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Diabetes Mellitus :: Medical Surgical Nursing :: Review For Nursing Licensure Examination Slide Transcript
Slide 1: Nurse Licensure Examination Review Diabetes Mellitus

Slide 2: Diabetes Mellitus A group of metabolic diseases  characterized by elevated levels of glucose in the blood resulting from defects in insulin secretion, insulin action, insulin receptors or any combination of conditions.

Slide 3: Diabetes Mellitus A chronic disorder of impaired  glucose metabolism, protein and fat metabolism

Slide 4: Diabetes Mellitus  BASIC PATHOLOGY : Insulin problem (deficiency or impaired action)

Slide 5: Diabetes Mellitus Insulin is a hormone secreted  by the BETA cells of the pancreas  Stimulus of insulin- HYPERGLYCEMIA

Slide 6: Diabetes Mellitus  Action of insulin: it promotes entry of Glucose into the body cells by binding to the insulin receptor in the cell membrane

Slide 7: INSULIN : Physiology Insulin Metabolic Functions:  1. Transports and metabolizes GLUCOSE  2. Promotes GLYCOGENESIS  3. Promotes GLYCOLYSIS  4. Enhances LIPOGENESIS  5. Accelerates PROTEIN SYNTHESIS

Slide 8: Diabetes Mellitus RISK FACTORS for Diabetes Mellitus  1. Family History of diabetes  2. Obesity  3. Race/Ethnicity

Slide 9: Diabetes Mellitus RISK FACTORS for Diabetes Mellitus  4. Age of more than 45  5. Previously unidentified IFG/IGT  6. Hypertension

Slide 10: Diabetes Mellitus RISK FACTORS for Diabetes Mellitus  7. Hyperlipidemia  8. History of Gestational Diabetes Mellitus

Slide 11: Diabetes Mellitus CLASSIFICATION OF DM 1. Type 1 DM Insulin dependent Diabetes Mellitus  2. Type 2 DM Non-insulin dependent Diabetes Mellitus  3. Gestational DM Diabetes Mellitus diagnosed during pregnancy  4. DM associated with other conditions or syndromes

Slide 12: Diabetes Mellitus CLASSIFICATION OF DM 1. Type 1 DM  Insulin dependent Diabetes Mellitus

Slide 13: Diabetes Mellitus CLASSIFICATION OF DM 2. Type 2 DM  Non-insulin dependent Diabetes Mellitus

Slide 14: Diabetes Mellitus CLASSIFICATION OF DM 3. Gestational DM  Diabetes Mellitus diagnosed during pregnancy

Slide 15: Diabetes Mellitus CLASSIFICATION OF DM 4. DM associated with other conditions or syndromes

Slide 16: Diabetes Mellitus Other types of DM  1. Impaired Glucose Tolerance  2. Impaired Fasting Glucose  3. Pre-diabetes

Slide 17: TYPE 1- Diabetes Mellitus This type of DM is characterized by the destruction of the pancreatic beta cells

Slide 18: TYPE 1- Diabetes Mellitus Etiology: 1. Genetic susceptibility- HLA DR3 and DR4 2. Autoimmune response 3. Toxins, unidentified viruses and environmental factors

Slide 19: TYPE 1- Diabetes Mellitus PATHOPHYSIOLOGY  Destruction of BETA cells decreased insulin production  uncontrolled glucose production by the liver hyperglycemia  signs and symptoms

Slide 20: TYPE 1- Diabetes Mellitus PATHOPHYSIOLOGY CLASSIC P’s  Polyuria  Polydipsia  Polyphagia

Slide 21: TYPE 2- Diabetes Mellitus A type of DM characterized  by insulin resistance and impaired insulin production

Slide 22: TYPE 2- Diabetes Mellitus Etiology: 1. Unknown 2. Probably genetic and obesity

Slide 23: TYPE 2- Diabetes Mellitus PATHOPHYSIOLOGY  Decreased sensitivity of insulin receptor to insulin  less uptake of glucose  HYPERGLYCEMIA

