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107 Cards in this Set

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What is the difference between type 1 and type 2 diabetes?
Diabetes occurs when inadequate insulin results in high blood sugar. Patients with type 1 diabetes stop making insulin. A combination of genetic predisposition and an environmental trigger, possibly a viral infection, causes autoimmune destruction of pancreatic islet B cells. These patients are generally young and slender. In type 2 diabetes, insulin secretion is not absent and may actually be elevated, but is not sufficient to overcome insulin resistance. Patients are usually obese and older than age 30.
What is the major risk factor for type 1 diabetes?
The major risk factor for type 1 diabetes is an identical twin with type 1 diabetes.
What is the major risk factors for type 2 diabetes?
1. Prior gestational diabetes or newborn greater than 9 lb
2. Overweight
3. Inactivity
4. Race (Native American, Hispanic, African American, Asian American, or Pacific Islander)
5. Hypertension
6. Family history of type 2 diabetes
7. Dyslipidemia
8. Polycystic ovary syndrome
9. History of glucose intolerance
What types of drugs can exacerbate glucose intolerance?
1. steroids
2. thiazide diuretics
3. niacin
4. protease inhibitors
5. glucosamine
6. beta-blockers
How does diabetic ketoacidosis occur?
DKA occurs in type 1 diabetes when glucose cannot be utilized due to lack of insulin, causing accelerated starvation that forces the body to make ketones for fuel.
What are the key features of DKA?
Key features include:
1. hyperglycemia
2. elevated ketones
3. anion-gap acidosis
What are some common precipitants of DKA?
1. infection (50%)
2. lack of insulin
3. new diabetes
What is hyperglycemia hyperosmolar nonketotic coma (HHNC)?
When patients with type 2 diabetes get extremely hyperglycemic, they become hyperosmolar. High glucose draws free water out of cells and creates an osmotic diuresis, leading to dehydration and altered mental status. Many patients with HHNC are elderly and unable to drink enough fluids to compensate. Coma occurs in 10% and mortality is 10%-17%.
Is DKA common in type 2 diabetes?
No, ketoacidosis is uncommon because patients have enough insulin to prevent ketone production.
What are common precipitants of HHNC?
1. infection
2. heart attack
3. stroke
4. uremia
5. pancreatitis
6. parenteral nutrition
How do I diagnose diabetes?
1. a single plasma glucose greater than or equal to 200 mg/dL with symptoms such as polydipsia, polyuria, polyphagia and weight loss
2. a fasting plasma glucose greater than or equal to 126 mg/dL on two occasions.
Can you use glycosylated hemoglobin (HgbA1C) for diagnosing diabetes?
No, "A1C" is too insensitive.
How do you screen for gestational diabetes?
You do an oral glucose tolerance test.
Patients have type 2 diabetes on average of how many years prior to being diagnosed?
10-12 years
Who should be screened for diabetes?
The ADA recommends screening those with one or more risk factors beginning at age 30. Screening includes risk factor evaluation and fasting plasma glucose.
How do patients under 20 years old with type 1 diabetes usually present?
The presentation is often abrupt. Often, it can be ketoacidosis precipitated by an acute stressor such as a bacterial infection. Some patients with type 1 diabetes present with more gradual onset of malaise, weight loss, polydipsia, polyuria, or blurred vision.
How does DKA present?
Ketoacidosis may be accompained by:
1. Coma (10%)
2. Kussmaul breathing (rapid deep breaths in response to acidosis)
3. Fruity breath from elevated acetone
4. Dehydration
5. Hypotension
6. Tachycardia
How do patients with type 2 diabetes commonly present?
They usually present with obvious symptoms, or within weeks to months of polyuria, polydipsia, weight loss, or symptoms of end-organ complications. Patients with diabetes can also experience recurrent infections such as boils, carbuncles, and vaginal yeast infections. Elderly patients with new onselt type 2 diabetes may be in life-threatening hyperosmolar coma.
What are some presentations of end-organ damage in diabetes?
1. altered vision (retinopathy)
2. peripheral edema (nephropathy)
3. sensory changes in the distal extremities (neuropathy)
Because patients with type 1 diabetes may have autoimmune destruction of other endocrine glands, what lab value should you check?
Among patients with type 2 diabetes, 10%-15% have neuropathy, 37% have retinopathy, and 50% have CAD at diagnosis. So what should you ask during the history to detect complications?
1. duration of symptoms
2. polyuria, polydipsia
3. current diet/exercise pattern
4. CV symptoms
5. CV risk factors
6. Fhx of diabetes
7. vision disturbance
8. sensory changes in extremities
9. medications
Among patients with type 2 diabetes, 10%-15% have neuropathy, 37% have retinopathy, and 50% have CAD at diagnosis. So what should you do on physical exam to detect complications?
1. BP
2. BMI
3. funduscopic exam (for retinopathy)
4. thyroid exam (concurrent autoimmune disease)
5. carotid, femoral, abdominal renal artery bruits (for atherosclerotic disease)
6. sensory exam with monofilament (neuropathy)
7. extremities for edema and ulcers
8. skin (fungal infections may provide portal of entry for cellulitis)
9. acanthosis nigricans
A1C estimates average blood glucose over the prior three months. How often should you get this lab?
Obtain a baseline A1c and repeat every 6 months in patients who are stable at target. But repeat every 3 months in patients who are above target or who are changing therapy.
How are the cardiovascular risk factors?
1. cigarette use
2. cholesterol
3. hypertension
4. family history of CV disease
What type of questions should you ask in a history during a follow-up exam on a diabetic?
1. hyper- or hypoglycemia symptoms
2. glucose monitoring results
3. changes in vision
4. changes in food sensation
5. daily self exam of feet
6. medication tolerance
7. diet and exercise habits
What tests are appropriate for patients with DKA or hyperosmolar coma?
1. electrolytes
2. renal function
3. arterial blood gas
4. complete CBC
5. UA
6. blood & urine cultures and CXR (to look for precipitating infection, even if patient is afebrile)

