Diabetics complications Year 4 Internal Medicine Notes

Diabetics complications Year 4 · Internal Medicine Collection: 4TH YEAR ALL NOTES / IMED / I MED BEAUTIFUL NOTES / HEMAT -- Diabetes complications\n435 medicine teamwork\n[ ​Important​ ​ ​ ​Notes ​ ​ ​Extra​ ​ ​Editing file​ ]\n\nlecture objectives:\n⇨ not given.\n\n Done By​: ​Dalal Al Huzaimi & Fahad AlAbdullatif\nEdited by​: ​Rahaf Binabbad\nRevised by​: L\n​ uluh Alzeghayer\nReferences: Lecture notes, Step up, Kumar’s & Davidson’s \n\n ★ Recall: Blood glucose levels\nPre-diabetes Diabetes Therapeutic goals (HbA1c)\nFasting plasma glucose = (​110-125​) Fasting plasma glucose = ​≥126​ mg/dL Early on in diabetes: ​6.5%​ or less.\nmg/dL or Plasma glucose in random sample or later in older patients: ​7.5%​ or less.\n2 hrs after a 75 g glucose load​ ≥ 200\nmg/dL\n\n ★ Diabetic complications​ ​A leading cause of morbidity & mortality. Chronic complications\nencompass ​Microvascular disease​ (neuropathy, retinopathy & nephropathy) & ​Macrovascular\ndisease (vasculopathy). What is the #1 cause of mortality among diabetics? Heart diseases.\n\nAcute Complications\n1. ​Hypoglycemia:\n❏ Hypoglycemia is really due to an imbalance between glucagon and insulin\n❏ The primary organ at risk in hypoglycemia is ​the brain​, unlike other tissues, the brain cannot use free fatty\nacids as an energy source.\n❏ its prevalence more than the hyperglycemia and it’s ​not​ associated with mortality1.​ hyperglycemia​ is\nassociated with mortality.\n\n Hypoglycemia \nCauses: - Either ​more drug ​or ​less food​ or​ more exercise\n● Drug-induced​ (Taking too much insulin)\n● Factitious hypoglycemia2 ‫ ﻣﺜﻞ‬،‫ﯾﺄﺧﺬون أدوﯾﺔ ﺗﺤﻔﺰ إﻓﺮاز اﻻﻧﺴﻮﻟﯿﻦ زﯾﺎدة ﻋﻠﻰ ﻋﻼﺟﻬﻢ اﻷﺳﺎﺳﻲ‬\nsulfonylureas\n● Ethanol ingestion​, through two mechanisms:\n○ Poor nutrition that leads to decreased glycogen\n○ Metabolism of alcohol that lowers nicotinamide adenine dinucleotide levels and\ndecreases gluconeogenesis\n● Post gastric surgeries. ​Remember dumping syndrome?\n● Adrenal insufficiency\n● Liver failure\n● Critical illness\n● Disorders of carbohydrate metabolism (e.g., glycogen storage diseases)\n● Idiopathic\n\n 1\n‫اﻟﺤﺎﻟﺔ اﻟﻠﻲ ﯾﻜﻮن ﻓﯿﻬﺎ اﻟﻤﺮﯾﺾ وﻗﺖ ﻫﺒﻮط اﻟﺴﻜﺮ ﻫﻲ ﺳﺒﺐ اﻟﻮﻓﺎة ﻓﻲ ﺑﻌﺾ اﻟﺤﺎﻻت ﻣﺜﻞ وﻫﻮ ﯾﺴﻮق أو وﻫﻮ ﯾﺴﺒﺢ وﻣﺤﺪ ﺣﻮﻟﻪ ﯾﺴﺎﻋﺪه‬\n“ doing the wrong activity in the wrong place at the wrong time “\n2\n​ actitious​ (or factitial) ​hypoglycemia​ occurs secondary to the surreptitious use of insulin or insulin secretagogues\nF\n(sulfonylureas, meglitinides). \n\nClinical Features: ● Symptoms occur at a blood glucose ​level of 40 to 50 mg/dL.\n● Elevated epinephrine​ levels cause ​sweating, tremors, increased BP and pulse, anxiety,\nand palpitation\n● Neuroglycopenic symptoms—decreased​ glucose for the brain (CNS dysfunction),\nresulting in irritability, behavioral changes, weakness, drowsiness, headache,\nconfusion, convulsions, coma, and even death Diagnosis: ● Symptoms generally begin when levels drop below 50. However, there is ​no cutoff\nvalue to define hypoglycemia.\n● Whipple’s triad:\n○ Hypoglycemic symptoms brought on by fasting\n○ Blood glucose <50 mg/dL​ during symptomatic attack\n○ Glucose administration brings relief of symptoms \nTreatment \n- not major but very serious if you didn’t treat. Acute treatment​: ​If the patient can eat, give sugar-containing foods; if not, give 1/2 to 2 ampules of D50W intravenously if the patient is alcoholic give thiamine before administering glucose to avoid ​Wernicke’s encephalopathy​.\n\n2. ​Hyperglycemia:\na. ​DKA:\n❏ Diabetic Ketoacidosis is an ​acute, life-threatening​ medical emergency that can occur in both type I and type II\ndiabetic patients (​more common in type I​).\n❏ Consequences of DKA include hyperglycemia, ketonemia, metabolic acidosis, and volume depletion.\n❏ Greatly raised ( 5 mmol/L) ketone levels Precipitating factors:\n❖ Any type of ​stress​ or ​illness​ (e.g., infectious process, trauma, myocardial infarction, stroke, recent surgery,\nsepsis, GI bleeding)\n❖ Inadequate administration of insulin\n\n Diabetic Ketoacidosis Pathogenesis: ● It’s secondary to ​insulin deficiency and glucagons excess​, both of which contribute to\naccelerated severe hyperglycemia and accelerated ketogenesis.\n● Severe hyperglycemia leads to an ​osmotic diuresis​, which causes ​dehydration​ and\nvolume depletion​.\n● In parallel, rapid ​lipolysis​ occurs, leading to ​→ ​elevated circulating free fatty-acid\nlevels ​→​ The free fatty acids are broken down to ​acetyl-coenzyme A (CoA)​ within the\nliver cells ​→​ in turn, it’s converted to ketone bodies within the ​mitochondria ​→\nAccumulation of ketone bodies produces a ​metabolic acidosis. Clinical Features: ● Nausea and vomiting\n● Kussmaul’s respiration3\n● Abdominal pain (more common in children) that may mimic acute abdomen\n● “Fruity” (acetone) breath odor\n● Marked dehydration, orthostatic hypotension, tachycardia—volume depletion is\nalways present\n● Polydipsia, polyuria, polyphagia, weakness\n● Altered consciousness, drowsiness, and frank coma may occur if not trea