DISEASES OF THE
ENDOCRINE SYSTEM
PART 2
DISEASES OF THE
PARATHYROID GLANDS
HYPERPARATHYROIDISM
HYPOPARATHYROIDISM
Thyroid/Parathyroid glands
1=normal thyroid gland
2 and 3=parathyroid gland
4=enlarged thyroid gland
Parathyroid gland
 Secretion: Parathyroid hormone (PTH,
Parathormone)
 Function: ↑ plasma Ca2+ concentration
 1. ↑ osteoclast activity
 2. ↑ Ca++ absorption from GI tract
 3. ↑ Ca++ reabsorption from kidney tubules
 Hyperparathyroidism →hypercalcemia
 Hypoparathyroidism →hypocalcemia
Hyperparathyroidism
 Causes:
 1º hyperparathyroidism—adenoma or carcinoma
 2º hyperparathyroidism—poor diet; low Ca intake; renal
disease
 Clinical signs:
 Many animals show no clinical signs
 signs occur as organ dysfunction occurs
urinary/renal calculi (high plasma Ca++)
 cardiac arrhythmias, tremors (Ca++ necessary
for normal muscle contraction)
 Anorexia, vomiting, constipation
 weakness

Hyperparathyroidism
Dx:
 Routine chemistry panel


↑ blood Calcium (normal: ~8-10 mg/dl))
+/- ↓ blood Phosphorus
 PTH assay
 normal PTH: dogs ~20 pg/ml, cats ~17 pg/ml

In a normal animal: if blood Ca++ is high, PTH is low (neg feedback)

1º Hyperparathyroidism: Ca++ high, PTH elevated
 Ultrasound of neck – enlarged glands, abdomen -
uroliths
Hyperparathyroidism
Tx:
1. Surgical removal of diseased parathyroid
Other options:
2. Ultrasound-guided chemical (ethanol) ablation
3. Ultrasound-guided heat (laser) ablation
Post-Op Care:
1. Hospitalize for 1 wk; ↓PTH may predispose animal to
hypocalcemia
2. Calcium therapy (oral tabs, liquid)
3. Vit D supplements (promotes Ca intestinal
absorption)
Hyperparathyroidism
Client Info
1. Most hyperparathyroid animals show no
signs when first diagnosed
2. Run yearly chem panels on all normal,
older animals
Hypercalcemia: Other causes
 Causes
 Neoplasia (lymphoma, perianal gland
tumors)
 Renal failure
 Hypoadenocorticism
 Vitamin D rodenticide
 Drugs or artifacts
 Clinical signs vary with cause
 PU/PD, anorexia, lethargy, vomiting,
weakness, stupor/coma (severe), uroliths
Hypercalcemia
 Treatment
 Fluids: 0.9% NaCl
No Ca2+ containing fluids
 Diuretics (furosemide)
 Steroids
 Complications
 Irreversible renal failure
 Soft tissue calcifications
Hypocalcemia
Causes:
1. Puerperal Tetany (Eclampsia)—late gestation thru postpartum period
a.
b.
c.
Improper prenatal nutrition
Heavy lactation
Inappropriate Ca++ supplementation
2. Parathyroid disease
a.
b.
Inadvertent removal of parathyroid during thyroidectomy
(most common cause
1º Hypoparathyroidism (uncommon in animals)
3. Chronic renal failure—
a.
b.
Vit D normally activated in kidney
Protein-losing nephropathy results in loss of albumin-bound Ca
http://www.thepetcenter.com/gen/eclampsia.html#The_video
Hypocalcemia
Clinical Signs:
1.
2.
3.
4.
Restlessness, muscle tremors, tonicclonic contractions, seizures
Tachycardia with excitement;
bradycardia in severe cases (Ca++ is
necessary for proper muscle
contractions)
Hyperthermia
Stiffness, ataxic
Hypocalcemia
Dx:
Total serum <6.5 mg/dl
Tx:
1.
2.
3.
4.
IV infusion of 10% Ca gluconate solution
(monitor HR and rhythm during
infusion)
Diazepam (IV) to control seizures
Oral supplements of Ca (tabs, caps,
syrup)
Improve nutrition
Hypocalcemia
Client info:
Well-balanced diet; increase
volume as pregnancy progresses
2. Signs in pregnant animal is
emergency; call vet immediately
3. May recur with subsequent
pregnancies
4. Early weaning is recommended
1.
DISEASES OF THE
PANCREAS
DI A B E TE S M E L L I TUS
I N SUL I N O M A
E XO C R I N E P A N C R EA TI C
I N SUF F I C I EN C Y
Review of pancreas functions
 Long flat organ near duodenum and
stomach
 Exocrine function (the majority of the
pancreas):

