Focus on Diabetes Mellitus Part 1 notes- Chronic Complications
Complications of Feet and Lower Extremities People with diabetes are at high risk for foot ulcerations and lower extremity amputations. - The development of diabetic foot complications can be the result of a combination of microvascular and macrovascular diseases that place the patient at risk for injury and serious infection (Fig. 49-15). -Sensory neuropathy and peripheral artery disease (PAD) are risk factors for foot complications. In addition, clotting abnormalities, impaired immune function, and autonomic neuropathy also have a role. -Smoking is deleterious to the health of lower extremity blood vessels and increases the risk for amputation. Sensory neuropathy is a major risk factor for lower extremity amputation in the person with diabetes. -Loss of protective sensation (LOPS) often prevents the patient from being aware that a foot injury has occurred. Improper footwear and injury from stepping on foreign objects while barefoot are common causes of undetected foot injury in the person with LOPS. -Because the primary risk factor for lower extremity amputation is LOPS, annual screening using a monofilament is important. -This is done by applying a thin, flexible filament to several spots on the plantar surface of the foot and asking the patient to report if it is felt. Insensitivity to a monofilament has been shown to greatly increase the risk for diabetic foot ulcers that can lead to amputation. -PAD increases the risk for amputation by causing a reduction in blood flow to the lower extremities. - When blood flow is decreased, oxygen, white blood cells, and vital nutrients are not available to the tissues. -Wounds take longer to heal, and the risk for infection increases. -Signs of PAD include intermittent claudication, pain at rest, cold feet, loss of hair, delayed capillary filling, and dependent rubor (redness of the skin that occurs when the extremity is in a dependent position). -The disease is diagnosed by history, ankle-brachial index (ABI) (see and angiography. Management includes control or reduction of risk factors, particularly smoking, high cholesterol intake, and hypertension. - Bypass or graft surgery is indicated in some patients. (PAD is discussed in Chapter 38.) If the patient has LOPS or PAD, aggressive measures must be taken to teach the patient how to prevent foot ulcers. -These measures include the selection of proper footwear, including prescription shoes. -The patient also must carefully avoid injury to the foot, practice diligent skin and nail care, inspect the foot thoroughly each day, and treat small problems promptly. -Guidelines for patient teaching are listed in Table 49-21. Proper care of a diabetic foot ulcer is critical for wound healing. Several forms of treatment can be used. - Casting can be done to redistribute the weight on the plantar surface of the foot. -Wound control for the ulcer can include debridement, dressings, advanced wound healing products (becaplermin [Regranex]), vacuum-assisted closure, ultrasound, hyperbaric oxygen, and skin grafting.
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two major categories of diabetic neuropathy are sensory neuropathy, which affects the peripheral nervous system, and autonomic neuropathy.
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16. Diabetic Neuropathy: Sensory- loss of sensation w/pain and paresthesias---> burning, itching ---> Tight glucose control is the only tx for it but neuropathic sx can be treated w/ topical creams like: 1. Capsaicin 2. TCAs 3. SSRI 4. SSNRI and 5. Antiseizures---> Gabapentin Pregabalin ---> important for you to know when your p.t is prescirbed Gabapentin it is a good idea to be sure it isn't for a seizure. Most of the time Dilantin or Keppra is used for seizures so be sure and check that.
17. Hypoglycemic unawareness and Gastroparesis(= reduces the ability of the stomach to empty out its contents): -20-40% of Diabetics -Delays the absorption of food so causes hypoglycemia or can cause hyperglycemia a very erratic movement of the stomach. -How do we treat it? In patients with Insulin Dependent Diabetes (IDDM) for > 10 years, they should do a GI workup tx: more frequent smaller volume meals and have those meals low in fat and fiber -multivitamins and liquid caloric supplements -moderate exercise -gastric electrical stimulation * Combination of the newer rapid acting insulin and long acting insulins will improve glycemic control and may be our best therapy yet to prevent this disorder.
18. Postural hypotension: 1. SGLT inhibitors (drug induced)-diabetes drugs 2.BP Drugs - Prevents the kidneys from recycling glucose--> They can't reabsorb it so it washes out and takes w/ it water, resulting in a relative dehydration.
20. Erectile Dysfunction: -Can be psychogenic -also women have more candidal infections and nonspecific vaginitis
21. Nuerogenic Bladder: Tx: is to empty bladder q3h-- use the Crede method-mild massage downward over the abdomen and lower bladder -- may need to self catherize
27. Types of Insulin: Basal-Bolus regimen that most closely mimics endogenous insulin production
30. < 60 GFR should not be in Metformin.