Slide 24: TYPE 2- Diabetes Mellitus PATHOPHYSIOLOGY  Decreased insulin production  diminished insulin action  hyperglycemia  signs and symptoms

Slide 25: TYPE 2- Diabetes Mellitus PATHOPHYSIOLOGY  BUT (+) insulin in small amount  prevent breakdown of fats  DKA is unusual

Slide 26: GESTATIONAL Diabetes Mellitus Any degree of glucose  intolerance with its onset during pregnancy  Usually detected between 24- 28 week gestation th

Slide 27: GESTATIONAL Diabetes Mellitus Blood glucose returns to normal  after delivery of the infant NEVER administer ORAL  HYPOGLYCEMIC AGENTS to PREGNANT MOTHERS!

Slide 28: Diabetes Mellitus ASSESSMENT FINDINGS  1. Classic 3 P’s  2. Fatigue  3. Body weakness

Slide 29: Diabetes Mellitus ASSESSMENT FINDINGS  4. Visual changes  5. Slow wound healing  6. Recurrent skin and mucus membrane infections

Slide 30: Diabetes Mellitus DIAGNOSTIC TESTS  1. FBS- > 126  2. RBS- >200  3. OGTT- > 200

Slide 31: Diabetes Mellitus DIAGNOSTIC TESTS  4. HgbA1- for monitoring!!  5. Urine glucose  6. Urine ketones

Slide 32: Diabetes Mellitus DIAGNOSTIC CRITERIA  1. FBS equal to or greater than 126 mg/dL (7.0mmol/L)  (Normal 8 hour FBS- 80- 109 mg/dL)

Slide 33: Diabetes Mellitus DIAGNOSTIC CRITERIA  2. OGTT value 1 and 2 hours post-prandial equal to or greater than 200 mg/dL  Normal OGTT 1 and 2 hours post-prandial- is  140 mg/dL

Slide 34: Diabetes Mellitus DIAGNOSTIC CRITERIA  3.RBS of equal to or greater than 200 mg/dL PLUS the 3 P’s

Slide 35: Diabetes Mellitus NURSING MANAGEMENT OF DM  The main goal is to NORMALIZE insulin activity and blood glucose level by:

Slide 36: Diabetes Mellitus NURSING MANAGEMENT OF DM 1. Nutritional modification 2. Regular Exercise 3. Regular Glucose Monitoring 4. Drug therapy 5. Client Education

Slide 37: Diabetes Mellitus The Patient with DM HISTORY  Symptoms and characteristics  PHYSICAL EXAMINATION  VS, BMI, Fundoscopy, Neuro  LABORATORY EXAMINATION  FBS, RBS, HgbA1c, lipid profile, ECG, UA  REFERRALS  Ophthalmologist, Podiatrist, Dietician, etc.. 

Slide 38: Diabetes Mellitus The Patient with DM HISTORY   Symptoms and characteristics PHYSICAL EXAMINATION   VS, BMI, Fundoscopy, and Neuro assessment

Slide 39: Diabetes Mellitus The Patient with DM LABORATORY EXAMINATION   FBS, RBS, HgbA1c, lipid profile, ECG, and Urinalysis REFERRALS   Ophthalmologist, Podiatrist, Dietician, etc..

Slide 40: DM Nutritional management

Slide 41: Diabetes Mellitus NUTRITIONAL MANAGEMENT  1.Review the patient’s diet history to identify eating habits and lifestyle  2. Coordinate with the dietician in meal planning for weight loss

Slide 42: Diabetes Mellitus NUTRITIONAL MANAGEMENT  3. Plan for the caloric intake distributed as follows- CHO 50-60%; Fats 20-30%; and Proteins 10-20%  4. Advise moderation in alcohol intake  5. Using artificial sweeteners is acceptable

Slide 43: DM Exercise management

Slide 44: Diabetes Mellitus EXERCISE Management  1. Teach that exercise can lower the blood glucose level  2. Diabetics must first control the glucose level before initiating exercise programs.

Slide 45: Diabetes Mellitus EXERCISE Management 3. Offer extra food /calories  before engaging in exercise 4. Offer snacks at the end of the  exercise period if patient is on insulin treatment.

