Cystitis, Urolithiasis, PID, BPH, Allergy, and SLE PDF

CYSTITIS  Cystitis Cystitis - is inf lammation of the bladder, usually caused by a bladder infection. It is a type of urinary tract infection Lower UTI (UTI), particularly in women....

CYSTITIS  Cystitis Cystitis - is inf lammation of the bladder, usually caused by a bladder infection. It is a type of urinary tract infection Lower UTI (UTI), particularly in women. Types: it usually result from an Cystitis – (bladder) ascending infection. Prostatitis – (prostate gland) Urethritis – (urethra) UTI – caused by pathogenic microorganisms in the urinary tract. Catheter-associated UTI – hospital acquired UTI. Pathophysiology  CAUSES OF LOWER UTI infection by gram negative Simultaneous infection an indwelling urinary fistula between the enteric bacteria, such as E. with multiple pathogens in catheter intestine and bladder coli, klebsiella, Proteus, a patient with neurogenic Enterobacter, bladder Pseudomonas, or Serratia enterovesical fistula  Causes: Routes (3 ways) Bacterial invasion of the Transurethral route urinary tract (ascending infection) – 2 Ref lux – obstruction to free- most common (fecal f lowing urine contamination) a. urethrovescial ref lux - ref lux Bloodstream of urine from urethra into the (hematogenous spread) bladder Fistula from the intestine b. vesicoureteral ref lux – (direct extension) backf low of urine from the bladder into one or both ureters. Clinical Manifestations: Burning on Assessment and urination Diagnostic Findings: Urinary frequency 1. Urine cultures Urgency 2. Cellular studies Nocturia a.Hematuria Incontinence b.Pyuria Suprapubic or c.X-rays/CT scan pelvic pain 3. Urinalysis Hematuria back pain fever  Nursing Interventions: Relieve pain Antispasmodic/analgesic drug Heat to the perineum Drink plenty of f luids Urinary irritants should be avoided (coffee, Nursing Diagnosis: tea, colas, citrus) Medical Management: Frequent voiding (every 2-3 hours) Acute pain associated with Antibacterial agent (Anti- infectives – cephalosporin, infection within the urinary 2. Monitoring and managing potential tract complications levof loxacin) Note: gram-negative sepsis – most common complications Monitor VS and LOC Antibiotic Increased f luid intake. UROLITHIASIS Urolithiasis Contributing factors: Infection stones (calculi) in the urinary Urinary stasis tract and kidney. Immobility - concentrations of substances Alter calcium metabolism or increased (calcium oxalate, calcium calcium formation of stones. phosphate and uric acid) Causes: Renal tubular acidosis Excessive intake of vit. D Excessive intake of milk and alkali Clinical Manifestations: 1. Infection (fever, chills and urinary frequency) 2. Excruciating pain and discomfort 3. Intense, deep ache and tenderness in the cost vertebral region (stones in renal pelvis) 4. Hematuria 5. Nausea and vomiting 6. Ureteral colic 7 Oxalate stones Assessment and Diagnostic Findings: 1. CT scan 2. Blood chemistries test (calcium, uric acid, creatinine, sodium pH) Interventional Medical Procedures: Management: Ureteroscopy Opioid analgesics Electrohydraulic lithotripsy NSAID’s ESWL- Extracorporeal Shock Wave Increased f luid intake Lithotripsy- non-invasive procedure to Limit oxalate intake (spinach, chocolate, breakdown stones in part of the urinary peanuts) system Surgical management – nephrolithotomy  Pelvic Infl a m m a t o r y Disease  Pelvic Inf lammatory Disease (PID) is an inf lammatory condition of the pelvic cavity that may begin with cervicitis and uterus (endometritis), fallopian tubes (salpin- gitis), ovaries (oophoritis), pelvic peritoneum, or pelvic vascular system. Causes: Virus Fungus parasite Gonorrheal/chlamydial organisms – common causes Types of PID Clinical Vaginal discharge Dyspareunia Manifestations: Dysuria Pelvic or lower abdominal pain Tenderness that occurs after menses and postcoital bleeding Fever General