Diabetes Flashcards
Antiglycemic agents, diagnostic and treatment guidelines, diabetes-related emergencies
Metformin MOA
- Decreases hepatic glucose production
- Improves insulin sensitivity
- Delays glucose absorption in gut
Biguanide
GLP1/GIP agonist MOA
- Increases glucose-dependent insulin secretion
- Decreases glucagon secretion
- Slows gastric emptying and increases satiety
Tirzepatide
GLP-1 agonist MOA
- Increases glucose-dependent insulin secretion
- Decreases glucagon secretion
- Slows gastric emptying and increases satiety
GLP-1 agonists
Liraglutide
Semaglutide
Dulaglutide
Exanatide
DPP-4s MOA
- Inhibt breakdown of incretin hormones (GLP-1 and GIP)
- Increases glucose-dependent insulin secretion
SGLT2i MOA
Increase urinary glucose excretion
DPP4s
Sitagliptin
Linagliptin
Saxagliptin
SGLT2 inhibitors
Canagliflozin
Dapagliflozin
Empagliflozin
“flows”
Sulfonylureas MOA
Stimulates pancreatic beta cells to release insulin
Sulfonylureas
Glipizide
Glyburide
Glimepiride
ride out
Thiazolidinediones MOA
Directly increase insulin sensitivity in muscle
Thiazolidinediones
Pioglitazone
Rosiglitazone
“azo”
Antiglycemic agents that cause weight loss
In order from greatest to least
Tirzepatide
GLP1s
SGLT2s
Metformin
Antiglycemic agents that cause weight gain
In order from greatest to least
Insulin
SUs
TZDs
Antigylcemic agents with very high A1c lowering power
Rough range
Tirzepatide
Semaglutide, dulaglutide
Insulin
1.5 to 2.5%
Antigylcemic agents with high A1c lowering power
Rough range
Metformin
Exenatide, liraglutide
SGLT2s
SUs
TZDs
0.5 to 1.5%
Antigylcemic agents with moderate A1c lowering power
Rough range
DPP4s
0.5 to 1%
Antiglycemic agents with ASCVD benefits
Liraglutide
Semaglutide (SQ)
Dulaglutide
Canagliflozin
Empagliflozin
“LSD” GLPs, “CE” SGLT2s
Antiglycemic agents with benefits in heart failure
Empagliflozin
Dapagliflozin
“ED” SGLT2s - canagliflozin has moderate benefits too
Antiglycemic agents contraindicated/cautioned in heart failure
TZDs
Saxagliptin
Antiglycemic agents with renal protective effects
Liraglutide
Semaglutide (SQ)
Dulaglutide
Canagliflozin
Dapagliflozin
“LSD” GLPs, “CkD” SGLT2s - empag has moderate benefits too
Metformin ADEs and CIs
GI effects - diarrhea, flatulence (titrate or ER)
Risk of lactic acidosis
CI: CKD, liver disease, heavy alcohol consumption
GLP1s (GLP1/GIPs) ADEs and CIs
N/V/D
Stomach pain
CI: Personal or family hx of medullary thyroid cancer or pancreatitis
DPP4s ADEs and CIs
Flu-like symptoms
Risk of pancreatitis
SGLT2s ADEs and CIs
UTIs, genital mycotic infections
Polyuria
CI: Hx of UTIs, bone fractures (cana)
Sulfonylureas ADEs and CIs
Hypoglycemia
Weight gain
CI: high-risk hypoglycemia, CKD or elderly (glyburide)
TZDs ADEs and CIs
Weight gain
Edema
Anemia
CI: Class 3-4 CHF
What is C-peptide measured for?
Produced 1:1 during insulin synthesis
Marker of insulin production
Rapid acting insulins
Lispro (Humalog)
Aspart (Novolog)
Short acting insulins
Humulin R
Novolin R
Intermediate acting insulins
Humulin N
Novolin N
Long acting insulins
Glargine (Lantus, Basaglar, Toujeo)
Degludec (Tresiba)
When to initiate insulin for T2DM
- A1C > 10%
- Active hyperglycemia symptoms
- Emergent symptoms of hyperglycemia
- Unable to meet A1c goals after 3 months of treatment
Initial insulin doses
T1 and T2
T1DM: 0.5 u/kg/day divided 50/50 basal/bolus
T2DM:
* Basal: 10 u/day OR 0.1-0.2 u/kg/day
* Bolus: 4 u/day or 10% of basal insulin dose
Use weight based dosing for T2 if FBG is really high
Insulin titration strategy
Bolus: adjust by 1-2 u/dose q3d
Basal: adjust by 2 u q3d
Hypoglycemic: decrease TDD by 10-20%
Signs of overbasalization and what to do
- Dose > 0.5 u/kg/day
- Elevated bedtime-morning and/or post-preprandial differential
- High variability in BG readings
- Frequent episodes of hypoglycemia
Add bolus insulin and/or switch to BID basal dosing
I:C ratio
insulin:carbs
500/TDD = carbs
ISF
Insulin sensitivity factor, add on to I:C calculation
Sensitive or rapid: 1800/TDD
Resistant or short: 1500/TDD
Symptoms of hyperglycemia
- Polyuria
- Polyphagia
- Polydipsia
- Fatigue
- Weight loss
phagia = hunger, dipsia = thirst
Complications of uncontrolled diabetes
- Peripheral neuropathy
- Hypertension
- Nephropathy
- Retinopathy
- Cardiovascular disease, stroke
- Cerebrovascular disease, cognitive impairment
- Periodontal disease
- Foot ulceration
Mechanism of diabetic ketoacidosis
Lack of insulin causes overproduction of ketones - glucagon has free reign to breakdown free fatty acids as energy sources
Mechanism of hyperosmolar hyperglycemic state
Severe dehydration due to high blood glucose levels and low fluid status, commonly triggered by illness
Kidneys cannot keep up to maintain fluid status
Symptoms of DKA vs HHS
Both: polyuria, polydipsia, weakness, lethargy, weight loss
DKA:
* Abdominal pain
* “fruity” breath - smell of ketones
* BG 250 - 600
HHS:
* Delirium
* BG > 600
* Dehydration
Likely patients DKA vs. HHS
DKA: T1DM, young
HHS: T2DM, elderly
Lab findings DKA vs HHS
DKA
* Acidotic pH (7-7.25)
* Urine or serum ketones
* Anion gap > 10
HHS:
* pH > 7.3
* No ketones
* serum osmolality > 320 mOsm/kg
Treatment of DKA and HHS
Fluid replacement:
1. NS for 1-2 hrs
2. If corrected Na level is normal/high, switch to 1/2 NS
3. Once BG < 200 (DKA) or < 300 (HHS), switch to D5W+1/2NS
IV Insulin: do not initiate if K < 3.3
* Give 0.1u/kg bolus, then 0.1 u/kg/hr
* Only decrease gluc by 50-75 mg/dL/hr, risk of cerebral edema
* Maintain BG 150-200 (DKA) or 250-300 (HHS)
DKA only: if pH < 7, give bicarb
Diagnostic criteria for T2DM
A1C ≥ 6.5%
FBG ≥ 126
Criteria for pre-diabetes
A1c: 5.7-6.4%
FBG: 100-125
Treatment goals
A1c < 7%
FBG 80-130
2hr pp < 180
Comprehensive care considerations for diabetes
- Statin for 1º prevention
- ASA for 2º prevention
- Annual eye, foot, and kidney exam
- Immunizations: HepB, PPSV23, flu, COVID
Treatment of prediabetes
Lifestyle mod
Metformin if BMI ≥ 35, age 25 - 59, or hx of gestational diabetes
Monitor annually
