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Block 10 Week 2 > Pancreas-Usera > Flashcards

Pancreas-Usera Flashcards

1
Q

THe endocrine pancrease is made up of a million clusters of cells called the (blank)

A

islets of langerhans

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2
Q

What are the four main cells types of the islets of langerhans?

A
  • β: secretes insulin
  • α: secretes glucagon
  • δ: secretes somatostatin
  • PP: secretes pancreatic polypeptide
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3
Q

What are the 2 minor cell types of the islets of langerhans?

A
  • D1: secrete VIP (slows muscle contraction)

* Enterochromaffin cells: secrete serotonin

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4
Q

What does glucagon look like?

A

alpha granules-round, dense, with a thin halo

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5
Q

What does insulin look like?

A

beta granules-crystalline core with a wide halo

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6
Q

What does somatostatin look like?

A

delta granules-round, less dense core with a thin halo (somastostatin)

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7
Q

What does pp look like?

A

small, hyperdense cores

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8
Q

What is diabetes mellitus?

A
  • dysfunction or loss of pancreatic B-cells

- decreased secretion of insulin

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9
Q

What is a pancreatic endocrine tumor?

A

abnormal proliferation of pancreatic islet cells

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10
Q

Diabetes mellitus (DM) is not a single disease entity, but rather a (blank) of metabolic disorders sharing the common underlying feature of hyperglycemia

A

group

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11
Q

DM results from defects in (Blank)

A

insulin secretion or insulin action OR more commonly both

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12
Q

Chronic hyperglycemia and associated metbaolic dysregulation may be associated with secondary organ damage, especially in the (Blank x 4)

A

kidneys
eyes
nerves
blood vessels

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13
Q

DM affects greater than (blank) million children and adults

A

20

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14
Q

App. (blank) million cases of DM are diagnoses each year

A

1.5

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15
Q

DM is the leading cause of (blank), adult onset (blank) and non-traumatic lower extremity amputation

A

end-stage renal disease

adult onset blidness

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16
Q

(blank) million adults are pre-diabetic (elevated blood sugar not meeting criteria for diagonsis of DM

A

54

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17
Q

For individuals born in the US, the estimated lifetime risk of being diagnosed with diabetes mellitus is (blank) in males and (blank) in females

A

1/5

2/5

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18
Q

DM is 2 to 5 times higher in the (blank X) population as compared to non-hispanic whites

A

AA, hispanic, native americans

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19
Q

It is one of the most common noncommunicable disease?

A

DM (number of affected individual is expected to double)

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20
Q

How can you make the diagnosis of DM?

A

Random blood glucose> 200 mg/dL with classical signs and symptoms
Fasting blood glucose>126 mg/dL
Abnormal glucose tolerance test w/ blood glucose > 200 mg/dL after a standard carb load

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21
Q

What is normal blood sugar?

A

less than 100 mg/dL fasting

less than 140 mg/dL for a glucose tolerance test

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22
Q

What is prediabetic blood sugar?

A

greater than 100 but less than 126 mg/dL fasting

greater than 140 and less than 200 mg/dL glucose tolerance test

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23
Q

What is type 1 DM?

A
  • absolute deficiency of insulin caused by an autoimmune destruction of B cell mass
  • T-lymphocytes mount an immune response against pancreatic B cell antigens
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24
Q

What is type 2 DM?

A

-peripheral resistance to insulin action
-relative insulin deficiency (inadequate secretion by pancreatic B cells)
Accounts for 90-95% of
-most are overweight -but its not necessary

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25
Q

(blank) locus on 6P21; contributes over 50% of the genetic susceptibility for type I diabetes

A

HLA

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26
Q

90-95% of whites with DM type I have either (blank or blank) haplotypes

A

HLA-DR3 or HLA-DR4

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27
Q

What are the non-HLA genes that can have mutations and cause Type I diabetes?

A
  • insulin (VNTR)
  • CTLA4 (cytotoxic T lymphocyte antigen 4)
  • PTPN22 (protein tyrosine phosphatase)
  • CD25 (decreases activity of IL2R)
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28
Q

Viral infections can cause type I DM, what infections can cause this?
How?

A
  • Mumps, rubella, coxsackie B, CMV, and others
  • viral infection induces islet cell injury/inflammation
  • molecular mimicry
  • precipitating virus
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29
Q

How does a viral infection induce islet cell injury/inflammation?

A

leading to exposure of self B cell antigens and activation of autoreactive T-cells

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30
Q

How does molecular mimicry cause type I DM?

A

viral proteins mimic B cell antigens and the immune response cross reacts

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31
Q

How does a precipitating virus cause type I DM?

