Endo-glucose metabolism Flashcards
Screening criteria for DM?
How often should you screen?
Screening of adults in primary care setting with at least one of the following risk factors:
- Age >45
- Overweight or Obese
- First degree relative with DM
- History of GDM
- History of PCOS
- High risk ethnicity: Black, alaskan native, asian American, hispanic
Screen every 3 years.
Diagnostic criteria for DM
Random plasma glucose >200
Fasting plasma glucose >126
Plasma glucose during a 2hr 75g OGTT >200
Hemoglobin A1C >6.5%
Diagnostic criteria for metabolic syndrome?
1) waist circumference >40 in men and >35 in women
2) Fasting TG >150 or on drug therapy for TGs
3) HDL cholesterol: Men <40, Women <50
4) BP: Systolic >130, DS >85, or on drug therapy for hypertension
5) Fasting glucose >100
What is the best way to prevent a prediabetic from getting diabetes?
Lifestyle modifications! It has proven to decrease the risk of patients with prediabetes developing type 2 diabetes by 41-58%
What are the thiazolidinediones?
They are: troglitazone, rosiglitazome, pioglitazone
What are strategies to prevent or delay onset of type II DM?
- Diet and exercise
- Smoking cessation
- Bariatric surgery
- Metformin
- Lipase inihibitors (Orlistat)
- Thiazolidoinediones (troglitazome, rosiglitazone, pioglitazone)
Are ACEI or ARBS effective at preventing DM?
No!
What is the A1C goal for…
- Healthy adults?
- Complex health issues?
- Older adults?
- Pregnant women?
- Healthy adults: 7%
- Complex Health issues: 8% without severe recurrent hypoglycemia
- Older adults: 7-8.5% depending on how impaired they are as an older adult
- Pregnant women: >6% without severe recurrent hypoglycemia
When should you self-monitor BG?
for multiple daily insulin injections…. for once daily or non-insulin regimens, wouldn’t worry too much about it
Look at page 8, insulin pharmacokinetics
! Look
INSULIN
Mechanism of action?
Effect on weight?
Risks and Concerns?
Long-term studies on definitive outcomes?
Mechanism of action?: decreases hepatic glucose production, increases peripheral glucose uptake
Effect on weight?: increases
Risks and Concerns?: hypoglyemia
Long-term studies on definitive outcomes?: decrease in microvascular and microvascular events
SULFONYLUREAS
Mechanism of action?
Effect on weight?
Risks and Concerns?
Long-term studies on definitive outcomes?
Mechanism of action?: stimulate insulin secretion
Effect on weight?: increase
Risks and Concerns?: hypoglycemia
Long-term studies on definitive outcomes?: decrease microvascular events but possible increase in microvascular
What are the sulfonylureas?
glipize, glyburide, glicazide, glimepiride
METFORMIN
Mechanism of action?
Effect on weight?
Risks and Concerns?
Long-term studies on definitive outcomes?
Mechanism of action? decrease hepatic glucose production, increase insulin mediated uptake of glucose in muscles
Effect on weight?: neutral
Risks and Concerns? diarrhea and abdominal discomfort, lactic acidosis
Long-term studies on definitive outcomes?: decrease micro and microvascular
THIAZOLIDINEDIONES
Mechanism of action?
Effect on weight?
Risks and Concerns?
Long-term studies on definitive outcomes?
Mechanism of action? increase peripheral glucose uptake
Effect on weight? neutral
Risks and Concerns? fluid retention
Long-term studies on definitive outcomes? may be harmful?
GLP-1 mimetics
Mechanism of action?
Effect on weight?
Risks and Concerns?
Long-term studies on definitive outcomes?
Mechanism of action?: slows gastric emptying, suppress glucagon secretion, increase satiety
Effect on weight? decrease
Risks and Concerns? hypoglycemia, nausea, pancreatitis
Long-term studies on definitive outcomes? none
GLP-1 mimetics
exenatide and liraglutide
DPP-4 inhibitors
sitagliptin, saxagliptin, vildagliptin, linagliptin, alogliptin
DPP-4 INHIBITORS
Mechanism of action?
Effect on weight?
Risks and Concerns?
Long-term studies on definitive outcomes?
Mechanism of action?: slows gastric emptying
Effect on weight?: neutral
Risks and Concerns? hypoglycemia
Long-term studies on definitive outcomes? none, but also increased risk of hospitalization for heart failure with saxagliptin
SGLT2 inhibitors
dapaglifozin and canagliflozin
SGTL2 inhibitors
Mechanism of action?
Effect on weight?
Risks and Concerns?
Long-term studies on definitive outcomes?
Mechanism of action? increases kidney excretion of glucose
Effect on weight? Decrease
Risks and Concerns? hypoglycemia, kidney impairment
Long-term studies on definitive outcomes?none
Inpatient blood glucose targets?
<140 premeal
<180 random
What is the differential diagnosis of spontaneous fasting hypoglycemia in patient w/o diabetes?
insulinoma
surreptitious use of sulfonylureas
surreptitious use of insulin
insulin autoimmune hypoglycemia
What is a sign of surreptitious insulin use
C-peptide will be low!
