Endocrine 3 – Pancreas Flashcards

1
Q

Main pancreatic outputs

A
  • Exocrine: >90%
  • Endocrine islets: 10%
    o Beta-cells (60-70%): insulin
    o Alpha-cells (20%): glucagon
    o Delta-cells (5%): somatostatin
    o Pancreatic polypeptide cells (10%)
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2
Q

Hypoglycemia

A
  • *young animals=big issue
  • Impair brain function: potentially causing seizures, coma and death
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3
Q

Type I diabetes mellitus

A
  • Insulin-dependent (“Juvenile”)
  • Destruction of beta-cells with progressive loss of insulin secretion
    o Insulin required for life after diagnosis
  • May present with KETOACIDOSIS
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4
Q

Type II diabetes mellitus

A
  • Develops due to insufficient insulin secretion relative to metabolic demand
  • *most common form in humans and CATS
  • Middle to older cats
  • *usually a gradual presentation
    o Insulin resistance and/or dysfunction of beta cells
    o Resistance is often secondary to obesity
  • Start with a little bit of insulin and then become dependent on it
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5
Q

Islet amyloid polypeptide (IAPP): amyloidosis

A
  • Produced by pancreatic beta-cells
  • Co-processed with insulin in response to glycemia
  • *Common in obese cats, but does NOT mean they have diabetes
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6
Q

What are the top causes of secondary diabetes mellitus

A
  • *1. Dogs and cats with chronic, relapsing pancreatitis (ex. get pancreatic atrophy)
    o Destruction=leads to Type 1 DM
  • *2. HIGH CORTISOL
    o Dogs with Cushing’s
    o Chronic steroid therapy
    1. Cats with GH excess (GH secreting pituitary tumor)
    1. Glucagon (glucagonomas)
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7
Q

What are the lesions with diabetes mellitus?

A
  • PU/PD/PP
  • Weight loss, weakness
  • Hepatic lipidosis: cats need to be overweight and anorexic
  • Increased omental fat and TG formation
  • *cataract=dogs
  • Blood vessels: glomeruli highly susceptible to damage
  • Peripheral demyelinating neuropathies occasionally seen: toe amputation
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8
Q

Cushing’s and DM

A
  1. Cushing’s can induce secondary DM
  2. Cushing’s can complicate treatment of primary DM
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9
Q

Adrenal diabetes

A
  • Increase gluconeogenesis and decrease glucose use LEADS TO secretion of insulin LEADS TO adrenal diabetes
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10
Q

Steroid hepatopathy

A
  • Increased cortisol: decrease glucose usage, increased glycogen storage
  • Diffusely enlarged at least 50%
  • Histo: light colour=glycogen accumulation
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11
Q

Hepatic lipidosis

A
  • Yellow
  • Floats in formalin
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12
Q

Beta cell neoplasms=insulinomas

A
  • *mostly in adult dogs and ferrets
  • Often functional: producing excess insulin
  • Adenomas are encapsulated
  • Carcinomas: larger with features of malignancy and may metastasize
  • Clinical: high serum insulin, low blood glucose and one ore more nodules on pancreas (often present with seizures)
  • *single discrete tumor
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13
Q

Glucagonomas

A
  • Rare (maybe dogs)
  • Produce excess glucagon
    o Secondary DM
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14
Q

Gastrinomas

A
  • Rare (dogs and cats)
  • APUD cells in pancreas
  • Produce excess gastrin: gastric ulcers
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15
Q

Pancreatic nodular hyperplasia

A
  • EXOCRINE hyperplasia
  • Multifocal and very common
    o Usually moderate (some are extreme)
  • Variable fibrosis from damage
  • *may develop DM due to destruction
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16
Q

Aortic body carcinoma OR chemodectoma

A

diagnosis made via histo between these 2

17
Q

Ferrets: common PM findings, diseases

A
  • Lymphosarcoma: spleen or lymph nodes
  • Adrenal tumors: *excrete estrogen (ex. alopecia: hair loss) LEFT
  • Insulinoma: drop in blood glucose, weak
  • Gastric ulcers
  • IBD
  • Cyst: RIGHT (still get estrogen excretion)
  • Choroma: tumor at end of tail