Diabetes/GI System & Disorders Exam Review Guide to A+

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I. DIABETES:  Function of Pancreas: o Secretes Insulin  2 Types of Diabetes: o Mellitus and Insipidus  3 Types of Diabetes Mellitus: o Type 1, Type 2, and gestational o More prevalent ... in men than women o Occurs more in African Americans and Hispanic populations o Has wide ranging systemic effects and is a contributing factor to the development of cardiovascular disease, hypertension, kidney disease, neuropathy, retinopathy, peripheral vascular disease and stroke.  Role of Insulin: o Insulin allows for the metabolism or uptake of glucose into the body’s cells.  Type 1 Diabetes Mellitus: o A metabolic disorder resulting from inadequate production of insulin. o An autoimmune dysfunction involving the destruction of beta cells, which produce insulin in the islet of Langerhans of the pancreas. o No insulin is produced by the pancreas o Usually genetic/inherited and occurs early on in life, child diabetes o Viruses- destruction of beta cells o Auto antibodies against insulin o Pathophysiology:  Stages – Genetic predisposition – Environmental Trigger – Active Autoimmunity – Progressive Beta cell destruction – Overt Diabetes Mellitus  Type 2 Diabetes Mellitus: o A progressive condition due to increasing inability of cells to respond to insulin (insulin resistance) and decreased production of insulin by the beta cells. o Insulin production is less or use is impaired or reduces insulin sensitivity o Hereditary – major role o Linked to obesity, sedentary lifestyle, diet, and hereditary o Pathophysiology:  Causes – leading to high glucose  Stages – Desensitization – Failure of beta cells to respond to high glucose levels  Insulin Resistance – Production of glucose by liver despite of high glucose levels  Inability of fat and muscle tissue to take up glucose – peripheral insulin resistance o These patients usually have blood glucose levels around 160 o Insulin takes the glucose into the cell, as well as potassium because they follow each other, where it can be metabolized and used. o Patient Teaching: Eat healthy (1200 calories/day maximum, eat smaller more frequent meals), exercise 30-45 mins a day, get away from sedentary lifestyle, take oral antidiabetic medications, and then if these interventions don’t control the diabetes, then give insulin. o 3 P’s of hyperglycemia of type 2 diabetes: Polyurea, polydipsia, polyphagia  Polyuria: Excessive urination  Polydipsia: Excessive thirst  Polyphagia: Excessive hunger o Diagnostic Methods: HgbA1C or give patient glucometer and have him record his glucose levels for 3 days and report (cheaper than A1c), run lipid profile, CBC, CMP, RLT, check eyes for glaucoma, check toes for neuropathy, wounds that do not heal? Frequent infections?  Clinical manifestations plus high glucose = Diabetic  Gestational Diabetes: o Occurs during a woman’s pregnancy and usually goes away after birth o Pregnant woman also experience the 3 P’s, so run OGTT (oral glucose tolerance test):  fasted over night, take her blood, then give her 100mg glucose, then take her blood after 30 mins and 2 hrs o Pregnant women get OGTT, not HgbA1C  Clinical Manifestations: o Hyperglycemia S/S: Fatigue, Blurred vision, Slow wound healing, Itchy skin-“Hot and dry, blood sugar high”-3 P’s o Hypoglycemia S/S: Sweating, Hunger, Trembling, Anxiety, Confusion, Blurred vision-“Cool and clammy, need some candy” o Weight loss o Ketone bodies- Diabetic Keto Acidosis o Fruit breath odor, headache, N,V, Abd. Pain, fatigue, weakness, slow wound healing o Nonspecific symptoms  Classic symptoms of type 1 may manifest o Fatigue o Recurrent infection o Recurrent vaginal yeast or candida infection o Prolonged wound healing o Visual changes  Complications of Diabetes: o Neuropathy:  Caused by damage to sensory nerve fibers resulting in numbness and pain  Is progressive, can affect every aspect of the body, and can lead to ischemia and infection  Provide foot care, lotion on feet (not toes), powder in toes, trim nails straight, and put powder in between toes, and buy larger sized shoes  Neuropathy - Desensitization of peripheral nerve endings.  Microvasculature that supplies nerves is damaged  Due to decreased circulation, myelin sheet is damaged Nerve conduction is reduced o Nephropathy:  Damage to the kidneys from prolonged elevated blood glucose levels and dehydration  Increased polyuria, Glycosuria and changes in kidney vasculature leads to renal failure.  