31. Nursing Management nursing implementation: * What types of surgery would require contrast medium? ERCP, any surgery where a C-arm is used Hold Metformin on day of surgery/procedure and for -48 hours- afterwards. Serum Blood test to check: (serum creatinine has been checked and is normal) * When caring for an unconscious surgical p.t (When they are under anesthesia they can have a hypoglycemic episode) receiving insulin, the nurse must be alert for hypoglycemic signals such as sweating, tachycardia, and tremors.
33. Etiology and Pathophysiology: -Although liver cells are not considered insulin-dependent tissue, insulin receptor sites on the liver facilitate the hepatic uptake of glucose and its conversion to glycogen * Counter regulatory hormones: --> Glucagon, epinephrine, growth hormone, cortisol - these increase blood glucose levels -provide regulated release of glucose for energy -help maintain normal blood glucose levels. * abnormal production of any or all of these hormones may be present in diabetes-- ?what does it mean to oppose the effects of insulin? Answer: not drive glucose into storage.
36. A1c (%) to eAG (mg/dl) The Math: 28.7 x A1C - 46.7=
5.Secondary diabetes: (another medical condition you can get this); (Usually resolves when underlying condition is treated) Adrenal Gland Disorder: Cushings Thyroid Gland Disorder: Hyperthyroidism Triglycerides also high: Pancreatitis Feed the P.T w/out GI tract access: TPN (Total Parenteral Nutrition) Covered in Pedi Unit: Cystic Fibrosis Also a cause of Chronic liver Disease: Hemochromatosis (when your body absorbs too much iron from the food you eat-hereditary)
5.Secondary Diabetes: *Drugs that raise your glucose levels: 1. Corticosteroids (Prednisone)- 2. Thiazides/loop diuretics: lasix ---> can potentiate hyperglycemia by inducing Potassium loss 3. Phenytoin (Dilantin)-antiseizers 4. Atypical antipsychotics (clozapine)- 5. Caffeine 6. ca blockers 7. questeran 8. lithium 9. marijuana 10. oral contraceptives 11.
5.Secondary Diabetes: Alcohol inhibits gluconeogenesis (breakdown of glycogen to glucose) by the liver. - This can cause severe hypoglycemia in p.t on insulin or oral hypoglycemic medications that increase insulin secretion. -Acetaminophen (Tylenol) lowers blood glucose levels -NSAIDS (ibuprofen) lowers BG -allopurinol -Potassium salts -salicylic aspirin
5.Secondary Diabetes: Beta blockers: Metoprolol ---> lols -they mask Sx of hypoglycemia but prolong hypoglycemic effects of insulin.
6. The risk for stroke is also 2 to 4 times higher among people w/diabetes: Leading cause of: 1. End-stage renal disease 2. Adult blindness 3. non-traumatic lower limb amputations Major contributing factor: 1. Heart Disease 2. Stroke
7. Complications from diabetes are primary those of end organ disease from damage to blood vessels or angiopathy secondary to hyperglycemia
Sensory Neuropathy- The most common form of sensory neuropathy is distal symmetric polyneuropathy, which affects the hands and/or feet bilaterally. - This is sometimes referred to as stocking-glove neuropathy. -Characteristics of distal symmetric polyneuropathy include loss of sensation, abnormal sensations, pain, and paresthesias. -The pain, which is often described as burning, cramping, crushing, or tearing, is usually worse at night and may occur only at that time. -The paresthesias may be associated with tingling, burning, and itching sensations. The patient may report a feeling of walking on pillows or numb feet. -At times the skin becomes so sensitive (hyperesthesia) that even light pressure from bed sheets cannot be tolerated. -Complete or partial loss of sensitivity to touch and temperature is common. -Foot injury and ulcerations can occur without the patient ever having pain (Fig. 49-14). -Neuropathy can also cause atrophy of the small muscles of the hands and feet, causing deformity and limiting fine movement. Control of blood glucose is the only treatment for diabetic neuropathy. - It is effective in many, but not all, cases. Drug therapy may be used to treat neuropathic symptoms, particularlypain. -Medications commonly used include topical creams (e.g., capsaicin [Zostrix]), tricyclic antidepressants (e.g., amitriptyline [Elavil]), selective serotonin and norepinephrine reuptake inhibitors (e.g., duloxetine [Cymbalta]), and antiseizure medications (e.g., gabapentin [Neurontin], pregabalin [Lyrica]). - Capsaicin is a moderately effective topical cream made from chili peppers. -It depletes the accumulation of pain-mediating chemicals in the peripheral sensory neurons. - The cream is applied three or four times a day. -At the start of therapy, symptoms usually increase, followed by relief of pain in 2 to 3 weeks. - Tricyclic antidepressants are moderately effective in treating the symptoms of diabetic neuropathy. - They work by inhibiting the reuptake of norepinephrine and serotonin, which are neurotransmitters believed to play a role in the transmission of pain through the spinal cord. - Duloxetine is thought to relieve pain by increasing the levels of serotonin and norepinephrine, which improves the body's ability to regulate pain. -Antiseizure medications decrease the release of neurotransmitters that transmit pain.
