Lecture 38-Complications of Diabetes (2nd update) Year 4

Lecture 38-Complications of Diabetes (2nd update) Year 4 · Internal Medicine Collection: 4TH YEAR ALL NOTES / IMED / I MED BEAUTIFUL NOTES / CVS -- MEDICINE 432 Team 38 Complications of Diabetes\n\n Done By: Reviewed By:\nMohammad Alsari Asma Al-Mohizea\n\n COLOR GUIDE: • Females' Notes • Males' Notes • Important • Additional \n\n432MedicineTeam Complications of Diabetes\n\n Objectives\nNot given.\n\nNote:\n• Due to the unavailability of the lecture’s PowerPoint, the\ncontents of this file are based on the Diabetes chapters in\nboth Kumar & Davidson’s.\n\n 1 \n\n432MedicineTeam Complications of Diabetes\n\nDiabetic patients are at risk of a wide variety of complications and have a considerably reduced life expectancy (T1DM reduces it by 11-13yrs) when compared to non-diabetics. Complications can be divided into acute and chronic.\nNote:\nRegarding the management The general pathophysiology: of hyperosmolar non-ketotic Related to hyperglycemia and its consequences via the following comas, the doctor mechanisms: emphasized giving 0.45%\nsaline to manage they\n• Non-enzymatic glycosylation: accumulation of advanced\nhypernatremia while the\nglycosylated end products, causing inflammation and injury. books advice starting 0.9%:\nGlucose binding to protein increases with exposure like Kumar: avoid 0.45% saline\nhemoglobin A1c. because the rapid dilution of\nblood may cause more\n• Polyol pathway: increased glucose metabolism via aldose\ncerebral damage than a few\nreductase causes the accumulation of sorbitol and fructose. hours of hypernatremia.\nWhich affect vascular permeability and cellular structure. Like Davidson: switch to 0.45%\nwhat happens in the eyes. saline only of osmolality is\nincreasing while giving 0.9%\nsaline.\n\nAcute Complications: They are usually caused by either hypoglycemia or hyperglycemia:\nA) Hypoglycemia: can lead to palpitations, confusion & loss of consciousness. \nB) Hyperglycemia: can lead to:\n Type 1 diabetes: DKA & hypovolemia\n Type 2 diabetes: hyper-osmolar non ketotic coma\n\nChronic Complications: Diabetics have a higher risk of developing vasculopathies, retinopathies, nephropathies & neuropathies among other systemic manifestations. Vasculopathies: Diabetic microangiopathy: \n• Thickening of the capillary basement membrane associated increased vascular\npermeability throughout the body \n• This form of vascular injury affects multiple systems, leading to diabetic\nretinopathy, nephropathy, neuropathy and accelerated atherosclerosis\n\n 2 \n\n432MedicineTeam Complications of Diabetes\n\nNeuropathies: Pathophysiology: Due to insulin deficiency or resistance, the Schwann cells on the neural axons are forced use the polyol pathway as their source of ATP, which processes glucose into sorbitol. The sorbitol increases the cell’s viscosity. This leads to an influx of fluids into the cell (‫)الخاصية األسموزية‬, increasing its size and pressure on the axon. If the process continues, the cell might rupture. Symptoms include: \n• Symmetrical sensory polyneuropathy: \no Loss of vibration perception (usually first) \no Numbness and paresthesia \no Acute in lower limbs \no Weakness and atrophy in the lower limbs may occur. Especially the\ninterosseous muscles \n• Diabetic Amyotrophy: \no Painful muscle wasting \no Usually asymmetrical \no Quadriceps and shoulders are commonly affected \no Resolves with time and proper glycemic control \n• Mononeuropathies: \no Severe and rapid with eventual recovery \no Palsies are most likely to occur in the 3rd and 6th cranial nerves \no Lesions in compression areas are also common \n• Autonomic Neuropathy: \nThe sympathetic and parasympathetic systems may be affected in one or more\nsystems. Symptoms depend on the affected region. \no Cardiovascular: \n▪ Postural hypotension \n▪ Resting tachycardia \n▪ Fixed heart rate \no Gastrointestinal: \n▪ Esophageal atony (decreased motility) causing dysphagia\n\n 3 \n\n432MedicineTeam Complications of Diabetes\n\n ▪ Colonic atony causing constipation \n▪ Nocturnal diarrhea or fecal incontinence (inability to control\ndefecation) \n▪ Nausea and vomiting, feeling full, delayed gastric emptying \no Genitourinary: \n▪ Urinary incontinence \n▪ Recurrent bladder infections due to bladder atony \n▪ Erectile dysfunction \no Pupillary: \n▪ Delayed reflexes to light \n▪ Small pupil size\n\nNephropathies: Pathophysiology: \n• Increase in glomerular filtration rate due to hyperglycemia causes glomerular\nhypertrophy \n• Vasodilation of afferent vessels, further increase in filtration rate \n• This increase in intraglomerul pressure damages the glomerular capillaries and leads\nto hypertrophied mesangial cells. \n• If the process continues (no glycemic control) it may lead to glomelular sclerosis \n• Which causes progressive leaking of large molecules (proteins) into the urine Retinopathies:\n• Cataracts: \no Defined as denaturation of proteins and other lens components, causing the\nlens to be opaque (‫)شبه شفاف‬ \no Can