Digestive enzymes
 Endocrine function – islets of Langerhans
 Alpha cells => glucagon
 Beta cells => insulin
 Delta cells => somatostatin
Pancreas
Pancreas: beta
cells
Review
 Insulin
 Moves glucose into cells to be used for energy
 Decreases blood glucose
 Glucagon
 Raises blood glucose
 Stimulates liver to release glucose
 Stimulates gluconeogenesis
 Other hormones from other glands perform
similar functions (hyperglycemic effect)
 Growth hormone
 Glucocorticoids
Insulin/Glucagon Balance
Endocrine Pancreas
 Hyperglycemia
 Definition:
Excessively high blood
glucose levels
Normal in dogs: 60-120 mg/dl
Normal in cats: 70 -150 mg/dl
Diabetes Mellitus
 Definition: Disorder of carbohydrate, fat and
protein metabolism caused by an absolute or
relative insulin deficiency
 Type I – Insulin Dependent DM – very low
or absent insulin secretory ability
 Type II – Non insulin dependent DM
(insulin insensitivity) – inadequate or
delayed insulin secretion relative to the
needs of the patient
Diabetes mellitus
Incidence:
Dogs: ~100% Type I (Insulin dependent)
Cats: ~ 50% Type I and 50% Type II
-non-insulin dependent cats
can sometimes be managed with
diet and drug therapy
Causes:
Chronic pancreatitis
Immune-mediated disease
-beta cell destruction
Predisposing/risk factors:
Cushing’s Disease
Acromegaly
Obesity
Genetic predisposition
Drugs (steroids)
Diabetes mellitus
 Age/sex:
Dogs: 4-14 yrs, females 2x more likely to be
affected
 Cats: all ages, but 75% are 8-13yrs, neutered
males most affected

Poodles, Schnauzers,
Keeshonds, Cairn Terriers,
Dachshunds, Cockers, Beagles
 Breeds:
DIABETES MELLITUS
 Pathophysiology
 Insulin
deficiency => impaired ability
to use glucose from carbohydrates,
fats and proteins
 Impaired
glucose utilization +
gluconeogenesis => hyperglycemia
Diabetes mellitus
 PATHOPHYSIOLOGY:
 Clinical
signs develop when:
 Exceeds
capacity of renal tubular cells to
reabsorb
 Dogs – BG > 180-220 mg/dl
 Cats - BG > 200-280 mg/dl
 Glucosuria
 Osmotic
develops
diuresis
 Polyuria/polydipsia
 UTI
 Suppress immune system
DIABETES MELLITUS
 SYSTEMS AFFECTED:

Endocrine/metabolic: electrolyte depletion and metabolic acidosis

Hepatic: liver failure 2° to hepatic lipidosis (mobilization of
free fatty acids to liver leads to hepatic lipidosis and
ketogenesis)

