Diabetes mellitus Flashcards
current recommendations for diabetes mellitus screening
universal screening is not recommended, but is generally more accepted in folks who are
- obese
- >45 yo
- (+) family hx
- certain ethnic groups (black, hispanic, pima indian)
mandatory in pregnancy!
When are the tests and criteria for diagnosing diabetes
- a glucose ≥ 126 mg/dL after an overnight (or 8-hour) fast on two separate occasions
- a random glucose level > 200 mg/dL
- an oral glucose tolerance test > 200 mg/dL after two hours after receiving a 75g oral dose of glucose
- Hb A1c ≥ 6.5% on two separate occasions
What are the classic differences between type I and II diabetes in terms of:
What are the post-prandial and fasting glucose level goals of treatment in terms of glucose levels?
postprandial glucose levels < 180 mg/dL
fasting glucose levels between 70 - 130 mg/dL.
What is a good measure of long-term diabetes control?
A1c levels < 7%
fyi: A rough rule of thumb is that HbA1c x 20 = average blood glucose level
When a nondiabetic patient presents with hypoglycemia, how can you distinguish between factitious disorder (exogenous insulin) and an insulinoma (endogenous insulin)?
measure C-peptide level
C-peptide is produced whenever the body makes insulin, but it is absent in prescription insulin preparations.
Therefore, C-peptide is high with an insulinoma and low with factitious disorder
What should you remember before giving IV iodinated contrast material to a patient with diabetes or a patient with renal insufficiency?
Diabetic patients and patients with renal insufficiency are prone to acute renal failure from the intravenously administered iodinated contrast agents
If you must give contrast, first hydrate the patient with IV fluids to avoid renal shutdown. Acetylcysteine and bicarbonate may decrease the risk of contrast nephropathy in patients at high risk.
The concerns about IV iodinated contrast do not apply to oral contrast agents (e.g., barium).
What is diabetic ketoacidosis (DKA)?
What usually precipitates this?
How do these patients classically present?
How is it treated?
DKA is a medical emergency that occurs in Type I diabetics when their insulin levels become depleted; commonly due to non-compliance with insulin therapy or infection
Presentation: Kussmaul breathing (deep, rapid respirations), dehydration, hyperglycemia, acidosis (due to excessive ketone formation), and increased ketones in the serum (fruity breath) and urine.
Treatment: IVF, insulin, electrolyte replacement (K and Phosphate); do not use bicarbonate to correct acidosis!
What is nonketotic hyperglycemic hyperosmolar state?
How is it treated?
Hyperglycemic hyperosmolar state - medical emergency that occurs predominantly in Type 2 diabetics, where hyperglycemia + hyperosmolar serum are present in the absence of ketones and acisois; results in severe dehydration +/- mental status changes
Treatment: fluids, fluids, fluids! insulin + electrolytes
What are the classic presenting symptoms of new-onset diabetes?
Polyuria, polydipsia, and polyphagia
candidal infections (thrush vs candiasis)
weight loss (due to xs urination)
blurry vision (prolonged hyperglycemia causes lens to swell -> myopic)
older folks may claim that they no longer need reading glasses (presbyopia is temp. corrected by lens swelling)
What are the common long-term complications of diabetes mellitus?
LOTS
- Atherosclerosis, CAD, MI
- Retinopathy - #1 cause of blindness < 50 yo in US
- Nephropathy - #1 cause of ESRD requiring hemodialysis (HTN is a close second).
- Peripheral vascular disease - #1 cause of limb amputation; may lead to claudication, strokes, and impotence.
- Peripheral neuropathy - causes “silent” heart attacks, numbness in the feet, and other findings
- Increased risk for infection - WBC do not function as well in a hyperglycemic environments; moreover, clogged arteries cannot deliver them to the site of an early infection and patients with diabetes have decreased ability to sense pain, leading to increased risk for infection.
All of these complications can be delayed or even prevented by good glucose control.
What problems may result from diabetic peripheral neuropathy?
LOTS
- Gastroparesis - the stomach does not empty well, patients experience early satiety and vomiting. Treat with motility enhancers, such as metoclopramide.
- Charcot joints - deformed joints secondary to lack of sensation; patients may break a bone and not feel it.
- Impotence - due to neuropathy and atherosclerosis.
- Cranial nerve palsies (esp CN 3, 4, and 6) - diplopia and extraocular muscle paralysis, which should resolve within 8 weeks without treatment.
- Orthostatic hypotension - occurs even when the patient is well hydrated because the arteries do not “clamp down” when the patient stands up, and the heart rate fails to increase appropriately.
- Pressure ulcers in the feet - lack of sensation leads to overuse or failure to rest an injured/tired foot
- Neurogenic bladder
Describe the treatment for diabetic retinopathy.
Panretinal laser photocoagulation - for proliferative retinopathy (neovascularization or new, irregular vessel formation)
Focal (limited) laser photocoagulation - for nonproliferative retinopathy only when symptoms are present (from macular edema).
Describe the onset, peak, and duration of action of each of the insulin preparations.