malaise Anorexia Nausea Headache Vomiting Intense tenderness of the uterus or cervix 01 02 03 Complications: Medical Management: Nursing Management: Peritonitis Broad spectrum antibiotic VS and MIO Abscess strictures MIO (ceftriaxone, doxycycline, Record the characteristics and Fallopian tube obstruction metronidazole) amount of vaginal discharge resulting to: Analgesics Ectopic pregnancy Infection control practices- sterility meticulous handwashing Adhesions  BENIGN PROSTATIC HYPERTROPHY/HYPERPLASIA  Risk factors: Smoking Benign Prostatic Heavy alcohol Hypertrophy/Hyperplasia (BPH) consumption noncancerous enlargement Obesity or hypertrophy of the prostate. Reduced activity level common diseases in aging men (over 40 years old) Hypertension Heart disease Western diet ( high in animal fat and CHON and ref ined CHO) Clinical Manifestations: Urinary frequency, urgency Nocturia, hesitancy in starting urination Decreased and intermittent force of stream Sensation of incomplete bladder emptying Abdominal straining with urination Decrease in the volume and force of the urinary stream Recurrent UTI Azotemia – due to chronic urinary retention and large residual volumes Assessment and Diagnostic Findings: 1.Voiding diary 2.Urinalysis 3.PSA level 4.UTZ 5.Urethrocystoscopy Medical Management: 1. Cystostomy – incision in the bladder surgical creation of an opening into the bladder. Pharmacologic Therapy: Alpha adrenergic blockers (alfuzosin, terazosin) - relax the smooth muscle of the bladder neck and prostate. Side effects: Dizziness Headache Asthenia/fatigue Orthostatic hypotension Rhinitis Sexual dysfunction 5-alpha-reductase inhibitors (finasteride)- prevent the conversion of testosterone to DHT and decrease the prostate size. Side effects: a. Decreased libido b.Ejaculatory/erectile dysfunction c. Gynecomastia d. Flushing  Surgical Management: 1. Transurethral resection of the prostate (TURP) A L L E R G Y HY P E R S E N S IT I V IT Y OCTOBER 2020  Allergy – inappropriate and often harmful immune system response to substances that are normally harmless. Hypersensitivity – excessive or aberrant immune response to any type of stimulus. It is a reaction that follows a re- exposure after sensitization, or buildup antibodies in predisposed person. Types of hypersensitivity reactions: Anaphylactic (Type 1) hypersensitivity -most severe and rapid hypersensitivity reaction. Characteristics: Edema (larynx) Hypotension Bronchospasm Cardiovascular collapse Primary chemical mediators – responsible for the symptoms (skin, lungs and GIT) 2. Cytotoxic (Type 11) Hypersensitivity -Occurs when antibodies are directed against antigens on cells or basement membranes of tissues. -lead to cell lysis and tissue damage. e.g. hemolytic transfusion 3. Immune Complex (Type 111)Hypersensitivity -damaging inflammatory reaction caused by insoluble immune complexes formed by antigens that bind to antibodies. e.g. rheumatoid arthritis 4. Delayed (Type IV) Hypersensitivity or delayed hypersensitivity -T cell-mediated immune reaction after exposure to an antigen. -occurs 24-48 hours after exposure to an antigen. e.g. (PPD) antigen from Mycobacterium tuberculosis 01 02 03 Assessment: Diagnostic Evaluation: Types of Skin tests: Comprehensive allergy history CBC Prick Thorough physical examination Eosinophil Count – increased Scratch Allergy assessment Total serum immunoglobulin E intradermal levels – high (allergy) Skin tests – most accurate conf irmation of allergy  Note: Corticosteroid and antihistamines, over the counter allergy drugs, Interpretation: suppress the skin test Positive reaction – urticarial reactivity. wheal 48-96 hours before testing should be stopped. DEFINITIONS: Hypersensitivity- exaggerated or inappropriate immune reaction resulting in tissue damage Allergy- Hypersensitivity reaction to an extrinsic (often innocuous) antigen. Autoimmunity- immune response with