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Endocrinology Flashcards

1
Q

predisposition of canine hypothyroidism

A

middle and older, medium and large

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2
Q

cause of canine hypothyroidism

A
  • primary (thyroid): due to lymphocytic thyroiditis, idiopathic atrophy, thyroids gland neoplasia, irradiation, anti-thryo medications
  • secondary (hypophysis): due to: pituitary neoplasia, corticosteroid intake, hyperadrenocorticism
  • tertiary (hypothalamus): rare
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3
Q

signs of hypothyroidism

A

lethargy, depressed, sensitive to coldness, fat, hairless, prone to skin and ear problems
- metabolic: lethargy, weight gain, tiredness, dullness, bradycardia, weakness
- cutaneous: dry, thin, brittle hair, alopecia, pyoderma, otitis, dry/oily seborrhoea
- neuromuscular: polyneuropathy, peripheral vestibular syndrome, CNS disorder
- cardiovascular: DCM, arrhythmia, low QRS
- goitre

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4
Q

diagnosis of hypothyroidism

A
  • routine lab: haematocrit and total erythrocyte count, within the lower reference limits
  • biochemical:
    o severe hyperlipidaemia with triglycerides 20 and more mmol/L
    o slight increase in AP and GGT
    o slight increase in CK
  • endocrinological
    o T4 (falls in hypothyroidism) and TSH (pituitary hormone, in primary hypothyroidism, concentration is higher than normal)
    o low T4 with elevated TSH with 95% confidence confirms diagnosis
    o fT4 (metabolically active form of T4), most accurate insight into thyroid function so in hypothyroidism it falls
    o TgAA: suitable for some breeds prone to autoimmune lymphocytic thyroiditis (English setter, Dalmatian, boxer, retriever)
    o T3 no value in diagnostics
  • TSH stimulation test
    o performed by high dose of TSH
    o should increase in concentration of stimulated T4, but hypothyroidism = T4 low
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5
Q

treatment of hypothyroidism

A
  • thyroxine supplementation
  • synthetic levothyroxine
  • starting dose is 20ug/kg every 24 hours, serum c of T4 reassessed after 2 weeks
  • dose adjustment = take blood 6 hours after taking tablet (expected highest concentration)
  • take tablet at lowest concentration  6 hr later thyroxine should be 50-60nmol/L,
    o if < 35nmol/L = not good response
    o if > 90nmol/L = decrease dose
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6
Q

prognosis of hypothyroidism

A

excellent

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7
Q

3 characteristic signs of hypothyroidism

A

o coldness intolerance
o tragic face expression
o hairless “rat” tail

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8
Q

predisposition of hyperthyroidism

A

older cat, Siamese and Himalayans less likely to have it

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9
Q

cause of hyperthyroidism

A

benign tumours (adenoma), secondary hyperthyroidism due to increased TSH secretion

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10
Q

pathogenesis of hyperthyroidism

A

concentration of thyroid hormone in the body is increased

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11
Q

signs of hyperthyroidism

A

weight loss, hyperactivity, PUPD, vomiting, diarrhoea, steatorrhea, tachycardia, heart murmur, ventroflexion of the neck, alopecia, messy hair, goitre

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12
Q

diagnosis of hyperthyroidism

A

every old skinny cat
- haematological and biochemical tests
- cardio consult and thyroid hormones
- confirmed by an increase in T3, T4 and fT4 concentrations

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13
Q

treatment of hyperthyroidizsm

A
  • surgical removal of part or all of the thyroid gland
  • carbimazole and methimazole (2.5-5mg per cat every 12 hours), lasts until patient is stabilised and physiological concentration of T4 is reached
  • if surgery isn’t possible, treatment continued 5mg carbimazole every 12hr or 5mg methimazole (24)
  • radioactive treatment: iodine is given IV
  • aim = achieve T4 in lower half of reference range (15-30nmol/L)
  • control every 3-6 months
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14
Q

diabetes mellitus

A
  • dogs get type 1 = Absolute/relative lack of insulin due to decreased production or tissue resistance to insulin
  • cats get type 2 = insulin resistance + dysfunction of B cells of Langerhans islets
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15
Q

predisposition of.DM

A

all, Samoyed, poodles, schnauzers
- in cats: old, make, neutered  obesity  adipokines increased  insulin resistance

