Acute & chro. complications of d. m.


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Complications of Diabetes Mellitus
Acute Complications of Diabetes
Chronic complications of Diabetes

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  • Stage I:This stage is usually not clinically evident
    Stage II:Renal lesions are found on biopsy
    Stage III:Without intervention the average increase in albuminuria in patients with type 1 DM is 20% per year. Blood pressure usually starts to increase once fixed albuminuria exist
    Stages I – III are reversible
  • Stage 3:Overt diabetic nephropathy
    After 15 – 25 years in 35% of diabetic patients
    Pronounced abnormalities of the glomeruli
    GFR decline by 10 ml/min/year
    Progressive clinical proteinuria
    BP increase by 5 mmHg per year
    Nor reversible but progression can be slowed by good glucose control and use of ACE inhibitor
    Stage 4:ESRD
    Final outcome after 25-30 years
    Glomerular closure
    GFR < 10 ml/min
    Invariably hypertensive
  • Stage I:This stage is usually not clinically evident
    Stage II:Renal lesions are found on biopsy
    Stage III:Without intervention the average increase in albuminuria in patients with type 1 DM is 20% per year. Blood pressure usually starts to increase once fixed albuminuria exist
    Stages I – III are reversible
  • Thoracoabdominal radiculopathy. Truncal radiculopathies are rare but can present at the initial diagnosis of diabetes.2 Nerve roots T8 through T12 are commonly affected. Patients complain of a tight bandlike or constricting pain in the chest or abdomen. The chest or abdominal wall skin becomes sensitive to the touch.2 Motor involvement may lead to abdominal muscle weakness, which may lead to herniation and an asymmetric bulge in the abdominal wall.3 Examination of spinal fluid may show an increase of protein.4 Prognosis is generally good; most patients recover within several months.
  • Sudomotor Dysautonomia
    Patients often complain of hyperhidrosis or anhidrosis of the extremities, venous congestion, pain and redness of the feet, and gustatory sweating.5 Gustatory sweating is common in patients with cervical sympathetic denervation, demonstrated by profuse sweating of the face, neck, and upper trunk while eating.12
  • PMN leukocyte function is depressed, particularly when acidosis is also present. Leukocyte adherence, chemotaxis, and phagocytosis may be affected. Antioxidant systems involved in bactericidal activity may also be impaired.
  • A standardized filament is pressed against part of the foot. When the filament bends, its tip is exerting a pressure of 10 grams (therefore this monofilament is often referred to as the 10gram monofilament). If the patient cannot feel the monofilament at certain specified sites on the foot, he/she has lost enough sensation to be at risk of developing a neuropathic ulcer. The monofilament has the advantage of being cheaper than a biothesiometer, but to get results which can be compared to others, the monofilament needs to be calibrated to make sure it is exerting a force of 10 grams
  • Acute & chro. complications of d. m.

    2. 2. Complications of diabetes mellitus I. Acute complications:  diabetic ketoacidosis  hypoglycemia  diabetic nonketotic hyperosmolar coma II. Chronic complications:  a. Microvascular  retinopathy nephropathy neuropathy diabetic foot dermopathy b. Macrovascular Cerbrovascular. Cardiovascular. peripheral vascular disease. DR. RAHUL GARG
    3. 3. Diabetic ketoacidosis (DKA) May be the 1st presentation of type 1 DM. Result from absolute insulin deficiency or increase requirement. Mortality rate around 5%. DR. RAHUL GARG
    4. 4. Pathogenesis  Insulin decrease ↓  Counter-regulatory hormone increase: Glucagon, catecholamines, cortisol & growth hormone ↑  Hepatic glucose production increase ↑  ↓glucose utilization of peripheral tissue  => glycosuria, osmotic diuresis & dehydra-tion  lead to the release of free fatty acid into circulation from fatty tissue.  Unrestrained hepatic fatty acid oxidation to ketone bodies (β-hydroxybutyrate, acetone, acetoacetate)  => resulting in ketonemia and metabolic acidosis. DR. RAHUL GARG
    5. 5. Diagnosis of DKA Hyperglycemia Ketonuria and ketonemia Acidosis (PH< 7.3 ) DR. RAHUL GARG
    6. 6. Predisposing factors for DKA Infection Trauma Myocardial Infarction Stroke Surgery Emotional stress DR. RAHUL GARG
    7. 7. Clinical presentation of DKA Polyuria and polydipsia. Nausea and vomiting. Anorexia and abdominal pain. Tachycardia. Fruity odor of the breath. Hypotonia, stupor and coma. Sign of dehydration. DR. RAHUL GARG
