Discussion Week 3: Chronic disease management
Discussion Week 3: Chronic disease management
The student should be able to:
List the major causes of morbidity and mortality in diabetes mellitus.
Recognize the basic management of hypertension and hyperlipidemia in the diabetic patient. Perform a diabetic foot exam.
Counsel patient on behavior change.
Recognize value of a team approach to the management of diabetes.
Appreciate the impact diabetes mellitus has on a patient’s quality of life, well-being, ability to work, and the family.
It is important at each visit to ask diabetic patients if they have experienced any hypoglycemic symptoms or events that required the assistance of another person.
Often times, when a patient is hypoglycemic, he does not write it down because he is preoccupied treating the hypoglycemia.
It is estimated that 50% of patients with diabetes will eventually struggle with one or more neuropathies related to their diabetes.
Axonal loss and atrophy are responsible for the majority of clinical symptoms and loss of function in patients with neuropathy. There can also be evidence of demyelination and remyelination, with the actual number of large nerve fibers being reduced, while small nerve fibers increase.
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Distal polyneuropathy is the most common type of diabetic neuropathy. It is the progressive loss of sensation in the classic stocking/glove distribution. Diabetic foot ulcer incidence is greatly increased in patients with distal polyneuropathy.
Autonomic neuropathy can take many forms and affect one or many organs. Specific types include:
cardiovascular (orthostatic hypotension, resting sinus tachycardia, postprandial hypotension) gastrointestinal (gastroparesis, chronic constipation, esophageal motility disorders) genitourinary (sexual dysfunction, neurogenic bladder) abnormal pupillary responses and disorders of hidrosis Discussion Week 3: Chronic disease management
Diabetic retinopathy, a microvascular diabetic complication, is the leading cause of preventable blindness in the developed world.
Two large prospective trials (DCCT with Type 1 diabetics and UKPDS with Type 2 diabetics) revealed that intensive glucose management resulted in prevention or delayed onset and progression of diabetic retinopathy.
Coexisting hypertension, nephropathy, and tobacco abuse also contribute to retinopathy onset and progression.
Two types of diabetic retinopathy
1. Non-proliferative diabetic retinopathy
Involves cotton wool spots, hard exudates, microaneurysms, and retinal hemorrhages.
Vision loss usually results from severe macular edema, a thickening of the retina with resultant edema of the macula.
2. Proliferative diabetic retinopathy
Involves neovascularization of the retinal vessels or optic disc, retinal hemorrhage (dot-blot, flame), retinal fibrosis with traction detachment, and vitreous hemorrhage. Macular edema can occur as well.
Image of proliferative retinopathy with neovascularization
Development of diabetic retinopathy is directly related to disease duration and is generally not seen in patients who have had diabetes less than five years. The exception is Type 2 diabetic patients who were likely hyperglycemic more than five years prior to their diabetes diagnosis.
Annual dilated eye exams by an ophthalmologist are recommended for all Type 1 diabetic patients within five years of diagnosis and shortly after diagnosis in patients with Type 2 diabetes. Patients with progressive retinopathy are often seen quarterly or biannually.
Panretinal laser photocoagulation is the treatment of choice for proliferative diabetic retinopathy and severe cases of nonproliferative retinopathy. Screening is done aggressively due to the well-documented efficacy of laser photocoagulation in the prevention of vision loss. Ranibizumab, an anti-vascular endothelial growth factor, injected into the vitreous showed noninferiority to laser therapy and can also be used.
Diabetic nephropathy occurs in 20% to 40% of diabetic patients and is the most common etiology of end-stage renal disease in the U.S.
Risk factors associated with the progression of diabetic nephropathy include: obesity, increasing age, African American race, and tobacco abuse.
Kidney insult appears to originate with glomerular hypertension and hyperfiltration. Chronic hyperglycemia leads to mesangial expansion, deposition of matrix, increased amount of VEG-F and other cytokines, local inflammation, and activation of protein kinase C.
Prevention / Treatment
Two large prospective trials (DCCT with type 1 diabetics and UKPDS with Type 2 diabetics) revealed that intensive glucose management resulted in prevention or delayed onset and progression of diabetic nephropathy.
