Endocrine- Pancreas Pathology

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  1. Glucagon _________ insulin; insulin ________ glucagon.
    stimulates; inhibits
  2. Glucagon _________ somatostatin; somatostatin _________ glucagon.
    stimulates; inhibits
  3. Juvenile onset of hypofunction of pancreatic islets is __________, characterized by... (2)
    type I diabetes mellitus; lack of beta cells and insulin
  4. Type I DM is ________, making patients prone to _________.
    insulin-dependent; ketosis
  5. Type I DM is initiated by a ___________ combined with _______ to... (3)
    genetic predisposition; viral exposure; coxsackievirus, mumps, rubella (induces immune reaction against islets)
  6. Type I DM is seen in ________ (vetmed); it initially steams from __________ destruction of islets.
    keeshond pups; immune-mediated lymphocytic inflammatory
  7. Inherited DM in Keeshonds exhibits __________ inheritance; clinical signs include... (5)
    autosomal recessive; stunted growth, hyperglycemia, hypercholesterolemia, hypoinsulinemia, normal blood glucagon
  8. Why does Type I DM lead to stunted growth in keeshond pups?
    hypoinsulinemia causes decreased protein anabolism and decreased AA uptake by muscle cells
  9. Type II DM is ________; insulin conc is ________ and blood glucose is _________.
    insulin-independent; normal to increased; increased
  10. Describe the condition of pre-diabetes.
    increased insulin, normal blood glucose; beta cells are hyperfunctioning trying to overcome insulin resistance
  11. Type II DM is characterized by _________.
    insulin resistance
  12. ______  (species) are very prone to type II DM.
    Cats
  13. Horses often have pre-diabetes/metabolic syndrome associated with ________.
    PPID
  14. What is the primary mechanism of insulin resistance with type II DM? What are its repercussions in the patient? (3)
    down-regulation of insulin receptors; obesity, cortisol/GH excess, damage to pancreas
  15. When is accelerated insulin degradation a major source of insulin resistance?
    gestational diabetes
  16. What is unique about rat islets?
    rat islets can proliferate beta cells, leading to higher production of insulin--> makes rats less susceptible to Type II DM
  17. What is the current theory on betatropin gene function?
    stimulates insulin secretion and beta cell hyperplasia in rats
  18. What is the progression to type II DM?
    insulin resistance--> beta cells make more insulin to overcome--> stress on beta cells--> death/atrophy of beta cells
  19. How has the degeneration of islets been described in diabetic cats?
    early on, islets swell; then, islets become vacuolated, vacuoles contain glycogen; finally, glycogen degeneration of the islets
  20. What processes play a role in islets atrophy in type II DM? (3)
    degeneration of islet cells, inflammation, macrophages
  21. In cats, ________ may predispose them to type II DM.
    amyloidosis
  22. Amyloidosis is a(n) _________ lesion in cats.
    age-related
  23. What is the most common islet lesion in cats with clinical diabetes?
    amyloidosis
  24. Amylin lowers _________ and increases _________.
    glycogen synthesis; hepatic glucose output
  25. Type III DM involves _________ of islets due to... (5)
    destruction; [chronic] chronic pancreatitis or cancer of exocrine pancreas, [acute] pancreatitis with hemorrhage and necrosis
  26. Chronic relapsing pancreatitis ultimately leads to... (4)
    necrosis, fibrosis, atrophy, type III DM
  27. What are secondary lesions associated with DM? (5)
    weight loss, cystitis, skin infections, liver cirrhosis, cataracts
  28. Describe cataracts associated with DM. (3)
    bilateral opacity of lens, asteroidal, diffuse
  29. Diabetic hepatomegaly occurs because lack of insulin leads to __(2)__; also, there is toxic injury due to ___________.
    lipolysis, increased mobilization of fat; hyperketonemia
  30. What are the 2 components of cirrhosis of the liver due to DM?
    fibrosis and regenerative hyperplasia
  31. Cirrhosis of the liver is a sequelae to __________.
    chronic fatty liver necrosis
  32. Pancreatic endocrine tumors are usually _________, ie. _________.
    beta cell adenoma; functional insulinoma
  33. Insulinoma may result in the following functional disturbances... (2)
    convulsive seizures due to hypoglycemia (exercise or fasting), favorable response to exogenous glucose
  34. Pancreatic endocrine tumors occur most commonly in... (3)
    dogs, ferrets, cattle
  35. Pancreatic endocrine tumors are usually _________ carcinomas with a __________ that may take years to develop.
    well-differentiated; high incidence of metastasis
  36. Clinical signs of insulinoma in ferrets. (6)
    weight loss, pytalism, muscle tremors, hind limb weakness, hypoglycemia, hyperinsulinemia
  37. In ferrets insulinoma has a ______ of metastasis and a high incidence of...
    low; recurrence in the pancreas after excision.
  38. Insulinoma in cattle is often found at slaughter as distant metastases in the _______ and ________.
    regional lymph nodes; liver
  39. You see white nodules in the pancreas of an aged cat upon necropsy/exploratory surgery. What's going on?
    exocrine nodular hyperplasia- common aging change, ESP in cats- NOT NEOPLASIA
  40. DM is a relative or absolute _____________, resulting in... (3)
    insulin deficiency; chronic hyperglycemia, abnormal fat/protein metabolism, and damage to various organs.
  41. DM etiology has a spectrum from __________ to __________.
    pure insulin resistance; complete lack of insulin production
  42. In order to diagnose DM, hyperglycemia must be documented __________ and best must be done to rule out _________ in cats.
    consistently; stress hyperglycemia
  43. What are the consequences of hyperglycemia? (4)
