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Outpatient DM Management
Terms in this set (33)
Who should be screened for diabetes?
- Adults with BMI >/=25 (23 if Asian) PLUS one other risk factor
- All adults >/= 45 yo regardless of risk factors
How often should they be re-screened?
- if normal, every 3 years
- if pre-diabetes, every year
What are the cutoffs for pre-diabetes diagnosis for: fasting plasma glucose? A1C? 2-hr glucose tolerance?
- fasting plasma glucose: 100-125
- A1C: 5.7-6.4
- 2hr tolerance: 140-199 (pregnant women!)
What are the cutoffs for diabetes diagnosis for: fasting plasma glucose? A1C? 2-hr glucose tolerance? symptoms of hyperglycemia?
- fasting plasma glucose: >/= 126
- A1C: >/= 6.5
- 2hr tolerance: >/= 200
- hyperglycemia sx: >/= 200 RANDOM glucose
How many abnormal test(s) needed to diagnose pre-DM or DM?
need at least TWO abnormal test results!
What are some disadvantages of the A1C as a test?
- less sensitive than fasting glucose
- affected by hemoglobin variants (sickle cell) and RBC turnover (anemia)
When can metformin be given in a patient who does NOT have a diagnosis of diabetes?
When patient has a high risk of development of diabetes! Ex:
- A1C >6%
- Family history of DM
- BMI >35
- Age <60
What are the general treatment goals for diabetics? (note: not true for everyone and must be individualized!)
- A1C <7%
- Fasting glucose 80-130
- 2 hr post prandial < 180
Which of those treatment goals is predictive of decreased amount of microvascular complications?
A1C <7 => decreased microvascular complications (retinopathy, nephropathy, neuropathy)
Which patient factors would lead you to aim for a lower A1C? (A1C goal <6)
- more recent diagnosis of DM
- more motivated patient
- longer life expectancy
- no/less comorbidities
- no/less microvascular and macrovascular complications
- lower risk of hypoglycemia
- better support systems
Patients with opposite? Probably aim for A1C <8
GLUT4 is in the membranes of which types of tissues?
Peripheral tissues! Especially adipose and muscle
How does glucose uptake have different effects in the liver vs in muscles vs in adipose tissue?
- liver: increased glycogenesis and decreased glycogenolysis
- muscle: increased protein synthesis and glycogen storage
- adipose tissue: increased triglyeride storage
How do insulin and glucose differ in their affects on serum K?
Insulin drives K into cells; glucose drives it into serum
(remember that you have to give K to patients you are treating for DKA because you are giving them lots of insulin, which will deplete their serum K and may cause hypokalemia!)
What are the short acting insulins?
GIRLS AND LADS
15-45 mins; used in meal-times
What are the intermediate acting insulins?
- regular insulin
What are the long acting insulins?
Can last up to 24hrs
Sulfonylureas: MOA? Name a few? SE's?
- MOA: close the K channels and cause endogenous release of insulin
- name: glyburide, glipizide, glimepiride, -glinides
- SE: weight gain, hypolgycemia, sulfa allergy, disulfiram-like reaction with alcohol
GLP1-agonists: MOA? Name a few? SE's?
- MOA: activate GLP1 => increased insulin release and satiety, decreased glucagon release (which then lowers serum glucose levels) and gastric emptying
- name: -TIDE, exenatide, liraglutide
- SE: decreased gastric emptying, pancreatitis, N/V, injection site reactions, risk of CVD and medullary thyroid cancer, weight loss
do NOT cause hypoglycemia
DPP-4 inhibitors: MOA? Name a few? SE's?
- MOA: inhibit DPP4, which normally breaks down GLP1, so in turn they increase GLP1
- name: "clipped clothespins", - GLIPTINS, sitagliptin, linagliptin, saxagliptin
- SE: decreased gastric emptying, URI's, nasopharyngitis
do NOT cause hypoglycemia
Metformin: MOA? SE's?
- MOA: decreased hepatic gluconeogenesis, increased insulin sensitivity
- SE's: lactic acidosis esp in renal insufficiency, GI effects (N/V/D), modest weight loss, vitamin B12 deficiency in long-term use
TZD's: MOA? Name a few? SE's?
- MOA: increase insulin sensitivity through PPAR-y, upregulate GLUT4
- name: -glitazones
- SE's: weight gain, decreased triglycerides, fluid retention/peripheral edema, exacerbated CHF, decreased bone mineral density (esp in women)
Amylin analogues: MOA? Name a few? SE's?
- MOA: decreased glucagon
- name: pramlintide
- SE: decreased gastric emptying, hypoglycemia, GI effects
good for both T1 and T2! good for post-prandial spike
Acarbose: MOA? SE's?
- MOA: delay carb absorption in GI
- SE: GI effects
good for post-prandial spike
SGLT2-inhibitors: MOA? Name a few? SE's?
- MOA: reabsorb glucose in proximal tubule to release glucose in urine
- Name: -FLOZIN (floss), canagliflozin, dapagliflozin
- SE: UTI's, vaginal candidal infection, hypotension (d/t osmotic diuresis) - can be beneficial in people with HTN!, weight loss, contraindicated in renal insufficiency
Brand names for SGLT2 inhibitors?
- Farxiga (dapagliflozin)
- Jardiance (empagliflozin)
- Invokana (canagliflozin)
Brand names for GLP1-agonists?
- Dulaglutide (Trulicity)
- Exenatide (Byetta)
- Liraglutide (Victoza)
- Lixisenatide (Adlyxin)
- Semaglutide (Ozempic)
Brand names for DPP4-inhibitors?
- Linagliptin (Tradjenta)
- Saxagliptin (Onglyza)
- Sitagliptin (Januvia)
Brand names for TZD's?
When to consider insulin in a patient with Type 2 DM?
- when A1C >10, symptomatic, or glucose toxicity
- not at goal despite oral meds or injections
What regimen is insulin started on?
Start basal (NPH, glargine, or detemir) once daily, usually at 10 units per day. Then increase the dose by 2 units every 3 days until they achieve target fasting glucose (80-130)
When would you start a meal-time insulin?
What regimen do you start at?
If fasting blood glucose is at goal but A1C is not.
Start at 2-4u of aspart or lispro with largest meal. (does not need to be TID from the start). Increase dose by 1-2u until achieve post-prandial target (<180 at 2 hrs post-prandial)
What is the name of the pre-mixed insulin? (mixed long and short acting)
Novolin! It's 70/30 of NPH/regular
How often do you test A1C in a diabetic?
Every 6 months if at goal. Every 3 months if changing therapy or not at goal.
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