Diabetes Mellitus

Question 1

Outline the current recommendations for DM screenings

Answer 1

Universal screening is not generally recommended.
Screening is accepted in patients who are obese, over 45 y/o, with a family history, certain minority groups (blacks, Hispanics, Pima Indians).
Screening in pregnancy is mandatory.

Question 2

Does DM1 or DM2 develop ketoacidosis? Hyperosmolar state?

Answer 2

DM1: ketoacidosis
DM2: hyperosmolar state

Question 3

What is the level of endogenous insulin in DM1 vs. DM2?

Answer 3

DM1: low to none
DM2: normal to high (insulin resistance)

Question 4

What is the twin concurrence in DM1 vs. DM2? Is there an HLA association in either one?

Answer 4

DM1: 50%, NO HLA association

Question 5

Does DM1 or DM2 respond to oral hypoglycemics?

Answer 5

DM2 responds to oral hypoglycemics

Question 6

Does DM1 or DM2 have antibodies to insulin?

Answer 6

DM1 has antibodies to insulin at diagnosis

Question 7

Is DM1 or DM2 at risk for diabetic complications?

Answer 7

BOTH

Question 8

What is the islet-cell pathology in DM1 vs. DM2?

Answer 8

DM1: insulitis (loss of most B cells)
DM2: normal number, but with amyloid deposits

Question 9

What are the goals of treatment in terms of glucose levels?

Answer 9

Keep postprandial glucose levels less than 180 mg/dL and fasting glucose levels 70-130 mg/dL
Attempts at stricter control may result in hypoglycemia; watch for symptoms of SNS activation and mental status changes

Question 10

What is a good measure of long-term diabetes control?

Answer 10

Hemoglobin A1c measures “average” control of blood glucose level over the prior 2-3 months. Current recommendation is to keep it below 7.
Rough rule of thumb: Hg A1c x 20 = average blood glucose level

Question 11

When a nondiabetic patients presents with hypoglycemia, how can you distinguish between factitious disorder (exogenous insulin) and an insulinoma (endogenous insulin)?

Answer 11

C-peptide level. C-peptide is produced whenever the body makes insulin, but is absent in prescription insulin. C-peptide will be high with an insulinoma and low with factitious disorder.

Question 12

What should you remember before giving IV iodinated contrast material to a diabetic patient or a patient with renal insufficiency?

Answer 12

Prone to acute renal failure from IV contrast used for pyelography, angiography, or CT. Weigh the risk-benefit ratio. If you give contrast, hydrate patient well with IV fluids to avoid renal shutdown. Acetylcysteine and bicarbonate may decrease the risk of contrast nephropathy in high risk patients. These concerns do not apply to oral contrast agents (e.g. barium).

Question 13

What is diabetic ketoacidosis?

Answer 13

All type I diabetics will die without insulin, DKA happens before they die. Look for Kussmaul breathing (deep, rapid respirations), dehydration, hyperglycemia, acidosis (due to excessive ketone formation), and increased ketones in the serum (often associated with a fruity odor of the breath) and urine.

Question 14

What is the treatment for DKA?

Answer 14

IV fluids, insulin, electrolyte replacement (esp. potassium and phosphate).
Mortality rate of DKA with current treatment efforts is less than 10%.

Question 15

What is the most common cause of DKA?

Answer 15

1. Insulin therapy noncompliance

2. Infection

Question 16

What is nonketotic hyperglycemic hyperosmolar state? How is it treated?

Answer 16

It is what happens to type II diabetics before they die. Hyperglycemia and increased serum osmolarity in the absence of ketones and acidosis.
Most patients are severely dehydrated; first three treatments are thus “fluids, fluids, fluids” (IV hydration with NS). Insulin and electrolyte replacement is also required. Mortality rate can approach 50% if mental status changes are present at the time of diagnosis.

Question 17

What are the classic presenting symptoms of new-onset diabetes?

Answer 17

Polyuria, polydypsia, and polyphagia (pee a lot, drink a lot, and eat a lot).
Also be suspicious if patient presents with candidal infections (e.g. thrush or vaginal yeast), weight loss (due to excessive urination), or blurry vision.
Prolonged hyperglycemia causes lenses in eyes to swell, and patient may become myopic. Older patients may even claim that they no longer need their reading glasses (i.e. presbyopia is temporarily corrected by lens swelling).

Question 18

What are the most common long-term complications of DM?

Answer 18

• Atherosclerosis, CAD, MI. Often have “silent” heart attacks (no chest pain due to autonomic neuropathy).
• Retinopathy. Leading cause of blindness in U.S. for persons under 50 y/o.
• Nephropathy. #1 cause of ESRD requiring hemodialysis (30% of cases, HTN is a close second).
• Peripheral vascular disease. Leading cause of limb amputation and may lead to claudication, stroke, and impotence.
• Peripheral neuropathy
• Increased risk of infection. WBC do not function as well in hyperglycemic environment. This plus inability to sense pain and clogged arteries that cannot deliver white cells to site of infection.