    8. 8. Treatment of DKA Fluid replacement. Insulin therapy for hyperglycemia. Electrolyte correction. Acidosis correction. Treatment of precipitating cause. DR. RAHUL GARG
    9. 9. Complication of DKA Cerebral edema Vascular thrombosis Infection M I Acute gastric dilatation Respiratory distress syndrome DR. RAHUL GARG
    10. 10. Hypoglycemic coma Hypoglycemia is the most frequent acute complication in diabetes.  Hypoglycemia is the level of blood glucose at which autonomic and neurological dysfunction begins DR. RAHUL GARG
    11. 11. Clinical manifestations of hypoglycemia:  Autonomic dysfunctions: 1. Hunger 2. Tremor 3. Palpitation 4. Anxiety 5. Pallor 6. Sweating DR. RAHUL GARG
    12. 12. Neurologic dysfunctions: 1. Impaired thinking 2. Change of mood 3. Irritability 4. Headache 5. Convulsion 6. Coma DR. RAHUL GARG
    13. 13. Predisposing factors Missed meal Change in physical activity Alterations or errors in insulin dosage Alcohol ingestion DR. RAHUL GARG
    14. 14. Treatment of hypoglycemia In mild cases oral rapidly absorbed carbohydrate In sever cases (comatose patient) iv hypertonic glucose 25% or 50% concentration Glucagons injection DR. RAHUL GARG
    15. 15. Chronic Complications of DM A. Macrovascular Complications: B. Microvascular Complications: DR. RAHUL GARG
    16. 16. Macro-vascular Complications: Ischemic heart diseases. Cerebrovascular diseases. Peripheral vascular diseases. Diabetic patients have a 2 to 6 times higher risk for development of these complications than the general population DR. RAHUL GARG
    17. 17. Macro-vascular Complications:  Accelerated atherosclerosis involving the aorta and large- and medium-sized arteries.  Myocardial infarction, caused by atherosclerosis of the coronary arteries, is the most common cause of death in diabetics.  Gangrene of the lower extremities.  Hypertension due to Hyaline arteriolosclerosis. DR. RAHUL GARG
    18. 18. Hypertension in DM Type 2 Type 1  present after several years of     DM affects about 30% of patients. Secondary to nephropathy Activation of the Renin angiotensin system DR. RAHUL GARG     Mostly present at diagnosis Affects about 60% of patients Secondary to insulin resistance Activation of the sympathetic nervous system
    19. 19. Dyslipidaemia in DM Most common abnormality is ↓ HDL and ↑ Triglycerides A low HDL is the most constant predictor of Cardiovascular disease in DM. DR. RAHUL GARG
    20. 20. Screening for Macrovascular Complications 1. 2. 3. 4. Examine pulses for cardiovascular diseases. lipid profile. ECG. Blood pressure. DR. RAHUL GARG
    21. 21. Microvascular Complications Microvascular complications are specific to diabetes and related to longstanding hyperglycaemia. Both Type1 DM and Type2 DM are susceptible to microvascular complications. The duration of diabetes and the quality of diabetic control are important determinants of microvascular abnormalities. DR. RAHUL GARG
    22. 22. Pathophysiology of microvascular disease In diabetes, the microvasculature shows both functional and structural abnormalities. The structural hallmark of diabetic microangiopathy is thickening of the capillary basement membrane. changes in basement membrane composition including increased type IV collagen and its glycosylation (i.e binding of glucose to wall of blood vessels). DR. RAHUL GARG
    23. 23. The main functional abnormalities include increased capillary permeability, viscosity, and disturbed platelet function. These changes occur early in the course of diabetes and precede organ failure by many years. Increased capillary permeability is manifested in the retina by leakage of fluorescein and in the kidney by increased urinary losses of albumin which predict eventual renal failure. DR. RAHUL GARG
    24. 24.  Platelets from diabetic patients show an exaggerated tendency to aggregate, perhaps mediated by altered prostaglandin metabolism.  Plasma and whole blood viscosity are increased in diabetes.  These defects together with the platelet abnormalities may cause stasis in the microvaculature, leading to increased intravascular pressure and to tissue hypoxia.  There is abnormal production of von Willebrand factor and endothelial derived nitric oxide by endothelial cells which could contribute to tissue damage. DR. RAHUL GARG
    25. 25. 1- Diabetic retinopathy * Pathogenesis: Histologically the earliest lesion is thickening of the capillary basement membrane. On fluorescein angiography the first abnormality is the capillary dilatations (microaneurysms).  Microaneurysm may give rise to haemorrhage or exudate. Vascular occlusion, initially of capillaries and later of arteries and veins, leads to large ischaemic areas (cotton-wool spots). DR. RAHUL GARG
