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MUHAMMAD ZAMAN HABIB FINAL YEAR MBBS NISHTAR MEDICAL COLLEGE MULTAN
Mechanisms
Genetic susceptibility *Repeated acute changes in cellular metabolism Hyperglycemia **Cumulative long term changes in stable macromolecules Independent accelerating factors Tissue damage
Macro-vascular Complications
Diabetic patients have a 2 to 6 times higher risk for development of these complications than the general population
Macro-vascular Complications
The major cardiovascular risk factors in the non-diabetic population (smoking, hypertension and hyperlipidemia) also operate in diabetes, but the risks are enhanced in the presence of diabetes. Overall life expectancy in diabetic patients is 7 to 10 years shorter than non-diabetic people.
Macro-vascular Disease
Once clinical macro-vascular disease develops in diabetic patients they have a poorer prognosis for survival than normoglycemic patients with macrovascular disease The protective effect females have for the development of vascular disease are lost in diabetic females
2-3 fold increase in clinically evident atherosclerotic disease in diabetics women diabetics=male diabetics in terms of CAD mortality
5000 men with type 2 DM Followed for 12 years Men with type 2 DM had absolute risk of CAD-related death 3 times higher than nondiabetic cohort
50% have hypertension 30% have dyslipidemia Prospective study Newly detected type 2 DM:
UKPDS:
Risk of MI in Diabetes
UKPDS:
1441 patients, type 1 diabetes Randomized to intensive glycemic control vs. conventional therapy Monitored prospectively for 6.5 years Results:
Less retinopathy by 50% Macrovascular complications: 41% reduction (not statistically significant) -small number of events in young patient cohort
3867 patients with newly diagnosed type 2 DM Intensive vs. Conventional therapy 10 year follow-up Microvascular endpoints improved Trend only towards reduced incidence of MI ( p=0.052)
Effect of Hypertension
Mortality vs systolic blood pressure
70
60 50 40 30 20 10 0 110 120 130 140 150 160 Systolic Blood pressure (mmHg) Non-diabetic Diabetic
Type 2
Mostly present at diagnosis Affects at least 60% of patients
Pathophysiology of hypertension
Type 1 DM
Secondary to nephropathy Activation of the RAAS
Type 2 DM
Hyperinsulinemia Secondary to insulin resistance Activation of the sympathetic nervous system
Effect of Cholesterol
Serum cholesterol vs Mortality
Ten Year Mortality (per 1000)
70 60 50 40 30 20 10 0 4 5 6 7 s-Cholesterol (mmol/L)
Non-diabetic Diabetic
Dyslipidaemia in DM
Most common abnormality is s HDL and s Triglyserides A low HDL is the most constant predictor of CV disease in DM Target lipid values: LDL <2.6 mmol/l, HDL >1.15 mmol/l, TG < 2.5 mmol/l
Eye Complications
Cataracts
Non enzymatic glycation of lens protein and subsequent cross linking Sorbitol accumulation could also lead to osmotic swelling of the lens but evidence of involvement in cataract formation is less strong
Eye Complications
Retinopathy (stages) Background Pre-proliferative Proliferative Advanced diabetic eye disease Maculopathy Glaucoma
DR is the leading cause of blindness in the working population of the Western world The prevalence increase with the duration of the disease (few within 5 years, 80 100% will have some form of DR after 20 years) Maculopathy is most common in type 2 patients and can cause severe visual loss
Background Retinopathy
Micro aneurisms Scattered exudates Hemorrhages(flame shaped, Dot and Blot) Cotton wool spots (<5) Venous dilatations
Background retinopathy
Background retinopathy
Pre-Proliferative Retinopathy
Rapid increase in amount of micro aneurisms Multiple hemorrhages Cotton wool spots (>5) Venous beading, looping and duplication
Proliferative retinopathy
Proliferative Retinopathy
New vessels (on disc, elsewhere) Fibrous proliferation (on disc, elsewhere) Hemorrhages (preretinal, vitreous)
Panretinal photo-coagulation
Proliferative retinopathy
Vitreous Bleeding
Rubeosis Iridis
Retinal detachment with or without retinal tears Rubeosis iridis Neovascular glaucoma
Maculopathy
Maculopathy