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16
Q

cause of DM

A

genetic, immune mediated, pancreatitis, excess of GH, secondary hypothyroidism, amyloidosis, obesity

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17
Q

pathogenesis of DM

A

absolute or relative lack of insulin due to: decreased production of insulin or tissue resistance of insulin

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18
Q

signs of DM

A

anorexia, PUPD, glucosuria, persistent hyperglycaemia, weight loss, ketonuria, neurological signs

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19
Q

diagnosis of DM

A

simple, history
- stress hyperglycaemia: transient hyperglycaemia due to stress (never results in glucosuria), cats 25mmol/L, never results in glucosuria
- serum frucosamine

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20
Q

treatment of DM

A
  • control of DM (moderate hyperglycaemia 5-15mmol/L)
  • food for diabetics: increased content of fibres with soluble and insoluble fire ratio, 2x meals daily prior to insulin
    insulin according to duration
  • short acting = crystalline (regular)
  • middle acting = BPH, lente
  • long acting: protamine zinc, ultralente, glargine
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21
Q

monitor DM

A

serum frucosamine, urine glucose and serial blood glucose curve

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22
Q

complications of DM

A

diabetic ketoacidosis, acute pancreatitis, hyperosmolar coma, cataracts, vasculopathies, prolonged healing, UTI

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23
Q

diabetes insidious

A

Passage of large quantities of dilute urine (polyuria)

24
Q

predisposition of diabetes insipidus

A

rare in dogs

25
Q

types of D.I

A
  • central diabetes insipidus = lack of vasopressin to concentrate urine – hypothalamus doesn’t produce any or enough ADH
  • Nephrogenic diabetes insipidus – where kidneys don’t respond appropriately to ADH
26
Q

cause of D.I

A

pituitary neoplasm, head trauma or idiopathic

27
Q

signs of D.I

A

PUPD, USG of urine blow plasma, slight hypernatremia

28
Q

diagnosis of D.I

A
  • measure urine SG
  • water deprivation test with vasopressin administration
  • measure plasma vasopressin during osmotic stimulation by hypertonic saline
    o euhydrated animal infused through jugular for 2 hr with 20% NaCl at 0.03ml/kg/min, take blood to measure vasopressin in 120 mins
29
Q

treatment of D.I

A

desmopressin, nephrogenic (diuretics, low Na diet, hydrochlorothiazide)

30
Q

prognosis of d.I

A

good if no neoplasia if left without water, untreated

31
Q

differentials of D.I

A

PD = hyperactive young dogs left alone, nephrogenic DI = rare, congenital

32
Q

predisposition of addisons

A

: standard poodles, 1-12years

33
Q

cause of addisons

A

insufficient mineralocorticoids and/or glucocorticoids production (primary, most common) secondary can also be iatrogenic (drugs)

34
Q

signs of addison

A

inappetence, lethargy, weakness, vomiting, diarrhoea, melena, tremor, depression, hypovolemia, bradycardia, hypothermia, PUPD

35
Q

diagnosis of addisons

A
  • ECG = bradycardia, tall T waves, no P waves
  • biochemistry: hyperkalaemia, hyponatremia, hyperphosphatemia, increased BUN + creatinine
    ACTH stimulation
  • low baseline cortisol, no response to stimulation
    NA: K ratio (only applied to primary addisons)
  • majority of patients <27
  • <24 stronger suggests addisons
  • <15 is more suggestive
  • Na:L > 29 probably excludes addisons
    +/- endogenous ACTH
36
Q

treatment of addisons

A
  • correction of hypotension/hypolvemia: 20-40ml/kg/h for 1st 2-3 hours, followerd with 2-4ml/kg/h plasmolyte, bolus of colloids (HES) if hypoalbuminemic
  • correction of hypoglycaemia + hyperkalaemia
  • glucocorticoids: dexamethasone (0.5-2mg/kg), prednisolone (1-2mg/kg)
  • mineralocorticoids: DOCP (2mg/kg/h IM every 25-30 days), hydrocortisone/fludocortisone (10-30mcg/kg PO every 24hr)
37
Q

differentials of addisons

A

abdominal or thoracic effusions, cardiorespiratory disease, sepsis, DKA, kidney failure, perforating GI ulcer

