Endocrinology And Diabetes Chapter 26 Paauw

Front 1

What is the difference between type 1 and type 2 diabetes?

Back 1

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.

Front 2

What is the major risk factor for type 1 diabetes?

Back 2

The major risk factor for type 1 diabetes is an identical twin with type 1 diabetes.

Front 3

What is the major risk factors for type 2 diabetes?

Back 3

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

Front 4

What types of drugs can exacerbate glucose intolerance?

Back 4

1. steroids
2. thiazide diuretics
3. niacin
4. protease inhibitors
5. glucosamine
6. beta-blockers

Front 5

How does diabetic ketoacidosis occur?

Back 5

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.

Front 6

What are the key features of DKA?

Back 6

Key features include:
1. hyperglycemia
2. elevated ketones
3. anion-gap acidosis

Front 7

What are some common precipitants of DKA?

Back 7

1. infection (50%)
2. lack of insulin
3. new diabetes

Front 8

What is hyperglycemia hyperosmolar nonketotic coma (HHNC)?

Back 8

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%.

Front 9

Is DKA common in type 2 diabetes?

Back 9

No, ketoacidosis is uncommon because patients have enough insulin to prevent ketone production.

Front 10

What are common precipitants of HHNC?

Back 10

1. infection
2. heart attack
3. stroke
4. uremia
5. pancreatitis
6. parenteral nutrition

Front 11

How do I diagnose diabetes?

Back 11

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.

Front 12

Can you use glycosylated hemoglobin (HgbA1C) for diagnosing diabetes?

Back 12

No, "A1C" is too insensitive.

Front 13

How do you screen for gestational diabetes?

Back 13

You do an oral glucose tolerance test.

Front 14

Patients have type 2 diabetes on average of how many years prior to being diagnosed?

Back 14

10-12 years

Front 15

Who should be screened for diabetes?

Back 15

The ADA recommends screening those with one or more risk factors beginning at age 30. Screening includes risk factor evaluation and fasting plasma glucose.

Front 16

How do patients under 20 years old with type 1 diabetes usually present?

Back 16

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.

Front 17

How does DKA present?

Back 17

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

Front 18

How do patients with type 2 diabetes commonly present?

Back 18

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.

Front 19

What are some presentations of end-organ damage in diabetes?

Back 19

1. altered vision (retinopathy)
2. peripheral edema (nephropathy)
3. sensory changes in the distal extremities (neuropathy)

Front 20

Because patients with type 1 diabetes may have autoimmune destruction of other endocrine glands, what lab value should you check?

Back 20

TSH

Front 21

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?

Back 21

History:
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

Front 22

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?

Back 22

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

Front 23

A1C estimates average blood glucose over the prior three months. How often should you get this lab?

Back 23

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.

Front 24

How are the cardiovascular risk factors?

Back 24

1. cigarette use
2. cholesterol
3. hypertension
4. family history of CV disease

Front 25

What type of questions should you ask in a history during a follow-up exam on a diabetic?

Back 25

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

Front 26

What tests are appropriate for patients with DKA or hyperosmolar coma?

Back 26

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.

Front 27

Serum osmolarity greater than what can cause altered mental status?

Back 27

greater than 330

Front 28

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?

Back 28

Get a head CT and LP

Front 29

What are the target A1C for diabetics?

Back 29

less than or equal to 6.5% (normal is 4% to 6%)

Front 30

What is the goal fasting blood glucose for diabetics?

Back 30

Fasting blood glucose should be less than 110 mg/dL

Front 31

What is the goal for 2 hour postprandial glucose for diabetics?

Back 31

It should be less than 140 mg/dL

Front 32

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?

Back 32

50%-75% less likely to develop end-organ complications.

Front 33

How do I choose a starting dose of insulin for a type 1 diabetic?

Back 33

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.

Front 34

What is the glargine/lispro combination regimen?

Back 34

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.

Front 35

For less intensive insulin therapy, you can give 2 shots per day. What can you use?

Back 35

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).

Front 36

If treating diabetics, what if nighttime hypoglycemia becomes a problem? What do you do?

Back 36

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.

Front 37

Most patients with type 2 diabetes require diet and an oral agent. What proportion will eventually need insulin?

Back 37

About a third of type 2 patients will eventually need insulin; many patients feel better and achieve better glycemic control on insulin.

Front 38

When can diet and exercise take place of medications in patients with type 2 diabetes?

Back 38

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.