Autonomic Neuropathy- Autonomic neuropathy can affect nearly all body systems and lead to hypoglycemic unawareness, bowel incontinence and diarrhea, and urinary retention. -Gastroparesis (delayed gastric emptying) is a complication of autonomic neuropathy that can produce anorexia, nausea, vomiting, gastroesophageal reflux, and persistent feelings of fullness. -Gastroparesis can trigger hypoglycemia by delaying food absorption. -Cardiovascular abnormalities associated with autonomic neuropathy are postural hypotension, resting tachycardia, and painless myocardial infarction. -Assess patients with diabetes for postural hypotension to determine if they are at risk for falls. Instruct the patient with postural hypotension to change from a lying or sitting position slowly. -Diabetes can affect sexual function in men and women. -Erectile dysfunction (ED) in diabetic men is well recognized and common, often being the first manifestation of autonomic neuropathy. - ED in diabetes is also associated with other factors, including vascular disease, poor metabolic control, endocrine disorders, psychogenic factors, and medications. -Decreased libido is a problem for some women with diabetes. -Candidal and nonspecific vaginitis is also common. ED or sexual dysfunction requires sensitive therapeutic counseling for both the patient and the patient's partner. -A neurogenic bladder may develop as the sensation in the inner bladder wall decreases, causing urinary retention. -Apatient with retention has infrequent voiding, difficulty voiding, and a weak stream of urine. -Emptying the bladder every 3 hours in a sitting position helps prevent stasis and subsequent infection. - Tightening the abdominal muscles during voiding and using the Credé maneuver (mild massage downward over the lower abdomen and bladder) may also help with complete bladder emptying. -Cholinergic agonist drugs such as bethanechol (Urecholine) may be used. The patient may also need to learn self-catheterization
Type 1 Diabetes- get an eye exam 5 years after dx Type 2 diabetes: get an eye exam at the time of dx - This is because the earliest and most treatable stages of retinopathy produce no changes in vision at all
Diabetic Nephropathy: 14. A ratio greater than 30 mg of Albumin to 1 gm of creatinine signals chronic kidney disease. Why are these BP medications preferred? -They decrease Proteinuria -The kidneys filter the blood to remove wastes and keep our fluids and electrolytes in balance -But they should not be filtering out Albumin ---> if it does appear in the urine that means the kidneys are allowing it to go through - Doing the Albumin and Creatinine ratio we can pick this up early and prescribe the: 1. ACE-I or the ARBS
Macrovascular complications are diseases of the large and medium-size blood vessels that occur with greater frequency and with an earlier onset in people with diabetes. Macrovascular diseases include: cerebrovascular, cardiovascular, and peripheral vascular disease. Women with diabetes have a four to six times increased risk for CVD, and men with diabetes have a two to three times increased risk for CVD compared with those without diabetes. Patients with diabetes can decrease several risk factors associated with macrovascular complications, such as: obesity -smoking, -hypertension, -high fat intake, and sedentary lifestyle. - Smoking, which is detrimental to health in general, is especially injurious to people with diabetes and significantly increases their risk for blood vessel and cardiovascular disease, stroke, and lower extremity amputation. -The ADA recommends yearly screening of diabetic patients for CVD risk factors. Optimizing BP control in patients with diabetes is significant for the prevention of cardiovascular and renal disease. -Treating hypertension in diabetic patients results in a decrease in macrovascular and microvascular complications. -Hypertension in people with diabetes causes an increase in mortality greater than for those with hypertension without diabetes. - A target BP of less than 130/80 mm Hg is recommended for most patients with diabetes. -Patients with diabetes have an increase in lipid abnormalities. - This contributes to the increase in CVD seen in this population. - The ADA recommends target values of LDL cholesterol less than 100 mg/dL (2.6 mmol/L), triglycerides less than 150 mg/dL (1.7 mmol/L), and HDL cholesterol greater than 40 mg/dL (1.0 mmol/L) in men and greater than 50 mg/dL (1.3 mmol/L) in women. The ADA advocates lifestyle interventions, including nutritional therapy, exercise, weight loss, and smoking cessation to treat hyperlipidemia. -Medications (primarily statins) are recommended for those who do not reach lipid goals with lifestyle modifications and for people over 40 years of age with other CVD risk factors regardless of their baseline lipid levels. -Insulin resistance has an important role in the development of CVD and is implicated in the pathogenesis of essential hypertension and dyslipidemia. -The role of insulin resistance in the pathogenesis of CVD is not well understood, but it seems to combine with dyslipidemia in contributing to greater risk of CVD in patients with diabetes mellitus. -All patients with diabetes should be screened for dyslipidemia at the time diabetes is diagnosed.