Slide 46: Diabetes Mellitus EXERCISE Management  5. Advise that exercise should be done at the same time every day, preferably when blood glucose levels are at their peak

Slide 47: Diabetes Mellitus EXERCISE Management 6. Regular exercise, not sporadic  exercise, should be encouraged. 7. For most patient, WALKING  is the safe and beneficial form of exercise

Slide 48: Glucose Self Monitoring

Slide 49: Diabetes Mellitus GLUCOSE MONITORING Self-monitoring of blood glucose  (SMBG) enables the patient to adjust the treatment regimen to obtain optimal glucose control

Slide 50: Diabetes Mellitus GLUCOSE MONITORING  Most common method involves obtaining a drop of capillary blood applied to a test strip.  The usual recommended frequency is TWO-FOUR times a day.

Slide 51: Diabetes Mellitus When is it done?  At the peak action time of the medication to evaluate the need for adjustments.  To evaluate BASAL insulin  test before meals

Slide 52: Diabetes Mellitus When is it done?  To titrate bolus or regular and lispro test 2 hours after meals.  To evaluate the glucose level of those taking ORAL hypoglycemics  test before and two hours after meals.

Slide 53: Diabetes Mellitus Monitoring therapy Testing the glycosylated  hemoglobin (HbA1c) This glycosylated hemoglobin  refers to the blood test that reflects the average blood glucose over a period of TWO to THREE months.

Slide 54: Diabetes Mellitus Monitoring therapy  Normal value is 4 to 6 %  No patient preparation is needed for this testing  Done to monitor therapy

Slide 55: Diabetes Mellitus Urine testing for glucose  Benedict’s test 

Slide 56: Diabetes Mellitus Urine testing for ketones   Ketones are by-products of fat breakdown

Slide 57: Diabetes Mellitus Urine testing for ketones   This is performed whenever TYPE 1 DM have glucosuria or persistent elevation of blood glucose, during illness, and in gestational diabetes

Slide 58: DM Drug therapy

Slide 59: Diabetes Mellitus DRUG THERAPY and MANAGEMENT Usually, this type of management is  employed if diet modification and exercise cannot control the blood glucose level.

Slide 60: Diabetes Mellitus DRUG THERAPY and MANAGEMENT Because the patient with TYPE  1 DM cannot produce insulin, exogenous insulin must be administered for life.

Slide 61: Diabetes Mellitus DRUG THERAPY and MANAGEMENT TYPE 2 DM may have  decreased insulin production, ORAL agents that stimulate insulin production are usually employed.

Slide 62: Diabetes Mellitus PHARMACOLOGIC INSULIN This may be grouped into several  categories according to: 1. Source- Human, pig, or cow 2. Onset of action- Rapid-acting, short-acting, intermediate-acting, long-acting and very long acting

Slide 63: Diabetes Mellitus PHARMACOLOGIC INSULIN This may be grouped into several  categories according to: 3. Pure or mixed concentration 4. Manufacturer of drug

Slide 64: Diabetes Mellitus GENERALITIES  1. Human insulin preparations have a shorter duration of action than animal source

Slide 65: Diabetes Mellitus GENERALITIES  2. Animal sources of insulin have animal proteins that may trigger allergic reaction and they may stimulate antibody production that may bind the insulin, slowing the action

Slide 66: Diabetes Mellitus  3. ONLY Regular insulin can be used INTRAVENOUSLY!

Slide 67: Diabetes Mellitus 4. Insulin are measured in  INTERNATIONAL UNITS or “iu” 5. There is a specified insulin  injection calibrated in units

Slide 68: Diabetes Mellitus RAPID ACTING INSULIN  Lispro (Humalog) and Insulin Aspart (Novolog)  Produces a more rapid effect and with a shorter duration than any other insulin preparation

Slide 69: Diabetes Mellitus RAPID ACTING INSULIN  ONSET- 5-15 minutes  PEAK- 1 hour  DURATION- 3 hours  Instruct patient to eat within 5 to 15 minutes after injection

