DIABETES MELLITUS
Case vignette
A 58-year-old female presents with nausea and vomiting in the background of progressive exertional dyspnoea.She is a smoker with a 10-pack per year history. She was diagnosed with diabetes 2 years ago and has been managed on metformin 500 mg twice daily. On examination she has coarse crepitations in the lung bases bilaterally. She has an S3 gallop in the precordium. She is obese and has moderate bipedal pitting oedema. Blood pressure is 140/90 mmHg. On the ECG, ST segment depression is observed in the lateral leads. Her fasting blood sugar levels are 11.2 mmo/L with an Hb A1c of 8.2%. Serum troponin level is not elevated.
Approach to the patient
Diabetes is a very commonly encountered condition in the long case setting. Most diabetic patients have multiple associated medical conditions, and this makes them favourite long case material. A candidate is expected to be able to address diabetic cases thoroughly and extensively. Ascertain whether the patient has the metabolic syndrome (see box) that is associated with high cardiovascular risk. The following is a discussion of the integral issues that should never be missed in any diabetic case.
(Adapted from International Diabetes Federation 2006 Consensus worldwide definition of metabolic syndrome. Online. Available: http://www.idf.org/webdata/docs/MetS_def_update2006.pdf)
(Adapted from International Diabetes Federation 2006 Consensus worldwide definition of metabolic syndrome. Online. Available: http://www.idf.org/webdata/docs/MetS_def_update2006.pdf)
History
Ask about:
• when and how the diagnosis was made, and symptoms at presentation, such as loss of weight, polyuria, polydypsia, and other associated presenting features such as diabetic ketoacidosis, hyperosmolar coma and infection
• initial treatment, subsequent treatment and the current medical regimen
• age at disease onset
• the type of diabetes the patient has—this has implications for the risk of diabetic ketoacidosis and for the therapeutic regimens
• the insulin treatment, such as previous and/or current regimens, types of insulin, dose and frequency of administration, who injects the insulin, the method of delivery (pen or syringe) and adverse effects associated with insulin treatment
• medication history, in detail—note the different classes of drugs that have been used to treat the diabetes, and also other medications that would interfere with adequate glycaemic control
• the patient’s knowledge of and compliance with the diabetic diet, and knowledge of the concept of the glycaemic index of various carbohydrate-containing foods
• who monitors the blood sugar levels and how often this is done—ask for the most recent readings
• episodes of ketoacidosis, hyperosmolar coma and other acute events that have necessitated hospitalisation
• whether the patient suffers from hypoglycaemic episodes and how he or she recognises early warning signs, and what remedial measures the patient takes in such situations
• other vascular risk factors, such as smoking, hyperlipidaemia and hypertension
• diabetic complications:
– macrovascular complications—ischaemic heart disease, heart failure, intermittent claudication and stroke (remember that diabetic cardiomyopathy may dominate the picture, leading to silent ischaemic episodes)
– microvascular complications:
ocular complications—such as diabetic retinopathy. Ask how often the patient visits the ophthalmologist and the current level of vision and any visual symptoms. Ask about any laser therapy for diabetic retinopathy. While discussing the eye, ask about cataracts.
neurological complications—ask about peripheral paraesthesias, painful peripheries, burns, neuropathic ulcers and Charcot’s joints. Ask whether the patient has ever had nerve conduction studies done. Enquire about symptoms of autonomic neuropathy, such as persistent postural dizziness, bloating, nocturnal diarrhoea, impotence and incontinence.
nephropathy—ask whether the patient has any urinary symptoms, such as frequency, polyuria and nocturia. Has the patient observed peripheral oedema that would suggest early-stage renal failure? Enquire about any previous investigations, such as 24-hour urinary collection for proteinuria, and whether the patient is aware of their level of renal function.