specificity for self antigen Autoimmune disease- disease in which an autoimmune response plays a pathogenetic role. Systemic Lupus Erythematosus SLE Chronic multi-system collagen disorder inflammatory, autoimmune disorder that affects nearly every organ in the body. Characterized by remissions and exacerbations A chronic inflammatory disorder of the connective tissue, SLE affects multiple organ system, as well as the skin, and can be fatal. Increased incidence in females, 15 to 40 years old 50% - 10 year survival rate CAUSES Unknown Autoimmune Drugs Viral infection Genetic susceptibility Drug induced (phenergan, apresoline, dilantin, quinidine, isoniazid, pronestyl) PROGNOSIS The prognosis improves with early detection and treatment but os poor for patient who develops CV, Renal, or neurologic complications or severe bacterial infection Clinical Manifestations: Fever Fatigue Skin rashes Joint pain and swelling Systems involve: Mucocutaneous – papulo squamous or annular polycyclic lesions, discoid rash , erythematous papules or plaques and scaling causing scarring and pigmentation. - lesions worsens – during exacerbations and provoked by sunlight or artificial ultra violet light. - oral ulcers, splinter hemorrhages, alopecia, Raynaud’s phenomenon Musculoskeletal system - joint pain and swelling - morning stiffness Renal system -nephritis Nervous system -psychosis, cognitive impairment, seizures, peripheral and cranial neuropathies, transverse myelitis, strokes Cardiovascular system -chest pain, myocarditis, hypertension, cardiac arrhythmias, valvular incompetence Respiratory system -pleural effusion  CBC – pancytopenia Elevated ESR (erythrocyte sedimentation rate) Diagnostic ANA (Anti-nuclear antibodies) Tests Anti-DNA (most specif ic)- antibody that develops against the patient’s own DNA LE factor (Lupus erythematosus cells)  Weakness Anorexia Nursing Malaise Fatigue Assessment Joint pains Fever Oral/ Nasopharyneal ulcerations Alopecia Photosensitivity Butterfly rash over nose & cheeks (malar rash) Neuropathy Seizures Psychosis Renal/ CNS/ Cardiopulmonary involvement (pleural effusion) FACTORS THAT MAY genetic predisposition INCREASE THE RISK OF stress streptococcal or viral infection SLE EXACERBATION exposure to sunlight or UV light immunization pregnancy abnormal estrogen metabolism medications that increase the risk of SLE: procainamide, hydralazine, anticonvulsant, less coomonly, penecillin, sulfa drugs, and hormonal contraceptives Collaborative Management Nursing Interventions: ◉Rest – relieve muscle and joint pains ◉ROM exercises ◉Prevent infection ◉Avoid exposure to sunlight ○Sunblock ○Long-sleeved clothing ○Hats ○Sunglasses ◉High calorie, high protein diet Pharmacotherapy ◉Acetylsalicylic acid (Aspirin) ◉Steroids ◉NSAIDs ◉Anti-malarial drugs ◉Cytotoxic agents (Cyclophosphamide/ Methotrexate) ◉Plasmapheresis MULTIPLE SCLEROSIS  MULTIPLE SCLEROSIS immune-mediated progressive Results from progressive demyelinating disease of the It progress rapidly, disabling demyelination of the white CNS characterized as a chronic, is a major cause of chronic patients by early adulthood or matter of the brain and spinal progressive, and non- disability in young adults. causing death within months of cord and is cahracterized by contagious disease. onset. remission and exacerbation Demyelination – destruction of myelin – fatty and protein material that surrounds nerve f ibers in the brain and spinal cord resulting in impaired transmission of nerve impulses.  