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Zak, Endo/Repro 2 > Endocrine Pancreas Pathology > Flashcards

Endocrine Pancreas Pathology Flashcards

1
Q

Which ethnicities are more likely to develop DM?

A

Native Americans
African Americans
Hispanics

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2
Q

What are the criteria for Dx of DM?

A

Fasting glucose ≥ 126
Random glucose ≥ 200
2-hour glucose ≥ 200 during OGTT
HbA1C ≥ 6.5%

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3
Q

What is the pathogenesis of DM1?

A

Islet cell destruction caused by immune effector cells reacting against endogenous ß-cell Ags

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4
Q

What are the potential autoAg targets in DM1?

A

Insulin
ß-cell enzyme Glutamic Acid decarboxylase (GAD)
Islet cell autoAg 512 (ICA512)

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5
Q

What HLA’s are associated with DM1?

A

HLA-DR3, HLA-DR4

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6
Q

Which other HLA mutation gives the highest risk for DM1?

A

HLA-DR8

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7
Q

Which chromosome are the HLA’s on for DM1?

A

Chrom 6p21

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8
Q

Which polymorphisms are seen in DM1?

A

CTLA4
PTPN22
AIRE
Wasinsulin

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9
Q

What is the classic Sx triad for DM1?

A

Polyuria
Polydipsia
Polyphagia

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10
Q

What is the “honeymoon” period?

A

Endogenous insulin secretion is enough to need little exogenous insulin

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11
Q

Is DKA more likely in DM1 or DM2?

A

DM1

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12
Q

When does DM1 typically present?

A

< 18 yo

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13
Q

What is the biggest risk factor for DM2?

A

Central/Visceral obesity

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14
Q

What is the pathogenesis of DM2?

A

Insulin resistance –> decreased response of peripheral tissues to insulin

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15
Q

How does insulin resistance affect the liver?

A

Failure to inhibit gluconeogenesis –> high fasting blood glucose

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16
Q

How does insulin resistance affect the SkM?

A

Failure of glucose uptake and glycogen synthesis after a meal –> high post-prandial blood glucose

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17
Q

How does insulin resistance affect adipose tissue?

A

Failure to inhibit activation of lipase –> excess TG breakdown and high circulating FFA’s

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18
Q

When does DM2 typically present?

A

> 40 yo

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19
Q

What are the main Sx’s of DM2 at presentation?

A

Fatigue
Dizziness
Blurred vision

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20
Q

What is Hyperosmolar Hyperosmotic Syndrome (HHS)?

A

Severe dehydration from sustained osmotic diuresis

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21
Q

What type of pts typically get Hyperosmolar Hyperosmotic Syndrome?

A

Older pts disabled by stroke or infection

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22
Q

What is the blood glucose range for pts with Hyperosmolar Hyperosmotic Syndrome?

A

600-1200 mg/dL

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23
Q

What is Lipoatrophic diabetes?

A

Hyperglycemia along with loss of adipose tissue in subQ fat

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24
Q

Pregnant women with pregestational DM that isn’t controlled put their fetuses at increased risk for?

A

Stillbirth

Congenital malformations

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25
Q

Why do pregnant women develop gestational DM?

A

Pregnancy is a diabetogenic state where the hormones favor a state of insulin resistance

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26
Q

Do pregnant women who get gestational DM have a increased risk of developing overt DM?

A

Yes, 10-20 years later

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27
Q

What factors can trigger DKA?

A

Failure to take insulin*
Infection, Illness
Trauma
Drugs

28
Q

What is the typically serum glucose level in DKA?

A

250-600 mg/dL

29
Q

What are the major Sx’s of DKA?

A

Fatigue, N/V, ab pain, fruity breath, labored breathing (Kussmaul), CNS depression

30
Q

What is the MOA of DKA?

A

Insulin deficiency –> stimulation of lipases –> increased FFA’s in serum –> increased fatty acyl-CoA production in liver –> oxidation of fatty acyl-CoA into ketone bodies

31
Q

What are the two ketone bodies of concern in DKA?

A

Acetoacetic acid

ß-hydroxybutyric acid

32
Q

How does metabolic ketoacidosis occur?

A

Dehydration –> decreased urinary excretion of ketone bodies

33
Q

What is the Tx for DKA?

