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CVNT 2 > Endocrine > Flashcards

Endocrine Flashcards

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
Q

clinical signs of hyperthyroidism

A

increased:
- metabolic rate, CO, HR, BP, GI motility, CNS activity
decreased:
- sleep, body weight
- palpably enlarged thyroid glands
- polyphagia, polyuria, polydipsia

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26
Q

handling the feline hyperthyroidism patient

A
  • hands-off approach
  • consider gabapentin 2hrs before travel
  • quiet, dark room
  • give time to acclimatise in consult, nursing room
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27
Q

diagnosis of feline hyperthyroidism

A
  • compatible clinical signs
  • screening tests
  • confirmatory tests
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28
Q

screening tests for feline hyperthyroidism

A
  • haematology
  • biochemistry (elevated liver enzymes)
    • look for concurrent disease (chronic kidney disease)
  • urinalysis (look for concurrent disease)
  • BP measurement
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29
Q

confirmatory diagnostic test for feline hyperthyroidism

A
  • serum total thyroxine (TT4)
  • false negatives are possible (can fluctuate over 24hr day, can be falsely low in patients with concurrent disease)
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30
Q

treatments for feline hyperthyroidism

A
  • anti-thyroid drugs
  • iodine restricted diet
  • surgery
  • radioactive iodine
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31
Q

anti-thyroid drugs for hyperthyroidism

A
  • 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
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32
Q

advantages of anti-thyroid drugs

A
  • readily available
  • effective
  • inexpensive
  • practical (bioavailable)
  • no GA or hospitalisation
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33
Q

disadvantages of anti-thyroid drugs

A
  • lifelong (expensive)
  • long-term resistance
  • compliance
  • side effects
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34
Q

side effects of anti-thyroid drugs

A
  • vomiting, anorexia, lethargy (10-20%)
  • GI irritant, leukopenia, anaemia, dermatitis, hepatopathy, myasthenia gravis
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35
Q

iodine-restricted diet for feline hyperthyroidism

A
  • 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
Q

thyroidectomy

A
  • 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
37
Q

advantages of thyroidectomy

A
  • curative
  • rapidly effective
  • short hospitalisation period
38
Q

disadvantages of thyroidectomy

A
  • GA risks
  • cost
  • complications
  • depends of location of adenoma
  • recurrence
39
Q

complications of thyroidectomy

A
  • damage to parathyroid tissue (post-op hypoparathyroidism)
  • damage to recurrent laryngeal nerve
  • damage to sympathetic nerve (horner’s syndrome)
  • possible recurrence
40
Q

Iatrogenic hypoparathyroidism

A
  • associated with bilateral thyroidectomy
  • removal of parathyroid glands prevents TTH production which causes hypocalcaemia
41
Q

clinical signs of iatrogenic hypoparathyroidism

A
  • inappetence
  • weakness, tremors
  • hypersalivation
    monitor serum calcium BID if bilateral thyroidectomy
42
Q

Iatrogenic hypoparathyroidism treatment

A
  • hospitalisation
  • IV 10% calcium gluconate
    • avoid bicarbonate, lactate, phosphate fluids as precipitates calcium
  • ECG to monitor for arrythmia and bradycardia
43
Q

radioiodine treatment for feline hyperthyroidism

A
  • 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
Q

advantages of radioactive iodine therapy

A
  • curative
  • simple procedure
  • no GA, minimally invasive
  • can treat carcinoma
45
Q

disadvantages of radioactive iodine therapy

A
  • limited availability
  • isolation treatment
  • irreversible
  • may take time to achieve euthyroid
  • high initial cost (cheaper long term)
46
Q

monitoring of feline hyperthyroid patient

A
  • 6 monthly check-ups once stabilised
  • recurrence (history, clinical signs, blood test)
  • hypertension
  • chronic kidney disease (urinalysis, urea- creatinine)
47
Q

hyperthyroidism and chronic kidney disease

A
  • hyperthyroidism may mask underlying CKD, treatment will uncover CKD
  • consider medical management before curative treatment
48
Q

canine thyroid neoplasia

A
  • 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
Q

canine hypothyroidism clinical signs

A
  • 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
Q

diagnosis of canine hypothyroidism

A
  • compatible clinical signs
  • haematology and biochemistry
  • confirmatory tests
  • low T4, high TSH
  • anti-thyroglobulin antibodies
51
Q

total T4 (TT4) test

A
  • 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
Q

Canine TSH (cTSH)

A
  • increased in hypothyroidism due to lack of negative feedback
  • good specificity: largely non-affected by non-thyroidal illness or drugs
53
Q