Front 39

When are diet and oral agents not enough to control type 2 diabetes? Meaning you have to initiate insulin therapy.

Back 39

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.

Front 40

Which oral agent should I use for nonobese patients who need more than dietary treatment?

Back 40

They should start with a sulfonylurea to stimulate pancreatic insulin secretion and decrease insulin resistance.

Front 41

Which oral agent should I use for overweight patients or patients with high triglycerides?

Back 41

They do well on metformin, which lowers lipids and doesn't cause the weight gain common with sulfonylureas and insulin.

Front 42

When is metformin contraindicated?

Back 42

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.

Front 43

When should metformin be temporarily stopped?

Back 43

1. sepsis
2. hypoxia
3. dehydration
4. patients undergoing surgery
5. proceures requiring intravenous contrast dye.

Front 44

Oral agents lower A1C by how much?

Back 44

Oral agents lower the A1C by 1%-2%, except acarbose (0.5% reduction)

Front 45

What should I do if one oral agent is not enough?

Back 45

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.

Front 46

The combination of metformin and glyburide lowers the A1C by how much?

Back 46

about 3%

Front 47

When would a patient with type 2 diabetes on oral agents need insulin (when they normally don't need insulin)?

Back 47

Acute illness or medications such as prednisone can exacerbate hyperglycemia, necessitating short-term insulin use.

Front 48

How can I prevent nephropathy and renal failure?

Back 48

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

Front 49

When is ACEi contraindicated?

Back 49

1. pregnancy
2. if ACEi causes hyperkalemia
3. if ACEi causes angioedema

Front 50

Elevated creatinine alone should not prevent ACEi use. At what creatinine levels is ACEi use for HTN (in a diabetic) still "safe"?

Back 50

Cr of 3 to 4

Front 51

What do you do if a patient has a creatinine higher than 3 or 4 and they are taking ACEi?

Back 51

They are at increased risk for hyperkalemia. Monitor their electrolytes and keep them volume replete. Be sure they do not take potassium supplements.

Front 52

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.

Back 52

T

Front 53

A patient with type 2 diabetes is on sulfonylurea. He is ill or fasting for a procedure. How do I adjust therapy?

Back 53

Patients with type 2 diabetes can hold or decrease sulfonylurea doses and monitor chemsticks.

Front 54

A patient with type 2 diabetes is on metformin. He is ill or fasting for a procedure. How do I adjust therapy?

Back 54

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.

Front 55

A patient with type 1 diabetes is ill or fasting for a procedure. How do I adjust therapy?

Back 55

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.

Front 56

How do I treat hypoglycemia?

Back 56

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.

Front 57

T or F: Hypoglycemia is the most common endocrine emergency.

Back 57

T

Front 58

What are the risk factors for hypoglycemia?

Back 58

1. intensive therapy

2. decreased clearance of insulin or sulfonylureas

Front 59

How does someone with hypoglycemia present?

Back 59

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.

Front 60

What are common reasons to hospitalize patients with diabetes?

Back 60

1. DKA
2. hyperosmolar coma
3. severe infections
4. severa nausea and vomiting
5. cardiac ischemia

Front 61

What do you do when a diabetic patient has cellulitis and foot ulcers?

Back 61

Give IV antibiotics

Front 62

A patient with DM has malignant otitis externa, an uncommon but life-threatening pseudomonal infection of the external ear. What do you do?

Back 62

Give IV antibiotics

Front 63

What are some other life-threatening infections seen with diabetes?

Back 63

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).

Front 64

How do I treat patients with DKA initially?

Back 64

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.

Front 65

What is the screening test for retinopathy? How often should it be performed?

Back 65

Opthalmology referral.

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

Type 2: yearly starting at diagnosis

Front 66

What is the treatment for retinopathy?

Back 66

laser therapy

Front 67

What is the screening test for nephropathy? How often should it be performed?

Back 67

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

Front 68

What is the treatment for nephropathy?

Back 68

1. ACEi
2. ARB
3. BP control

Front 69

What is the screening test for neuropathy? How often should it be performed?

Back 69

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

Front 70

What is the treatment for neuropathy?

Back 70

1. tricyclic antidepressants
2. gabapentin
3. carbamazepine
4. capsaicin cream

Front 71

What is the screening test for heart disease? How often should it be performed?

Back 71

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

Front 72

What is the treatment for heart disease?

Back 72

1. lower lipids with statin to LDL less than 100

2. beta-blockers post-MI.