A

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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32
Q 
What is this:
Slow progressive destruction of islet cells prior to any signs or symptoms
Greate than (blank)% of the B cells have been destroyed before hyperglycemia and ketosis occur
A

Type 1 diabetes

90%

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33
Q

What is the fundamental immune abnormality in type 1 diabetes?

A

failure of tolerance to self

NOTE: autoantibodies to islet cells are present in patients and their family members.

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34
Q

What is the pathogenesis of type 2 DM?

A

-environmental factos:
sedentary lifestyle, diet, obesity
-Genetic factors

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35
Q

What are the genetic factors that contribute to type 2 DM?

A
  • 35-60% concordance in monozygotic twins
  • risk more than doubled if both parents affected
  • strongest association to TCF7L2 (10q)
  • not linked to HLA genes
36
Q

What are the 2 metabolic defects of type 2 diabetes

A
  • Insulin resistance

- B cell dysfunction (relative insulin deficiency)

37
Q

What is insulin resistance?

A

decreased ability of peropheral tissues to respond to insulin

38
Q

What is b-cell dysfunction (relative insulin deficiency)?

A

inadequate insuline secretion in the face of hyperglycemia

39
Q

In type 2 diabetes, usually (blank) is the primary event and predates hyperglycemia, followed by increasing degrees of b-cell dysfunction

A

insulin resistance

40
Q

What is the normal function of insulin on adipose tissue?

A

increased glucose uptake
increased lipogenesis
decreased lipolysis

41
Q

what is the normal function of insulin on striated muscle?

A

increased glucose uptake
increased glycogen synthesis
increased protein synthesis

42
Q

What is the normal function of insulin on liver?

A

decreased gluconeogensis
increased glycogen synthesis
increased lipogenesis

43
Q

Visceral obesity is present in (blank) percent of diabetic patients. Insulin resistance is present in obesity unaccompanied by hyperglyemia

A

80%

44
Q

What is this:

failure of target tissues to respond normally to insulin

A

insulin resistance

45
Q

In states of insulin resistance, insulin secretion is initially higher for each level of (blank)

A

glucose

46
Q

When (blank) compensation becomes inadequate, diabetes develops

A

B cell

47
Q

What can cause B cell compensation to become inadequate?

A
  • intrinisc predisposition
  • TCF7L2 allelic variants associated with reduced insulin secretion
  • Amyloid replacement of islet cells
48
Q

Diabetes genes, adipokines, inflammation, hyperglycemia, FFAs all cause (blank)

A

b cell dysfunction and insulin resistance

49
Q

Obesity will lead to adipocytes secreting.. (blank X 3). This will result in (blank)

A

adipokines, FFAs and inflammation

-insulin resistance

50
Q

What is persistant hyperglycemia?

A

glucotoxicity

51
Q

What is the best assessment of glycemic control?

A

HGBA1C (glycosylated hemoglobin)

52
Q

What is this:
• Formed by nonenzymatic covalent addition of glucose moities to hemoglobin in RBCs
• Provides a measure of glycemic control over the lifespan of a RBC (120 days)

A

HGBA1C

53
Q

A non-diabetic patient has a HGBA1C of less than (blank)

A

6.5%

54
Q

What is this:
form when non-enzymatic reaxns occur b/w glucose and the amino groups of intra and extracellular proteins
The rate of age formation is accelerated in (blank)

A

Advanced Glycosylation End (AGE) products

Hyperglycemia

55
Q

AGES can directly cross-link to extracellular matrix proteins and cause….?

A

decreases vascular elasticity
enhances protein deposition
entrap non-glycated plasma and interstitial proteins (LDL)

56
Q

Tissues that do not require insulin for glucose transport are most affected by (blank)

A

hyperglycemia

57
Q

Increased intracellular glucose-> reduced (blank) production-> increased susceptibility to (blank)

A

glutathione

oxidative stress

58
Q

In neurons, hyperglycemia causes (blank)

A

diabetic neuropathy (glucose neurotoxicity)

59
Q

In DM, accelearted atherosclerosis involving (blank) and (blank) arteries, (blank) of the lower extremities, (blank) arteriosclerosis associatd with HTN

A

aorta and large-medium sized arteries
gangrene
hyaline

60
Q

What is the most common cause of death in diabetic patients?

A

myocardial infarctions due to atherosclerosis of coronary arteries (equally common in diabetic women and men, increased ris of prediabetics)

61
Q

What is this:

diffuse thickening of the BM, most evident in the capillaries

A

Diabetic microangiopathy

62
Q

Diabetic capillaries are more leakly than normal to (Blank)

A

plasma proteins

63
Q

What underlies development of diabetic nephropathy, retinopathy, and some forms of neuropathy?