Anti-thyroglobulin antibodies

A
  • 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
Q

treatment of canine hypothyroidism

A
  • synthetic T4
    • available in tablet and liquid forms
  • bioavailability is halved with food
    • try give on empty stomach
55
Q

monitoring of hypothyroidism patient

A
  • 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
Q

canine hypoadrenocorticism (addison’s disease)

A
  • 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:
57
Q

aldosterone

A
  • 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
Q

clinical signs of canine hypoadrenocorticism

A
  • polydipsia and polyuria
  • addisonian crisis:
    • collapse, severe dehydration, hypovolaemia, pre-renal azotaemia, cardiac arrhythmias due to hyperkalaemia
59
Q

screening tests for hypoadrenocorticism

A
  • 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
60
Q

confirmation tests of hypoadrenocorticism

A

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
Q

treatment of canine hypoadrenocorticism (addisonis crisis)

A
  • 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
Q

long-term therapy of canine hypoadrenocorticism

A

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
Q

monitoring of canine hypoadrenocorticism patient

A
  • 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
64
Q

hyperadrenocorticism

A
  • 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)
65
Q

pituitary dependent hyperadrenocorticism

A
  • 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
Q

adrenal dependent hyperadrenocorticism

A
  • 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
67
Q

common clinical signs of cushing’s disease

A
  • dermatological signs (skin thinning, alopecia)
  • excessive panting
  • polyuria, polydipsia, polyphagia
  • pendulous (loose) abdomen
68
Q

screening tests for hyperadrenocorticism

A
  • 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
69
Q

haematology findings as indicators for cushing’s

A
  • mild erythrocytosis (elevated RBCs)
  • mild thrombocytosis (elevated platelets)
  • stress/steroid leukogram
    • increased neutrophils, monocytes
    • decreased eosinophils, lymphocytes
70
Q

biochemistry findings as indicators of cushings

A
  • increase in ALKP
  • increased ALT
  • hypercholesterolaemia, hypertriglyceridemia due to lipolysis
  • hyperglycaemia due to insulin antagonism
  • increased bile acids
71
Q

urinalysis findings as indicators of cushings

A
  • dilute urine <1.015 USG (cortisol inhibits ADH)
  • proteinuria, glycosuria (prolonged steroids can damage kidneys)
  • urolithiasis
72
Q

test of HPA axis for hyperadrenocorticism

A
  • 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
73
Q

sensitivity definition

A

probability of a positive result if the patient is affected

74
Q

sensitivity definition

A

probability of a positive result if the patient is affected
- Sn N out: high sensitivity, negative result, rule out

75
Q

specificity definition

A

probability of a negative result if the patient is not affected
- Sp P in: high specificity, positive result, rule in

76
Q

ACTH stimulation test for cushings

A
  • 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
77
Q

advantages and disadvantages of ACTH stimulation test

A
  • 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
Q

low dose dexamethasone suppression test (LDDST)

A
  • collect serum for basal cortisol concentration
  • inject 0.01mg/kg IV dexamethasone
  • collect serum sample 4 and 8 hours after injection
79
Q

LDDST test findings to indicate cushings

A
  • 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
Q

advantages and disadvantages of LDDST test

A
  • 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
Q

urine cortisol:creatinine ratio

A
  • highly sensitive, not very specific
    • false positives common
  • urine sample collected at home, not after stressful event (low stress)
    • pooled samples
82
Q

tests to differentiate PDH from ADH

A
  • LDDST
  • HDDST (high dose dexamethasone)
    • most pituitary dependant cases have V shape cortisol concentration trend
  • imaging
    • adrenal glands in ADH are asymmetrical
83
Q

treatment of cushings

A
  • medical
    • trilostane
  • surgery
    • hypophysectomy for PDH
    • adrenalectomy for ADH
  • radiation therapy
84
Q

trilostane as treatment of cushings

A
  • give with food SID or BID
  • monitor through clinical signs or ACTH stim test
85
Q

hypophysectomy as treatment for pituitary dependant hyperadrenocorticism

A
  • complete removal of pituitary gland
  • 75% canine patients experience long-term cure
  • life long hormonal supplementation after surgery
86
Q

adrenalectomy as treatment for adrenal dependant hyperadrenocorticism

A
  • can cause haemorrhage, iatrogenic hypoadrenocorticism
87
Q

radiation therapy as treatment for cushings

A
  • reduces the size of macroadenomas to help eliminate neurological signs
  • reduction of ACTH is variable so often concurrent treatment with trilostane is needed

CVNT 2 (33 decks)

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