Slide 70: Diabetes Mellitus REGULAR INSULIN  Also called Short-acting insulin  “R”  Usually Clear solution administered 30 minutes before a meal

Slide 71: Diabetes Mellitus REGULAR INSULIN  ONSET- 30 minutes to 1 hour  PEAK- 2 to 3 hours  DURATION- 4 to 6 hours

Slide 72: Diabetes Mellitus INTERMEDIATE ACTING INSULIN  Called “NPH” or “LENTE”  Appears white and cloudy

Slide 73: Diabetes Mellitus INTERMEDIATE ACTING INSULIN  ONSET- 2-4 hours  PEAK- 4 to 6-12 hours  DURATION- 16-20 hours

Slide 74: Diabetes Mellitus LONG- ACTING INSULIN  “UltraLENTE”  Referred to as “peakless” insulin

Slide 75: Diabetes Mellitus LONG- ACTING INSULIN  ONSET- 6-8 hours  PEAK- 12-16 hours  DURATION- 20-30 hours

Slide 76: Diabetes Mellitus HEALTH TEACHING Regarding Insulin SELF- Administration  1. Insulin is administered at home subcutaneously

Slide 77: Diabetes Mellitus HEALTH TEACHING Regarding Insulin SELF- Administration  2. Cloudy insulin should be thoroughly mixed by gently inverting the vial or ROLLING between the hands

Slide 78: Diabetes Mellitus HEALTH TEACHING Regarding Insulin SELF- Administration  3. Insulin NOT IN USE should be stored in the refrigerator, BUT avoid freezing/extreme temperature

Slide 79: Diabetes Mellitus 4. Insulin IN USE should be  kept at room temperature to reduce local irritation at the injection site

Slide 80: Diabetes Mellitus 5. INSULIN may be kept at  room temperature up to 1 month

Slide 81: Diabetes Mellitus 6. Select syringes that match  the insulin concentration.  U-100 means 100 units per mL

Slide 82: Diabetes Mellitus  7. Instruct the client to draw up the REGULAR (clear) Insulin FIRST before drawing the intermediate acting (cloudy) insulin

Slide 83: Diabetes Mellitus 8. Pre-filled syringes can be  prepared and should be kept in the refrigerator with the needle in the UPRIGHT position to avoid clogging the needle

Slide 84: Diabetes Mellitus 9. The four main areas for  insulin injection are- ABDOMEN, UPPER ARMS, THIGHS and HIPS

Slide 86: Diabetes Mellitus Insulin is absorbed fastest in the  abdomen and slowest in the hips Instruct the client to rotate the areas  of injection, but exhaust all available sites in one area first before moving into another area.

Slide 87: Diabetes Mellitus 10. Alcohol may not be used to  cleanse the skin  11. Utilize the subcutaneous injection technique- commonly, a 45-90 degree angle.

Slide 88: Diabetes Mellitus 12. No need to instruct for  aspirating the needle  13. Properly discard the syringe after use.

Slide 89: Diabetes Mellitus T-I-E Test blood Inject insulin  Eat food

Slide 90: Diabetes Mellitus COMPLICATIONS OF INSULIN THERAPY 1. Local allergic reactions  Redness, swelling, tenderness and induration appearing 1-2 hours after injection  Usually occurs in the beginning stage of therapy

Slide 91: Diabetes Mellitus COMPLICATIONS OF INSULIN THERAPY 1. Local allergic reactions  Disappears with continued use  Antihistamine can be given 1 hour before injection time  Porcine and bovine insulin preparations have a higher tendency to produce this reaction.