ocular complications—such as diabetic retinopathy. Ask how often the patient visits the ophthalmologist and the current level of vision and any visual symptoms. Ask about any laser therapy for diabetic retinopathy. While discussing the eye, ask about cataracts. neurological complications—ask about peripheral paraesthesias, painful peripheries, burns, neuropathic ulcers and Charcot’s joints. Ask whether the patient has ever had nerve conduction studies done. Enquire about symptoms of autonomic neuropathy, such as persistent postural dizziness, bloating, nocturnal diarrhoea, impotence and incontinence. nephropathy—ask whether the patient has any urinary symptoms, such as frequency, polyuria and nocturia. Has the patient observed peripheral oedema that would suggest early-stage renal failure? Enquire about any previous investigations, such as 24-hour urinary collection for proteinuria, and whether the patient is aware of their level of renal function.• other complications:
– infections/sepsis—ask about previous or current oral or vaginal candidiasis, impetigo, ulcers, abscesses, carbuncles, furuncles and recurrent urinary tract infections
– diabetic foot—the presence of painful callosities, corns or ulcers. Any anatomical foot deformities that predispose to foot injury should be enquired into. Ask whether the patient sees a podiatrist and, if so, how often.
The social and occupational impact of diabetes on the patient should be discussed in detail. Talk about impotence, if relevant to the patient. Social and marital issues associated with this condition should be dealt with in detail. Check for a family history of diabetes mellitus and obtain details thereof.
Exclude possible secondary causes for the diabetes, such as chronic pancreatitis, cystic fibrosis, Cushing’s syndrome, acromegaly, polycystic ovary syndrome and consumption of drugs such as corticosteroids, thiazides and the oral contraceptive pill (see box).
Causes of secondary diabetes mellitus
1. Medications—glucocorticoids, diazoxide, thiazides, oral contraceptive pill
2. Cushing’s disease
3. Acromegaly
4. Polycystic ovary syndrome
5. Pancreatic insufficiency (e.g. chronic pancreatitis, cystic fibrosis)
6. Obesity
7. Gestation
8. Haemochromatosis
9. Ataxia telangiectasia
10. Glucagonoma/vipoma
Examination
1. Body habitus—particularly looking for obesity, endocrinopathic appearance suggesting Cushing’s syndrome (see box), polycystic ovary syndrome or acromegaly (see box), and evidence of recent weight loss or weight gain. Measure the waist circumference and calculate the body mass index (BMI). Patients who have had type 1 diabetes from an early age may have stunted growth.
2. Postural blood pressure and postural pulse (postural response is absent in autonomic neuropathy)
3. State of hydration, injection marks, amputations, impetigo, acanthosis nigricans
4. Eye examination—looking for cataract, visual acuity, diabetic retinopathy and oculomotor nerve palsy with pupillary sparing
5. Oral cavity—for hygiene, periodontal disease and candidiasis
6. Abdomen—for hepatomegaly associated with diabetic fatty liver
7. Peripheral neuropathy (motor and sensory) and diabetic amyotrophy (in the quadriceps femoris musculature)—the 10 g Semmes-Weinstein monofilament test, looking for peripheral neuropathy (assesses the foot at risk)
8. Cutaneous stigmata—such as diabetic dermopathy, necrobiosis lipoidica diabeticorum and lipodystrophy associated with frequent injections (particularly in patients with poor technique)
