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Block 10 Week 2 > Usera: Endocrine Pancreas > Flashcards

Usera: Endocrine Pancreas Flashcards

1
Q

The endocrine pancreas is made up of 1 million clusters of cells called the (blank)

A

islets of langerhans

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2
Q

What are the four main cells types found in the endocrine pancreas, and what does each secrete?

A

beta cells: secrete insulin
alpha cells: secrete glucagon
delta cells: secrete somatostatin
PP cells: secrete pancreatic polypeptide

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3
Q

What are the two minor cells found in endocrine pancreas, and what does each secrete?

A

D1 cells: secrete VIP

enterochromaffin cells: secrete 5HT

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4
Q

Round, dense granules with a thin halo

A

alpha granules (secrete glucagon)

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5
Q

Crystalline core with a wide halo

A

beta granules (secrete insulin)

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6
Q

Round, less dense core with a thin halo

A

delta granules (secrete somatostatin)

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7
Q

Small, hyperdense cores

A

PP granules

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8
Q

What are the two main disorders of the pancreatic islet cells?

A

Diabetes mellitus

pancreatic endocrine tumors

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9
Q

Dysfunction or loss of pancreatic B-cells

Decreased secretion of insulin

A

DM

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10
Q

Abnormal proliferation of pancreatic islet cells

A

pancreatic endocrine tumors

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11
Q

Not a single disease entity, but rather a group of metabolic disorders sharing the common underlying feature of hyperglycemia.
Results from defects in insulin secretion, insulin action or most commonly, both.

A

Diabetes mellitus

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12
Q

Chronic hyperglycemia and associated metabolic dysregulation may be associated with secondary organ damage, especially in these organs…

A

kidneys
eyes
nerves
blood vessels

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13
Q

Diabetes mellitus is the leading cause of these three conditions

A

end-stage renal disease
adult-onset blindness
non-traumatic lower extremity amputation

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14
Q

What is the estimated lifetime risk of being diagnosed with DM in individuals born in the US, males vs females?

A

1 in 3 males

2 in 5 females

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15
Q

What are 3 ways to diagnose DM?

A
  1. random blood glucose greater than 200mg/dL with classical signs & symptoms
  2. fasting blood glucose greater than 126mg/dL more than once
  3. abnormal glucose tolerance test with blood glucose greater than 200mg/dL after a carb load
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16
Q

What is the fasting blood glucose of a prediabetic? What is the glucose tolerance testing like?

A

fasting blood glucose: 100-126 (less than 100 in healthy individuals)
glucose tolerance testing: 140-200 (less than 140 in healthy individuals)

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17
Q

What is type 1 DM?

A

absolute deficiency of insulin caused by autoimmune destruction of beta-cell mass
T-lymphocytes mount an immune response against pancreatic beta-cell antigens

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18
Q

What is type 2 DM?

A

peripheral resistance to insulin action or relative insulin deficiency (inadequate secretion by pancreatic B cells)

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19
Q

This makes up 90-95% of diabetes cases

A

type II DM

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20
Q

Most people with type II DM are (blank)

A

overweight

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21
Q

What is the major gene associated with type I DM?

A

HLA-DR3 and HLA-DR4

**HLA contributes to over 50% of the genetic susceptibility
90-95% of whites with DM type 1 have either HLA DR3 or DR4 haplotypes
40-50% of DM type i are combined DR3 & DR4 heterozygotes

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22
Q

Some non-HLA genes associated with DM 1 include the following…

A

insulin (VNTR)
CTLA4
PTPN22
CD25 (decreases activity of IL2R)

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23
Q

This is one way that you can get type 1 DM…

A

viral infection induces islet cell injury & inflammation –> leads to exposure of self B cell antigens and activation of autoreactive T-cells

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24
Q

Two ways in which a virus can lead to type 1 DM…

A

molecular mimicry: viral proteins mimic B cell antigens & the immune response cross reacts

precipitating virus: viral infection early in life could persist in tissue –> subsequent infection with a similar virus could elicit an immune response against infected islet cells

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25
Q

In type 1 DM, there is slow, progressive destruction of islet cells. About what percentage of the beta cells must be destroyed before hyperglycemia & ketosis occur?

A

greater than 90%

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26
Q

These are present in patients with type 1 DM and in their family members

A

autoantibodies to islet cells

27
Q

What are some environmental factors contributing to type 2 DM?

A

sedentary lifestyle
diet
obesity

28
Q

What are some genetic factors contributing to type 2 DM?

A

strongest association with TCF7L2
35-60% concordance in monozygotic twins!!
lifetime risk for offspring is more than doubles if both parents are affected
not linked to HLA genes

29
Q

What are the TWO metabolic defects of type 2 diabetes? Which happens first?

A
  1. insulin resistance - decreased ability of peripheral tissues to respond to insulin
  2. beta-cell dysfunction - inadequate insulin secretion in the face of hyperglycemia

**the insulin resistance is usu the primary event

30
Q

What effects does insulin have on the following?

adipose tissue
striated muscle
liver

A

adipose tissue: increases glucose uptake & decreases lipolysis

striated muscle: increases glucose uptake & glycogen synthesis, increases protein synthesis

liver: decreases gluconeogenesis & increases glycogen synthesis & lipogenesis

31
Q

(blank) is present in about 80% of type 2 DM patients

A

visceral obesity

32
Q

(blank) is present in obesity unaccompanied by hyperglycemia. In other words, in states of fatty excess, there is a fundamental abnormality in (blank)

A

insulin resistance; insulin signaling

33
Q

The failure of target tissues to respond normally to insulin

A

insulin resistance

34
Q

Discuss how beta cell dysfunction evolves with insulin resistance leading to diabetes

A

in states of insulin resistance, insulin is initially higher for each level of glucose
higher levels of insulin compensate for peripheral insulin resistance to maintain normal blood glucose levels
once beta cell compensation becomes inadequate, diabetes developes

35
Q

(blank) allelic variants associated with reduced insulin secretion

A

TCF7L2

36
Q

So initially, pancreatic beta cells secrete normal amounts of insulin, and blood glucose remains normal. Then, as insulin resistance begins to develop, beta cells compensate by producing more insulin. Ultimately, the beta cells will (blank), leading to decreased insulin production & (blank)

A

fail; diabetes mellitus

37
Q

What is the best assessment of glycemic control in DM?