Question 19

What is the characteristic renal pathology in DM when viewed under micrograph?

Answer 19

Acellular Kimmelstiel-Wilson nodules
Hyalinization of arterioles which can be seen in HTN but characteristically affects BOTH efferent and afferent arterioles (vs. only afferent arterioles in HTN).

Question 20

What problems may result from diabetic peripheral neuropathy?

Answer 20

• Gastroparesis. Because the stomach does not empty well, patients experience early satiety and vomiting. Treat with motility enhances (e.g. metoclopramide).
• Charcot joints. Deformed secondary to lack of sensation. Patients may break a bone and not feel it.
• Impotence
• Cranial nerve palsies (esp. CN III, IV, and VI). Patients present with diplopia and extrocular muscle paralysis, which should resolve within 8 weeks without treatment.
• Orthostatic hypotension. When patient is well hydrated but arteries do not “clamp down” when stands up and heart rate fails to increase.
• Pressure ulcers in feet. Lack of sensation leads to overuse or failure to rest an injured or tired foot. Should all wear socks and comfortably fitting shoes and inspect feet regularly.

Question 21

Describe the treatment for diabetic retinopathy.

Answer 21

• Proliferative (neovascularization or new, irregular vessel formation) - panretinal laser photocoagulation. Laser beam is used to burn tiny spots around the periphery of the retina, sparing the central retina, to prevent progression to blindness.
• Symptomatic (macular edema) nonproliferative - focal (limited) laser photocoagulation

Question 22

What is the difference in onset of action, action peak, and total duration of action between regular insulin and NPH insulin?

Answer 22

Regular insulin: starts to work in 45 minutes, action peaks around 3-4 hours after injection, duration of action is 6-8 hours
NPH insulin: start to work in 1-1.5 hours, action peaks at 6-8 hours, duration of action is 12-20 hrs

Question 23

If the patient has high (or low) glucose at 7 AM, what insulin adjustment should you make?

Answer 23

Increase (or decrease) NPH insulin at dinner the night before

Question 24

If the patient has high (or low) noon glucose, what insulin adjustment should you make?

Answer 24

Increase (or decrease) the AM dose of regular insulin

Question 25

If the patient has high (or low) glucose at 5 PM, what insulin adjustment should you make?

Answer 25

Increase (or decrease) the AM dose of NPH insulin

Question 26

If the patient has high (or low) glucose at 9 PM, what insulin adjustment should you make?

Answer 26

Increase (or decrease) the dinner-time dose of regular insulin

Question 27

Define the Somogyi effect

Answer 27

Body’s reaction to hypoglycemia. If too much NPH insulin is given at dinner, the glucose level at 3 AM on the morning will be low. The body reacts to this by releasing stress hormones, which cause a high glucose level at 7 AM. The treatment is to decrease evening (NPH) insulin.

Question 28

Define the dawn phenomenon

Answer 28

Hyperglycemia caused by normal secretion of growth hormone early in the morning. Glucose level is high at 7 AM and normal or high at 3 AM (no hypoglycemia). The treatment is to increase evening (NPH) insulin.

Question 29

How do you manage diabetic patients who are not allowed to eat because they are scheduled for surgery?

Answer 29

Generally, 1/3-1/2 of the normal dose of insulin is given. Glucose is monitored intra- and postoperatively by the anesthesiologist. Regular IV insulin can be given to control glucose levels.

Question 30

What is the deal with beta blockers, hypoglycemia, and diabetics?

Answer 30

If you give a beta blocker to a diabetic patient, you will mask the classic symptoms of hypoglycemia (tachycardia, diaphoresis), which are caused by catecholamine release. You must weight the risk-benefit ratio of using these in diabetics. If the patient is having or has had a previous MI, the benefits outweigh the risks.

Question 31

What are the best oral agents to use in type 1 diabetes?

Answer 31

None. Patients with type 1 DM require insulin. Currently available oral agents do not work for them.

Question 32

What is the first treatment for type 2 diabetes?

Answer 32

Weight loss, because it may reduce glucose levels by reducing insulin resistance. Oral agents are tried first, typically metformin. Other agents include insulin secretagogues (glipizide, glimepiride, nateglinide, glyburide, repaglinide), thiazolidinediones (rosiglitazone, pioglitazone), alpha-glucosidase inhibitors (acarbose, miglitol), incretin mimetics (exenatide), incretin enhancers (saxagliptin, sitagliptin), and amylin analogues (pramlintide). Many type 2 diabetics eventually require insulin.