    26. 26. DR. RAHUL GARG
    27. 27. Background Retinopathy Micro aneurysms Scattered exudates Hemorrhages(flame shaped, Dot and Blot) Cotton wool spots (<5) Venous dilatations Background retinopathy DR. RAHUL GARG
    28. 28. Cotton wool spots DR. RAHUL GARG
    29. 29. Proliferative Retinopathy New vessels (on disc, elsewhere) Fibrous proliferation (on disc, elsewhere) Hemorrhages (preretinal, vitreous) Panretinal photo-coagulation DR. RAHUL GARG
    30. 30. Other Eye Complications - Cataracts. - Glaucoma - Macular edema. -Ischaemic maculopathy. -Proliferative retinopathy. -Vitreous Bleeding. -Rubeosis Iridis DR. RAHUL GARG
    31. 31. Vitreous Bleeding DR. RAHUL GARG
    32. 32. DR. RAHUL GARG
    33. 33. Proliferative retinopathy. Note the abnormal capillaries and haemorrhages. DR. RAHUL GARG
    34. 34. 2- Diabetic Nephropathy (DN) - Diabetic nephropathy is defined by persistent albuminuria (>300 mg/day), decrease glomerular filtration rate and rising blood pressure. - About 20 – 30% of patients with diabetes develop diabetic nephropathy DR. RAHUL GARG
    35. 35. Risk factors of DN Duration of DM.  Family History of hypertension. Cardiovascular disease, nephropathy.  Hyperglycemia.  Hypertension.  Microalbuminuria.  Male gender.  Cigarette smoking.  DR. RAHUL GARG
    36. 36. Pathogenesis: The glomerular and vascular lesions are linked to hyperglycemia. Nonenzymatic glycosylation to glomerular proteins results in accumulation of irreversible advanced glycosylation end products in the glomerular mesangium and glomerular basement membrane. This alteration leads to proteinuria and eventually glomerulosclerosis DR. RAHUL GARG
    37. 37. Pathological pattern of DN Diffuse form (more common): consist of thickining of glomerular basement membrane with generalized mesangial thickenings. The nodular form (the Kimmelstiel-Wilson lesion): (accumulation of periodic acid schiff positive material are deposit in the periphery of glomerular tufts. DR. RAHUL GARG
    38. 38. Diabetic nephropathy • The glomerulus shows sclerotic nodules in the center of the lobules or segments. DR. RAHUL GARG
    39. 39. DR. RAHUL GARG
    40. 40. Stages of DN Stage I ↑ glomerular filtration and kidney hypertrophy Stage II u-albumin excretion < 30mg/24h Stage III Microalbuminuria (30 – 300 mg/24h) Stage IV Overt nephropathy (> 300mg/24h, positive u dipstick) Stage V ESRD characterized by ↑ blood urea and creatinine levels, hyperkalaemia and fluid overload DR. RAHUL GARG
    41. 41. Treatment to prevent progression to DN Glycaemic control. ACE inhibitor . Blood pressure control. Smoking cessation. Proteins restriction. Lipid reduction. DR. RAHUL GARG
    42. 42. 4. Diabetic Neuropathy 1. Sensorimotor neuropathy. 2. Autonomic neuropathy. DR. RAHUL GARG
    43. 43. Sensorimotor Neuropathy Numbness, paresthesias. Feet are mostly affected, hands are seldom affected. Complicated by ulceration (painless), charcot arthropathy. DR. RAHUL GARG
    44. 44. Complications of Sensorimotor neuropathy DR. RAHUL GARG
    45. 45. Autonomic Neuropathy Symptomatic Postural hypotension Gastroparesis Diabetic diarrhea Neuropathic bladder Erectile dysfunction Neuropathic edema Charcot arthropathy Gustatatory sweating DR. RAHUL GARG Subclinical abnormalities Abnormal pupillary reflexes Esophageal dysfunction Abnormal cardiovascular reflexes Blunted counter-regulatory responses to hypoglycemia Increased peripheral blood flow
    46. 46. Mononeuropathies Cranial nerve palsies (most common are n. IV,VI,VII) Truncal neuropathy (rare) DR. RAHUL GARG
    47. 47. 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 DR. RAHUL GARG
    48. 48. DR. RAHUL GARG
    49. 49. DR. RAHUL GARG
    50. 50. 5. Infections  Community acquired pneumonia  Acute bacterial cystitis  Acute pyelonephritis  Pyelonephritis  Perinephric abscess  Fungal cystitis. DR. RAHUL GARG
    51. 51. foot care Patient should check feet daily Wash feet daily Keep toe nails short Protect feet Always wear shoes Look inside shoes before putting them on Always wear socks Break in new shoes gradually DR. RAHUL GARG
    52. 52. Foot ulcer DR. RAHUL GARG
    53. 53. DR. RAHUL GARG
    54. 54. Screening for Neuropathy 128 Hz tuning fork for testing of vibration perception 10g Semmers monofilament The main reason is to identify patients at risk for development of diabetic foot DR. RAHUL GARG
    55. 55. Using of the Monofilament DR. RAHUL GARG
    56. 56. The end DR. RAHUL GARG