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3. Sys Path 2 > Endocrinology 3 The endocrine pancreas > Flashcards

Endocrinology 3 The endocrine pancreas Flashcards

1
Q

Islets of Langerhans:
- endocrine-involved cells and what they produce

A
  • alpha cells -glucagon
  • beta cells –insulin
  • delta cells - somatostatin
  • F cells -pancreatic polypeptide
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2
Q

pancreas response to low blood glucose

A
  • glucagon released by alpha cells of pancreas
    > liver releases glucose into blood
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3
Q

pancreas response to high blood glucose

A
  • insulin released by beta cells of pancreas
    > fat cells take in glucose from blood
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4
Q

effects of insulin in skeletal muscle, liver, and adipose tissue

A

skeletal muscle:
- increase amino acid reflux
- increase protein synthesis
- increase glycogen synthesis
<><>
liver:
- decrease gluconeogenesis
- increase lipgenesis
- increase glycogen synthesis
<><>
Adipose tissue:
- decrease lipolysis
- increase lipogenesis

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5
Q

Diabetes - primary
- Type 1 vs type 2

A

Type I (Insulin Deficient Diabetes, IDD) = loss of b cells, young to middle age, fairly sudden onset, dependent on insulin treatment (insulin-dependent diabetes mellitus, IDMM)
<><><><>
Type II (Insulin Resistant Diabetes, IRD) = insulin resistance of tissues and/or “dysfunctional” b cells,
gradual onset, may be non-insulin dependent for a while

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6
Q

Secondary hyperglycemia (diabetes)
- causes

A
  • Carbohydrate intolerance secondary to insulin antagonists (epinephrine, cortisol, glucagon, growth hormone)
  • Transient diabetes that may resolve or become sub- clinical
  • High progesterone states i.e.diestrus in the dog, or cats treated with megesterol acetate
  • Gestational diabetes
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7
Q

Type I diabetes
- what is it in people?
- is it common in dogs?
- age?
- breeds?
- association to other conditions?

A
  • People: genetics + environmental factors > immune- mediated insulitis > impaired insulin secretion > overt diabetes with complete b cell destruction.
  • Virtually all canine diabetes is type I, onset middle age
  • Genetic predisposition - Keeshonds, Cairn terriers, Min. Pinscher, Min. Schnauzers, dachshunds, small poodles
  • Role of pancreatitis in dogs?
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8
Q

Type II diabetes
- how common? in cats?
- pathogenesis
- associations?

A
  • 30-50% of feline DM is non- or variably insulin-dependent
  • Likely pathogenesis: muscle and adipose tissue are glucose intolerant due to obesity or concurrence of GH hypersecretion > chronic over-secretion of insulin > co- secretion of islet amyloid polypeptide (IAPP) > transformation to insoluble amyloid > partial or complete destruction of b cells
  • Strong association of typeII DM with obesity in cats (and people)
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9
Q

Type II diabetes
Pathophysiology:

A

Downregulation of insulin receptors, decreased affinity of receptor for insulin, reduced action of intracellular insulin in obesity
= carbohydrate intolerance

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10
Q

Glucose tolerance test in type II diabetes –

A
  • In healthy cats, injection of a bolus of glucose causes a rapid release of insulin from pancreatic islets, which quickly returns the blood glucose concentration to normal limits.
  • In cats with subclinical (pre-diabetic) type II diabetes and insulin resistance, injection of a bolus of glucose causes a delayed and greater release of insulin, which corresponds to a longer period of hyperglycemia.
  • Cats with insulin resistance usually overproduce insulin for months to years before they are diagnosed as diabetic.
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11
Q

Diabetes
Pathophysiology (type I)

A
  • Insulin deficiency results in decreased tissue utilization of glucose, amino acids, and fatty acids.
  • Persistent glucosuria develops once plasma glucose >10-12 mmol/L (dog) and >16 mmol/L (range 11-18) (cat)
  • Persistent hyperglycemia
  • Osmotic diuresis = PU/PD
  • Lack of satiety response from cells in hypothalamus = polyphagia
  • Metabolism of protein and fat = weight loss
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12
Q

Diagnosis of diabetes
- signalment
- history
- PE

A
  • Signalment: female dogs and male cats slightly more frequently affected
  • History: polydipsia/polyuria, polyphagia, weight loss, sudden blindness (cataracts), ketoacidotic crisis
  • Physical exam: Hepatomegaly, neuropathy
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13
Q

Diagnosis of diabetes mellitus
- lab abnormalities

A
  • Hyperglycemia & glucosuria
  • Increased liver enzymes
  • Increased pancreatic enzymes - pancreatitis
  • Azotemia – rare
  • Hyperlipidemia - increased lipolysis, decreased lipoprotein lipase activity
  • Urinary tract infection - glucosuria, proteinuria, pyuria
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14
Q