Risk factors: Virus Environmental – obesity, lack of vitamin D exposure, high salt diet in teenage year Age- younger adults Gender- women Causes: Geographic area- Europe, New Zealand, Autoimmune Southern Australia, Northern US, South Canada Genetic predisposition- presence of human leukocyte antigen on the cell wall  Clinical Manifestations: Frequently affected areas: Primary, progressive ??1. Optic nerve chiasm course and tracts a. Quadriparesis ?2. Cerebrum? b. Cognitive dysfunction 3. Brain stem and c. Visual loss cerebellum d. Brain stem syndromes ?4. Spinal cord 2. Progressive, relapsing a. relapses with continuous, disabling progression between exacerbations 3. Secondary progressive course a. disease progression occurs with or without relapses Primary Symptoms commonly reported: Fatigue Depression Weakness Numbness Difficulty in coordination Loss of balance Pain Blurring of vision Diplopia Scotoma Total blindness Paresthesias  13. Dysethesias 14. Loss of Proprioception 15. Spasticity 16. Loss of abdominal reflexes 17. Cognitive and * Exacerbations and phychological problems remissions are 18. Ataxia characteristic of MS 19. Emotional lability and euphoria 20. Bladder, bowel and sexual dysfunction  SECONDARY COMPLICATIONS 1.UTI 2.Constipation 3.Pressure ulcers 4.Contracture deformities 5.Dependent pedal edema 6.Pneumonia 7.Reactive depression 8.osteoporosis Assessment and Diagnostic Findings: 1. MRI 2. CSF Electrophoresis 3. Evoked potential studies 4. Urodynamic studies 5. Neuropsychological testing 6. Sexual history  *Individual treatment program for signs and symptoms continuing support are provided. No cure exist for MS MEDICAL * Goals of treatment : MANAGEM 1. Delay the progression of the disease 2. Manage chronic symptoms ENT 3. treat acute exacerbations Pharmacologic Therapy Disease Modifying Therapies Reduce frequency and duration of relapse, reduces sizes of plaques 1. Interferon beta -1a (Rebif) 2. Glatiramer acetate (Copaxone ) 3. IV methylprednisolone 4. Mitoxantrone Symptom Management: 1. Baclofen – use to treat spasticity 2. Valium, Zanaf lex, and Dantrium – may also use to treat spasticity 3.Symmetrel and Cylert – use to treat fatigue 4. Inderal, neurontin and Klonopin – use to treat ataxia 5. Anticholinergic agents, alpha-adrenergic blockers and antispasmodic agents – may be used to treat bladder dysfunction 6. Vitamin C – to acidify the urine, making bacterial growth less likely 7. Antibiotic – prescribed when appropriate  Nursing Process: Assess for the following: 1. Neurologic def icits 2. Secondary complications 3. Impact of disease on the patient and the family 4. Balance and mobility (risk for falling) 5. Assess for weakness, spasticity, visual impairment, incontinence, swallowing and speech disorder 6. Patient lifestyle, coping and improvement Nursing Diagnosis: 1. Impaired bed and physical mobility related to weakness, muscle paresis, and spasticity 2. Risk for injury related to sensory and visual impairment 3. Impaired urinary and bowel elimination related to nervous system dysfunction 4. Impaired verbal communication and risk for aspiration related to cranial nerve involvement 5. Disturbed thought processes related to cerebral dysfunction 6. Ineffective individual coping related to uncertainty of course of MS 7. Impaired home maintenance management related to physical, psychological, and social limits imposed by MS 8. Potential for sexual dysfunction related to lesions or psychological reaction  Planning Goals: 1. Promotion of physical mobility 2. Avoidance of injury 3. Achievement of bladder and bowel continence 4. promotion of speech and swallowing mechanism 5. Improvement of cognitive function 6. Development of coping strengths 7. Improved home maintenance management 8. Adaptation to sexual dysfunction  Nursing Intervention: 1. Promoting physical mobility Relaxation and coordination exercises Exercise-walking improves gait; may use assistive device 2. Minimizing spasticity and contractures Warm packs Avoid hot bath (risk for burn injury) 3. Activity and rest Encourage work and exercise (avoid fatigue) Avoid strenuous exercise 4. Minimizing effects of immobility 5. Preventing injury Patient is taught how to walk Taught to watch the feet while walking 6. Enhancing bladder and bowel control Bedpan and urinal