9. Presence or absence of all peripheral pulses
10. A detailed diabetic foot examination.
Clinical features of Cushing’s syndrome
• Weight gain leading to central obesity
• Moon facies
• Excessive sweating
• Telangiectasia, straie, increased skin fragility (easy bruising)
• Hyperpigmentation
• Proximal myopathy
• Hirsutism
• Buffalo hump
• Decreased libido, impotence, amenorrhoea
• Mood disturbances (euphoria, depression and delirium)
• Hypertension
• Diabetes
Clinical features of acromegaly
• Enlargement of the hands and feet
• Protrusion of eyebrows and jaw
• Arthritis, carpal tunnel syndrome
• Increased spacing between the teeth
• Macroglossia
• Compression of the optic chiasma leading to bitemporal hemianopia
• Diabetes mellitus
• Hypertension
• Increased palmar sweating and seborrhea of the face
Investigations
Investigations that should be performed in the diabetic patient include:
1. Blood sugar level (capillary or venous)
2. Glycosylated haemoglobin (Hb A1c) level
3. Serum fructosamine level (not a very reliable test)
4. Full blood count
5. Fasting serum lipid profile
6. Electrolyte profile and the renal function indices—looking for evidence of renal impairment
7. Spot urine specimen—for proteinuria and for albumin-to-creatinine ratio (a ratio of > 2.5 is considered significant). If urine is positive for protein, a 24-hour urine collection should be carried out, looking for microalbuminuria. An albumin excretion of 30–300 mg over 24 hours is defined as microalbuminuria and is predictive of early diabetic nephropathy. The positive tests should be repeated within 3 months, and if there is persistent microalbuminuria on two occasions the patient should be commenced on an ACE inhibitor.
8. ECG—for evidence of ischaemic heart disease
Management
Discussion of therapeutic options revolves around the diabetic diet, regular physical exercise, oral hypoglycaemic agents and their side effects, and insulin therapy. Objectives of diabetes management include: 1) adequate control of the blood sugar level (fasting levels to be maintained below 6.1 mmol/L and postprandial levels below 7.8 mmol/L) and the glycosylated haemoglobin level (should be maintained below 7% in most cases, based on the patient’s clinical status); 2) prevention of end-organ complications; and 3) control of other vascular risk factors.
1. Hypoglycaemic agents—If the diabetic diet and physical exercise fail to provide adequate glycaemic control in the patient with type 2 diabetes, consider commencing an oral hypoglycaemic agent. Commonly used agents are:
• biguanides—metformin is the most common and the first line of pharmacotherapy in type 2 diabetes. Act to enhance peripheral insulin sensitivity. Side effects of this class of drugs include diarrhoea, nausea, impaired vitamin B12 absorption and lactic acidosis, particularly in patients with hepatic or renal failure.
• sulfonylureas—act via stimulation of pancreatic insulin secretion. Side effects of this class of drugs include hypoglycaemia, weight gain, rash and, very rarely, bone marrow suppression and cholestasis. Sulfonylureas have been associated with an increased mortality rate in post myocardial infarction patients.
• thiazolidinediones—rosiglitazone and pioglitazone are the thiazolidinediones currently available. These agents act mainly by improving insulin sensitivity and preserving pancreatic beta cell function. These agents have beneficial effects on cardiovascular health and have been observed to be able to prevent in-stent restenosis. According to the guidelines these agents are considered third-line therapy in difficult-to-control diabetes and should be added to the regimen when glycaemic control is suboptimal on biguanides and sulfonylureas. First-generation agent troglitazone was associated with hepatotoxicity, but other agents of this class (e.g. rosiglitazone) are believed to be safe. Thiazolidinediones give good blood sugar control when used in combination with insulin, metformin or sulfonylureas, but have a tendency to cause weight gain. In heart failure patients these agents may contribute to an exacerbation of the condition and they also have a negative impact on bone density, contributing to osteoporosis. It is very important to avoid this agent in patients with heart failure. Peripheral oedema is another commonly observed side effect. Rosiglitazone can elevate LDL as well as HDL levels, while pioglitazone has a neutral effect on LDL levels and a beneficial effect on HDL levels.
• meglitinides—repaglinide is a short-acting agent that acts by stimulating pancreatic insulin secretion, but can cause weight gain and hypoglycaemia. This agent can be given in combination with metformin.
• alpha-glucosidase inhibitor agents such as acarbose act to inhibit the activity of intestinal glucosidase enzymes. Their side effect profile includes bloating, abdominal discomfort, diarrhoea and flatulence.
2. Insulin therapy
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