Slide 92: Diabetes Mellitus 2. SYSTEMIC ALLERGIC REACTIONS  Very rare  Generalized urticaria is the manifestation  Treatment is desensitization

Slide 93: Diabetes Mellitus COMPLICATIONS OF INSULIN THERAPY 3. INSULIN DYSTROPHY  A localized reaction in the form of lipoatrophy or lipohypertrophy

Slide 94: Diabetes Mellitus Lipoatrophy- loss of  subcutaneous fat usually caused by the utilization of animal insulin

Slide 95: Diabetes Mellitus  Lipohypertrophy- development of fibrofatty masses, usually caused by repeated use of injection site

Slide 96: Diabetes Mellitus 4. INSULIN RESISTANCE  Most commonly caused by OBESITY  Defined as daily insulin requirement of more than 200 units  Management- Steroids and use of more concentrated insulin

Slide 97: Diabetes Mellitus 5. MORNING HYPERGLYCEMIA  Elevated blood sugar upon arising in the morning  Caused by insufficient level of insulin  DAWN phenomenon  SOMOGYI effect  INSULIN WANING

Slide 98: Diabetes Mellitus DAWN PHENOMENON  Relatively normal blood glucose until about 3 am, when the glucose level begins to RISE  Results from the nightly surges of GROWTH HORMONE secretion  Management: Bedtime injection of NPH

Slide 99: Diabetes Mellitus SOMOGYI EFFECT  Normal or elevated blood glucose at bedtime, decrease blood glucose at 2-3 am due to hypoglycemic levels and a subsequent increase in blood glucose (rebound hypergycemia)

Slide 100: Diabetes Mellitus SOMOGYI EFFECT  Nocturnal hypoglycemia followed by rebound hyperglycemia

Slide 101: Diabetes Mellitus SOMOGYI EFFECT  Due to the production of counter regulatory hormones- glucagon. cortisol and epinephrine  Management- decrease evening dose of NPH or increase bedtime snack

Slide 102: Diabetes Mellitus INSULIN WANING Progressive rise in blood glucose  from bedtime to morning Seen when the NPH evening dose is  administered before dinner Management: Move the insulin  injection to bedtime

Slide 103: Diabetes Mellitus ORAL HYPOGLYCEMIC AGENTS These may be effective when  used in TYPE 2 DM that cannot be treated with diet and exercise These are NEVER used in  pregnancy!

Slide 104: Diabetes Mellitus ORAL HYPOGLYCEMIC AGENTS  There are several agents:  Sulfonylureas  Biguanides  Alpha-glucosidase inhibitors  Thiazolidinediones  Meglitinides

Slide 105: Diabetes Mellitus SULFONYLUREAS  MOA- stimulates the beta cells of the pancreas to secrete insulin  Classified as to generations- first and second generations

Slide 106: Diabetes Mellitus SULFONYLUREAS  FIRST GENERATION- Acetoheximide, Chlorpropamide, Tolazamide and Tolbutamide  SECOND GENERATION- Glipizide, Glyburide, Glibenclamide, Glimepiride

Slide 107: Diabetes Mellitus: Sulfonylureas The most common side –effects  of these medications are Gastro- intestinal upset and dermatologic reactions. HYPOGLYCEMIA is also a  very important side-effect

Slide 108: Diabetes Mellitus: Sulfonylureas Chlorpropamide has a very long  duration of action. This also produces a disulfiram-like reaction when taken with alcohol Second generation drugs have  shorter duration with metabolism in the kidney and liver and are the choice for elderly patients

Slide 109: Diabetes Mellitus BIGUANIDES  MOA- Facilitate the action of insulin on the peripheral receptors  These can only be used in the presence of insulin

Slide 110: Diabetes Mellitus BIGUANIDES= “formin”  They have no effect on the beta cells of the pancreas  Metformin (Glucophage) and Phenformin are examples

Slide 111: Diabetes Mellitus: Biguanides The most important side effect  is LACTIC ACIDOSIS!  These are not given to patient with renal impairment

Slide 112: Diabetes Mellitus: Biguanides These drugs are usually given  with a sulfonylurea to enhance the glucose-lowering effect more than the use of each drug individually

Slide 113: Diabetes Mellitus ALPHA-GLUCOSIDASE INHIBITORS  MOA- Delay the absorption of glucose in the GIT  Result is a lower post-prandial blood glucose level  They do not affect insulin secretion or action!  Side-effect: DIARRHEA and FLATULENCE

Slide 114: Diabetes Mellitus Examples of AGI are Acarbose  and Miglitol They are not absorbed  systemically and are very safe They can be used alone or in  combination with other OHA