Diabetes has become the most common cause of end stage renal failure in the US and Europe About 20 30% of patients with diabetes develop evidence of nephropathy The prevalence of DN is higher in Black Americans than in Whites (Figures for South Africa is not available)
Stages of DN
Stage I glomerular filtration and kidney hypertrophy Stage II u-albumin excretion < 30mg/24h Stage III Microalbuminuria (30 300 mg/24h)
Stages of DN (cont)
Stage IV Overt nephropathy (> 300mg/24h, positive u dipstick) Stage V ESRD characterized by blood urea and creatinine levels, hyperkalaemia and fluid overload
Diabetic Neuropathy
Sensorimotor neuropathy (acute/chronic) Autonomic neuropathy Mononeuropathy Spontaneous Entrapment External pressure palsies Proximal motor neuropathy
Sensorimotor Neuropathy
Patients may be asymptomatic / complain of numbness, paresthesias, allodynia or pain Feet are mostly affected, hands are seldom affected In Diabetic patients sensory neuropathy usually predominates
Autonomic Neuropathy
Symptomatic Postural hypotension Gastroparesis Diabetic diarrhea Neuropathic bladder Erectile dysfunction Neuropathic edema Charcot arthropathy Gustatatory sweating Subclinical abnormalities Abnormal pupillary reflexes Esophageal dysfunction Abnormal cardiovascular reflexes Blunted counter-regulatory responses to hypoglycemia Increased peripheral blood flow
Mononeuropathies
Cranial nerve palsies (most common are n. IV,VI,VII) Truncal neuropathy (rare)
Entrapment Neuropathies
Carpal tunnel syndrome (median nerve) Ulnar compression syndrome Meralgia paresthetica (lat cut nerve to the thigh) Lat Popliteal nerve compression (drop foot) All the above are more common in diabetic patients
Diabetic Amyotrophy
Thoracoabdominal Radiculopathy
Sudomotor Dysautonomia
Summary
Diabetic neuropathy is a common complication, and result in significant morbidity Diabetic neuropathy present in numerous ways Hyperglycemia is the cause of diabetic neuropathy
Summary (cont)
Diabetic neuropathy have bad consequences Diabetic neuropathy can be prevented in only one way Once diabetic neuropathy is present it can only be managed symptomatically Early diagnosis and aggressive management can prevent progression
Infections
The association between diabetes and increased susceptibility to infection in general is not supported by strong evidence However, many specific infections are more common in diabetic patients and some occur almost exclusively in them Other infections occur with increased severity and are associated with an increased risk of complications
Infections (cont)
Several aspects of immunity are altered in patients with diabetes There is evidence that improving glycemic control patients improves immune function
Specific Infections
Community acquired pneumonia Acute bacterial cystitis Acute pyelonephritis Emphysematous pyelonephritis Perinephric abscess Fungal cystitis
Rhino-Cerebral Mucormycosis
Microalbuminuria
Increased risk for overt nephropathy Increased cardiovascular mortality Increased risk of Retinopathy Increased all-cause mortality Thus Microalbuminuria is an indication for screening for possible vascular disease and aggressive intervention to reduce all cardiovascular risk factors
Normal
30 30 - 299
20 20 - 199
30 30 - 299
300
200
300
Begin with puberty Start screening at the Diagnosis of After 5 years diabetes duration of disease Should be done Should be done annually there after annually there after
Management of Nephropathy
Improvement of glycemic control Treatment of hypertension Treatment with angiotensin converting enzyme inhibitors Restriction of dietary intake of protein Once persistent elevation in u-Albumin is found refer to a Internist or Nephrologist
Management of Neuropathy
Burning pain TADs / Capsaicin Lancinating pain Anticonvulsants / TAD / Capsaicin Painful cramps Quinidine sulphate Restless legs - Clonazepam
check feet daily Wash feet daily Keep toenails short Protect feet Always wear shoes Look inside shoes before putting them on Always wear socks Break in new shoes gradually
Conclusion
This is just an outline of the major diabetic complications, and doesn't aim to be comprehensive All complications are preventable with good glycaemic control The progression of most complications can be halted if detected early and appropriate therapy instituted