A

HGBA1c

38
Q

What is HgbA1c? What does it tell you?

A

formed by nonenzymatic covalent addition of glucose moities to hemoglobin in RBCs

**provides a measure of glycemic control over the lifespan of the RBCs (120 days)

39
Q

What should the HgbA1c be in non-diabetics?

A

less than 7%

40
Q

Form when nonenzymatic reactions occur between glucose and the amino groups of intra- and extracellular proteins

A

advanced glycosylation end products (AGEs)

41
Q

The rate of AGE formation is accelerated in hyperglycemia. When AGEs directly cross-link to extracellular matrix proteins, what happens?

A

Decreases vascular elasticity
Enhances protein deposition
Entrap non-glycated plasma and interstitial proteins (LDL)

42
Q

What happens to peripheral tissues (tissues that do not require insulin for glucose transport i.e. nerves, lenses, kidneys, blood vessels) with persistent hyperglycemia?

A

increased intracellular glucose –> reduced glutathione production –> increased susceptibility to oxidative stress

43
Q

In neurons, hyperglycemia causes (blank)

A

diabetic neuropathy

44
Q

This is a hallmark of DM

Accelerated atherosclerosis involving aorta and large- and medium-sized arteries

A

macrovascular disease

45
Q

This is most common cause of death equally common in diabetic women and men
There is an increased risk in prediabetics

A

Myocardial infarction due to atherosclerosis of coronary arteries

46
Q

What types of symptoms would you see when you have macrovascular disease in DM?

A

gangrene of the lower extremities

hyaline arteriolosclerosis –> HTN

47
Q

Diffuse thickening of the basement membranes, most evident in the capillaries
Diabetic capillaries are more leaky than normal to plasma proteins
Underlies development of diabetic nephropathy, retinopathy and some forms of neuropathy

A

microvascular disease

48
Q

(blank) secondary to microvascular disease is 2nd most common cause of death in DM

A

renal failure

49
Q

So what are the top two leading causes of death in diabetic patients?

A
  1. MI due to atherosclerosis of coronary arteries

2. renal failure

50
Q

What type of vascular problems do you see in the kidneys of diabetic patients?

A

glomerular lesions - capillary basement membrane thickening

hyaline arteriolosclerosis

51
Q

You will see these histologically in the glomerulus of diabetic patients

A

Kimmelsteil-Wilson nodules

52
Q

What happens to the eyeballs in DM?

A

diabetic retinopathy

53
Q

What happens to the mouth in DM?

A

dental caries –> due to diet & decreased salivary flow
salivary dysfunction
oral mucosal diseases –> lichen planus, aphthous stomatitis
oral infections –> candidiasis
gingivitis & periodontal disease
taste & other neurosensory disorders

54
Q

Recap the longterm complications of DM

A 
microangiopathy, cerebral vascular infarcts
HTN
retinopathy, cataracts, glaucoma
MI
atherosclerosis
nephrosclerosis, arteriolosclerosis
peripheral nephropathy
peripheral vascular atherosclerosis --> gangrene
55
Q

What are the dominant clinical features of type 1 DM?

A

occurs in the young

polyuria, polydipsia, polyphagia, ketoacidosis

56
Q

What are the dominant clinical features of type 2 DM?

A

older patients
obese
ketoacidosis is infrequent

57
Q

How is the diagnosis of type 2 diabetes usu made?

A

after routine blood or urine testing in an asymptomatic patient

58
Q

Why don’t you usu see ketoacidosis in type 2 DM?

A

higher portal vein insulin levels prevents unchecked fatty acid oxidation, keeps formation of ketone bodies in check

59
Q

This occurs in type 2 diabetics when they are severely dehydrated from hyperglycemic polyuria, and they are not compensating
Do not experience nausea, vomiting, resp symptoms that occur in ketoacidosis though

A

hyperosmotic nonketotic coma

60
Q

Finally, compare type 1 to type 2 diabetes…everything you know…

A

type 1: young patient, not obese, absolute lack of insulin, autoantibodies, HLA linkage, ketoacidosis, insulitis, beta cell depletion, islet atrophy

type 2: adults, obese, relative lack of insulin, no autoantibodies, no HLA linkage, nonketotic hyperosmolar coma (usu not DKA), amyloid deposition within islets

61
Q

Most common of the pancreatic endocrine neoplasms
May produce enough insulin to cause clinical hypoglycemia
Most common of pancreatic endocrine neoplasms
May produce enough insulin to cause clinical hypoglycemia

A

insulinoma (neoplastic proliferation of beta cells)

62
Q

What differentiates hypoglycemia caused by an insulinoma from exogenous insulin injection?

A

with an insulinoma, you will get elevation in both insulin & C peptide levels
If exogenous insulin, no C peptide

**proinsulin is cleaved into insulin & C-peptide

63
Q

What are some other rate pancreatic endocrine neoplasms?

A

alpha cell tumors (glucagonomas)
delta cell tumors (somatostatinomas)
vipoma

Block 10 Week 2 (8 decks)

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