Slide 115: Diabetes Mellitus Side-effect if used with other  drug is HYPOGLYCEMIA  Note that sucrose absorption is impaired and IV glucose is the therapy for the hypoglycemia

Slide 116: Diabetes Mellitus THIAZOLIDINEDIONES  MOA- Enhance insulin action at the receptor site  They do not stimulate insulin secretion

Slide 117: Diabetes Mellitus THIAZOLIDINEDIONES Examples- Rosiglitazone, Pioglitazone  These drugs affect LIVER  FUNCTION Can cause resumption of OVULATION  in peri-menopausal anovulatory women

Slide 118: Diabetes Mellitus MEGLITINIDES  MOA- Stimulate the secretion of insulin by the beta cells  Examples- Repaglinide and Nateglinide

Slide 119: Diabetes Mellitus MEGLITINIDES They have a shorter duration  and fast action Should be taken BEFORE meals  to stimulate the release of insulin from the pancreas

Slide 120: Diabetes Mellitus MEGLITINIDES  Principal side-effect of meglitinides- hypoglycemia  Can be used alone or in combination

Slide 121: Diabetes Mellitus ACUTE COMPLICATIONS OF DM  Hypoglycemia  Diabetic ketoacidosis  Hyperglycemic hyperosmolar non- ketotic syndrome (HHNS)

Slide 122: Diabetes Mellitus CHRONIC COMPLICATIONS OF DM Macrovascular complications- MI,  Stroke, Atherosclerosis, CAD, and Peripheral vascular disease Microvascular complications- micro-  angiopathy, retinopathy, nephropathy Peripheral neuropathy 

Slide 124: Diabetes Mellitus HYPOGLYCEMIA Blood glucose level less than 50 to 60  mg/dL Causes: Too much insulin/OHA, too  little food and excessive physical activity Mild- 40-60  Moderate- 20-40  Severe- less than 20 

Slide 125: HYPOGLYCEMIA ASSESSMENT FINDINGS 1. Sympathetic manifestations-  sweating, tremors, palpitations, nervousness, tachycardia and hunger

Slide 126: HYPOGLYCEMIA ASSESSMENT FINDINGS 2. CNS manifestations- inability to  concentrate, headache, lightheadedness, confusion, memory lapses, slurred speech, impaired coordination, behavioral changes, double vision and drowsiness

Slide 128: HYPERGLYCEMIA

Slide 129: HYPOGLYCEMIA DIAGNOSTIC FINDINGS  RBS- less than 50-60 mg/dL level

Slide 130: HYPOGLYCEMIA Nursing Interventions  1. Immediate treatment with the use of foods with simple sugar- glucose tablets, fruit juice, table sugar, honey or hard candies

Slide 131: HYPOGLYCEMIA Nursing Interventions  2. For unconscious patients- glucagon injection 1 mg IM/SQ; or IV 25 to 50 mL of D50/50

Slide 132: HYPOGLYCEMIA Nursing Interventions  3. re-test glucose level in 15 minutes and re-treat if less than 75 mg/dL  4. Teach patient to refrain from eating high-calorie, high-fat desserts

Slide 133: HYPOGLYCEMIA Nursing Interventions  5. Advise in-between snacks, especially when physical activity is increased  6. Teach the importance of compliance to medications

Slide 134: Diabetic Ketoacidosis This is cause by the absence of insulin  leading to fat breakdown and production of ketone bodies Three main clinical features:   1. HYPERGLYCEMIA  2. DEHYDRATION & electrolyte loss  3. ACIDOSIS

Slide 135: DKA PATHOPHYSIOLOGY  No insulin reduced glucose breakdown and increased liver glucose production  Hyperglycemia

Slide 136: DKA PATHOPHYSIOLOGY  Hyperglycemia kidney attempts to excrete glucose  increased osmotic load  diuresis  Dehydration

Slide 137: DKA PATHOPHYSIOLOGY  No glucose in the cell fat is broken down for energy  ketone bodies are produced Ketoacidosis

Slide 138: DKA Risk factors  1. infection or illness- common  2. stress  3. undiagnosed DM  4. inadequate insulin, missed dose of insulin

