| How can we diagnose diabetes mellitus type 2? | Fasting Blood Glucose (if <100 normal, if 100-125 impaired fasting glucose (IFG) prediabetes, if >125 diabetic)
2h Plasma Glucose (if <140 normal, if 140-200 impaired glucose tolerance (IGT) prediabetes, if >200 diabetic)
Random plasma glucose (if >200 diabetic- indeterminant if below) |
| How can we diagnose metabolic syndrome? | Abdominal Obesity (men >94cm , women >80cm)
TG (>150 mg/dl)
HDL (men <40 mg/dl, women <50 mg/dl)
BP >130/85
Fasting Glucose >100 (IFG) |
| Is HbA1C a screening method for diabetes? | can be used for dx, but some still don't use it.
If >6.5% DM, if 5.7-6.5% glucose intolerance
can be repeated for confirmation, and pt w/hemoglobinopathies need other dx parameters. |
| How is natural history of T2DM? | First we have normal glucose tolerance w/ diabetes genes, increased obesity, lipogenesis, waist cirumference, atherogenesis, hyperinsulinemia, insulin resistance, arterial HTN and increased TG w/decreased HDL
Then we get impaired glucose tolerance (insulin secretion deficiency, decreased glucose transport, increased glucose prodcution, postprandial plasma glucose increase)
These lead to macroangiopathy and microangiopathy leading finally to T2DM. |
| What are the risk factors for getting T2DM? | HTN, hx of gestational DM, baby weight >9lb, high risk ethnic groups, HDL<35, TG>250, 1st degree relative w/DM, hx of vascular disease, habitual inactivity, visceral fat and increased waist circumference (strongest obesity-related parameter associated w/metabolic risk factor- can be used as a risk marker of CV risk) |
| What is the routine screening recommendations for pre-diabetes? | Age>45 years w/BMI>25, Age <45 w/BMI>25 +risk factor.
FPG or 2hour OGTT can be used, done as a part of healthcare office visit, rescreening 3 years. |
| Why is abdominal obesity harmful? | Since it is associated w/CV risk factors and metabolic disease.
Adipocytes are metabolically active endocrine organs that exert actions on brain, liver, muscles, pancreas. Leads to HTN (angiotensinogen), Leptin release (reproductive disorder, energy balance), cytokines (immune function), LPL stimulating factors (lipid metabolism), |
| How is pathophysiology of metabolic syndrome leading to atherosclerotic CVD? | Genetics and environmental causes lead to abdominal obesity, thus adipocytes release adipokines and cytokines lead to liver release of inflammatory markers, which cause insulin resistance and metabolic syndrome.
Metabolic syndrome causes increase BP, TG and decrease HDL which lead to atherosclerosis, plaque rupture/thrombosis and cardiovascular event |
| How is pathophysiology of insulin resistance? | Increased free fatty acid, lead to increase glucose production in liver and decreased glucose uptake (glycogen), leads to increased insulin secretion, less insulin sensitivity (muscle), increased Na+ reabsorption causing HTN.
Another path is increased proinflammatory cytokines by adipose leading to increased FFA and same mechanism above.
Dangers caused by insulin resistance include hyperinsulinemia, IGT, Dyslipidemia, HTN, coagulopathy. |
| What is IGT and IFG? | Stage in natural hx of disoder in glucose metabolism, lead to any type of diabetes, increased risk of progression to diabetes, increased risk of CVD, little or no risk of microvascular disease, some may revert to normoglycemia. |
| What is post-prandial hyperglycemia? | Early warning for DM, IGT, normal HbA1C and fasting glucose, increase risk of CV when overt diabetes develops, when we measure post-prandial glucose we can identify at-risk pt. |
| What are clinical presentations seen at dx of DM? | 20-30% diabetic eye disease, 10-20% diabetic kidney dysfunction, 30-40% HTN, 50-80% increased fats in blood, 80-100% vascular dysfunction |
| What are other tests that can be used in metabolic? | Microalbumin, hyperleptinemia, PAI-1, ApoB LDL, hyperuricemia, fatty liver, insulin resistance, CRP, adiponectin. (serum uric acid risk factor for diabetes) |
| How is tx of DM? | Lifestyle behaviors and meds.
Aiming to maintain glycemia and weight (by diet and exercise)
Medications include those in case of CV risk (in case of HF give SGLT2i, in case of CKD give SGLT2i or GLP-1 RA if SGLT2i not tolerated, if HbA1C above normal give both, in case of high risk of CV complication give GLP-1RA or SGLT2i or both in case A1C above target)
In case of maintenance of glycemia if HbA1C above normal(for glycemic management give metformin, very high efficacy (dulaglutide, semaglutide, tirzepatide, insulin combination oral or injectable) high efficacy for metformin, SGLT2i, GLP1-RA...)
Weight loss if HbA1C above normal (very high efficacy (semaglutide and tirezepatide), high efficacy (dulaglutide and liraglutide) intermediate (GLP1RA and SGLT2i) neutral metformin and DPP-4i |