made readily available Set up voiding time schedule Adequate f luids, dietary f iber Bowel training program 7. Enhancing communication and managing swallowing dif ficulties Speech therapy evaluation Teach patient and family to adhere to the plan Ready suction apparatus Careful feeding Proper positioning during eating 8. Improving sensory and cognitive function Vision-eye patch or covered eye glasses lens 9. Cognition and emotional responses Make the family aware of the degree of cognitive impairment Family and friend support is needed 10. Strengthening coping mechanism Nurse initiates home care Coordinate network services Help patient def ine and understand the problem Help develop alternatives management/solution Maintain planning and f lexibility in action 11. Improving home management Avoid exposure to heat Recommend air condition room 12. Promoting sexual 13. Promoting home and functioning community-based care Collaborate between patient, family and Teaching patient self care health care Continuing care encourage sharing and communication of feelings Planning for sexual activity Exploring alternative methods of sexual expression Gouty arthritis A systemic disease caused by deposition of urate crystals in the joint and body tissues Affects more men than women urate deposits leads to painful arthritic joints. It can affects any joint but occurs most commonly in the feet and legs. Gout follows an intermittent course and commonly leaves patients symptom-free for years between attacks. It can lead to chronic disability and rarely, severe hypertension and progressive renal disease. Prognosis is good with treatment CAUSES: 1. Primary gout- disorder of Purine metabolism thus increase serum uric acid 2. Secondary gout- excessive uric acid in the blood due to another disorder such as leukemia, CRF &DKA. Also caused by certain drugs such as diuretics & antituberculosis drugs. Alcohol beverages also increase uric acid level. Normal: 2.4-7.0mg/dL GOUT DEVELOPS IN 4 STAGES: Asymptomatic Acute Intercritical Chronic  In gout, increased concentration of uric acid leads to tophi (urate deposit) in joints or tissue. These crystals trigger an immune response, causing local necrosis or fibrosis ASSESSMENT FINDINGS ACUTE ATTACK 1. Severe pain in the involved joints, initially the big toe 2. red, hot, swollen, painful & tender 3. inf lammation of the joint, fever, chills and general malaise. CHRONIC ATTACK 3. TOPHI- yellowish-whitish, irregular deposits in the skin, cartilage, synovial membranes, tendons & soft tissues that break open and reveal a gritty appearance Tophi can be developed also in the heart and form a uric acid stones in the kidney. 4. PODAGRA-big toe  DIAGNOSTIC TEST Elevated levels of uric acid in the blood Uric acid stones in the kidney (+) urate crystals in the synovial f luid Medical management 1. Colchicine Prevents urate crystals formation Used for acute attacks 2. Allupurinol (ZYLOPRIM) Rash signif ies allergic reaction Reduce uric acid formation Take with food 3. Probenecid (BENEMID) Increase uric acid excretion 4. Febuxostat tablet Nursing Intervention 1. Provide a diet with LOW purine Avoid Organ meats, aged and processed foods STRICT dietary restriction is NOT necessary 2. Encourage an increased f luid intake (2-3L/day) to prevent stone formation 3. Instruct the patient to avoid alcohol 4. Provide alkaline ash diet to increase urinary ph (cranberry/prune juice, meat, eggs, poultry products & vitamin C) 5. Provide bed rest during early attack of gout 6. Elevate the affected joint and hot or cold compresses for comfort 7. A liberal f luid intake (3 or more LPD) 8. Sodium bicarbonate or potassium citrate to minimize uric acid renal stones. 