Slide 139: DKA ASSESSMENT FINDINGS  1. 3 P’s  2. Headache, blurred vision and weakness  3. Orthostatic hypotension

Slide 140: DKA ASSESSMENT FINDINGS  4. Nausea, vomiting and abdominal pain  5. Acetone (fruity) breath  6. Hyperventilation or KUSSMAUL’s breathing

Slide 141: HYPERGLYCEMIA

Slide 142: Hyperglycemia

Slide 143: DKA LABORATORY FINDINGS  1. Blood glucose level of 300- 800 mg/dL  2. Urinary ketones

Slide 144: DKA LABORATORY FINDINGS  3. ABG result of metabolic acidosis- LOW pH, LOW pCO2 as a compensation, LOW bicarbonate  4. Electrolyte imbalances- potassium levels may be HIGH due to acidosis and dehydration

Slide 145: DKA NURSING INTERVENTIONS  1. Assist in the correction of dehydration  Up to 6 liters of fluid may be ordered for infusion, initially NSS then D5W  Monitor hydration status  Monitor I and O  Monitor for volume overload

Slide 146: DKA NURSING INTERVENTIONS  2. Assist in restoring Electrolytes  Kidney function is FIRST determined before giving potassium supplements!

Slide 147: DKA NURSING INTERVENTIONS  3. Reverse the Acidosis  REGULAR insulin injection is ordered IV bolus 5-10 units  The insulin is followed by drip infusion in units per hour  BICARBONATE is not used!

Slide 148: HHNS A serious condition in which  hyperosmolarity and extreme hyperglycemia predominate Ketosis is minimal  Onset is slow and takes hours to  days to develop

Slide 149: HHNS PATHOPHYSIOLOGY  Lack of insulin action or Insulin resistance  hyperglycemia  Hyperglycemia osmotic diuresis  loss of water and electrolytes

Slide 150: HHNS PATHOPHYSIOLOGY  Insulin is too low to prevent hyperglycemia but enough to prevent fat breakdown  Occurs most commonly in type 2 DM, ages 50-70

Slide 151: HHNS Precipitating factors  1. Infection  2. Stress  3. Surgery  4. Medication like thiazides  5. Treatment like dialysis

Slide 152: HHNS ASSESSMENT FINDINGS  1. Profound dehydration  2. Hypotension  3. Tachycardia  4. Altered sensorium  5. Seizures and hemiparesis

Slide 153: HHNS DIAGNOSTIC TESTS  1. Blood glucose- 600 to 1,200 mg/dL  2. Blood osmolality- 350 mOsm/L  3. Electrolyte abnormalities

Slide 154: HHNS NURSING INTERVENTIONS  Approach is similar to the DKA  1. Correction of Dehydration by IVF  2. Correction of electrolyte imbalance by replacement therapy

Slide 155: HHNS NURSING INTERVENTIONS  3. Administration of insulin injection and drips  4. Continuous monitoring of urine output

Slide 156: MACROVASCULAR CX Nursing management  1. Diet modification  2. Exercise

Slide 157: MACROVASCULAR CX Nursing management  3. Prevention and treatment of underlying conditions such as MI, CAD and stroke  4. Administration of prescribed medications for hypertension, hyperlipidemia and obesity

Slide 158: MICROVASCULAR CX Retinopathy- a painless deterioration  of the small blood vessels in the retina, may be classified as to background retinopathy, pre-proliferative and proliferative retinopathy Permanent vision changes and  blindness can occur

Slide 159: MICROVASCULAR CX Retinopathy-ASSESSMENT FINDINGS  Blurry vision  Spotty vision  Asymptomatic

Slide 160: MICROVASCULAR CX Retinopathy: Diagnostic findings  1. Fundoscopy  2. Fluorescein angiography  Painless procedure  Side-effects- discoloration of the skin and urine for 12 hours, some allergic reactions, nausea  Flash of camera may be slightly uncomfortable

Slide 161: MICROVASCULAR CX NURSING INTERVENTIONS  1. Assist in diagnostic procedure  2. Assist in the preparation for surgery- laser photocoagulation

