Glucose is the main source of energy in the body - for the brain , heart , all cells etc.
Diabetes Mellitus -dm- is a disease in which there is excess of glucose . Excess glucose sticks on to red cells and forms hba1c -glycated hemoglobin and this may block the small blood vessels in the nerves ie microvascularature-miv- causing damage - neuropathy eg foot tingling and sensation loss , the film of the eye -retinopathy and the kidneys - nephropathy , initally causing microalbuminuria and then gross protein loss . Dm is diagnosed if the glucose after an overnight fast is above 7mmol and hba1c is also above 7. Keeping the a1c levels below 7 can prevent miv damage and problems . Levels of fasting glucose between 6 and 7 are called impaired glucose tolerance -igt . Igt can also cause damage which can be delayed by a drug called metformin.
Excess glucose also accelerates atheroscelerosis where cholestrol is deposited in the big vessel walls and leads to macrovascular -mav- problems of stroke , heart attack and peripheral vascular disease. Mav can be ameliorated by cholestrol lowering agents .
Insulin is the hormone produced by the beta cells of the pancreas . At lower levels insulin stops the mainly night time glucose release by the liver and at higher levels secreted after meals it stimulates glucose uptake by the muscle and fat cells .
Type 1 dm is caused by a viral attack on beta cells .It mainly affects the young. There is a massive or total loss of insulin production and the patient -p - will need regular insulin injections. Main damage is miv . There is need for tight a1c control to slow this damage .
Type 2 dm mainly afflicts overweight middle aged people . Constant snacking may initially cause continuous insulin release and this tends to cause insulin resistance in muscle and fat cells , so less glucose goes into them and instead circulates in the blood. Insulin resistance is also thought to be due to the toxic effect of high blood fats. Eventually the beta cells become exhausted and blood glucose and a1c start to rise. Type 2 is now considered a cardiovascular disease as the damage is mainly to large arteries ie macrovascular - mav. Tight lipid control with statins may prevent mav damage.
The main symptoms of type 2 dm maybe nothing for a long time but once insulin levels are insufficient to keep glucose under control , its blood level rises and the p suffers frequency and dehydration as the kidney tries to get rid off the excess sugar. Type 2 may also present as resistant candidal or other genital infection . Elderly can have silent infarcts due to pain nerve denervation . Autonomic nerve dysfunction can cause gastric and bladder paresis , erectile dysfunction and orthostatic hypotension and abnormal sweating on eating.
On examination one should check the weight , bp, waist circumference which should be less than 102cm -40in for men and 88 cm -35in for women . South asians who typically have high tg and low hdl levels and are more at risk of heart attacks should be less than 94cm men and 33in women . Bmi should be under 25.
The fundii should be checked for retinopathy . vrmny.comThe first signs are background retinopathy with micro aneurysms of the arteries and small intraretinal hemorrhages called blots - both dots and blots tend to look the same . Flame shaped where bleeding tracks along the axons.Hard lipid depositis can form a ring pattern near the macular interfering with vision . Macular oedema can cause blurred vision and loss of acuity of more than two lines on the snellen chart and may need laser. 6/9 means a p can read the 9 line when a normal eyed patient can read the 6 line at that distance . 6 month checks are done.
Pre prolferative retinopathy has soft cotton wool exudates with indistinct edges as ischameia worsens. Dye -fluoresciene injection in the arm outlines these changes.
Proliferative retinopathy happens when new arteries grow from the optic disc and other areas . These vessels are fragile and can bleed into the vitreous causing floaters and also cause retinal detachment .Emergency lasering is indicated. Also check for cataracts and glaucoma.
Partial blindness if best corrected vision is less than 6/60, and blind if less than 3/60 and will bring financial aid , guide dogs etc.
Carotid bruits may signal risk of strokes. The heart may be enlarged in heart failure .
Measure weight -bmi- should be less than 25 , and abdominal circumference which should be less than 102cm -40in for men and 88cm- 35in for women , in south asians 94cm -37in men and 83m -33in women. Femoral , popliteal , posterior tibial and dorsalis pedis pulses are checked with doppler if necessary.
