Pancreas-Usera

Question 1

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

Answer 1

islets of langerhans

Question 2

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

Answer 2

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

Question 3

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

Answer 3

• D1: secrete VIP (slows muscle contraction)

* Enterochromaffin cells: secrete serotonin

Question 4

What does glucagon look like?

Answer 4

alpha granules-round, dense, with a thin halo

Question 5

What does insulin look like?

Answer 5

beta granules-crystalline core with a wide halo

Question 6

What does somatostatin look like?

Answer 6

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

Question 7

What does pp look like?

Answer 7

small, hyperdense cores

Question 8

What is diabetes mellitus?

Answer 8

• dysfunction or loss of pancreatic B-cells

- decreased secretion of insulin

Question 9

What is a pancreatic endocrine tumor?

Answer 9

abnormal proliferation of pancreatic islet cells

Question 10

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

Answer 10

group

Question 11

DM results from defects in (Blank)

Answer 11

insulin secretion or insulin action OR more commonly both

Question 12

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

Answer 12

kidneys
eyes
nerves
blood vessels

Question 13

DM affects greater than (blank) million children and adults

Answer 13

20

Question 14

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

Answer 14

1.5

Question 15

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

Answer 15

end-stage renal disease

adult onset blidness

Question 16

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

Answer 16

54

Question 17

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

Answer 17

1/5

2/5

Question 18

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

Answer 18

AA, hispanic, native americans

Question 19

It is one of the most common noncommunicable disease?

Answer 19

DM (number of affected individual is expected to double)

Question 20

How can you make the diagnosis of DM?

Answer 20

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

Question 21

What is normal blood sugar?

Answer 21

less than 100 mg/dL fasting

less than 140 mg/dL for a glucose tolerance test

Question 22

What is prediabetic blood sugar?

Answer 22

greater than 100 but less than 126 mg/dL fasting

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

Question 23

What is type 1 DM?

Answer 23

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

Question 24

What is type 2 DM?

Answer 24

-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

Question 25

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

Answer 25

HLA

Question 26

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

Answer 26

HLA-DR3 or HLA-DR4

Question 27

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

Answer 27

- insulin (VNTR) - CTLA4 (cytotoxic T lymphocyte antigen 4) - PTPN22 (protein tyrosine phosphatase) - CD25 (decreases activity of IL2R)

Question 28

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

Answer 28

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

Question 29

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

Answer 29

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

Question 30

How does molecular mimicry cause type I DM?

Answer 30

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

Question 31

How does a precipitating virus cause type I DM?

