| What are the types of chronic complications of DM? | Vascular Complications (microvascular: retinopathy, nephropathy, neuropathy; macrovascular: CAD, CVD, Peripheral artery disease (PAD)) Most common are microvascular
Non-vascular Complications |
| How is the prevelance of chronic complications of DM? | They are generally more prominent for pt with T2DM than T1 (US: 1/3 of pt T2DM have them while 1/10 of T1DM accoding to NHANES) |
| Describe the relationship between insulin resistance and diabetes development? | Early diabetes we have increased insulin resistance compensated by insulin level increase.
With time beta cells start failing so decrease insulin (IFG and IGT) and get diabetes type 2 level of sugar.
Risk of complications start with the diagnosis and increases with the progression of the disease.
We should start intervention with the increase in IFG and IGT. |
| What are the possible pathways of developing vascular complications of T2DM? | Sorbitol pathway decreases antioxidants and thus increases free radicals and thrombotic effect.
Glucose auto oxidation results in a state of oxidative stress.
AGE pathway (CVD, stroke, neuropathy and amputation, nephropathy and retinopathy) |
| What affects the CC of DM? | Risk increases with the duration of DM.
Microvascular increases with the duration of DM, macro is less conclusive.
Genetics, comorbidities smoking and obesity increase the risk as well |
| What is the DCCT study? | It is a study on T1DM pt clinical trial, showed that good glycemic control reduces the risk for complications and this risk increases with increased HbA1c
Randomized intensive and conventional treatment, follow up 6.5 years later and then EDIC 17 years later reduction of MI, stroke or death was seen |
| What is UKPDS study? | 5000 pt T2DM, conventional and intensive group, each 1% reduced HbA1C reduces risk of retinopathy by 35%
Post trial after 10 years, |
| What is the conclusion from UKPDS? | Intervention should start from diagnosis to benifit from legacy effect in later years
Early glycemic control results in long term benifits |
| What is kumamoto study? | Japanese on T2DM same results as UKPDS |
| What are ADVANCE, ACCORD, and VADT studies? | long term comparisons between standard treatment and intensive one for T2DM
Early treatment didnot reduce macrovascular complications of T2DM
No difference in occurance of MI/strokes
No difference in occurence of CVD and macrovascular complications with intensive glucose control |
| What should be the history of DM? | FBS <110
PPG (postprandial glucose) <140-180
HbA1C <6.5%
(different for each healthcare educator ADA/EASD...)
HbA1C target is individualized (one size doesn't fit all) |
| What are the ADA standards of medical care? | According to the HbA1C levels we have more disease duration, risk of hypoglycemia, life expectancy, comorbidities, vascular complications, and treament efforts ,support system (modifiable) |
| What are the new classes in treatment of T2DM? | SGLT2 inhibitors (Sodium gluc inhibitor - EMPA-REG, CANVAS, DECLARE-TIMI)
GLP1 RAs (LEADER, SUSTAIN 6 & PIONEER 6, REWIND) |
| What are the ophthalmic complications of DM? | Blindness, progressive retinopathy and macular edema, two stages proliferative and non-proliferative
Non-proliferative (increased capillary permeability, dilation, microaneurysms, AV shunts, hemorrhages, cotton-wool spots, hard exudate)
Proliferative (new vessels, scar, vitreal hemorrhage, Retinal detachment)
Risk factor is HTN, duration of DM, genetics.
Almost all pt with DM <20 years develope non-proliferative. |
| What is the treatment of ophthalmic complications of DM? | Prevention, intensive glycemic and BP control, if advanced control isn't necessary, regular eye examination and laser photocoagulation very successful. |
| What are the renal complications of DM? | Diabetic nephropathy is leading end-stage renal disease (ESRD) mortality.
proteinuria increases risk of CVD
microalbuminemia, accelerated by HTN and smoking |
| What is the treatment of diabetic nephropathy? | Prevention, early detection of microalbuminemia is imp
control of glycemia and BP (more if with proteinuria), ACE inhibitors, and dyslipidemia tx
Restriction of proteins, once overt then ESRD.
Hemodialysis, renal transplant or combined with a kidney and pancreas |
| What are the diabetic neuropathies? | Poly/mono/autonomic neuropathy
Correlates with duration of DM and glycemic control |
| What is the tx of diabetic neuropathy? | Glycemic control, avoid neurotoxins, vitamins, NSAIDs, Tricyclic anti depressants, orthostetic hypotension tx |
| What are the GI and UT complications of diabetes? | GI (delayed gastric emptying, altered intestinal motility)
UT (cystopathy, erectile dysfunction and female sexual dysfunction
Rx: glycemic control, symptomatic measure |
| What are the cardiovascular complications of DM? | PAD, CAD, MI, sudden death...
Glycemic control doesn't have an effect on CV complications. |
| What is the tx of CV complications of DM? | SGLT2 inhibitors and GLP1 RAs, revascularization (PCI and CABG), ACE inhibitors, BB, Antiplatelets, aspirin) |
| What are the lower extremity complications of DM? | Amputation due to neuropathy, PAD, abnormal foot mechanics, poor wound healing
Risk (male, DM>10 years, PAD, smoking, poor control)
Rx: prevention and management, Abx, peripheral bypass surgery if needed |
| Why do diabetics have a greater frequency of infections? | Abnormal immunity, hyperglycemia, diminished vascularization. |
| What are the dermatological complications of DM? | Protracted wound healing and skin ulceration, diabetic dermopathy (pigmented peritibial papules) from minor trauma
Acanthosis nigricans, granuloma and scleredema, lipoatrophy, xerosis and pruritis |