Note: an elevated WBC (12-15), glucose greater than 250 mg/dL, elevated potassisum due to cellular shifts and anion gap acidosis with compensatory respiratory alkalosis are expected.
Serum osmolarity greater than what can cause altered mental status?
greater than 330
If serum osmolarity is less than 330 with altered mental status, or if mental status does not reverse after several hours of treatment, what should you do?
Get a head CT and LP
What are the target A1C for diabetics?
less than or equal to 6.5% (normal is 4% to 6%)
What is the goal fasting blood glucose for diabetics?
Fasting blood glucose should be less than 110 mg/dL
What is the goal for 2 hour postprandial glucose for diabetics?
It should be less than 140 mg/dL
In the Diabetes Control and Complications Trial (DCCT), type 1 patients treated with intensive therapy were how much less likely to have progression of retinopathy, nephropathy and neuropathy than those treated with conventional therapy?
50%-75% less likely to develop end-organ complications.
How do I choose a starting dose of insulin for a type 1 diabetic?
Type 1 diabetics need multiple daily subQ insulin injections: short-acting to cover meals (prandial) and long-acting for basal requirements.

Estimate total daily insulin dose by weight, starting at 0.5 to 1.0 U/kg/day.
What is the glargine/lispro combination regimen?
Basal (glargine)/prandial (lispro) combination regiments give half of the insulin as basal and the other half prior to meals as lispro. The lispro is based on pre-meal glucose level and the anticipated amount to be eaten.
For less intensive insulin therapy, you can give 2 shots per day. What can you use?
Use neutral protamine Hagedorn (NPH) and regular or lispro insulin.

Give two-thirds the dose in the AM (2/3 NPH, 1/3 regular) and one-third in the evening (split 1/2 NPH, 1/2 regular).
If treating diabetics, what if nighttime hypoglycemia becomes a problem? What do you do?
There are two options:

1. Give NPH at bedtime instead of with dinner so the peak effect occurs later when early AM growht hormone and cortisol levels naturally increase blood sugar.