Slide 162: MICROVASCULAR CX NURSING INTERVENTIONS  3. Health teaching regarding prevention of retinopathy by regular ophthalmic examinations, good glucose control and self- management of eye care regimens  4. Maintain client safety

Slide 163: MICROVASCULAR CX DIABETIC NEPHROPATHY  Progressive deterioration of kidney function

Slide 164: MICROVASCULAR CX DIABETIC NEPHROPATHY  HYPERGLYCEMIA causes the kidney filtration mechanism to be stressed  blood proteins leak into the urine  Pressure in the kidney blood vessels increases stimulate the development of nephropathy

Slide 165: MICROVASCULAR CX ASSESSMENT findings for diabetic nephropathy  1. Albuminuria  2. Anemia  3. Acidosis

Slide 166: MICROVASCULAR CX ASSESSMENT findings for diabetic nephropathy  4. Fluid volume overload  5. Oliguria  6. Hypertension  7. UTI

Slide 167: MICROVASCULAR CX NURSING MANAGEMENT 1. Assist in the control of hypertension- use of ACE inhibitor 2. Provide a low sodium and low protein diet 3. Administer prescribed medication for UTI

Slide 168: MICROVASCULAR CX NURSING MANAGEMENT  4. Assist in dialysis 5. Prepare patient for renal transplantation, if indicated

Slide 169: MICROVASCULAR CX Diabetic Neuropathy  A group of disorders that affect all type of nerves including the peripheral, autonomic and spinal nerves

Slide 170: MICROVASCULAR CX Diabetic Neuropathy  Two most common types of Diabetic Neuropathy are sensori-motor polyneuropathy and autonomic neuropathy

Slide 171: MICROVASCULAR CX Peripheral neuropathy- ASSESSMENT findings  1. paresthesias- prickling, tingling or heightened sensation  2. decreased proprioception  3. decreased sensation of light touch  4. unsteady gait  5. decreased tendon reflexes

Slide 172: MICROVASCULAR CX Peripheral neuropathy- Nursing Management  1. Provide teaching that good glucose control is very important to prevent its development  2. Manage the pain by analgesics, antidepressants and nerve stimulation

Slide 173: MICROVASCULAR CX Autonomic Neuropathy- ASSESSMENT findings  1. Silent, painless ischemia  2. delayed gastric emptying  3. orthostatic hypotension  4. N/V and bloating sensation  5. urinary retention  6. sexual dysfunction

Slide 174: MICROVASCULAR CX Autonomic Neuropathy-Nursing management  1. Educate about the avoidance of strenuous physical activity  2. Stress the importance of good glucose control to delay the development

Slide 175: MICROVASCULAR CX Autonomic Neuropathy-Nursing management  3. Provide LOW-fat, small frequent feedings  4. Administer bulk-forming laxatives for diabetic diarrhea  5. Provide HIGH-fiber diet for diabetic constipation

Slide 176: MICROVASCULAR CX MANAGEMENT OF FOOT AND LEG PROBLEMS Soft tissue injury in the foot/leg formation of fissures and callus  poor wound healing  foot/leg ulcer

Slide 177: MICROVASCULAR CX RISK FACTORS for the development of foot and leg ulcers  1. More than 10 years diabetic  2. Age of more than 40  3. Smoking  4. Anatomic deformities  5. History of previous leg ulcers or amputation

Slide 178: MICROVASCULAR CX MANAGEMENT of Foot Ulcers  Teach patient proper care of the foot  Daily assessment of the foot  Use of mirror to inspect the bottom

Slide 179: MICROVASCULAR CX MANAGEMENT of Foot Ulcers  Inspect the surface of shoes for any rough spots or foreign objects  Properly dry the feet  Instruct to wear closed-toe shoes that fit well, recommend use of low-heeled shoes

Slide 180: MICROVASCULAR CX MANAGEMENT  Instruct patient NEVER to walk barefoot, never to use heating pads, open-toed shoes and soaking feet  Trim toenails STRAIGHT ACROSS and file sharp corners  Instruct to avoid smoking and over-the counter medications and home remedies for foot problems




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