Differential diagnosis of hyperglycemia:

A
  • DM (has glucosuria)
  • Stress (cat) – epinephrine-induced, may be as high as 22 mmol/L, generally no glucosuria
  • HAC – insulin antagonism of glucocorticoids
  • Pancreatitis – glucose commonly <15 mmol/L
  • Acromegaly – GH secreting pituitary tumor (cats)
  • Diestrus, pheochromocytoma, postprandial
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15
Q

Diagnosis of diabetes
- steps we should follow

A
  1. Establish diagnosis of DM from general laboratory data.
  2. Differentiate IDDM from NIDDM: severity of hyperglycemia, presence of ketoacidosis, response to insulin administration
  3. Specific tests: rarely needed
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16
Q

Diagnosis of diabetes
Intravenous glucose tolerance test (IVGTT, rarely needed):

A
  1. 24 hr hospital acclimatization
  2. IV catheter
  3. Fast overnight
  4. Baseline blood sample
  5. Administer 0.5 g of 50% dextrose/kg body weight iv over 30 sec
  6. Blood samples for glucose and insulin determination at 1, 5, 10, 20, 30, 45, 60, 90 and 120 min.
17
Q

Glucose/insulin curve

A
  • Concurrent glucose and insulin measurements over 24 hours to assess the response to insulin
  • Measurement of insulin by RIA > needs to be validated for species
  • Human and dog insulin almost identical, therefore human kits work well in dogs
  • Cat insulin different from dog and human, only a few kits designed for humans work with cat samples
18
Q

Glycated proteins
1. Glycosylated hemoglobin (gHb, HbA1c):
- what it tells us

A
  • insulin-independent binding of glucose to hemoglobin in red blood cells
  • expressed as % of total hemoglobin
  • consider hematocrit and red cell lifespan for interpretation
  • not readily available for animals but mainstay of long-term monitoring in people
    <><><><>
  • RBC life span: 60-70 days in the cat, ~120 days in the dog
  • Therefore: amount of gHb indicates glycemic control over 2-4 months
19
Q

Glycated proteins
2. Fructosamine
- what is this?
- what can we learn from blood levels?
- things that can interfere

A
  • Generic name for glycated serum proteins (ketoamines)
  • Mainly albumin; not all serum proteins are susceptible to glycation
  • Reflects glycemic control over 2-4 week period (T1/2 of albumin)
  • Automated colorimetric assay
  • Interference with severe hypoalbuminemia and hypertriglyceridemia
    > Glycated protein concentration is not influenced by transient hyperglycemia.
20
Q

Diabetic ketoacidosis
- pathogenesis

A

insufficient of absent insulin
- cells are starving for glucose > breakdown of protein, fat, and glycogen
<><>
> increased glucagon
> fat cells mobilized: glycerol, fatty acids
> muscle cells break down into amino acid constituents
> all of this stuff plus other substrates moves to the liver
> glycogenolysis, gluconeogenesis, ketogenesis
<><>
- increased ketone and glucose production
> increased ketone and glucose in bloodstream
> Osmotic diuresis, acidosis ketonuria, glucosuria
> dehydration
> Hypovolemia, acidosis, shock

21
Q

“Ketone bodies”
- what are they?
- tests?

A
  • acetoacetate > acetone, beta-hydroxybutyrate
    <><><><>
  • Ketone bodies are produced by the liver from fatty acids and some amino
    acids, and used as an energy source when glucose is not available (diabetes).
  • Most ketone tests detect mainly acetoacetate, to a lesser degree acetone, and no b-hydroxybutyrate, although the latter is the main product during ketosis.
22
Q

Diabetic ketoacidosis (DKA)
- pathophysiology

A
  • Hyperglycemia and glucosuria > osmotic diuresis and concomitant electrolyte loss
  • Accumulation of ketone bodies > metabolic acidosis
  • Nausea and/or vomiting > exacerbation of ketone production and acidosis
  • Increase in plasma osmolality > cellular dehydration > cerebral edema
  • H+-K+ shift leading to whole body hypokalemia
23
Q

Pancreatic endocrine neoplasms

A
  1. Insulinoma
  2. Gastrinoma
  3. Glucagonoma
24
Q

Insulinoma
- what is this?
- how bad? effects?
- diagnosis?

A
  • Tumor of pancreatic b cells
  • Insulin production
  • Malignant tumors – metastasis common at the time of diagnosis
  • Release of insulin despite hypoglycemia > weakness, seizures
    <><><><>
    Diagnosis: fasting hypoglycemia (<3.3 mmol/L) with normal or high insulin concentration
25
Q

Differential diagnosis for hypoglycemia:

A
  • hepatic portosystemic shunt
  • severe liver disease
  • hypoadrenocorticism
  • tumors producing hypoglycemic substance (hepatic or intestinal tumors)
  • sepsis
26
Q

Insulinomas in ferrets
- common?
- same presentation as what other condition
- can it be cured?

