Sams Endocrine Review Vet 436

Front 1

Canine Diabetes Mellitus (Type 1)
-Hx and CS

Back 1

One of 3 situations
-Uncomplicated=well dog w/ mild signs
-Diabetic ketoacidosis
-Non-ketotic hyperosmolar DM (rare

Front 2

Uncomplicated diabetes mellitus
-CS

Back 2

-PU/PD
-weight loss despite
-Polyphagia

Front 3

Diabetes ketoacidosis
-CS

Back 3

1. 'well' DKA:
-recent PU/PD
-weight loss
-polyphagia
-ketonuria
-hypoinsulinaemia
'sick' DKA:
-marked lethargy
-weakness
-vomiting
-dehydration
-anorexia

Front 4

Lab findings in Diabetes mellitus

Back 4

(blood for CBC, FBE, urine for UA for investigation of PU/PD)
-glycosuria w/ hyperglycaemia
-anemia (cats)
-increased choloesterol
-hypertriglyceridaemia
-decreased Na (urinary loss)
-Decreased K (urinary loss, vomiting)
-decreased Phosphate (urinary loss)

Front 5

Diabetes Mellitus
-Dx

Back 5

-CS
-lab data
-always check for signs of concurrent disease(s) and precipitating cause of DKA
+/- test fructosamine (esp cats)

Front 6

Diabetes Mellitus
-Tx

Back 6

1. Insulin
-Caninsulin-twice daily preferable at same time as food (0.5 unit/kg)
**Hospitalise the dog for the first 24h for observation and to check the response to insulin by BLOOD GLUCOSE CURVE (measure glucose after insulin and plot concentration)
2. OHE in entire females
3. low fat diet high in complex carbohydrates and soluble fibre (weight control diets)

Front 7

Managing DKA

Back 7

1. Well:
-fluid therapy as required
-short acting insulin + offer food
-monitor blood glucose q 2 h
-switch to maintenence insulin at earliest opportunity
2. 'Sick' Diabetic ketoacidotic dog:
(refer)
-fluid therapy: 0.9% saline-depletion of sodium and chloride
run fluids at 3-4X maintenence before starting insulin
add potassium after initial re-hydration is complete (DO NOT EXCEED 0.5mmol/kg/h)
-add phosphate if available and hypophosphatemia is present
Other therapy: a/b, sodium bicarb; monitor urine output

Front 8

Insulin therapy for DKA:
-Intermittent IM/SC protocol

Back 8

1. rehydrate w/ 0.9% NaCl for 2 hours, then check blood glucose
2. regular insulin injections hourly
3. monitor blood glucose hourly
4. blood glucose =10-15mmol/L, STOP hourly insulin
5. monitor glucose hourly and change to giving insulin every 6 hours SC
6. Morning: switch to caninsulin (if eating)

Front 9

List complications associated w/ managing diabetic dogs and cats

Back 9

-hypoglycaemia (insulin overdose)
-recurrent infections
-cataracts

Front 10

Feline Diabetes Mellitus
-Difference to dogs

Back 10

-type II=potentially curable
-amyloidosis and glucose toxicity in pathogenesis
-correct diet more important (low carb, high protein=catkins diet)

Front 11

Feline Diabetes Mellitus
-Pathogenesis

Back 11

-insulin resistance (w/ obesity)
-increased insulin secretion (early-response to resistance)
-later: reduced (to zero) secretion of insulin by Beta cells

Front 12

Feline Diabetes Mellitus
-Dx

Back 12

-plantigrade stance and weakness
-hyperglycaemia and glucosuria +/- ketonuria
-persistent hyperglycaemia (stress)
-concurrent abnormalities common: moderate anaemia, hypophosphatemia, hepatic enzyme elevations, hyponatremia and hypokalemia, ketoacidosis, pancreattis

Front 13

Feline Diabetes Mellitus
-Tx

Back 13

1) stable (uncomplicated):
-search for underlying disease and manage as indicated
-most cats require rehydration
-start w/ caninsulin
2) ketoacidotic cats:
-full lab assessment to determine extent of metabolic derangement
-fluid therapy and IV/IM regular insulin, glucose measured every 2 hours
3) Feeding:
-feed Hill's m/d