Aggressive blood pressure lowering is critical for treatment of increased urinary albumin excretion. In patients with hypertension with increased urinary albumin excretion, an ACE inhibitor or ARB therapy is recommended to delay the onset and decrease progression of diabetic nephropathy. Discussion Week 3: Chronic disease management
Referral to nephrology is appropriate if the cause of kidney disease is not certain, and or there are challenging management issues present, such as resistant hypertension or electrolyte derangement. The threshold for referral to nephrology varies across providers; however, nephrology should be consulted if Stage 4 or greater chronic kidney disease (GFR < 30 ml/min per 1.73 m2) develops since this has been found to reduce cost, improve quality of care, and keep people off dialysis longer. Diabetes Patient Resources in Spanish The ADA website has excellent resources for Spanish-speaking patients and their families. When to Perform the Diabetic Foot Exam It is important to do a thorough foot exam in a diabetic patient on an annual basis for low-risk patients and more often in patients at high risk for foot ulcer formation. Patients at High Risk for foot Ulcer Formation Patients with known diabetic polyneuropathy, sensory or vascular deficits, patients who smoke, and patients with a prior history of diabetic foot ulcer or amputation. Foot Exam in Patients with Diabetes Visually inspect the feet for callus formation, ulceration, nail infections, and bony deformities. Assess skin integrity, especially between toes and under metatarsal heads. Palpate the dorsalis pedis and posterior tibialis pulses to screen for peripheral vascular disease and look for signs of peripheral Clinical Skills vascular disease, such as hair loss. Check sensation using a 128 Hz tuning fork (vibration) and a cool metal object, potentially the same tuning fork (temperature). Check pressure sensation using a 10-g monofilament: Show the monofilament to the patient and try it on their hand to show them it will not hurt. Ask the patient to close their eyes or look at the ceiling and tell you each time they feel the monofilament touch their foot. Randomly place the end of the monofilament on the 9 different areas of the foot (see image to the right) with enough pressure to bend the monofilament. If the patient does not say “yes” at a particular site, continue to the next site and re-test that site at the end. Check Achilles reflexes. Effectiveness of Intravenous Insulin for Blood Glucose Control Blood sugar control in critically ill patients has been the subject of considerable investigation. Previous research suggested that tight control (80-120 mg/dL) was desirable, but more recent research shows that aggressive blood sugar control can be associated with higher mortality. Hypoglycemia (serum glucose concentration <70 mg/dL), with rates as high as 40% in some studies, is associated with tight glycemic control. A meta-analysis of 29 controlled trials involving more than 8,000 adult ICU patients showed no difference in inhospital mortality between the group assigned to tight glucose control versus usual care. The current recommended blood glucose target for most hospitalized patients is 140 to 180 mg/dL. Thiazolidinediones Pioglitazone (D), a member of the class of drugs known as thiazolidinediones (TZD), is not recommended for use in patients who have newly developed heart failure and in those with known NYHA Class III and IV heart failure. The same is true for rosiglitazone, another TZD that has been associated with an increased risk of cardiovascular disease. Management Diabetes Chronic Disease Management Evaluate for and optimize prevention of diabetic complications Discussion Week 3: Chronic disease management Macrovascular complications: Cardiovascular disease Cerebrovascular disease Microvascular complications: Retinopathy Nephropathy Neuropathy In particular, cardiovascular disease is the No. 1 cause of mortality for people with diabetes, and one of the top causes of morbidity. Hypoglycemia, infections, foot ulcers, and amputations are additional causes of morbidity and mortality in patients with diabetes. The American Diabetes Association publishes annual guidelines to assist in the management of a patient with diabetes. Remember the large role that the psychosocial aspects of a diabetes diagnosis play in management Non-adherence with medical recommendations could be due to economic, work-related, religious, social, or linguistic barriers to care. Care must be taken to assess the psychosocial status of each person with diabetes at each clinic visit to ensure that barriers to successful diabetes care are minimized. ADA Recommendations to Minimize the Risk of Cardiovascular Disease in Patients with Diabetes Smoking cessation, daily aspirin, blood pressure control, and lipid control are all recommended to reduce the risk of cardiovascular disease. Please note that as of 2018, ADA recommendations were published with the older definition of hypertension (140/90). It always takes time before multiple different organizations agree on the same thresholds. Daily low dose aspirin is recommended for primary prevention of cardiovascular disease in diabetic patients with a 10-year risk of atherosclerotic cardiovascular disease of >10%. It is also recommended for secondary prevention of all diabetic patients with a history of atherosclerotic disease.