9. Administer anti-gout medication and analgesics (NSAIDs) ASA is C/I cause interfere uric acid excretion. Rheumatoid arthritis A type of chronic systemic inf lammatory arthritis and connective tissue disorder affecting more women (ages 35 -45) than men RA is a chronic, systemic inf lammatory disease that primarily attacks peripheral joints and surrounding muscles, tendons, ligaments, and blood vessels. Spontaneous remission and u npredictable exacerbation mark the course of the disease. It is potentially crippling and requires lifelong treatment and sometimes surgery Prognosis worsens with the development of nodules, vasculitis, and high titers of Rheumatoid Factor FACTORS: Genetic Auto-immune connective tissue disorders with unknown cause. Fatigue, emotional stress, cold, infection ASSESSMENT FINDINGS Joint: 1. PAIN, swelling, tenderness; usually PIP and MCP joints of f ingers, wrists, knees, ankles & toes. Limited range of motion. Morning stiffness lasting more than 1 hour Joint destruction & deformity Swan neck deformity: f lexion of DIP joint with hyperextenion of PIP joint Boutonniere deformity: hyperextension of DIP joint with f lexion of PIP joint Ulnar deviation and subluxation of Metacarpophalageal joints Carpal tunnel syndrome Hallux valgus (foot deformity) and hammertoe deformities of the foot Systemic Fatigue, weakness Anorexia, weight loss Low-grade fever Anemia Rheumatoid nodules: f irm SQ tissue nodules over elbow, MCP joints, toes.  RA is currently believe to have autoimmune basis, although the casue remains unknown. cartilage damage resulting from inflammation triggers further immune responses, including compliment activation. Compliment, in turn, attracts polymorphonuclear leukocytes and stimulates the release of inflammatory mediators, which exacerbates joint destruction ASSESSMENT FINDINGS Joint involvement is SYMMETRICAL and BILATERAL Characteristically beginning in the hands, wrist and feet Joint STIFFNESS occurs early morning, lasts MORE than 30 minutes, not relieved by movement, diminishes as the day progresses Diagnostic test 1. X-ray Shows bony erosion 2. Blood studies reveal (+) rheumatoid factor, elevated ESR and CRP and ANTI-nuclear antibody 3. Arthrocentesis shows synovial f luid that is cloudy, milky or dark yellow containing numerous WBC and inf lammatory proteins MEDICAL MANAGEMENT 1. Therapeutic dose of NSAIDS and Aspirin to reduce inf lammation 2. Chemotherapy with methotrexate, antimalarials, gold therapy and steroid 3. For advanced cases- arthroplasty, synovectomy 4. Nutritional therapy GOLD THERAPY: IM or Oral preparation Takes several months (3-6) before effects can be seen Can damage the kidney and causes bone marrow depression Nursing MANAGEMENT 1. Relieve pain and discomfort USE splints to immobilize the affected extremity during acute stage of the disease and inf lammation to REDUCE DEFORMITY Administer prescribed medications Suggest application of COLD packs during the acute phase of pain, then HEAT application as the inf lammation subsides 2. Decrease patient fatigue Schedule activity when pain is less severe Provide adequate periods of rests 3. Promote restorative sleep 4. Increase patient mobility Advise proper posture and body mechanics Support joint in functional position Advise ACTIVE ROME Nursing Management 5. Provide Diet therapy Patients experience anorexia, nausea and weight loss Regular diet with caloric restrictions because steroids may increase appetite Supplements of vitamins, iron and PROTEIN 6. Increase Mobility and prevent deformity: Lie FLAT on a f irm mattress Lie PRONE several times to prevent HIP FLEXION contracture Use one pillow under the head because of risk of dorsal kyphosis NO Pillow under the joints because this promotes f lexion contractures OSTEOARTHRITIS The most common form of degenerative joint disorde symptoms usually begins in middle age and may progress with age Disability depends on the site and severity of involvement and can range from minor limitation of the f ingers to severe disabiiity in people with hip or knee involvement Chronic, NON-systemic disorder