Front 14

Causes of secondary nephrogenic diabetes insipidus

Back 14

-hyperCa
-hyperA
-pyometra, protatic abscess
-

Front 15

Central Diabetes insipidus
-Hx and Cs

Back 15

-profound PU/PD
+/- incontinence
+/- CNS signs

Front 16

Central Diabetes insipidus
-Dx

Back 16

-water deprivation test (do not perform if dehydrated, azotemic or has any other abnormalities)

Front 17

Central Diabetes insipidus
-Management

Back 17

-synthetic vasopressin-analogue (nasal drops)

Front 18

Hyperadrenocorticism (dogs only)
-predisposition

Back 18

-poodle, daschund, small-breed dogs (toy, mini)
-middle aged (5-7y.o)

Front 19

Hyperadrenocorticism (dogs only)
-CS

Back 19

-**PU/PD
-**PP
-abdominal distention and pain
-weakness and lethargy
-truncal obesity
-skin signs (alopecia (non-pruritic), thin skin, calcinosis cutis,
comedones, demodecosis)
-reproductive abnormalities
-neuromuscular signs (blindness, circling, seizures)
-panting (acute resp. distress)

Front 20

Hyperadrenocorticism (dogs only)
-Diagnostic procedure

Back 20

-Hx and CS
-rule out steroid admin
-full screening lab evaluation (CBE, FBE, urinalysis)
-specific tests for adrenal function
-definitive testing to differentiate between PDH and AT

Front 21

Hyperadrenocorticism (dogs only)
-diagnostic findings

Back 21

1. Screening tests:
-stress leukogram (neutrophillia, eosinopaenia, lymphopaenia, monocytosis)
-increased ALP
-hypercholesterolaemia/hyperlipidaemia
-hyperglycaemia
-decresed BUN/creatinine
-hyposthenuria (causes nephrogenic diabetes insipidus)
-UTI

Front 22

Canine Hyperadrenocorticism
-Tests for the hypophyseal adrenal axis

Back 22

1. LDDST
-dogs with hyperA will either not suppress or 'escape' suppression after 8 hours
-low sensitivity, high specificity
2. ACTH stim test
-excessive release of cortisol to ACTH

Front 23

Canine Hyperadrenocorticism
-Other diagnostic tests

Back 23

1. radiography
-adrenal thickness >7.5mm in large dogs and >5mm in small dogs=PDH
-hepatomegaly
+/- full bladder
2. Plasma ACTH measurement
=AT, negative feedback from tumour will suppress ACTH concentrations to very low levels

Front 24

Canine Hyperadrenocorticism
-DDx

Back 24

-hypothyroidism (weight gain but no PU/PD)
-Diabetes Mellitus (may be concurrent)
-Sertoli cell tumour (alopecia)
-renal disease (PU/PD)
-liver disease (PU/PD)
-other causes of nephrogenic diabetes insipidus (hypercalcaemia, pyometra, psochogenic polydipsia, diabetes insipidus)

Front 25

Canine Hyperadrenocorticism
-Tx

Back 25

Iatrogenic=weaned off corticosteroids in a controlled manner
-pituitary dependent: trilostane or mitotane
-consider referral
Adrenal tumours: assess if metastasis (lungs) and abdominal imaging (liver)
-surgical therapy (+ anaesthetic screen + glucose and electrolytes)

Front 26

DDx
-non inflammatory symmetrical alopecia

Back 26

Male dogs:
-hyperoestrogenism (sertoli cell tumour)
Female dogs:
-hyperoestrogenism (polycystic ovaries or functional ovarian neoplasia)
Both sexes:
-hyperA
-hypothyroidism
-pituitary dwarfism
-Alopecia X
-Telogen effluvium
Cats:
-hyperthyroidism
-hyperA

Front 27

Obesity and weight gain:
-problem solving approach

Back 27

1. assess caloric intake
2. decide whether appetite is increased (if so, polyphagia)
3. some animals gain weight despite normal/decreased appetite (e.g. with hypothyroidism)
4. is the dog really obese or is the weight gain associated with abdominal distension?
5. Once you have ruled out pathological disease, a weight loss programme should be advised

