Diabetes Mellitus - Causes, Symptoms, and Treatments PDF
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Uploaded by RobustNessie6053
PHINMA Saint Jude College Manila
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Summary
This document provides a detailed overview of diabetes mellitus (DM). It discusses the disorder of the pancreas, types (Type I and Type II DI), pathophysiology and tests. The document covers the effects of insulin, hematological & urine studies and treatment, including diet, exercise, and pharmacological approaches. It explores both acute and chronic complications. Finally, it outlines nursing interventions.
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DISORDER OF THE PANCREAS GLUCAGON – maintains the normal blood glucose levels during fasting states ; stimulates GLYCOGENOLYSIS. INSULIN – hormone that controls the level of glucose in the blood by regulating the production & storage of glucose; stimulates GLYCOGENESIS – It in...
DISORDER OF THE PANCREAS GLUCAGON – maintains the normal blood glucose levels during fasting states ; stimulates GLYCOGENOLYSIS. INSULIN – hormone that controls the level of glucose in the blood by regulating the production & storage of glucose; stimulates GLYCOGENESIS – It increases glucose transport into cells & promotes conversion of glucose to _____ --> thus it _______ serum glucose FUNCTIONS OF INSULIN: 1. Transports & metabolizes glucose for energy 2. Stimulates storage of glucose in the liver & muscles (in the form of GLYCOGEN) 3. Enhances storage of energy of dietary fat in adipose tissue 4. Signals liver to STOP release of glucose A chronic hereditary disease characterized by hyperglycemia (abnormal increase level of blood glucose) due to relative insufficiency or lack of insulin that leads to abnormalities of CHO, CHON & FAT metabolism PREDISPOSING FACTORS: 1. Older individuals 2. Obese 3. Women 4. Hereditary TYPE I (IDDM) TYPE II (NIDDM) Gradual Rapid > 40 y/o < 40 y/o Genetic predisposition, ONSET JUVENILE TYPE (before Obesity 15 y/o) ADULT onset (insulin resistant) AUTOIMMUNE May be asymptomatic Absolute deficiency INSULIN Relative deficiency in insulin (or very little) TREATMENT INSULIN, diet, exercise Diet, exercise, OHA COMPLICATION DKA HHNK syndrome/coma PATHOPHYSIOLOGY DIGESTION ✔ Fats 🡪 Fatty Acid ✔ CHO 🡪 Glucose ✔ CHON 🡪 Amino Acid ↓ Stored in the Liver in the form of GLYCOGEN ↓ if INSULIN is deficient; it goes to the bloodstream ↓ HYPERGLYCEMIA HYPERGLYCEMIA ↓ decreased tubular reabsorption (POLYURIA) ↓ F/E imbalance ↓ intracellular DHN (hemoconcentration) ↓ hypothalamus stimulation (POLYDIPSIA) “STATE OF STARVATION” Glucose cannot enter cells d/t lack of insulin ↓ cellular starvation (POLYPHAGIA) ↓ GLUCONEOGENESIS ↓ Breakdown of CHON & fats ↓ FATS -- Lipid Accumulation CHON -- Cataract Formation, Diabetic Retinopathy FATS -- Lipid accumulation CHON ↓ ↓ Atherosclerosis Eyes ↓ ↓ Decreased blood supply to major Cataract formation organs ↓ ↓ Diabetic Retinopathy Heart: MI, Angina Pectoris Brain: CVA Lower Extremities: Decreased blood supply 🡪 Necrosis🡪 Gangrene HEMATOLOGICAL STUDIES 1. FASTING BLOOD SUGAR (FBS) Normal: 70 – 110 mg/ml (+DM if BGL >126 mg/dL after 2 consecutive readings) 2. 2-HOUR POST-PRANDIAL BLOOD SUGAR TEST (PPBS) A test that determines the ability of an individual to dispose carbohydrates load. A blood sugar measurement is made 2 hours after ingestion of predetermined amount of CHO. Usually 100 gm CHO or 100 gm of glucose level remains high after 2 hours if with DM. Normally the glucose should return to normal within this time. 3. ORAL GLUCOSE TOLERANCE TEST (OGTT) 🡪 May be used to confirm diagnosis when the blood test is borderline. (Also confirms Gestational DM) 3 days before the test: 150 mg of carbohydrate diet + Normal activity Immediately before the test: A. NPO for 10-12 hrs B. fasting baseline specimen of blood & urine 🡪 Glucose (75mg) given PO (if pt vomits = D/C) 🡪 Blood and urine specimen are taken at 30 minutes 1 and 2, 3 hours after ingestion of the glucose 4. GLYCOSYLATED HEMOGLOBIN (HbA1C) 🡪 maybe used to monitor average blood glucose over 2 – 3 months period 🡪 N = 3.8 – 6.4 mg/dl 🡪 GOAL (for DM pts):