38
Q

trick of Addison’s disease

A
  • Disguise as renal failure (elevated BUN, creatinine, vomiting, melena, GI ulcerations…)
  • Prerenal (hypovolemia), if not corrected – true renal failure
  • Very responsive to fluids – clinical and lab parameters improvement until the next episode
  • Recurring GI problem
  • Intolerances/allergies
39
Q

predisposition of cushin

A

all older dogs (more than 7yrs), males, poodles, daschunds, small terriers (pituitary dependent), large breeds: adrenal dependent

40
Q

cause of cushing

A

syndrome resulting from excessive production or administration of glucocorticoids

41
Q

pathogenesis of cushing

A

spontaneous (pituitary or adrenal) or iatrogenic

42
Q

signs of cushing

A

thirsty, alopecia, pedunculus abdomen, skin irritation, bad coat

43
Q

diagnosis of cushing

A
  • haematology = leucocytosis/leukopenia, moderate anaemia
  • biochemistry = borderline hyperglycaemia, AP and cholesterol increased
    ACTH stimulation
  • best, 85% of pituitary dependent and for treatment monitoring
  • great for differentiation between spontaneous and iatrogenic, but doesn’t differ between PDHAC and ADHAC
    1. blood sample (baseline cortisol),
    1. Synacthen 250mcg IV
    1. second blood sample after 1 hr (stimulates cortisol)
      Low dose dexamethasone suppression test
  • differentiation between ADHAC and PDHAC
    1. blood sample – baseline cortisol
    1. 0.01mg/kg dexamethasone
    1. blood sample after 4 hours
    1. blood sample after 8 hours
44
Q

treatment of cushing

A

: ADHAC = adrenalectomy, PDHAC = trilostan 2mg/kg/day SID or BID
- monitoring: ACTH stimulation (14 days, 4 weeks, 12 weeks, 3 months after last test)

45
Q

complication of cushing

A

infections (UTI), hypertension, blindness, neuro signs due to pituitary macroadenoma, cats can get fragile skin syndrome

46
Q

function of glucocorticoids

A
  • increase: insulin sensitivity in muscle, lipid storage and gluconeogenesis, adipogenesis, food intake, Na and fluid retention + decrease inflammation
47
Q

predisposition of insulinoma

A

no gender or breed predisposition, 4-13 years

48
Q

cause of insulinoma

A

malignant adenocarcinoma of B cell Langerhans inlets that excrete insulin independent of low glucose concentration

49
Q

symptoms of insuliunoma

A

: hypoglycaemia, lethargy, weakness, collapse, disorientation, ataxia, seizures, nerve paresis, hunger, tremor, nervousness

50
Q

diagnosis of inuslinoma

A
  • lab: only hypoglycaemia which isn’t permanent
  • slightly decreased BG  measuring BG in morning before meal, if <3.5mmol/L + insulin >70pmol/L
  • US – only 50% if cannot visualise, then exploratory laparotomy, then if not by this then partial resection
51
Q

treatment of insulinoma - emergency

A
  • IV or PO diazepam per rectum
  • glucose syrup or honey – gingival rubbing
  • place IV catheter, measure BG
  • 1st bolus 50% dextrose, diluted 1:3 with NaCl, followed by CRI 2.5-5% glucose until starts to eat
  • dexamethasone 0.1mg/kg IV BID (2x a day)
52
Q

treatment of insulinoma - stable patient

A
  • conservative: older dogs, metastases, concurrent diseases
  • prednisone: 0.25mg/kg BID, gradually increase dose to effect
  • diazoxide: benzothiadiazide derivative – reduces insulin excretion: 10-40mg/kg/day (BID, TID), with meal, slowly increase dose to effect (max 60mg/kg/day)
53
Q

prognosis of insulinom

A

variable – aware of metastasis
- most favourable = complete surgical removal and no metastasis (0 days – 5 years)
- surgery and conservative = 1315 days
- conservative = 452 days

54
Q

differentials of insulinoma

A

epilepsy, other neoplasia, sepsis, polycytemia, idiopathic, juveniles, iatrogenic, PSA, hypoadrenocortism, renal disease

55
Q

Whipple triad

A
  • neurological signs (affect excitement/ activity)
  • hypoglycaemia during symptoms
  • withdrawal of symptoms after glucose intake (IV or PO)

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