Front 28

Canine hypothyroidism
-General

Back 28

-common in dogs, rare in cats
-thyroid hormone deficiency
-may be: congenital, acquired (primary, secondary, tertiary), iatrogenic (thyroidectomy)
-most cases aquired=lymphocytic thyroiditis or idiopathic follicular atrophy

Front 29

Canine hypothyroidism
-Predisposition

Back 29

-congenital (rare)
-acquired: mid to large breed dogs
-no recognised age or sex predisposition

Front 30

Canine hypothyroidism
-CS

Back 30

-pansystemic disorder and causes dysfunction in potentially any organ
-disproportional dwarfism and mental retardation (cretinism) will result if treatment not started
-reflect decrease in metabolism:
--lethargy, inactivity, weakness
--weight gain (to obesity)
--dermatological signs (hair loss, skin thickening, seborrhoea)

Front 31

Canine hypothyroidism
-Diagnostic procedure

Back 31

1. blood sample for CBC and FBE and urine for FA screen
2. total T4 and free T4 assays and the endogenous TSH assay
3. clinical assessment of response to treatment

Front 32

Canine hypothyroidism
-typical screening lab findings

Back 32

-low total T4 (but can be low in other diseases)
-low fT4 and elevated TSH
-normocytic, normochromic anaemia
-hypercholesterolaemia, hypertriglyceridaemia

Front 33

Canine hypothyroidism
-DDx

Back 33

-NB hypothyroid dogs DO NOT present with polydipsia, polyuria or polyphagia (despite weight gain and obesity)

Front 34

Canine hypothyroidism
-Tx

Back 34

-synthetic thyroxine (higher dose than in humans)
-re-evaluate in 6 weeks following start of supplementation

Front 35

Approach to weight loss:

Back 35

1. ensure caloric intake is met
2. question about dysphagia, disorders of swallowing, regurgitation, persistent vomiting, anorexia or reduced appetite
3. weight loss despite increase in appetite: increased caloric loss may be from kidney or gut, increased calorig 'usage'-hyperthyroidism, neoplasia

Front 36

Feline hyperthyroidism (thyrotoxicosis)
-General

Back 36

-most common endocrine disease in older cats
-usually benign adenoma hyperplasia of the thyroid gland (one or both=palpable 'goiter')

Front 37

Feline hyperthyroidism (thyrotoxicosis)
-Hx and CS

Back 37

-weight loss despite good appetite (PP)
-palpable cervical mass
-hyperactivity
-cardiac disease signs: tachycardia, gallop rhythms, volume overload (fluid expansion), reduced systemic resistance, HCM (often w/ murmur)
-PU/PD
-failure to groom
-diarrhoea (usually foul and steatorrhoea-DDx=intestinal lymphoma/other intestinal neoplasia)

Front 38

Feline hyperthyroidism (thyrotoxicosis)
-diagnostic procedure

Back 38

-thorough physical exam
-full lab screening
-'old cat profile' which includes T4 measurement
-marked tachycardia, gallop rhythm or a heart murmur

Front 39

Feline hyperthyroidism (thyrotoxicosis)
-Dx

Back 39

-CS
-elevated serum T4
-other lab tests non-specific:
-increased PCV, haemoglobin, RBC count
-increased ALT/ALP
-Azotemia
-mild hypocalcaemia/hyperphosphatemia

Front 40

Feline hyperthyroidism (thyrotoxicosis)
-Tx

Back 40

1. Antithyroid drug medication
-carbimazole
**-transdermal methimazole
2.Management of cardiac disease and heart failure:
-frusemide, atenolol, ACEi
3. Management of renal insufficiency of hyperthyroidism:
-cats w/ pre-existing kidney failure should probably NOT be treated for their hyperthyroidism since the reduction in BP and GFR may be enough to cause ARF.
4. Surgical management:
-intracapsular thyroidectomy
5. radioiodine therapy=curative

Front 41

Hyponatremia
-causes

Back 41

-hypoadrenocorticism (failure of mineralocorticoids=Na loss, water follows)
-loop diuretic use
-GI loss (vomiting and diarrhoea)
-loss to a third space (e.g pleural fluid)
-excess gain in water:
-liver disease
-CHF
-SIADH
-hypoproteinaemic states
-primary polydipsia