Answer 31

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

Question 32

``` 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 ```

Answer 32

Type 1 diabetes | 90%

Question 33

What is the fundamental immune abnormality in type 1 diabetes?

Answer 33

failure of tolerance to self NOTE: autoantibodies to islet cells are present in patients and their family members.

Question 34

What is the pathogenesis of type 2 DM?

Answer 34

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

Question 35

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

Answer 35

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

Question 36

What are the 2 metabolic defects of type 2 diabetes

Answer 36

- Insulin resistance | - B cell dysfunction (relative insulin deficiency)

Question 37

What is insulin resistance?

Answer 37

decreased ability of peropheral tissues to respond to insulin

Question 38

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

Answer 38

inadequate insuline secretion in the face of hyperglycemia

Question 39

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

Answer 39

insulin resistance

Question 40

What is the normal function of insulin on adipose tissue?

Answer 40

increased glucose uptake increased lipogenesis decreased lipolysis

Question 41

what is the normal function of insulin on striated muscle?

Answer 41

increased glucose uptake increased glycogen synthesis increased protein synthesis

Question 42

What is the normal function of insulin on liver?

Answer 42

decreased gluconeogensis increased glycogen synthesis increased lipogenesis

Question 43

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

Answer 43

80%

Question 44

What is this: | failure of target tissues to respond normally to insulin

Answer 44

insulin resistance

Question 45

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

Answer 45

glucose

Question 46

When (blank) compensation becomes inadequate, diabetes develops

Answer 46

B cell

Question 47

What can cause B cell compensation to become inadequate?

Answer 47

- intrinisc predisposition - TCF7L2 allelic variants associated with reduced insulin secretion - Amyloid replacement of islet cells

Question 48

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

Answer 48

b cell dysfunction and insulin resistance

Question 49

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

Answer 49

adipokines, FFAs and inflammation | -insulin resistance

Question 50

What is persistant hyperglycemia?

Answer 50

glucotoxicity

Question 51

What is the best assessment of glycemic control?

Answer 51

HGBA1C (glycosylated hemoglobin)

Question 52

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)

Answer 52

HGBA1C

Question 53

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

Answer 53

6.5%

Question 54

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)

Answer 54

Advanced Glycosylation End (AGE) products | Hyperglycemia

Question 55

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

Answer 55

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

Question 56

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

Answer 56

hyperglycemia

Question 57

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

Answer 57

glutathione | oxidative stress

Question 58

In neurons, hyperglycemia causes (blank)

Answer 58

diabetic neuropathy (glucose neurotoxicity)

Question 59

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

Answer 59

aorta and large-medium sized arteries gangrene hyaline

Question 60

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

Answer 60

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

Question 61

What is this: | diffuse thickening of the BM, most evident in the capillaries

Answer 61

Diabetic microangiopathy

Question 62

Diabetic capillaries are more leakly than normal to (Blank)

Answer 62

plasma proteins

Question 63

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

Answer 63

diabetic microangiopathy (diffuse thickening of BM)

Question 64

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

Answer 64

2nd

Question 65

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

Answer 65

Diabetic nephropathy

Question 66

What are glomerular lesions? | Where do you find glomerular lesions? Where do you find diffuse mesangiosclerosis?

Answer 66

capillary BM thickening-> widespread thickening of glomerular capillary basement membrane - Present in all cases of diabetic nephropathy - nephrotic syndrome

Question 67

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

Answer 67

kimmelsteil-wilson nodules

Question 68

What are the 2 stages of diabetic retinopathy?

Answer 68

proliferative and non proliferative

Question 69

What are the oral manifestations of DM?

Answer 69

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

Question 70

Candidiasis and periodontal disease are common in (blanK)

Answer 70

Diabetes mellitus

Question 71

What are the long term complications of DM?

Answer 71

- 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

Question 72

What are the clinical features of Type 1 DM?

Answer 72

- occurs in the young | - polyuria, polydipsia, polyphagia and ketoacidosis are the dominant clinical features.

Question 73

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?

Answer 73

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

Question 74

What are the clinical features of type 2 DM?

Answer 74

patients are older (>40 ) and obese | -diagnosis is usually made after routine blood or urine testing in an asymptomatic patient

Question 75

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.

Answer 75

higher portal vein insulin FA oxidation ketone bodies

Question 76

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.

Answer 76

higher portal vein insulin FA oxidation ketone bodies

Question 77

Type 1 DM patients get (blank) comas | TYpe 2 DM patients get (blank) comas

Answer 77

DKA | hyperosmotic nonketotic coma

Question 78

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

Answer 78

hyperglycemic polyuria

Question 79

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

Answer 79

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

Question 80

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

Answer 80

Type I diabetes

Question 81

What is this: - adults (usually > 40 yrs) - obese - relative lack of insulin - no autoantibodies - no HLA linkage - Usually not DKA - amyloid deposition within islets

Answer 81

Type 2 DM

Question 82

What are the major signs of hypoglycemia?

Answer 82

disorientation, confusion

Question 83

What are the most common causes of pancreatic endocrine neoplasms?

Answer 83

neoplastic proliferation of B cells (insulinomas)

Question 84

Pancreatic endocrin neoplasms may produce enough insulin to cause (blank0

Answer 84

clinical hypoglycemia

Question 85

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

Answer 85

c-reactive peptide and insulin

Question 86

What are rare pancreatic endocrine neoplasms?

Answer 86

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

Question 87

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

Answer 87

salt and pepper chromatin eosophilic -vomit lesions