A

diabetic microangiopathy (diffuse thickening of BM)

64
Q

Renal failures is the (blank) most common cause of death in DM

A

2nd

65
Q

What are these found in:
glomerular lesions
renal vascular lesions (primarily arteriolosclerosis)

A

Diabetic nephropathy

66
Q

What are glomerular lesions?

Where do you find glomerular lesions? Where do you find diffuse mesangiosclerosis?

A

capillary BM thickening-> widespread thickening of glomerular capillary basement membrane

  • Present in all cases of diabetic nephropathy
  • nephrotic syndrome
67
Q

If you have nodular diabetic glomerulosclerosis what can you see histologically?

A

kimmelsteil-wilson nodules

68
Q

What are the 2 stages of diabetic retinopathy?

A

proliferative and non proliferative

69
Q

What are the oral manifestations of DM?

A

Dental caries (diet, decreased salivary flow)
Salivary dysfunction (Xerostomia)
Oral mucosal diseases (lichen planus, apithous stomatitis)
Gingivitis and periodontal disease
Taste and othe rneurosensory disorders

70
Q

Candidiasis and periodontal disease are common in (blanK)

A

Diabetes mellitus

71
Q

What are the long term complications of DM?

A
  • microangiopathy, cerebrovascular infarcts, hemorrhage
  • retinopathy, cataracts, glaucoma
  • HTN
  • MI
  • Islet cell loss (type 1 (insulitis) type 2 (amyloid)
  • atherosclerosis
  • nephrosclerosis (glomerulosclerosis, arteriosclerosis, pyelonephritis)
  • peripheral neuropathy
  • autonomic neuropathy
  • gangrene
  • infections
  • peripheral vascular atherosclerosis
72
Q

What are the clinical features of Type 1 DM?

A
  • occurs in the young

- polyuria, polydipsia, polyphagia and ketoacidosis are the dominant clinical features.

73
Q

Since insulin is a major anabolic hormone, insulin deficiency results in a catabolic state affecting (blank X 3). What happens to glucose protein and fat?

A

glucose, protein and fat metabolism
increased blood glucose
muscle breakdown-> protein breakdown
Increased lipolysis

74
Q

What are the clinical features of type 2 DM?

A

patients are older (>40 ) and obese

-diagnosis is usually made after routine blood or urine testing in an asymptomatic patient

75
Q

Ketoacidosis is infrequent in type 2 DM because in type 2 you have (blank) levels that prevents unchecked (blank) and keeps formation of (blank) in check.

A

higher portal vein insulin
FA oxidation
ketone bodies

76
Q

Ketoacidosis is infrequent in type 2 DM because in type 2 you have (blank) levels that prevents unchecked (blank) and keeps formation of (blank) in check.

A

higher portal vein insulin
FA oxidation
ketone bodies

77
Q

Type 1 DM patients get (blank) comas

TYpe 2 DM patients get (blank) comas

A

DKA

hyperosmotic nonketotic coma

78
Q

Hyperosmotic nonketotic coma develops in type 2 DM because you get dehydrated from (blank)

A

hyperglycemic polyuria

79
Q

In type 2 DM does N/V and respiratory symptoms occur?

A

NO, this happens in type 1 pnts because it occurs with ketoacidosis

80
Q

What is this:

  • a young patient
  • not obese
  • absolute lack of insulin
  • autoantibodies HLA linkage
  • Ketotic hyperosmolar coma DKA
  • insulitis, B-cell depletion, islet atrophy
A

Type I diabetes

81
Q

What is this:

  • adults (usually > 40 yrs)
  • obese
  • relative lack of insulin
  • no autoantibodies
  • no HLA linkage
  • Usually not DKA
  • amyloid deposition within islets
A

Type 2 DM

82
Q

What are the major signs of hypoglycemia?

A

disorientation, confusion

83
Q

What are the most common causes of pancreatic endocrine neoplasms?

A

neoplastic proliferation of B cells (insulinomas)

84
Q

Pancreatic endocrin neoplasms may produce enough insulin to cause (blank0

A

clinical hypoglycemia

85
Q

Patients with an insulinoma have increased levels of (blank and blank) which differentiates this cause of acute hypoglycemia from exogenous injection of insulin

A

c-reactive peptide and insulin

86
Q

What are rare pancreatic endocrine neoplasms?

A

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

87
Q

What does a Pancreatic Endocrine Neoplasm Islet cell tumor look like histologically?

A

salt and pepper chromatin
eosophilic
-vomit lesions

Block 10 Week 2 (7 decks)

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