Front 42

Hyperkalemia
-causes

Back 42

-loss of free water or hypotonic fluids(DI-both CDI and renal/nephrogenic, heatstroke, water deprivation test)
-gain of ECF sodium (hypertonic fluid admin, hyperaldosteronism)
-CS: obtundation>>coma/convulsions

Front 43

Hypokalaemia
-causes

Back 43

-decreased intake for prolonged time (anorexia)
-alkalemia (K ions enter cells in exchange for H ions)
-excessive loss via GI or renal routes
-CS: muscle weakness (cats: ventroflexion of neck), tachycardia (+/- arrhythmia), PU/PD
-treat w. IVF or oral potassium
-cats: hypokalemic polymyopathy

Front 44

Hyperkalemia
-causes

Back 44

-uncommon if normal renal function
-impairment of urinary secretion of K (ARF (anuria), post-renal obstruction (calculi, FLUTD, ruptured bladder), hypoadrenocorticism (mineralocorticoid inactivity))
-muscle weakness, electical misconduction in heart

Front 45

Emergency therapy for hyperkalemia (i.e if >5mmol/L)

Back 45

1. Parenteral fluid therapy (K free)-reduce via plasma volume expansion
2. calcium gluconate-slow IV, calcium antagonises effect of K on heart
3. glucose-stimulates endogenous insulin release-moves K into cells
4. sodium bicarb-only if concurrent acidosis

Front 46

Canine hypoadrenocorticism
-general

Back 46

-Addison's disease
-deficiency of both mineralo and glucocorticoids
-primary:
occurs when 85-90% adrenal cortical function lost
principally mineralocorticoid deficiency
2. acquired
-sudden withdrawal of corticosteroids (failure of ACTH secretion=secondary hypoA)
-milotane overdose during treatment for Cushing's

Front 47

Canine hypoadrenocorticism
-Pathophysiology

Back 47

1. Mineralocorticoid deficiency results in:
-hyponatremia (PU/PD), hypovolemia, hyperkalemia(NM function, cardiac disturbance)
2. Glucocorticoid deficiency results in:
-GI signs (anorexia, vomiting, abdominal pain=cortisol maintains intestinal motility and Na absorption from colon)
-hypoglycaemia (shivering, nervousness, behaviour change, lethargy-cortisol stimulates gluconeogenesis and glycogenesis
-anaemia (cortisol stimulates erythropoeisis=mild, non-regenerative)

Front 48

Canine hypoadrenocorticism
-signalment

Back 48

-young to middle aged
-female

Front 49

Canine hypoadrenocorticism
-Hx

Back 49

-Acute collapse and weakness (Addisonian crisis)
OR
-progressive, vague, non-specific problems (chronic)
-anorexia, lethargy, vomiting, diarrhoea, PU/PD, depression
-signs worse when dog 'stressed'

Front 50

Canine hypoadrenocorticism
-CS

Back 50

-no consistent clinical signs unless the dog is 'ill'
-weakness, collapse, dehydration
-bradycardia and weak femoral pulses
-melena or haematochezia
-regurgitation
-shivering or shaking

Front 51

Canine hypoadrenocorticism
-Dx

Back 51

-Lab data and ECG
1.Lab data findings:
-hyponatremia
-hyperkalemia
-azotemia and isosthenuria
-hypochloremia
-acidosis
-hypoglycaemia (mild)
-hypercalcaemia (mild)
-normocytic, normochromic anemia (mild)
-eosinophillia and lymphocytosis (not expected in most sick dogs)
2. ACTH stim test
3. ECG changes [in order of increasing hyperkalameia] (tall, spike T waves, mild bradycardia, increased QRS duration and decreased R wave amplitude, decreased P wave amplitude, increased PR interval, loss of P wave and T wave spike=atrial standstill)

Front 52

Canine hypoadrenocorticism
-DDx

Back 52

DISTINGUISH FROM ARF (appear similar clinically and on lab tests)
-hyponatremia and hyperkalemia not specific other diseases incl: renal failure, urethral obstruction or urine leakage into abdomen; severe liver failure; severe acidosis (e.g. pancreatitis or DKA); massive tissue injury; CHF; whipworm or viral enteritis
-eosinophilia=other causes: parasitism, non-parasitic dermatological disease; mast cell tumours; eosinophilic (hypersensitivity) disorders

