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Type I diabetes mellitus
insulin dependent, decreased insulin secretion, dogs > cats
beta cell atrophy, causes - chronic pancreatitis, immune-mediated, idiopathic, vacuolar, genetic
Type II diabetes mellitus
insulin independent, insulin resistance ± decreased insulin secretion, cats > dogs
multifactorial causes
Diabetes mellitus clinical signs
caused by hyperglycemia
hepatic lipidosis, diabetic neuropathy, PU/PD
Insulinoma
beta cell tumor
ferrets common benign, dogs and cats less common malignant
hypoglycemia, weakness, seizures, collapse
Glucagonoma
alpha cell tumor
rare in all species
hyperglycemia, hepatomegaly, superficial necrolytic dermatitis in dogs
Hypothyroidism
decreased thyroid hormone production → hair follicle cycle slows → predominance of telogen phase → friction alopecia
dogs > cats
dogs - lymphocytic thyroiditis or idiopathic atrophy
cats - iatrogenic
Goiter
thyroid hyperplasia
Causes - ingestion of goitrogenic compounds, deficient dietary iodine, excess dietary iodine, congenital
large animals, fish > others
neonates - dystocia, prolonged gestation, weakness, high mortality rate
Cat hyperthyroidism
adenomatous hyperplasia, adenomas > carcinomas
unilateral or bilateral, functional
hyperthyroid associated cardiomyopathy
Dog hyperthyroidism
carcinomas > adenomas
unilateral or bilateral, nonfunctional, expansile and invasive
early metastasis to lungs
Heart based tumors in dogs
thyroid carcinoma, hemangiosarcoma
chemodectoma - brachycephalics, benign, incidental, expansile
C-cell hyerplasia/neoplasia
high Ca → hypercalcemia → C-cell hyperplasia → neoplasia
dairy bulls, horses > dogs
often incidental
Hypoparathyroidism
Decreased PTH
Idiopathic parathyroiditis, surgery, secondary destruction - decreased Ca
Vitamin D toxicosis - increased Ca → metastatic mineralization
Hyperparathyroidism
Increased PTH, Ca and P variable
Clinical signs - vomiting/anorexia, PU/PD, generalized muscle weakness/lethargy, fibrous osteodystrophy
Primary - dogs > cats, horses, Increased serum PTH and Ca, Decreased P
Secondary nutritional hyperparathyroidism
low Ca diet, high P diet, vitamin D deficiency
Chief cell hyperplasia - increased PTH, variable P and Ca
Secondary renal hyperparathyroidism
Decreased GFR → increased P → increased PTH → chief cell hyperplasia
Decreased calcitriol → decreased calcium → increased PTH → chief cell hyperplasia
Metastatic mineralization
Pseudohyperparathyroidism
Humoral hypercalcemia of malignancy
Normal PTH, increased PTHrp → increased Ca and decreased P
Common in lymphoma, AGASACA, SCC
Juvenile panhypopituitarism
pituitary dwarfism
dogs >> others, german shepherds - genetic component, signs around 2mo
Cyst, usually in pars distalis → compression → atrophy
Stunted growth, abnormal dentition, open epiphyseal lines, puppy coat → alopecia
Decreased TSH/ACTH → death
Diabetes insipidus
Central - pituitary dependent - damage to pars nervosa, Decreased ADH → PU/PD, Dogs >> others
Nephrogenic - kidneys can’t respond to ADH
Pars distalis hyperplasia
Dog, rats > others, adenomas most common
Dogs - increased ACTH → adrenocortical hyperplasia bilateral → increased cortisol
Rats - increased prolactin → mammary gland hyperplasia/neoplasia
Pars intermedia hyperplasia
Horses - pituitary pars intermedia dysfunction → not equine Cushing’s
Increased beta-endorphins → docile, unresponsive to pain
Compression of hypothalamus → Hirsutism, hyperpyrexia, polyphagia
Compression of pars nervosa → PU/PD
Idiopathic adrenocortical atrophy (Addison’s)
Dogs, middle-aged females >> others
All 3 layers affected, bilateral
Addisonian crisis - decreased mineralocorticoids → increased K and decreased Na → PU/PD → hypovolemia, bradycardia → shock
Hypercortisolism (Cushing’s )
Pituitary dependent - functional pituitary tumor, Most cases, Increased ACTH → increased cortisol
Adrenal dependent - functional adrenal tumor, Dogs > cows, hamsters > others, Middle-aged, geriatric, Adenomas > others, Contralateral atrophy
Iatrogenic - steroid administration