Reduction of cardiovascular risk is achieved with a goal of optimal glycemic control, as well as control of many other health factors that raise cardiovascular risk, such as tobacco use, obesity, poorly controlled hypertension, and hypercholesterolemia.
Mechanism of action: TZDs are peroxisome proliferator-activated receptor-gamma (PPARgamma) agonists.
Effects: TZDs decrease insulin resistance, increase glucose uptake in peripheral tissue, decrease hepatic glucose production, decrease vascular inflammation, redistribute visceral adipose tissue peripherally, and preserve beta cell function. Overall, they cause the A1c to decrease by 1% to 1.5%. Hypoglycemia is not associated with this medication class. TZDs have differing effects on lipids. Pioglitazone slightly reduces LDL levels and raises HDL. Rosiglitazone can increase LDL levels.
Side effects: The receptors that TZDs activate are ubiquitous and are abundant in the cells within the renal collecting tubules. Hence, TZDs increase sodium reabsorption, leading to increased water retention. Compared to placebo, all TZDs are associated with a statistically significant increase in edema and weight.
Warnings: Care should be used with these agents in patients with liver disease. Serum transaminases greater than 2.5 times the upper limit of normal is a contraindication to initiation of these agents, and a rise to greater than three times the upper limit of normal should lead to their discontinuation. Liver tests should be measured at baseline and periodically while the patient is on this class of medication.
Contraindications: The FDA has added a warning to the label of pioglitazone noting an increased risk of bladder cancer after more than one year of treatment. Pioglitazone is now contraindicated in patients with a history of bladder cancer or active bladder cancer. Patients should be counseled to tell their physician if they notice blood in their urine or a red tint to their urine.
When to Refer Patients with Diabetes to an Endocrinologist
If a patient is having recurrent or severe hypoglycemia (seizure, coma, or impairment that requires the aid of another person), an endocrinologist should be consulted. Hypoglycemia is defined as a blood glucose <70 mg/dL. Discussion Week 3: Chronic disease management Primary care physicians’ threshold for referral varies across providers. Other conditions that would warrant referral are when a patient’s A1c is 8% more than twice in a 12-month period, despite intensive treatment; for initiation of a complex multiple daily injection insulin regimen; or for initiation of continuous infusion insulin pump therapy. Self-Monitoring Glucose: Indications & Effectiveness Effectiveness of Self-Monitoring Blood Glucose Patients should be advised to check their blood sugar if they feel “low” because it is well recognized that people are not able to accurately detect hypoglycemia (blood glucose of < 70 mg/dL) by symptoms alone. Eating high carbohydrate food to treat perceived hypoglycemia rather than actual hypoglycemia leads to worsened overall glycemic control. Clinical studies have shown that self-monitoring of blood glucose (SMBG) may improve glycemic control, although for some patients self-monitoring increases depression and anxiety. It is important to evaluate patients’ abilities to use SMBG techniques to ensure they are using accurate data to evaluate their response to therapy and their degree of success in reaching blood-glucose targets. After receiving education, patients can use SMBG data to adjust their activity level, food intake and choice, as well as drug therapy to achieve optimal glycemic control. When to Self-Monitor Blood Glucose In patients on less frequent insulin injections, SMBG may be useful in achieving glycemic goals. Patients on an insulin pump and those using multiple daily insulin injections should self-monitor blood glucose at the following times: before each meal at bedtime when they have symptoms of hyper- or hypoglycemia after treating hypoglycemia to ensure return of euglycemia before exercise before critical activities, such as driving Discussion Week 3: Chronic disease management
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