Front 53

Canine hypoadrenocorticism
-Tx for Addisonian crisis

Back 53

Acute:
1. catheterise and establish IV line
2. draw blood for MDB and [resting cortisol]
3. check ECG if bradycardia
4. start IV fluids (0.9% NaCl) at shock rates
5. administer ACTH (start of ACTH stim test)
6. monitor for 1 hour, monitor [K] and HR closely
7. draw blood for second [cortisol] after 1 hour
8. give hydrocortisone and dexamethasone IV
9. continue to monitor [K] an ECG, slow rate of fluid infusion

Front 54

Canine hypoadrenocorticism
-Management of stable dogs

Back 54

1. Injectible DOCP +/- prednisolone q 22 days

Front 55

Hypoglycaemia
-DDx

Back 55

1.Neonates and younger animals:
-neonatal hypoglycaemia
-juvenile-onset
2. Adults
-Insulinoma
-Insulin overdose
-non-pancreatic tumours
-HypoA
-severe liver disease
-working dog hypoglycaemia
-severe sepsis

Front 56

Hypoglycaemia
-CS

Back 56

-weakness and seizures
-hunger, tachycardia
-depression, ataxia, muscle tremors, blindness and seizures

Front 57

Hypoglycaemia
-Dx

Back 57

-blood sample in FLUORIDE OXALATE tubes

Front 58

Insulinoma
-Dx

Back 58

-hypoglycaemia (NB use correct tube!)
-fasting amended insulin: glucose ratio
-U/S and thoracic radiographs

Front 59

Insulinoma
-Tx

Back 59

-surgical exploration
-debulking of non-resectable tumours usually leads to amelioration of signs
-parenteral fluid therapy w/ 0.45% saline + 2.5% dextrose
Medical:
(if surgery not possible and metastasis suspected)
1. Dietary therapy
-small meals q 4-6h
-limit exercise
2. Glucocorticoid therapy
-antagonise actions of insulin
3. Diazoxide ($$$)
-inhibits insulin secretion and stimulates gluconeogenesis

Front 60

Acute Hypoglycaemic crisis
-Emergency therapy

Back 60

At home:
-rub honey or sugar on gums
-feed a small meal once conscious
-seek veterinary assistance immediately
At hospital:
-est venous access and start fluid therapy
-give concentrated glucose solution slowly over 5-10 minutes
-monitor [K]
-on recovery, begin frequent admin of food
-observe closely for relapse
NB: IV glucose may exacerbate signs caused by an insulinoma

Front 61

Hypocalcaemia
-causes

Back 61

-eclampsia in post parturient dog
-ethylene glycol toxicity
-post-thyroidectomy
-admin of phosphate enemas
primary hypoparathyroidism (slower onset)

Front 62

Hypocalcaemia
-CS

Back 62

depends on rate of onset
Rapid:
-lethargy, anorexia, vomiting (early)
-weakness
-muscle tremor, pain and fasciculations>>tetanic contraction
-seizures (late=severe)
Slower:
-face rubbing**
-lenticular cataracts

Front 63

Eclampsia (puerperal tetany)
-general

Back 63

-excessive loss of calcium in the milk
-small breed dogs
-1-3 days after whelping
-stress precipitates

Front 64

Eclampsia (puerperal tetany)
-Hx and CS

Back 64

-recent whelping
-initial nervousness and muscle twitching>>>tetany and seizures

Front 65

Eclampsia (puerperal tetany)
-Tx

Back 65

Medical emergency:
-IV 10% calcium gluconate by slow injection TO EFFECT
-monitor HR and rhythm during injection (auscultation and ECG) and stop if bradycardia or VPCs occur

Front 66

Hypercalcaemia
-causes

Back 66

-Lab artefact (but always repeat test(
-Hypercalcaemia of malignancy
-hypoA
-primary hyperparathyroidism
-osteomyelitis or bone neoplasia
-vit D rodenticide toxicity
-ingestion of psoriasis medication

Front 67

Hypercalcaemia
-CS

Back 67

PU/PD
-anorexia, vomiting, constipation, lethargy
-calcium urolithiasis
-pathological fractures
-soft tisse mineralisation, arrhythmias, GI signs