2. Alternatively, substitue glargine for NPH since glargine provides twenty-four hours of basal insulin and is peakless and less likely to cause hypoglycemia.
Most patients with type 2 diabetes require diet and an oral agent. What proportion will eventually need insulin?
About a third of type 2 patients will eventually need insulin; many patients feel better and achieve better glycemic control on insulin.
When can diet and exercise take place of medications in patients with type 2 diabetes?
Asymptomatic patients near ideal body weight, with no complications, or with a fasting glucose level less than 200 mg/dL may do well with diet and exercise alone.
When are diet and oral agents not enough to control type 2 diabetes? Meaning you have to initiate insulin therapy.
For patients who are symptomatic, have complications, or have a fasting glucose greater than 300 mg/dL, diet and oral agents are usually not enough, so insulin is appropriate initial therapy.
Which oral agent should I use for nonobese patients who need more than dietary treatment?
They should start with a sulfonylurea to stimulate pancreatic insulin secretion and decrease insulin resistance.
Which oral agent should I use for overweight patients or patients with high triglycerides?
They do well on metformin, which lowers lipids and doesn't cause the weight gain common with sulfonylureas and insulin.
When is metformin contraindicated?
Metformin is contraindicated in patients...

1. older than age 80
2. CHF
3. liver disease
4. excessive alcohol use
5. creatinine greater than 1.4 mg/dL

*This is because of the risk of lactic acidosis.
When should metformin be temporarily stopped?
1. sepsis
2. hypoxia
3. dehydration
4. patients undergoing surgery
5. proceures requiring intravenous contrast dye.
Oral agents lower A1C by how much?
Oral agents lower the A1C by 1%-2%, except acarbose (0.5% reduction)
What should I do if one oral agent is not enough?
Many patients require combination therapy, either with a sulfonylurea plus metformin or an oral agent plus insulin.

Intermediate or long-acting insulin (0.1u/kg) can be added at bedtime.

Bedtime insulin decreases fasting glucose and causes less weight gain.
The combination of metformin and glyburide lowers the A1C by how much?
about 3%
When would a patient with type 2 diabetes on oral agents need insulin (when they normally don't need insulin)?
Acute illness or medications such as prednisone can exacerbate hyperglycemia, necessitating short-term insulin use.
How can I prevent nephropathy and renal failure?
1. Slow the progression of nephropathy by controlling HTN aggressively to BP less than 130/85.

2. Use ACEi when urine microalbumin is greater than 30 mg/L
When is ACEi contraindicated?
1. pregnancy
2. if ACEi causes hyperkalemia
3. if ACEi causes angioedema
Elevated creatinine alone should not prevent ACEi use. At what creatinine levels is ACEi use for HTN (in a diabetic) still "safe"?
Cr of 3 to 4
What do you do if a patient has a creatinine higher than 3 or 4 and they are taking ACEi?
They are at increased risk for hyperkalemia. Monitor their electrolytes and keep them volume replete. Be sure they do not take potassium supplements.
T or F: Beta-blockers and thiazide diuretics are strong choices for HTN, despite mild adverse effects on glycemic control and lipids. Patients with CAD gain greater benefit than harm from beta-blockers.
A patient with type 2 diabetes is on sulfonylurea. He is ill or fasting for a procedure. How do I adjust therapy?
Patients with type 2 diabetes can hold or decrease sulfonylurea doses and monitor chemsticks.
A patient with type 2 diabetes is on metformin. He is ill or fasting for a procedure. How do I adjust therapy?
Patients on metformin should stop this medication prior to procedures or surgery because of the small risk of lactic acidosis. Restart metformin after 48 hours if creatinine is stable.
A patient with type 1 diabetes is ill or fasting for a procedure. How do I adjust therapy?
Patients with type 1 diabetes always need insulin, regardless of food intake, to prevent keoacidosis. Since hepatic production accounts for about half of the serum glucose, give patients half their usual insulin in long-acting form, and monitor frequently. Alternatively, you may use an insulin drip.
How do I treat hypoglycemia?
Give oral glucose to conscious patients, and IV glucose and glucagon to unconcious patients. Hospitalize if the patient does not respond rapidly or if decreased renal clearance of insulin or sulfonylureas may cause recurrent symptoms of hypoglycemia.
T or F: Hypoglycemia is the most common endocrine emergency.
What are the risk factors for hypoglycemia?
1. intensive therapy