Clinical signs - follicular inactivity leading to alopecia, catabolic effects leading to thin skin and muscle atrophy, hepatomegaly, panting, PU/PD
Medulla pheochromocytoma
Dogs, ferrets > horses, cows, clouded leopards, Catecholamines
Weakness, tachypnea/tachycardia, arrhythmias, hypertension
Exocrine pancreatic insufficiency (EPI)
Pancreas doesn’t make enough digestive enzymes → maldigestion and malnutrition
Clinical signs at >90% damage
Polyphagia, weight loss with muscle wasting, increased fecal volume, frequent defecation
diagnosis - decreased TLI
causes - pancreatic acinar atrophy, chronic pancreatitis, obstruction of pancreatic duct by space-occupying mass
Pancreatic acinar atrophy
most common cause of EPI in dogs, clinical signs 6-36 mo
breeds - German shepherd, rough-coated collies, eurasians
may be autoimmune-mediated disease targeting acinar cells
Pancreatic exocrine nodular hyperplasia
Dogs, cats, cattle, Incidental finding
Cause - age-related, regenerative response to injury
Grossly - multifocal raised, small, pale tan, well-circumscribed hyperplastic nodules
Exocrine pancreatic adenoma
Rare, often clinically silent
Local compression may result in atrophy or pancreatitis
Usually single/solitary, multiple with nodular hyperplasia, well-demarcated and encapsulated
Exocrine pancreatic adenocarcinoma
Most exocrine pancreatic tumors malignant, aggressive, Older dogs and cats
Clinical signs - abdominal pain, vomiting, weight loss, abdominal mass, +/- jaundice, +/- ascites
Often advanced by time of diagnosis - Marked local tissue invasion, Transcoelomic (intraperitoneal) metastasis, Metastasis to lung, liver, spleen, kidney
Acute necrotizing pancreatitis
Dogs, cats, horses, pigs - mainly dogs
Dogs - lethargy, anorexia, vomiting, diarrhea, fever and signs of abdominal pain
Severe cases - shock, DIC, sudden death
Risk factors - middle to older age, obese, female, small breed, high-fat diet, dietary indiscretion, underlying endocrinopathy, trauma, drugs, toxins, infectious disease
Diagnosis - leukocytosis, PLI, TLI, lipase, amylase
Pathogenesis - autodigestion of the pancreas from premature activation of pancreatic enzymes, self-destructive and self-perpetuating
Grossly - hyperemia, hemorrhage and necrosis, fibrinosuppurative exudation, peripancreatic fat necrosis, fibrinous adhesions to adjacent structures and omentum
Outcomes of acute necrotizing pancreatitis
Trypsin inhibitors inactivate trypsin → mild, self-limiting disease
Trypsin activates additional proenzymes → autodigestion cascade and acute clinical pancreatitis → severe disease or recurring bouts of pancreatitis
Severe disease - inflammatory mediators and activated digestive enzymes → shock, respiratory distress, DIC, death
Repeated bouts of pancreatitis → fibrosis and atrophy → EPI and diabetes mellitus
Chronic pancreatitis
Recurrent, intermittent attacks → morphologic and functional destruction of the gland
necrotic/inflamed foci → liquefied, sequestered or replaced by fibrous connective tissue → loss of pancreatic parenchyma + fibrosis → reduces functional pancreatic mass → EPI or diabetes mellitus
Gross lesions - small, shrunken, firm and nodular pancreas due to fibrosis
Microscopic - loss of pancreatic acini with replacement by fibrous connective tissue
Equine pancreatitis
Clinical signs - colic +/- shock
Pathogenesis - severe strongyle infestation → migration of larvae through pancreas → eosinophilic granulomas and/of fibrosis → pancreatitis
Sequelae to pancreatitis
Bile duct obstruction → post-hepatic jaundice
Anorexia and vomiting → hepatic lipidosis in cats
Hepatic necrosis → activated enzymes → autodigestion of adjacent liver → elevated liver enzymes
Peripancreatic fat necrosis - saponification
Severe acute pancreatitis → +/- temporary diabetes mellitus
Chronic pancreatitis → +/- permanent diabetes mellitus
Liquefactive necrosis of pancreas → pseudocyst formation, ascending bacterial infection leading to abscess
Peripancreatic inflammation (peritonitis) → peripancreatic fibrous adhesions