of joints Pathophysiology Injury, genetic, Stimulate the chemicals will cause Previous joint chondrocytes to cartilage degeneration, damage, Obesity, release chemicals reactive inf lammation of Advanced age the synovial lining and bone stiffening Risk factors 1. Increased age 2. Obesity 3. Repetitive use of joints with previous joint damage 4. Anatomical deformity 5. genetic susceptibility OSTEOARTHRITIS: Assessment f indings 1. Joint pain Caused by –Inf lamed cartilage and synovium –Stretching of the joint capsule –Irritation of nerve endings 2. Joint stiffness commonly occurs in the morning after awakening Lasts only for less than 30 minutes DECREASES with movement, but worsens after increased weight bearing activitry Crepitation may be elicited 3. Functional joint impairment limitation The joint involvement is ASYMMETRICAL This is not systemic, there is no FEVER, no severe swelling Atrophy of unused muscles Usual joint are the WEIGHT bearing joints OSTEOARTHRITIS: Diagnostic f indings 1. X-ray Narrowing of joint space Loss of cartilage Osteophytes 2. Blood tests will show no evidence of systemic inf lammation and are not useful  OSTEOARTHRITIS: Medical management 1. Weight reduction 2. Use of splinting devices to support joints 3. Occupational and physical therapy 4. Pharmacologic management Use of PARACETAMOL, NSAIDS Use of Glucosamine and chondroitin Topical analgesics Intra-articular steroids to decrease inf lam OSTEOARTHRITIS: Nursing Interventions 1. Provide relief of PAIN Administer prescribed analgesics Application of heat modalities. ICE PACKS may be used in the early acute stage!!! Plan daily activities when pain is less severe Pain meds before exercising 2. Advise patient to reduce weight –Aerobic exercise –Walking 3. Administer prescribed medications –NSAIDS 4. Position the client to prevent f lexion deformity –Use of foot board, splints, wedges and pillows DIABETES MELLITUS  Diabetes Mellitus is a syndrome of impaired carbohydrate, fat, & protein metabolism caused by either lack of insulin secretion or decreased sensitivity of the tissues to insulin  Type 1 diabetes Two major Types also called insulin-dependent diabetes mellitus (IDDM) caused by lack of insulin secretion Type 2 diabetes also called non-insulin-dependent diabetes mellitus (NIDDM) caused by decreased sensitivity of target tissues to the metabolic effect of insulin This reduced sensitivity is often called insulin resistance  Gestational Diabetes Any degree of glucose intolerance with its onset during pregnancy. Develops in the 2nd and 3rd trimester due to secretions of placental hormones causing insulin resistance.  RISK FACTORS: OBESITY HISTORY OF GESTATIONAL DIABETES OR STRONG FAMILY HISTORY OF DM GLYCOSURIA ETHNIC GROUPS (HISPANIC AMERICANS, ASIAN AMERICANS) MANAGEMENT: DIETARY MODIFICATION BLOOD GLUCOSE MONITORING Type 1 DM Lack of insulin production by beta cells of the Pancreas Occurs at about 14 years of age Juvenile DM Plasma glucose of 300-1200mg/dL Causes Viral infections or autoimmune disorders Hereditary factor of beta cell degeneration  Causes loss of glucose in the urine excess glucose spills into the urine occurs when blood glucose rises 180mg/dL Causes DEHYDRATION glucose does not diffuse through the pores of cell membrane thus increase osmotic pressure loss of glucose in the urine causes OSMOTIC DIURESIS THUS, polyuria, intracellular & extracellular dehydration & increased thirst Causes utilization of Fats & Metabolic acidosis (ketones & dehydration) Causes depletion of the body’s proteins lWeight loss & asthenia (lack of energy) despite eating large amount of food (polyphagia)  Onset at 30 years old Type 2 DM Known as adult onset diabetes Causes Obesity Insulin resistance Cushing's syndrome General Assessment POLYPHAGIA POLYDIPSIA POLYURIA HYPERGLYCEMIA WEIGHT LOSS BLURRED VISION SLOW WOUND HEALING VAGINAL INFECTIONS WEAKNESS & PARESTHESIAS