Postprandial hypoglycemia
Most often occurs with a former bariatric surgery
Occurs within
Postprandial hypoglycemia
Most often occurs with a former bariatric surgery
Occurs within 5 hours of food consumption
How to diagnose postprandial hypoglycemia?
Diagnosis: measure glucose, insulin pro-insulin, and c-peptide levels prior to the meal and repeat 30 minute intervals after or at the time of symptomatic hypoglycemia
- if symptomatic hypoglycemia–> measure insulin Abs
- oral hypoglycemic screen test obtained
How is postprandial hypoglycemia treated?
involves small, frequent complex meals composed of protein, fat, and carbohydrate to avoid the sensation of hypoglycemia
What are some lab abnormalities of DKA?
urine and serum ketones elevated
beta-hydroxybutyrate
Elevated anion gap
glucose can be normal and up to 700
stress related mild leukocytosis is usually present
serum sodium levels low due to osmotic shifts
serum potassium elevated due to shifts
Lab abnormalities of HHS?
normal or small amounts of urine or serum ketones, plasma glucose is >700
serum osmolality is elevated an greater than 320 mOsm/kg
Management of DKA and HHS?
FLUIDS: give normal saline at first (1L/h) then switch to 1/2 normal saline at 250-500 mL/hr if corrected serum sodium level becomes normal or high–> when glucose reaches 200-300, then switch to D5-1/2normal
INSULIN:Insulin drip, 0.1 units/kg
POTASSIUM: If potassium <3.3 do not start insulin and give potassium IV until it is >3.3, then add 20-30mEq of potassium chloride to each tier of IV druids to keep potassium at 4-5. If potassium >5.2, then just start insulin
CORRECTION OF ACIDOSIS: if pH <6.9–give sodium bicarb and potassium over2 hrs. If pH 6.9 or greater, do not give sodium bicarb
How often do you screen for diabetic retinopathy?
- Type 1 DM
- Type 2 DM
- Pregnant women
- Type 1 DM: start 5 yrs after dx, do annually
- Type 2 DM: start at dx, do annually
- Pregnant women: every trimester and then closely for 1 year postpartum
How often do you screen for diabetic nephropathy? And how?
- Type 1 DM
- Type 2 DM
- Pregnant women
- Type 1 DM: 5 years after dx, albumin-cr ratio on random spot urine
- Type 2 DM: at diagnosis, albumin-cr ratio on random spot urine
How often do you screen for diabetic neuropathy? And how?
- Type 1 DM
- Type 2 DM
- Pregnant women
DMI: at 5 years after dx, use 19t monofilament, 128 Hz tuning fork, ankle reflexes
DMII: 10-g monofilament, 128 Hz tuning form, ankle reflexes
Health maintenance for diabetics
CV–monitor for hypertension at every visit!
Dyslipidemia-Annually with a fasting lipid profile
What is screening for women with a history of gestational diabetes?
For women with a history of gestational diabetes, diabetes screening using standard criteria should occur at 4 to 12 weeks postpartum and every 3 years thereafter.
How is diabetes treated in pregnant women?
LIFESTYLE MEASURES FIRST. The ADA 2018 Standards of Medical Care recommends insulin as the preferred agent for management of type 1 and type 2 diabetes in pregnancy.
Treatment of Type I DM
Lifelong insulin therapy is the first-line treatment for type 1 diabetes; physiologic insulin therapy reduces early microvascular disease by 34% to 76% in patients with type 1 diabetes mellitus compared with nonphysiologic regimens.
Continuous subcutaneous insulin infusion is a cost-effective treatment modality and should be considered for select patients with type 1 diabetes mellitus if adequate glycemic control is not achieved with adherence to multiple daily injection therapy.
What is first line for Type II DM?
For patients with type 2 diabetes mellitus, metformin is recommended first-line therapy and should be initiated in conjunction with lifestyle modifications; it has a lower incidence of hypoglycemia and weight gain compared with some of the other oral agents and insulin.
How does kidney functioning impact metformin prescribing?
The FDA now considers metformin to be safe for patients with mild chronic kidney disease and some patients with moderate kidney impairment using estimated glomerular filtration rate (eGFR) as a measure of kidney function. Metformin continues to be contraindicated in those with an eGFR less than 30 mL/min/1.73 m2.
In older patients with hypoglycemia… how do you control their DM?
In older patients with type 2 diabetes mellitus of longer disease duration, treatment of severe recurrent hypoglycemia should take precedence over controlling hemoglobin A1c values; the increased risks of hypoglycemia outweigh the risks of diabetes complications.
How is diabetic neuropathy managed?
Distal symmetric polyneuropathy (DPN) is the most common form of diabetic neuropathy, and it presents as a sensation of numbness or burning pain in a stocking-glove distribution; management may require one or more classes of drugs, including antidepressants (amitriptyline, venlafaxine, duloxetine, paroxetine), anticonvulsants (pregabalin, gabapentin, valproate), or capsaicin cream