ENDOCRINE: DIABETES, THYROID, Flashcards
drug causes dysglycemia
glucocorticoids BB atypical antipsychotics fluoroquinolone protease and calcineurin inhibitors statins ( HMG-CoA Reductase inhibitors)
the diagnosis of diabetes in Canada is established by
a random plasma glucose ≥11.1 mmol/L
a fasting plasma glucose (FPG) ≥7 mmol/L
2hPG in a 75-g OGTT ≥11.1 mmol/L
an HbA1c ≥6.5% (in adults)
what is the target for diabetes
FPG 4-7 mmol/L
2HPG 5-10 mmol/L OR 5-8 if A1C target not met
HBA1C <7% or <6.5% if patient has low hypoglycemia risk to reduce CKD & retinopathy
when is higher <8.5% A1C target indicated?
<8.5% in patient with history of severe hypoglycaemia, limited life expectancy, frail and/elderly with dementia
when is higher <8.0% A1C target indicated?
functionally dependent ( to avoid hypoglycaemia)
diabetes+ ASCVD ( acute MI, Coronary/ arterial vascularization, stroke, TIA, PAD)–> add?
GLP1 ( liraglutide, dulaglutide or SQ semaglutide)
SGLT2 ( empa, cana)
Diabetes + HF?
Dapa or empa
CKD+ DIABETES
SGLT 2 ( cana ( most evidence) then daga or empa)
ESRD + diabetes, what agent ??
ESRD < 15ml/min
DPP4 ( alogliptin, linagliptin, sitagliptin) or dulaglutide or repaglinide or SU (gliclazide) )insulin (low dose)
Which diabetes agent has benefit on weight loss
GLP1 and SGLT2I
which diabetes agent have reduce risk of hypoglycaemia
GLP1
SGLT2
acarbose or pioglitazone
when is appropriate to add insulin?
symptomatic hyperglycaemia, metabolic decompensation or antihyperglycemics insufficient
A1C >10%
Glucose >16.7 mmol/L
what is the recommended insulin basal starting dose
0.1-0.2 units/kg/day OR 5-10 units/ day , titrate 1 unit/day to taget BG ( FP <7 mmol/L
when it is appropriate to initiate bolus insulin?
how should bolus insulin be initiated?
BG not control despite being on basal + SGLT2 or GLP1 OR gylcemic values extremely high, may start basal/bolus right away
then add bolus
what is the renal cutoff in metformin, SGLT2-inhibitor
eGFR <30 ml/min
what is the MOA of biguanides and AE?
AI: increasing peripheral glucose uptake and insulin sensitivity and decreasing hepatic production
AE: upset stomach, N/V/, metallic taste, rhinitis, acidosis, B12 deficiency
MOA of a-glucosidase inhibitor and AE?
acarbose; inhibit a-glucosidase enzyme in SI, less glucose in absorbed since carbohydrates are B/D
AE: flatulence, diarrhea, abdominal pain ( dose related), hepatitis
sulfonylureas MOA and AE
gliclazide, glyburide, glimepiride, tobutamide
Meglitinides ( repaglnide)
depolarizes beta cells to stimulate insulin
hypoglycaemia ( higher with glyburide and eGFR <60 ml/min) weight gain headache dizziness GI effects
MOA of thiazolidinediones and AE
pioglitazone and rosiglitazone
increase PPAR-y sensitivity to insulin and decrease hepatic glucose production
ae: exacerbations/cause of HF, fluid retention, weight gain ( 2-2.5 kg), fractures, macular edema (rare), URI, headache
what are the CI of thiazolidinediones
HF, liver failure, bladder cancer( pioglitazone-rare), MI ( rosiglitazone- controversial)
DPP-4 inhibition MOA and adverse effects
“liptin” drug, sitagliptin, saxagliptin, linagliptin, alogliptin
DPP-4 inhibition leads to increase incretin levels
AE: headache, N/V/D, nasopharyngitis,
what should we be cautious of when initiating DPP-4 inhibition
**caution with history of pancreatitis or pancreatic cancer
what diabetic agent should we avoid in HF patient
DPP-4 I ( saxagliptin only)
thiazolidinediones,
what are the MOA of GLP-1 agonist and adverse effects
“tide drug”- exenatide, dulaglutide, liraglutide, lixisenatide, semaglutide
increased incretin concentrations
AE: N/V/D, weight loss
rare: acute pancreatitis, gallbladder