Foot examination is most important . If BP in the ankle is much lower than brachial there may be a risk .Vibration sense can be checked with a tuning fork over the big toe or a machine called a biothesiometer Foot care.
A 10g monofilament should be felt just before the wire bends (10g force) over the ten sites 1, 3 and 5 toe pulps , 1,3,and 5 metatarsal heads , medial and lateral aspects of plantar arches , center of heel and 1st dorsal web space .Foot site. A shorter test just over the first and fifth metatarsal plantar areas is just as good . Failed sensation can be considered as a risk factor for ulcers
. Loss of protective sensation generally is indicated by a patient's inability to feel the monofilament at 1 or more of the sites. Feet must be examined for inclawing due to damage to plantar fascia , pressure on metatarsal heads can cause callus and ulcers . Bleeding into a callus is a danger sign.Ulcers may heal with becalpermin cream which promotes platelet growth but may need a plaster cast with a window to keep the pressure off . Ampicillin , flucloxacillin and flagyl may be needed. If there is osteomyelitis clindamycin may help. Amputation is a last resort.
Investigations should include fbc , fbs , hba1c , ue , lft , tft , lipid profile . Microalbuminuria and if the albumin creatinie ratio is more than 2.5 , the patient needs to be put on an ace inhibitor to protect the kidneys. Rising creatinine levels above 150 indicate danger. Ecg , cxr etc.
Treatment Weight loss - each kg loss leads to a four month increase in life , low fat diet - less than 30% should be total fat and of this saturated fat should be less than 10% . Monounsaturates like olive oil are good as well as fresh foods and vegetables . Aerobic excercise eg 15min fast walk twice a day , and muscle building too increase blood supply and glucose uptake and are useful.
BP should be controlled to 130/80 . Every ten mm systolic lowering leads to a 30% fall in deaths.
The main drugs now used are insulin secretors - gliclazide , insulin itself and insulin resistance reducers eg metformin and rosiglitazones . Metformin is now the main oral drug of choice . It reduces insulin resistance and decreases hepatic glucose production . It cuts tg and stops wt gain but as it is excreted by the kidney , it needs good renal function , ie a creatinine less than 130. Start with 500 slow release and raise by 500mg every 2w until max of 2-3g per day is reached . Monitor fbs and a1c .Metformin lasts 12hrs . It raises hdl and fibrinolysis and cuts mi by 39% .
Sulfonylureas -su- bind to beta cell receptors , raise intracellular calcium in beta cells and cause release of insulin . Start on a low dose and increase every two weeks depending on fbs. May lose effect as beta cells start to decline. A 4kg wt gain may occur .They reduce a1c by about 1%. ue and lft need to be checked . Hypoglycaemic coma may be preceeded by hunger , tachycardia and sweating when bs is below 3 and aggression and confusion when the blood sugar falls below 2.7 and can be counteracted by hypostop gel or soft drinks . If in coma may need iv dextrose , insulin to get the glucose into brain cells and saline for rehydration . .
Insulin comes in 100 units per ml solution and is given sc , ie not into the skin or muscle , with the needle perpendicular . If the ac1c is more than 10 , one starts with 10u and if less than 8 with six and raise by 2u (1u in obese) daily, checking fbs each day . Its given as isophane insulin , two thirds of the units half hour pre breakfast and one third half an hr pre dinner. Pen injectors with dialled units are most popular . Humulin 30/70 mixtard is 30u short acting (onset 30mins , peak 3hrs and lasts 8hr) and 70u is intermediate isophane (onset 2hrs peak 8 lasts 18hrs) in each ml .
Only rapid (onset 10mins) -lispo , or short acting can be used iv. Rapid is given with meals . Lantus is long acting - onset 90mins , plateaus for a long time and lasts 24hrs , and can be used as a small bolus at night to cut down the night time hepatic glucose production. It can be combined with oral agents or short acting insulins during the day.
Rosiglitazones induces genes and so can take three months to start working .They reduces insulin resistance , cant be used in heart faliure but and can be combined with metformin and su , and in usa also with insulin.