Microvascular Complications- Microvascular complications result from thickening of the vessel membranes in the capillaries and arterioles in response to conditions of chronic hyperglycemia. -They differ from the macrovascular complications in that they are specific to diabetes. - Although microangiopathy can be found throughout the body, the areas most noticeably affected are the eyes (retinopathy), the kidneys (nephropathy), and the skin (dermopathy). -Microvascular changes are present in some patients with type 2 diabetes at the time of diagnosis.
Diabetic Retinopathy: Etiology and Pathophysiology- Diabetic retinopathy refers to the process of microvascular damage to the retina as a result of chronic hyperglycemia, nephropathy, and hypertension in patients with diabetes. -Diabetic retinopathy is estimated to be the most common cause of new cases of adult blindness. Retinopathy can be classified as nonproliferative or proliferative. - In nonproliferative retinopathy, the most common form, partial occlusion of the small blood vessels in the retina causes microaneurysms to develop in the capillary walls. -The walls of these microaneurysms are so weak that capillary fluid leaks out, causing retinal edema and eventually hard exudates or intraretinal hemorrhages. -Vision may be affected if the macula is involved. Proliferative retinopathy, the most severe form, involves the retina and the vitreous. -When retinal capillaries become occluded, the body compensates by forming new blood vessels to supply the retina with blood, a pathologic process known as neovascularization. -These new vessels are extremely fragile and hemorrhage easily, producing vitreous contraction. -Eventually light is prevented from reaching the retina as the vessels become torn and bleed into the vitreous cavity. -The patient sees black or red spots or lines. -If these new blood vessels pull the retina while the vitreous contracts, causing a tear, partial or complete retinal detachment will occur. - If the macula is involved, vision is lost. -Without treatment, more than half of patients with proliferative diabetic retinopathy will be blind. -Persons with diabetes are also prone to other visual problems. - Glaucoma occurs as a result of the occlusion of the outflow channels secondary to neovascularization. - This type of glaucoma is difficult to treat and often results in blindness. - Cataracts develop at an earlier age and progress more rapidly in people with diabetes.
Nephropathy: Diabetic nephropathy is a microvascular complication associated with damage to the small blood vessels that supply the glomeruli of the kidney. It is the leading cause of end-stage kidney disease in the United States and is seen in 20% to 40% of people with diabetes. *Risk factors for diabetic nephropathy include: hypertension genetic predisposition smoking chronic hyperglycemia. *Results of the DCCT and UKPDS research have demonstrated that kidney disease can be significantly reduced when near-normal blood glucose control is maintained. Patients with diabetes are screened for nephropathy annually with a random spot urine collection to assess for albuminuria and measure the albumin-to-creatinine ratio. - Serum creatinine is also measured to provide an estimation of the glomerular filtration rate and thus the degree of kidney function. Patients with diabetes who have microalbuminuria or macroalbuminuria should receive either angiotensin-converting enzyme (ACE) inhibitor drugs (e.g., lisinopril [Prinivil, Zestril]) or angiotensin II receptor antagonists (e.g., losartan [Cozaar]). - Both classifications of these drugs are used to treat hypertension and have been found to delay the progression of nephropathy in patients with diabetes. - Hypertension significantly accelerates the progression of nephropathy. Therefore aggressive BP management is indicated for all patients with diabetes. -Tight blood glucose control is also critical in the prevention and delay of diabetic nephropathy. (See Chapter 33 for a discussion of hypertension and Chapter 47 for a discussion of renal failure.)
Neuropathy- Diabetic neuropathy is nerve damage that occurs because of the metabolic derangements associated with diabetes mellitus. -About 60% to 70% of patients with diabetes have some degree of neuropathy. -The most common type of neuropathy affecting persons with diabetes is sensory neuropathy. -This can lead to the loss of protective sensation in the lower extremities, and, coupled with other factors, significantly increases the risk for complications that result in a lower limb amputation. -More than 60% of non traumatic amputations in the United States occur in people with diabetes. Screening for neuropathy should begin at the time of diagnosis in patients with type 2 diabetes and 5 years after diagnosis in patients with type 1 diabetes.
The pathophysiologic processes of diabetic neuropathy - The prevailing theory is that persistent hyperglycemia leads to an accumulation of sorbitol and fructose in the nerves that causes damage by an unknown mechanism. -The result is reduced nerve conduction and demyelinization. - Ischemic damage by chronic hyperglycemia in blood vessels that supply the peripheral nerves is also implicated in the development of diabetic neuropathy. -Neuropathy can precede, accompany, or follow the diagnosis of diabetes.
40-50 units of insulin are released in the body 70-120 insulin in your body
What do Type I and Type II share? Answer: Nutritional therapy is essential and vascular and neurologic complications are frequent.