Monitor BP, hydration, kidney function (I&O)  Teach the client to drink 2-3L/day fluid, avoid soda, alcohol and NSAIDS o Retinopathy:  Impaired vision and blindness  Cause hemorrhages in blood vessels of retina and cotton wool spots  Encourage yearly eye exams and management of blood glucose levels  Ophthalmic vasculature is damaged  Abnormal blood vessels proliferate and hemorrhage, clouding vision and destroying the retina o Circulatory Complications  Hypertension, MI, and stroke  Monitor BP  Encourage cholesterol level checks, exercise, weight loss, good diet/dietary consult o Delayed Wound Healing:  Development of gangrenes – FOOT CARE o Risk of infection:  Increased glucose and decreased nerve supply - Hub for bacteria  Opportunistic Infections – yeast, Candida  Circulatory Complications: o Heat and blood Vessels diseases – Stroke, Heart Attack, CAD  Microvascular complications: Retinopathy and/or nephropathy  Macrovascular Disease: Peripheral Artery Diseases  Diabetic Ketoacidosis: o Acute, Life threatening condition characterized by increased blood glucose (>300 mg/dL) resulting in breakdown of body fat for energy, dehydration, metabolic acidosis, and accumulation of ketones in the blood and urine. o Onset is rapid and high mortality rate. o Risks – Uncontrolled diabetes, missed insulin, stress, illness, trauma, increased steroids/epinephrine’s o DKA occurs acutely, and needs to be treated within 20 minutes o Give IV asap, give them bolus for dehydration 500ml/hr normal saline  Hyperglycemic-Hyperosmolar State (HHS): o HHS – Acute, life threatening condition characterized by profound hyperglycemia (>600 mg/dL) that leads to dehydration but absence of ketosis. Onset is generally over several days. o HHNKS (Hyperosmolar Hyperglycemic Non-Ketotic Syndrome) o Non-ketotic syndrome takes longer to develop than DKA (several days)  Treatment of HHS and DKA: o Treat the cause – infection/stress etc o First rapid Isotonic Fluid – followed by Hypotonic fluid o Monitor Vitals, Urine, Weight o Goal – Glucose – 250 – then start adding glucose to fluid o Regular Insulin – First Bolus – then IV o Monitor Potassium – First Hyper then Hypo o Cardiac Rhythm o Sod Bicarb if Acidosis o Do regular assessment, take CBC, ABG panel, then give fluids, don’t give anything NPO o When glucose goes down to 400, slow the insulin and fluids, once glucose goes to 280 stop the insulin  Diagnosis: o Fasting Blood Glucose or HbA1c  Nursing actions:  Hold antidiabetic medication until after blood is drawn.  Client education:  NPO 8hr. prior test. o Oral glucose tolerance test (OGTT):  Nursing actions:  Not a routine test  3 blood samples: o Fasting, then q 30min for 2 hr. (after glucola)  Client education:  Balanced diet x 3days  NPO 10-12 hr. prior test.  Only water during test. o Glycosylated Hb (HbA1C):  Normal : 4-6%  Diabetics: 6.5-8% (target goal <7%)  average BG for the past 120 days.  Client education:  Tx. Effectiveness & compliance.  Quarterly or twice a year o Urine Ketones:  >300 mg/dL associated with hyperglycemia  Medical emergency o Other Notes:  For a type 1 patient feeling feverish, drowsy, nauseas, with ketones in blood, with glucose around 350, eat, use the sliding scale, drink a lot and check glucose in 2 hrs.  If ketones go away, then you’re good, but if the ketones are still present, bring patient into ER (try to manage as much as possible before admitting them)  Assessment: Lab Tests o Lab Tests: o Diagnostic criteria include: • TWO findings (on separate days) of at least one of the above mentioned tests, OR • ONE of the above positive test + manifestations of diabetes  Specimen Collection for Glucose Monitoring: o Site selection:  Most common site?  Finger tips  Alternate sites? o Clean site with soap and water (NOT ALCOHOL) o Wipe away first drop of blood  Self-Monitoring of Blood Glucose: o Client Education –  Check the accuracy of the strips .  Use the correct code number in the meter to match the strip bottle number.  Store strips in the closed container in a dry location.  Hand hygiene.  Obtain an adequate amount of blood sample Use fresh lancets  Avoid sharing equipment to prevent infection.  Keep a record of the SMBG (Self Monitoring of blood glucose) that includes time, date, serum glucose level, insulin dose, food intake, and other events such as activity level or illness. o For an accurate reading, you need to make sure the patient has fasted for 6-8 hours and did their normal routine, and didn’t do anything different like exercise or start a new diet.  Medical Management of Diabetes: o INSULIN: o Promotes cellular uptake of glucose (decrease glucose levels) o Converts glucose into glycogen o Move K+ into cells o Uses: Type I, and some patients with Type II, and gestational diabetes o RAPID-, SHORT-, INTERMEDIATE-, AND LONG-ACTING o **Oral Hypoglycemic Agents – Discussed in Pharmacology  Insulin Types and Characteristics: o We expect the patient to be hypoglycemic during the peak hours, when insulin levels are the highest, the glucose is lowest. o If a patient gets insulin and does not eat, then you're going to be hypoglycemic and pass out. o Goal is to keep diabetic patients glucose between 120-130 o RN-mix regular (clear) then NPH (cloudy) and (inject air into NPH first then R) o Insulin ratio:70 (N)/30 (R) o Regular insulin is for Postprandial- 2 hrs after meal (less than 200-220) o U100- only regular insulin which can be mixed and pushed IV (not U500) [Show More]

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