Ophthalmic: cataracts (dogs) from glaucoma

Renal/urologic: UTI, osmotic diuresis

Nervous: peripheral neuropathy in cats

Musculoskeletal: Compensatory weight loss
Diabetes Mellitus
 Clinical Signs:
 Polyuria
 Polydipsia
 Polyphagia
 Weight
loss
 Dehydration
 Cataract formation-dogs
 Plantigrade stance-cats
Diabetes in Cats: Plantigrade posture
Diabetes Mellitus: Cataracts
Increase in sugar (sorbitol) in lens causes an influx
of water, which breaks down the lens fibers
Diabetic Ketoacidosis
2 metabolic crises:
↑ lipolysis in adipose tissue → fatty acids →ketone bodies →ketoacidosis →coma
(insulin normally inhibits lipolysis)
↑ hepatic gluconeogenesis (in spite of high plasma glucose levels)
(insulin normally inhibits gluconeogenesis)
Diabetic Ketoacidosis
 Definition: True medical emergency
secondary to absolute or relative insulin
deficiency causing hyperglycemia,
ketonemia, metabolic acidosis, dehydration
and electrolyte depletion
 DM
causes increased lipolysis => ketone
production and acidosis
Diabetic Ketoacidosis
 Diagnosed with ketones in urine or ketones in blood
 Can use urine dip stick with serum.
 Clinical Signs
 All of the DM signs
 Depression
 Weakness
 Tachypnea
 Vomiting
 Odor of acetone on breath
Diabetic Ketoacidosis
 IV fluids to rehydrate 0.9% NaCl
 Regular insulin to decrease blood
glucose
 Monitor
BG q 2-3 hrs
 When BG close to normal and patient
stable switch to longer acting insulin
DIABETES MELLITUS
 DIAGNOSIS:
 CBC: normal

Biochemistry panel:


Glucose > 200 mg/dl (dogs), >250 (cats)
UA
Glucosuria!!!! (causes UTI)
 Ketonuria
 USG – low


Electrolytes may be low due to osmotic diuresis

Fructosamine levels – mean glucose level for last 2-3
weeks (dogs)
 Ideal to test for regulation checks
Treatment:
INSULIN AND DIET
Table 1. Traditional insulin outline.
Insulin types
Duration/onset
category
Concentration
Rapid acting
Regular (Humulin R)
U-100 (100 units/ml)
Intermediate acting
NPH (Humulin N)
U-100
Lente (Vetsulin® by
Intervet)
U-40 (40 units/ml)
PZI (Idexx)
U-40
Insulin Detemir
U-100
Insulin Glargine
U-100
Long acting
Diabetes Mellitus:
Insulin therapy
Diabetes Mellitus: Insulin therapy

Beef-origin insulin is biologically
similar to cat insulin:

Porcine-origin insulin (porcine lente) is biologically
similar to dog insulin

Dogs and cats have responded well to human insulin
products


protamine zinc insulin (human recombinant PZI)
Insulin Glargine: not approved for use in cats and
PZI have same duration of action
DM: Insulin therapy
 INSULIN ADMINISTRATION:
 ALWAYS
USE THE
APPROPRIATE INSULIN
SYRINGE! (U-40 vs. U-100)
 Insulin
is given in units (insulin
syringes are labeled in units, not mL)
 30 units, 50 units, 100 units
DM: dietary management
 DIET
 DOGS: high fiber, complex carbohydrate diets
 Slows digestion, reduces the post-prandial glucose
spike, promotes weight loss, reduces risk of
pancreatitis
 Hill’s R/D or W/D

CATS: high protein, low carbohydrate diets
 Cats use protein as their primary source of energy
 Purina DM, Hill’s M/D
 Often a diet change in cats can dramatically reduce
or eliminate the need for insulin

This is particularly true for type II
Diabetes Mellitus
 ORAL HYPOGLYCEMICS:
o Sulfonylureas – Glipizide: cats
o
o
Direct stimulation of insulin secretion from the pancreas
Alpha-Glucosidase Inhibitors – Acarbose
o
Delays digestion of complex carbohydrates and delays
absorption of glucose from the intestinal tract.
 Insulin is more effective than oral
hypoglycemics
Diabetes Mellitus: Monitoring
Find an ear vein
Prick the ear to get
blood sample
Place drop of blood
on green tip; readout in
a few seconds
Diabetes Mellitus monitoring:
Urine glucose
Diabetes Mellitus monitoring:
Urine glucose
Diabetes Mellitus monitoring:
Urine glucose
DIABETES MELLITUS
 Client Education
 Lifelong insulin replacement therapy
 Insulin administered by injection
 Refrigerate insulin, mix gently (no
bubbles), single use syringes
 Vetsulin
may require vigorous shaking
 Consistent
diet and exercise
 Recheck BG or curve regularly or
fructosamine levels
 if animal does not eat- NO INSULIN