Diabetes Mellitus Flashcards
Outline the current recommendations for DM screenings
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.
Does DM1 or DM2 develop ketoacidosis? Hyperosmolar state?
DM1: ketoacidosis
DM2: hyperosmolar state
What is the level of endogenous insulin in DM1 vs. DM2?
DM1: low to none
DM2: normal to high (insulin resistance)
What is the twin concurrence in DM1 vs. DM2? Is there an HLA association in either one?
DM1: 50%, NO HLA association
Does DM1 or DM2 respond to oral hypoglycemics?
DM2 responds to oral hypoglycemics
Does DM1 or DM2 have antibodies to insulin?
DM1 has antibodies to insulin at diagnosis
Is DM1 or DM2 at risk for diabetic complications?
BOTH
What is the islet-cell pathology in DM1 vs. DM2?
DM1: insulitis (loss of most B cells)
DM2: normal number, but with amyloid deposits
What are the goals of treatment in terms of glucose levels?
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
What is a good measure of long-term diabetes control?
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
When a nondiabetic patients presents with hypoglycemia, how can you distinguish between factitious disorder (exogenous insulin) and an insulinoma (endogenous insulin)?
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.
What should you remember before giving IV iodinated contrast material to a diabetic patient or a patient with renal insufficiency?
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).
What is diabetic ketoacidosis?
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.
What is the treatment for DKA?
IV fluids, insulin, electrolyte replacement (esp. potassium and phosphate).
Mortality rate of DKA with current treatment efforts is less than 10%.
What is the most common cause of DKA?
- Insulin therapy noncompliance
2. Infection
What is nonketotic hyperglycemic hyperosmolar state? How is it treated?
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.
What are the classic presenting symptoms of new-onset diabetes?
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).
What are the most common long-term complications of DM?
- 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.
What is the characteristic renal pathology in DM when viewed under micrograph?
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).
What problems may result from diabetic peripheral neuropathy?
- 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.
Describe the treatment for diabetic retinopathy.
- 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
What is the difference in onset of action, action peak, and total duration of action between regular insulin and NPH insulin?
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
If the patient has high (or low) glucose at 7 AM, what insulin adjustment should you make?
Increase (or decrease) NPH insulin at dinner the night before
If the patient has high (or low) noon glucose, what insulin adjustment should you make?
Increase (or decrease) the AM dose of regular insulin