A

Insulin administration
Correct metabolic acidosis
Tx precipitating factor

34
Q

What is the most common acute metabolic complication in either type of DM?

A

Hypoglycemia

35
Q

What are the Sx’s of hypoglycemia?

A

Dizziness, confusion, sweating, palpitations, tachycardia

36
Q

What is used to assess glycemic control?

A

HbA1C

37
Q

Why does HbA1C help assess glycemic control?

A

The more glucose that has been around an RBC, the more HbA1C will be present

38
Q

What is the most common cause of death in DM pts?

A

MI

39
Q

Pts with DM have increased PAI-1 enzyme, meaning…

A

Increased inhibition of fibrinolysis = acts as procoagulatin

40
Q

Morphology = diffuse thickening of basement membranes of vessels with paradoxical increased leakiness of vessels

A

Diabetic microvascular disease

41
Q

What is the first sign of diabetic nephropathy?

A

Microalbuminuria

42
Q

What is a urinary marker for increased CV risk?

A

Albumin

43
Q

Which ethnicities (with DM2) are at greater risk for developing diabetic nephropathy?

A

Native Americans
African Americans
Hispanics

44
Q

What are the 3 major lesions seen in the kidney in diabetic nephropathy?

A

Glomerular lesions
Nodular Glomerulosclerosis
Pyelonephritis (necrotizing papillitis)

45
Q

What glomerular lesion is seen in diabetic nephropathy?

A

Thickening of the basement membrane

46
Q

What is seen in Diffuse Mesangial Sclerosis?

A

Increase mesangium with thickend GBM

47
Q

In Diffuse Meesangial Sclerosis, the matrix will stain + for?

A

PAS

48
Q

What is the name for nodules that enlarge and eventually obliterate the glomerular tuft in the kidney?

A

Nodular Glomerulosclerosis (Kimmelstiel-Wilson) disease

49
Q

What can happen to the afferent and efferent hilar arterioles in diabetic nephropathy?

A

Hyalinosis due to ischemia

50
Q

Which type of pyelonephritis is more common in pts with diabetic nephropathy?

A

Necrotizing papillitis

51
Q

Sx’s = motor and sensory dysfunction of the distal LE’s and UE’s

A

Diabetic neuropathy

52
Q

What are the Sx’s of autonomic neuropathy?

A

Bowel, bladder, and ED

53
Q

What are the Sx’s of mononeuropathy?

A

Sudden foot drop, wrist drop, or isolated CN palsies

54
Q

What is the pathogenesis of diabetic ocular complications?

A

Neovascularization from hypoxia-induced overexpression of VEGF in the retina

55
Q

What type of cells are involved in pancreatic neuroendocrine tumors?

A

Islet cells

56
Q

Islet cell tumors secreting insulin are mostly _____ while islet cell tumors secreting other hormones are mostly _____

A

Benign

Malignant

57
Q

What mutations are commonly seen in Pancreatic Neuroendocrine tumors?

A

MEN1, PTEN, TSC2
A-Thalaseemia/Mental retardation syndrome, X-linked (ATRX)
Death-domain Associated protein (DAXX)

58
Q

What is the most common pancreatic endocrine neoplasm?

A

Insulinoma

59
Q

What are the Sx’s of an Insulinoma?

A

Hypoglycemia with confusion, stupor, and LOC

60
Q

Morphology = small cells that look like giant cells with amyloid deposition

A

Insulinoma

61
Q

What lab value would indicate and Insulinoma?

A

High circulating insulin

High insulin:glucose ratio

62
Q

What is the Tx for an Insulinoma?

A

Surgical removal

63
Q

Sx’s = peptic ulcers, diarrhea, possible MEN1 syndrome

A

Gastrinoma (ZE)

64
Q

Sx’s = mild DM with skin rash and anemia in perimenopausal and postmenopausal women

A

a-cell tumors (Glucagonomas)

65
Q

Sx’s = DM, cholelithiasis, steatorrhea, and hypochlorhydria

A

d-cell tumors (Somatostatinomas)

66
Q

Sx’s = watery diarrhea, hypokalemia, achlorhydria (WDHA syndrome)

A

VIPoma

Zak, Endo/Repro 2 (33 decks)

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