2. decreased clearance of insulin or sulfonylureas
How does someone with hypoglycemia present?
Low serum glucose alters mental status and induces a catecholamine response: sweating, shakiness, weakness, nausea and anxiety.

Remember, beta-blockers blunt hypoglycemic symptoms except for sweating.
What are common reasons to hospitalize patients with diabetes?
1. DKA
2. hyperosmolar coma
3. severe infections
4. severa nausea and vomiting
5. cardiac ischemia
What do you do when a diabetic patient has cellulitis and foot ulcers?
Give IV antibiotics
A patient with DM has malignant otitis externa, an uncommon but life-threatening pseudomonal infection of the external ear. What do you do?
Give IV antibiotics
What are some other life-threatening infections seen with diabetes?
1. Rhinocerebral mucormycosis
2. Emphysematous cholecystitis (E. coli or Clostridium)
3. Emphysematous pyelonephritis (E. coli or other gram-negative rods)
4. Necrotizing fasciitis (mixed anaerobes and aerobes).
How do I treat patients with DKA initially?
1. Aggressive hydration with normal saline
2. IV insulin (regular insulin, 10 U/IV bolus, followed by an insulin drip for at least 12-24 hours, with hourly glucose checks; adjust as needed.
3. Electrolyte monitoring and replacement, check potassium and phosphate as these are often depleted. Serum potassium levels may not reflect total body depletion because acidosis causes a shift from cells to plasma.
What is the screening test for retinopathy? How often should it be performed?
Opthalmology referral.

Type 1: yearly beginning 5 years after diagnosis: at diagnosis if age greater than 30

Type 2: yearly starting at diagnosis
What is the treatment for retinopathy?
laser therapy
What is the screening test for nephropathy? How often should it be performed?
Urine protein/creatinine ratio or 24 hour urine (microabluminuria = 30-300 mg/24 hours)

Type 1: yearly beginning 5 years after diagnosis

Type 2: yearly
What is the treatment for nephropathy?
1. ACEi
2. ARB
3. BP control
What is the screening test for neuropathy? How often should it be performed?
Foot exam: deformity, lesions, and sensory testing with a 5.0 monofilament

For both type 1 and type 2:
1. daily patient self checks
2. foot exam at every visit
3. yearly sensory testing
What is the treatment for neuropathy?
1. tricyclic antidepressants
2. gabapentin
3. carbamazepine
4. capsaicin cream
What is the screening test for heart disease? How often should it be performed?
ECG at diagnosis in patients with type 2; purse testing if chest or respiratory complaints

Type 1: fasting lipids at diagnosis, then follow lipid screening guidelines

Type 2: fasting lipids yearly
What is the treatment for heart disease?
1. lower lipids with statin to LDL less than 100

2. beta-blockers post-MI.
What is the screening test for gastroparesis? How often should it be performed?
Ask about symptoms of early satiety, nausea, emesis.