Front 73

What is the screening test for gastroparesis? How often should it be performed?

Back 73

Ask about symptoms of early satiety, nausea, emesis.

Do an uppder GI series or nuclear medicine gastric emptying study.

Front 74

What is the treatment for gastroparesis?

Back 74

1. Metoclopramide
2. Erythromycin

Front 75

What does lag time refer to in terms of insulin therapy?

Back 75

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)

Front 76

What is the onset, peak and duration of Lispro (Humalog)?

Back 76

Action is immediate.
Onset: 5 to 15 minutes
Peak: 0.5 to 1.5 hours
Duration: less or equal to 5 hours

Front 77

What is the onset, peak and duration of Regular (Humulin R)?

Back 77

Action is rapid.
Onset: 30 to 60 minutes
Peak: 1 to 5 hours
Duration: 5 to 7 hours

Front 78

What is the onset, peak and duration of NPH (Humulin N)?

Back 78

Action is intermediate.
Onset: 3 to 4 hours
Peak: 6 to 12 hours
Duration: 18 to 28 hours

Front 79

What is the onset, peak and duration of Ultralente (Humulin U)?

Back 79

Action is prolonged.
Onset: 4 to 6 hours
Peak: 12 to 14 hours
Duration: 36 hours

Front 80

What is the onset, peak and duration of Glargine (Lantus)?

Back 80

Action is prolonged.
Onset: 2 hours
Peak: none
Duration: 24 hours

Front 81

What is the onset, peak and duration of 70/30 (Humulin 70%N/30%R)?

Back 81

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

Front 82

When would you use Humulin 75/25 versus Humulin 70/30?

Back 82

Humulin 75/25, 75% N and 25% Lispro is available and may be better for people with high carbohydrate diets.

Front 83

What is the primary action of sulfonylureas (e.g. glyburide)?

Back 83

Increased pancreatic insulin secretion

Front 84

What is the major side effect of sulfonylureas (e.g. glyburide)?

Back 84

hypoglycemia and weight gain

Front 85

What can sulfonylureas be used in combination with?

Back 85

metformin and insulin

Front 86

What is the dosage for sulfonylureas?

Back 86

1.25 to 10 mg/d

Front 87

What is the primary action of biguanides (e.g. metformin)?

Back 87

decrease gluconeogenesis

Front 88

What is the major side effect of biguanides (e.g. metformin)?

Back 88

GI intolerance and lactic acidosis

Front 89

What can biguanides be used in combination with?

Back 89

sulfonylurea

Front 90

What is the dosage for biguanides?

Back 90

1000 to 2550 mg/d divide bid to tid

Front 91

What is the primary action of meglitinides (e.g. repaglinide)?

Back 91

increase pancreatic insulin secretion

Front 92

What is the major side effect of meglitinides (e.g. repaglinide)?

Back 92

hypoglycemia and weight gain

Front 93

Meglitinides and sulfonylureas are similar in their primary action and major side effects, what are their differences?

Back 93

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.

Front 94

What can meglitinides be used in combination with?

Back 94

metformin

Front 95

What is the dosage for meglitinides?

Back 95

0.5 to 4 mg before each meal

Front 96

What is the primary action for thiazolidinediones (e.g. pioglitazone and rosiglitazone)

Back 96

increased uptake at the muscle

Front 97

What are the major side effects of the glitazones?

Back 97

edema, weight gain, CHF, possibly liver toxicity

Front 98

What can the glitazones be used in combination with?

Back 98

sulfonylurea, metformin, insulin

Front 99

What is the dosage for pioglitazone?

Back 99

15-45 mg/d

Front 100

What is the dosage for rosiglitazone?

Back 100

2-8 mg/d

Front 101

What is the primary action of alpha glucosidase inhibitors (e.g. acarbose)?

Back 101

slows down absorption

Front 102

What are the major side effects of alpha glucosidase inhibitors?

Back 102

intestinal gas and abdominal pain

Front 103

What can alpha glucosidase inhibitors be used in combination with?

Back 103

sulfonylurea and metformin

Front 104

What is the dosage for alpha glucosidase inhibitors?

Back 104

50-100 mg tid

Front 105

When treating a patient with DKA, what do you do when serum glucose drops down to 250?

Back 105

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.

Front 106

When treating a patient with DKA, when can insulin be changed to the outpatient regimen?

Back 106

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.

Front 107

How do I treat patients with hyperosmolar coma?

Back 107

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.