SIGNS OF INADEQUATE FEET CIRCULATION Diagnostic Test Plasma glucose level taken anytime of the day without regard to when last meal Eight hour fasting plasma glucose known as FBS (no food or fluid intake for 8 hours) Two hour Glucose test (during an OGTT) Common Type of Insulin Complications of Insulin Therapy: Local allergic reactions Systemic allergic Insulin lipodystrophy Lipohypertrophy Resistance to injected insulin Morning hyperglycemia – elevated blood glucose level on arising in the morning caused by insuf ficient insulin. Methods of Insulin Delivery: Insulin Pen Jet injectors Insulin pumps Transplantation of Pancreatic Cells Providing Patient Education Develop a diabetes education plan Organizing information Assessing the readiness to learn Educating experienced patients Determining education methods Educating patients to self-administer insulin Storing Insulin 1. whether it is short acting or long acting preparations – should be refrigerated. 2. Cloudy insulins should be thoroughly mixed by gently inverting the vial or rolling it between the hands before drawing the solution into a syringe or pen. 3. Inspect for flocculation in the bottles of intermediate acting insulin (whitish coating and frosted). If frosted – inactive and should not be used. Mixing Insulins When rapid or short acting insulin are to be given simultaneously with longer acting insulin – they are mixed together in the same syringe. The longer acting insulin must be mixed thoroughly before drawing into the syringe. Regular insulin should be drawn up first. Note: injecting cloudy insulin into a vial of clear insulin contaminates the entire vial of clear insulin and alters its action. Withdrawing Insulin Inject air into the bottle of insulin equivalent to the number of units of insulin to be withdrawn.- to prevent the formation of a vacuum inside the bottle, which would make it difficult to withdraw the proper amount of insulin. Selecting and Rotating the Injection Site A. Four main areas for injection: Abdomen – speed of absorption is greatest Upper arms (posterior surface) Thighs (anterior surface) Hips B. Systematic rotation of injection sites within an anatomic area – prevent lipodystrophy. C. Use all available injection sites within one area rather than randomly rotating sites from area to area - promote consistency in insulin absorb- tion. D. Don’t use the exact same site more than once in 2-3 weeks E.Insulin should not be injected into the limb that will be exercised – drug absorbed faster resulting to hypoglycemia. APPROACH TO DIABETES MELLITUS Diet Exercise OHA/ INSULIN  Sulfonylureas (stimulate pancreas to produce insulin) Chlorpropamide (Diabinase) OHA Tolbutamide (Orinase) glyburide (DIA BETA), Glimipiride (Amara) BIGUANIDES (improves glucose use in skeletal muscles) metformin (GLUCOPHAGE) ALPHA-GLUCOSIDE INHIBITORS (slows digestion & absorption of carbohydrates) Acarbose (PRECOSE) MEGLITINIDES (stimulates pancreas to secrete insulin) repaglinide (PRANDIN) THIOZOLIDINEDIONES (increases insulin sensitivity at receptor sites on liver, muscle, & fat cells) Rosiglitazone (Avandia) OHA Dipeptidyl-Peptidase 4 Inhibitors stimulate insulin secretin and inhibit glucagon secretion by elevating endogenous GLP-1 (stimulate insulin secretion & inhibit glucagon secretion thus limiting postprandial glucose excursions E.g. sitagliptin, saxagliptin, linagliptin, vildagliptin, alogliptin, gemigliptin  HYPOGLYCEMIA Complication DIABETIC KETOACIDOSIS (DKA) HYPERGLYCEMIC HYPEROSMOLAR NONKETOTIC SYNDROME (HHNS)  Sweating Tremor Tachycardia/palpitations Nervousness Signs of Hunger/anxiety Hypoglycemia Pale, cool skin Hypotension Decreased LOC headache Mild Hypoglycemia 60-70mg/dL Fast-acting glucose: 3 glucose tablets ½ cup of fruit juice or regular soda 8 oz of skim milk 6-8 life savers candies 2-3 tsp of sugar or honey Nursing alert: do not add sugar to fruit juice  Blood glucose