): - trial and error dosage to limit clinical signs of polyphagia, polyuria, polydipsia, weight gain - increase dose if lethargy, vomiting, diarrhoea mineralocorticoid: - desoxycortone pivalate (zycortal)
63
monitoring of canine hypoadrenocorticism patient
- ask for evidence of lethargy, vomiting, diarrhoea - blood testing for mineralocorticoid needs: - measure Na/K 10-14 days after DOCP injection (peak effect) - measure Na/K 25-30 days after DOCP injection (duration of effect) good prognosis but will need lifelong treatment
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hyperadrenocorticism
- Cushing's disease - due to excessive production of cortisol as a consequence of pituitary or adrenal tumours 3 causes: pituitary dependent, adrenal dependent, iatrogenic (excessive and sustained steroid admin)
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pituitary dependent hyperadrenocorticism
- most common cause of cushing's (85%) - adenoma of pars distalis of pituitary gland - results in the overproduction of ACTH which stimulates overproduction of cortisol - 10-20% can grow large (macroadenoma), causing neuro signs
66
adrenal dependent hyperadrenocorticism
- adenomas/carcinomas causing excess cortisol production - leads to negative feedback of production of ACTH of pituitary gland - one adrenal gland enlarged due to tumour, the other adrenal gland atrophied due to suppression of ACTH production
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common clinical signs of cushing's disease
- dermatological signs (skin thinning, alopecia) - excessive panting - polyuria, polydipsia, polyphagia - pendulous (loose) abdomen
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screening tests for hyperadrenocorticism
- haematology, biochemistry, urinalysis - ACTH stimulation test - no confirmatory test available - need to keep animal stress free to prevent increases in cortisol levels unrelated to cushings
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haematology findings as indicators for cushing's
- mild erythrocytosis (elevated RBCs) - mild thrombocytosis (elevated platelets) - stress/steroid leukogram - increased neutrophils, monocytes - decreased eosinophils, lymphocytes
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biochemistry findings as indicators of cushings
- increase in ALKP - increased ALT - hypercholesterolaemia, hypertriglyceridemia due to lipolysis - hyperglycaemia due to insulin antagonism - increased bile acids
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urinalysis findings as indicators of cushings
- dilute urine <1.015 USG (cortisol inhibits ADH) - proteinuria, glycosuria (prolonged steroids can damage kidneys) - urolithiasis
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test of HPA axis for hyperadrenocorticism
- essential that some clinical signs are apparent before pursuing a diagnosis - no recent steroid admin (minimise chance of false positives) - LDDST, ACTH stim, cortisol:creatinine ratio
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sensitivity definition
probability of a positive result if the patient is affected
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sensitivity definition
probability of a positive result if the patient is affected - Sn N out: high sensitivity, negative result, rule out
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specificity definition
probability of a negative result if the patient is not affected - Sp P in: high specificity, positive result, rule in
76
ACTH stimulation test for cushings
- cortisol before and 1hr post ACTH admin - collect serum for basal cortisol concentration - inject %mcg/kg of ACTH IV - collect second serum sample 1hr after
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advantages and disadvantages of ACTH stimulation test
- more specific but less sensitive than LDDST - good first line test (positive result can indicate cushings) - doesn't distinguish PDH from ADH (types of cushings) - used for monitoring response to treatment
78
low dose dexamethasone suppression test (LDDST)
- collect serum for basal cortisol concentration - inject 0.01mg/kg IV dexamethasone - collect serum sample 4 and 8 hours after injection
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LDDST test findings to indicate cushings
- normal dog= cortisol conc decreases over the 8hrs (dex injection inhibits CRH secretion from hypothalamus) - some pituitary dependant dog= cortisol decreases till 4hrs then rises - adrenal and pituitary dependant dog= flat line response
80
advantages and disadvantages of LDDST test
- more sensitive but less specific than ACTH stimulation test - affected by non-adrenal illness - shouldn't be used as sole diagnostic test - can distinguish PDH from ADH
81
urine cortisol:creatinine ratio
- highly sensitive, not very specific - false positives common - urine sample collected at home, not after stressful event (low stress) - pooled samples
82
tests to differentiate PDH from ADH
- LDDST - HDDST (high dose dexamethasone) - most pituitary dependant cases have V shape cortisol concentration trend - imaging - adrenal glands in ADH are asymmetrical
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treatment of cushings
- medical - trilostane - surgery - hypophysectomy for PDH - adrenalectomy for ADH - radiation therapy
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trilostane as treatment of cushings
- give with food SID or BID - monitor through clinical signs or ACTH stim test
85
hypophysectomy as treatment for pituitary dependant hyperadrenocorticism
- complete removal of pituitary gland - 75% canine patients experience long-term cure - life long hormonal supplementation after surgery
86
adrenalectomy as treatment for adrenal dependant hyperadrenocorticism
- can cause haemorrhage, iatrogenic hypoadrenocorticism
87
radiation therapy as treatment for cushings
- reduces the size of macroadenomas to help eliminate neurological signs - reduction of ACTH is variable so often concurrent treatment with trilostane is needed
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