Endocrinology Flashcards
predisposition of canine hypothyroidism
middle and older, medium and large
cause of canine hypothyroidism
- 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
signs of hypothyroidism
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
diagnosis of hypothyroidism
- 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
treatment of hypothyroidism
- 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
prognosis of hypothyroidism
excellent
3 characteristic signs of hypothyroidism
o coldness intolerance
o tragic face expression
o hairless “rat” tail
predisposition of hyperthyroidism
older cat, Siamese and Himalayans less likely to have it
cause of hyperthyroidism
benign tumours (adenoma), secondary hyperthyroidism due to increased TSH secretion
pathogenesis of hyperthyroidism
concentration of thyroid hormone in the body is increased
signs of hyperthyroidism
weight loss, hyperactivity, PUPD, vomiting, diarrhoea, steatorrhea, tachycardia, heart murmur, ventroflexion of the neck, alopecia, messy hair, goitre
diagnosis of hyperthyroidism
every old skinny cat
- haematological and biochemical tests
- cardio consult and thyroid hormones
- confirmed by an increase in T3, T4 and fT4 concentrations
treatment of hyperthyroidizsm
- 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
diabetes mellitus
- 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
predisposition of.DM
all, Samoyed, poodles, schnauzers
- in cats: old, make, neutered obesity adipokines increased insulin resistance
cause of DM
genetic, immune mediated, pancreatitis, excess of GH, secondary hypothyroidism, amyloidosis, obesity
pathogenesis of DM
absolute or relative lack of insulin due to: decreased production of insulin or tissue resistance of insulin
signs of DM
anorexia, PUPD, glucosuria, persistent hyperglycaemia, weight loss, ketonuria, neurological signs
diagnosis of DM
simple, history
- stress hyperglycaemia: transient hyperglycaemia due to stress (never results in glucosuria), cats 25mmol/L, never results in glucosuria
- serum frucosamine
treatment of DM
- 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
monitor DM
serum frucosamine, urine glucose and serial blood glucose curve
complications of DM
diabetic ketoacidosis, acute pancreatitis, hyperosmolar coma, cataracts, vasculopathies, prolonged healing, UTI
diabetes insidious
Passage of large quantities of dilute urine (polyuria)
predisposition of diabetes insipidus
rare in dogs
types of D.I
- 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
cause of D.I
pituitary neoplasm, head trauma or idiopathic
signs of D.I
PUPD, USG of urine blow plasma, slight hypernatremia
diagnosis of D.I
- 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
treatment of D.I
desmopressin, nephrogenic (diuretics, low Na diet, hydrochlorothiazide)
prognosis of d.I
good if no neoplasia if left without water, untreated
differentials of D.I
PD = hyperactive young dogs left alone, nephrogenic DI = rare, congenital
predisposition of addisons
: standard poodles, 1-12years
cause of addisons
insufficient mineralocorticoids and/or glucocorticoids production (primary, most common) secondary can also be iatrogenic (drugs)
signs of addison
inappetence, lethargy, weakness, vomiting, diarrhoea, melena, tremor, depression, hypovolemia, bradycardia, hypothermia, PUPD
diagnosis of addisons
- 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
treatment of addisons
- 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)
differentials of addisons
abdominal or thoracic effusions, cardiorespiratory disease, sepsis, DKA, kidney failure, perforating GI ulcer
trick of Addison’s disease
- 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
predisposition of cushin
all older dogs (more than 7yrs), males, poodles, daschunds, small terriers (pituitary dependent), large breeds: adrenal dependent
cause of cushing
syndrome resulting from excessive production or administration of glucocorticoids
pathogenesis of cushing
spontaneous (pituitary or adrenal) or iatrogenic
signs of cushing
thirsty, alopecia, pedunculus abdomen, skin irritation, bad coat
diagnosis of cushing
- 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
- blood sample (baseline cortisol),
- Synacthen 250mcg IV
- second blood sample after 1 hr (stimulates cortisol)
Low dose dexamethasone suppression test
- second blood sample after 1 hr (stimulates cortisol)
- differentiation between ADHAC and PDHAC
- blood sample – baseline cortisol
- 0.01mg/kg dexamethasone
- blood sample after 4 hours
- blood sample after 8 hours
treatment of cushing
: ADHAC = adrenalectomy, PDHAC = trilostan 2mg/kg/day SID or BID
- monitoring: ACTH stimulation (14 days, 4 weeks, 12 weeks, 3 months after last test)
complication of cushing
infections (UTI), hypertension, blindness, neuro signs due to pituitary macroadenoma, cats can get fragile skin syndrome
function of glucocorticoids
- increase: insulin sensitivity in muscle, lipid storage and gluconeogenesis, adipogenesis, food intake, Na and fluid retention + decrease inflammation
predisposition of insulinoma
no gender or breed predisposition, 4-13 years
cause of insulinoma
malignant adenocarcinoma of B cell Langerhans inlets that excrete insulin independent of low glucose concentration
symptoms of insuliunoma
: hypoglycaemia, lethargy, weakness, collapse, disorientation, ataxia, seizures, nerve paresis, hunger, tremor, nervousness
diagnosis of inuslinoma
- 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
treatment of insulinoma - emergency
- 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)
treatment of insulinoma - stable patient
- 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)
prognosis of insulinom
variable – aware of metastasis
- most favourable = complete surgical removal and no metastasis (0 days – 5 years)
- surgery and conservative = 1315 days
- conservative = 452 days
differentials of insulinoma
epilepsy, other neoplasia, sepsis, polycytemia, idiopathic, juveniles, iatrogenic, PSA, hypoadrenocortism, renal disease
Whipple triad
- neurological signs (affect excitement/ activity)
- hypoglycaemia during symptoms
- withdrawal of symptoms after glucose intake (IV or PO)
