Endo - Diabetes Mellitus

Front 1

What two clinical aspects do all DM presentations share?

Back 1

1) Abnormalities in CHO, protein, and fat metabolism as a result of a relative or absolute insulin deficiency
2) End-organ complications involving the eyes, kidneys, nerves and BVs.

Front 2

Using an oral glucose tolerance test, in what three categories are people placed?

Back 2

1) Diabetes: > (200 mg/dL)
2) Impaired Glucose Tolerance: 200 > x > 140
3) Impaired Fasting Glucose: 125 > x > 100

Front 3

Pre-diabetics are at risk for what medical complications?

Back 3

Pre-diabetics are at risk for heart disease, stroke, and developing T2DM

Front 4

Define "INCIDENCE" and "PREVALENCE"

Back 4

INCIDENCE - the rate at which new cases appear
PREVALENCE - proportion of a population afflicted

Front 5

Is hypoglycemia an early- or late-stage development of T1DM?

Back 5

Hypoglycemia is a late-stage development of T1DM.

Front 6

What is a major genetic marker/determinant of T1DM?

Back 6

HLA Short-arm Chromosome 6

Front 7

What new therapy was recently shown to preserve insulin secretion in newly-diagnosed patients?

Back 7

A monoclonal antibody directed against CD3 was shown to preserve insulin secretion in newly-diagnosed patients.

Front 8

On the molecular level, what are the most common causes of insulin resistance?

Back 8

Receptor Level - changes in the number, affinity, or transduction of insulin receptors.
Post-Receptor Level - loss of signal transduction by receptor.

Front 9

What insulin-related pathologies are required for the development of T2DM?

Back 9

Both insulin resistance and a relative insulin deficiency are required for the development of T2DM

Front 10

What are the functional characteristics of insulin secretion in T2DM?

Back 10

The beta cell lesions in T2DM is specific to glucose. Other agents, such as amino acids, may promote insulin release.

Front 11

What subset of T2DM is developed early in life?

Back 11

MODY - Maturity Onset Diabetes of Youth

Front 12

What are the hallmarks of DKA?

Back 12

1) Insulin deficiency
2) Glucagon excess
3) Volume depletion

Front 13

Can DKA occur in T2DM?

Back 13

Yes, but more common is a Nonketotic Hyperosmolar Coma.

Front 14

How is severe hypoglycemia defined?

Back 14

Severe hypoglycemia is defined as an episode requiring assistance from another person for treatment.

Front 15

What two physiologic alarm mechanisms for hypoglycemia are gradually lost in DM?

Back 15

1) After 5 years of T1DM, glucagon levels do not respond to hypoglycemia
2) After 10 years, the EPI response is blunted as well

Front 16

What are the four classes of diabetes complications?

Back 16

1) Microvascular
2) Macrovascular
3) Neuropathic
4) Miscellaneous

Front 17

Describe the microvascular pathology of diabetic retinopathy.

Back 17

Non-perfusion of retinal capillaries leads to weakness and hemorrhage. Blindness results from vitreal hemorrhage, retinal detachment, or edema.

Front 18

What histopathologic finding accompanies diabetic nephropathy?

Back 18

Thickening of the basement membrane, leading to glomerular hypertension and proteinuria.

Front 19

What pharmacotherapy is renal-sparing in DM?

Back 19

ACE or ARB and good glucose control may manage diabetic nephropathy.

Front 20

Why is diabetic neuropathy such a problem?

Back 20

Insensate feet are vulnerable to infection, ulceration, and gangrene, requiring surgical debridement or amputation.

Front 21

Has the relationship between MACROvascular complications and hyperglycemia been established?

Back 21

Not statistically, although a correlation has been seen.

Front 22

What medication attempts to reverse the damaging, excessive intracellular production of sorbitol in hyperglycemics?

Back 22

Aldose reductase inhibitors.

Front 23

What molecular inhibitor is under investigation for the prevention of diabetic retinopathy?

Back 23

Protein Kinase C inhibitors

Front 24

How do sulfonylurea receptors function?

Back 24

Sulfonylureas are responsible for drug binding and subsequent closure of an ATP-dependent K-Channel, promoting insulin secretion in beta islet cells.

Front 25

Sulfonylurea drugs...

Back 25

are economical, may cause hypoglycemia and weight gain, and are not effective long-term.

Front 26

Metformin is...

Back 26

Metformin (a biguanide) is as effective as sulfonylureas, does not cause hypoglycemia or weight gain. MF frequently causes GI upset. Lactic acidosis is the most serous side-effect.

Front 27

How does metformin work?

Back 27

Metformin reduces hepatic glucose production primarily through suppression of gluconeogenesis.

Front 28

Who may not take metformin?

Back 28

Metformin is contraindicated in people with liver or kidney malfunction.

Front 29

How do thazolinediones (TZDs) work?

Back 29

TZDs increase insulin sensitivity in target tissues, especially muscle, possibly through PPARs

Front 30

What are the major thazolinediones (TZD) side-effects?

Back 30

Edema, weight gain are common. Increased risk of CHF.

Front 31

How do the incretin drugs function?

Back 31

Incretins mimic gut hormones (Glucagon-like peptides, GLPs) released in response to a meal. They potentiate beta-islet cell insulin secretion.

Front 32

Do T1DMs make any amylin?

Back 32

No. Type 1 diabetics make no amylin.

Front 33

What functions have been attributed to amylin?

Back 33

Amylin has been shown to have several functions, including retardation of gastric emptying, post-prandial glucagon suppression, and suppression of appetite.