A
  • The most common tumor in ferrets!
  • Same clinical presentation due to hypoglycemia
  • But not as malignant as in dogs … surgery is often curative
27
Q

Gastrinoma
- what is this?
- effects?
- clinical signs
- dx
- prognosis

A
  • Gastrin in adult life is produced by
    gastric and intestinal epithelial cells
  • Gastrin causes excessive gastric acid secretion
  • Animals and persons with overproduction of gastrin have Zollinger-Ellison syndrome: vomiting, diarrhea, GI ulceration and pancreatic mass
  • Diagnosis: basal gastrin concentration (reliable) and gastrin stimulation tests
  • Prognosis: poor, metastasis common
28
Q

Glucagonoma
- what is it
- species
- what happens
- clinical signs

A
  • Tumor of pancreatic α cells
  • Dogs only
  • Superficial necrolytic dermatitis due to low blood amino acid concentration
  • Increased glucagon > gluconeogenesis, glycogenolysis, ketogenesis
  • Mild DM, venous thrombosis, glossitis/stomatitis, diarrhea
  • Metastasis?
29
Q

parathyroid gland - what does it do?

A

secretes parathyroid hormone (in response to low serum Ca)
- acts on kidney: 25-hydroxyvitamin D > 1,25-dihydroxyvitamin D > increased calcium absorption in the GI tract
- acts on bone > increased bone resorption
> overall, acts to increase serum Ca > negative feedback to secrete less PTH

30
Q

Hyperparathyroidism effects on kidney and bone, overall

A

Kidney:
­- increased re-absorption of Ca
- decreased re-absorption of P
- increased production of active
cholecalciferol
> Intestine: increased Ca and P absorption
<><><><>
Bone:
­- increased osteoclast activity, bone resorption > increased Ca and P
<><><><>
- Hypercalcemia = BAD!
> Kidney disease, soft tissue mineralization, GI abnormalities, ‘feeling bad’

31
Q

Calcitonin:
- where does it come from, what does it do?

A
  • Produced by parafollicular C cells in the thyroid gland in response to hypercalcemia.
  • Decreases bone re-sorption – limited effect
  • No effect on kidney or intestine.
32
Q

Hyperparathyroidism
- usual causes
- presentation, signs

A
  • Most commonly due to autonomously secreting adenoma of “chief” cells in parathyroid glands
  • Adenomas are rarely palpable in dogs
  • If palpable > consider carcinoma
  • Adenomas palpable in 50% of cats
  • Keeshond more commonly affected?
  • Presenting signs: non-specific, PU/PD, weakness
33
Q

Hyperparathyroidism dx

A

Diagnosis (fairly straightforward)
1. Marked and persistent hypercalcemia
2. Low or low-normal serum P concentration
3. Increased serum PTH “2-site” (intact) assay

34
Q

Hypercalcemia
Differential diagnosis:

A
  1. Hypercalcemia of malignancy
    - marked hypercalcemia and low to normal P concentration, low PTH concentration
  2. Chronic renal failure
    - variable serum Ca, normal or high P, low to normal Ca++, high PTH
  3. Hypervitaminosis D (cholecalciferol toxicosis)
    - hypercalcemia and hyperphospatemia
  4. Hypoadrenocorticism, nutritional 20 hyperparathyroidism, systemic mycotic disease
35
Q

Hyperparathyroidism in cats
- signs

A
  • Mass often palpable
  • PU/PD uncommon
  • Consistent marked hypercalcemia and hyperparathyroidemia, variable hypophosphatemia
36
Q

hyperparathyroidism in reptiles

A

Diet high in P and low in Ca > secondary hyperparathyroidism > removal of Ca from bones > fibrous dystrophy and pathologic fractures

37
Q

Hypoparathyroidism
- common?
- cause?
- age, sex…
- history

A
  • Uncommon disease
  • Cause? Likely autoimmune mechanism of destruction
  • Young to old animals affected, no sex predilection in dogs, but males more commonly in cats
  • History: abrupt neuromuscular abnormalities (seizures, tetany, facial rubbing, muscle fasciculations)
38
Q

Hypoparathyroidism Dx

A

Diagnosis:
* Persistent severe hypocalcemia and hyperphosphatemia in the absence of azotemia
* Undetectable serum PTH concentration with hypocalcemia

39
Q

Differential diagnosis for hypocalcemia:

A
  • Iatrogenic following thyroidectomy
  • Chronic renal failure (clinically silent)
  • Hypoalbuminemia
  • Acute pancreatitis
  • Ethylene glycol toxicity

3. Sys Path 2 (47 decks)

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