    glucose toxicity, cataracts, peripheral neuropathy, PU/PD
  44. PU/PD with DM is caused by ___________.
    osmotic diuresis
  45. Inability of peripheral tissues to use glucose leads to reliance on ________ and _________ as energy sources.
    FFAs; ketones
  46. Insulin deficiency leads to ________ in adipose tissue, _______ of fat, and _________. This leads to an immediate increase in serum __(2)__ and _________.
    lipolysis; breakdown; weight loss; FFA and cholesterol; fatty liver
  47. Insulin deficiency leads to decreased ____________, leading to muscle breakdown and __________.
    protein anabolism; weight loss
  48. How does insulin deficiency lead to polyphagia?
    satiety center in the brain has insulin dependent mediated uptake of glucose
  49. A decrease in the insulin:glucagon ratio in the liver leads to increased __________.
    ketone production
  50. Clinical signs/hallmarks of insulin deficiency. (4)
    polyuria, polydipsia, polyphagia, weight loss
  51. Diabetic _____ WILL develop cataracts; diabetic ______ usually do not.
    dogs; cats
  52. 75% of diabetic dogs will develop cataracts within _______ of diagnosis.
    1 year
  53. Glucose enters the lens freely; in a normal individual, it's used for energy; in a diabetic, the ________ is saturated, and glucose is metabolized through the _________ to __(2)__.
    glycolytic pathway; polyol pathway; fructose and sorbitol
  54. __(2)__ are not freely permeable in the lens and lead to _________ of lens fibers and _______.
    Fructose and sorbitol; swelling/rupture; cataracts
  55. Diabetic peripheral neuropathy is common in ________; it often presents as _________ with ___________.
    diabetic cats; plantigrade posture; hocks touching the ground
  56. Etiologies of DM. (4)
    inherited beta cell aplasia, beta cell destruction (drugs, viruses, pancreatitis, autoimmune), beta cell dysfunction, insulin resistance
  57. Type I DM results from _________ and loss of_________; there is often a _________; breed predisposition is ___________; ___________ breed are at low risk.
    autoimmune destruction; beta cells; genetic predisposition; terriers/small dogs; large breed/boxers
  58. Diabetic dogs are usually classified as __________ because most dogs are _______ at diagnosis.
    Type I DM; insulin-dependent DM
  59. In dogs, there is frequently an associated with DM and __________, which is _________.
    pancreatitis; Type III DM
  60. Type II DM is characterized by __________ and __________.
    beta cell dysfunction; insulin resistance
  61. Type II DM has a strong association with ________.
    visceral obesity
  62. Risk factors for type II DM include __(2)__.
    decreased physical activity, genetics
  63. Onset of Type II DM is usually ________ in life.
    mid to late
  64. Amyloid deposition occurs in ________ and affects beta cells by ________.
    cats and people; damaging them
  65. The proinsulin:insulin ratio is _________ in Type II DM and is an early marker of _________.
    increased; beta cell dysfunction
  66. Decreased proinsulin conversion to insulin may predispose to ____________.
    amyloid deposition
  67. In type II DM, insulin secretion is always at least ________ and in late disease is _________.
    relatively decreased (relative to hyperglycemia); absolutely decreased
  68. A key feature of type II DM, there is decreased sensitivity of _______ to _______ and defects in the _________, leading to decreased __(2)__.
    beta cells; glucose; incretin effect; GIP and GLP-1
  69. Glucose toxicity results from ___________; it causes... (4)
    chronic persistent hyperglycemia; impaired insulin secretion, down-reguation of glucose transport, beta cell injury/death, overt diabetes
  70. What populations of cats are at greater risk for type II DM? (6)
    male, neutered, obesity, old age, decreased physical activity, glucocorticoid and progestin administration
  71. Most cats are first presented as ________.
    insulin-dependent DM
  72. Insulin deficiency is present but it is typically not an _________, rather ___________.
    absolute deficiency; relative to the degree of insulin resistance
  73. In healthy individuals, insulin resistance results in...
    compensatory response and increased capacity to secrete insulin.
  74. In diabetic individuals, insulin resistance leads to...
    an abnormality in beta cells that does not allow an appropriate compensatory response.
  75. Insulin resistance occurs when a given concentration of insulin produces...
    less biologic response than normal.
  76. Physiologic causes of insulin resistance. (5)
    circulating insulin antagonists (counterregulatory hormones, cytokines), target tissue defects (receptor defects)
  77. Lifestyle causes of insulin resistance. (3)
    obesity, inflammation, stress
  78. Results of insulin resistance in the liver. (1)
    increased glucose output
  79. Results of insulin resistance in muscles/fat. (1)
    decreases glucose uptake
  80. Results of insulin resistance in the pancreas. (4)
    increased beta cell mass, increased insulin resistance, increased stress on beta cells, damage/death of beta cells
  81. If the pancreatic response to insulin resistance is normal, it results in _______ and ________ [insulin].
    euglycemia; increased
  82. If the pancreatic response to insulin resistance is abnormal, it results in _________ and ________ [insulin].
    hyperglycemia; slightly increased-low
  83. More obscure causes of DM. (4)
    endocrinopathy, drugs, gestation, pancreatitis

Card Set Information

Author:
 Mawad
ID:
 307552
Filename:
 Endocrine- Pancreas Pathology
Updated:
2015-09-10 02:31:07
Tags:
vetmed pancreas pathology endocrinology
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Description:
vetmed endocrinology
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