Do an uppder GI series or nuclear medicine gastric emptying study.
What is the treatment for gastroparesis?
1. Metoclopramide
2. Erythromycin
What does lag time refer to in terms of insulin therapy?
Lag time refers to the amount of time between an insulin injection and when a patient should eat. Lag time is approximately equal to onset of action (e.g., 30 minutes for regular insulin; little or no lagtime with Lispro)
What is the onset, peak and duration of Lispro (Humalog)?
Action is immediate.
Onset: 5 to 15 minutes
Peak: 0.5 to 1.5 hours
Duration: less or equal to 5 hours
What is the onset, peak and duration of Regular (Humulin R)?
Action is rapid.
Onset: 30 to 60 minutes
Peak: 1 to 5 hours
Duration: 5 to 7 hours
What is the onset, peak and duration of NPH (Humulin N)?
Action is intermediate.
Onset: 3 to 4 hours
Peak: 6 to 12 hours
Duration: 18 to 28 hours
What is the onset, peak and duration of Ultralente (Humulin U)?
Action is prolonged.
Onset: 4 to 6 hours
Peak: 12 to 14 hours
Duration: 36 hours
What is the onset, peak and duration of Glargine (Lantus)?
Action is prolonged.
Onset: 2 hours
Peak: none
Duration: 24 hours
What is the onset, peak and duration of 70/30 (Humulin 70%N/30%R)?
Action is a mix of intermediate (N) and rapid (R)
Onset: 30 to 60 minutes (R) and 3 to 4 hours (N)
Peak: 6 to 15 hours
Duration: 22 to 28 hours
When would you use Humulin 75/25 versus Humulin 70/30?
Humulin 75/25, 75% N and 25% Lispro is available and may be better for people with high carbohydrate diets.
What is the primary action of sulfonylureas (e.g. glyburide)?
Increased pancreatic insulin secretion
What is the major side effect of sulfonylureas (e.g. glyburide)?
hypoglycemia and weight gain
What can sulfonylureas be used in combination with?
metformin and insulin
What is the dosage for sulfonylureas?
1.25 to 10 mg/d
What is the primary action of biguanides (e.g. metformin)?
decrease gluconeogenesis
What is the major side effect of biguanides (e.g. metformin)?
GI intolerance and lactic acidosis
What can biguanides be used in combination with?
What is the dosage for biguanides?
1000 to 2550 mg/d divide bid to tid
What is the primary action of meglitinides (e.g. repaglinide)?
increase pancreatic insulin secretion
What is the major side effect of meglitinides (e.g. repaglinide)?
hypoglycemia and weight gain
Meglitinides and sulfonylureas are similar in their primary action and major side effects, what are their differences?
Repaglinide has a shorter half life, can be given with meals and skipped when meals are skipped. Possibly less hypoglycemia, but more expensive than sulfonylureas.
What can meglitinides be used in combination with?
What is the dosage for meglitinides?
0.5 to 4 mg before each meal
What is the primary action for thiazolidinediones (e.g. pioglitazone and rosiglitazone)
increased uptake at the muscle
What are the major side effects of the glitazones?
edema, weight gain, CHF, possibly liver toxicity
What can the glitazones be used in combination with?
sulfonylurea, metformin, insulin
What is the dosage for pioglitazone?
15-45 mg/d
What is the dosage for rosiglitazone?
2-8 mg/d
What is the primary action of alpha glucosidase inhibitors (e.g. acarbose)?
slows down absorption
What are the major side effects of alpha glucosidase inhibitors?
intestinal gas and abdominal pain
What can alpha glucosidase inhibitors be used in combination with?
sulfonylurea and metformin
What is the dosage for alpha glucosidase inhibitors?
50-100 mg tid
When treating a patient with DKA, what do you do when serum glucose drops down to 250?
IV fluids can be changed to D5 & 1/2 NS to prevent hypoglycemia and provide calories and free water. Before you were giving just NS to aggressively rehydrate.
When treating a patient with DKA, when can insulin be changed to the outpatient regimen?
When the bicarbonate normalizes, you can make the switch. The patient can also eat at this time. Continue the insulin drip at least one hour after the first subcutaneous injection to prevent recurrent ketone production.
How do I treat patients with hyperosmolar coma?
1. hydration with isotonic saline is the mainstay of therapy.
2. Insulin may be needed in lower doses than for DKA (5-10 U/IV bolus and 0.1 U/kg/h).
3. As with DKA, look for and treat any precipitating infection.