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NCM 112- MED SURG
Thou Who Shall Not Be Named | 2 RA 10173 🙂 Inflammatory Disorders ● Diabetes Mellitus (DM) ● Urinary System ○ Cystitis ○ Urolithiasis ● Reproductive System ○ Pelvic Inflammatory Dse (PID) ○ Benign Prostatic Hypertrophy ● Skin ○ Hypersensitivity/ Allergy ● Immunologic Disorder ○ Systemic Lupus Erythematosus ○ Multiple Sclerosis ○ Rheumatoid Arthritis ○ Transplant Rejection INFLAMMATORY DISORDER URINARY SYSTEM CYSTITS ● is inflammation of the bladder, usually caused by a bladder infection. ● It is a type of urinary tract infection (UTI), particularly in women. ● it usually result from an ascending infection. UTI - caused by pathogenic microorganisms in the urinary tract Catheter-associated UTI - hospital acquired UTI. Lower UTI Types:
- Cystitis - (bladder)
- Prostatitis - (prostate gland)
- Urethritis - (urethra) CAUSES OF LOWER UTI
- infection by gram negative enteric bacteria, such as E. coli, klebsiella, Proteus, Enterobacter, Pseudomonas, or Serratia
- Simultaneous infection with multiple pathogens in a patient with neurogenic bladder
- an indwelling urinary catheter
- fistula between the intestine and bladder Causes:
- Bacterial invasion of the urinary tract 2 Reflux - obstruction to free-flowing urine a. urethrovescial reflux
- reflux of urine from urethra into the bladder b. vesicoureteral reflux
- backflow of urine from the bladder into one or both ureters. Routes (3 ways) ● Transurethral route (ascending infection) - most common (fecal contamination) ● Bloodstream (hematogenous spread) ● Fistula from the intestine (direct extension) Clinical Manifestations: o Burning on urination o Urinary o frequency o Urgency o Nocturia o Incontinence o Suprapubic or pelvic pain o Hematuria back pain fever Assessment and Diagnostic Findings:
- Urine cultures 2 Cellular studies
a. a.Hematuria
b. b.Pyuria c. c.X-rays/CT scan
- Urinalysis Medical Management Psalm 145:9 | 1
ü Antibacterial agent (Anti-infectives - cephalosporin, levofloxacin) Nursing Diagnosis ü Acute pain associated with infection within the urinary tract Nursing Interventions: Relieve pain o Antispasmodic/analgesic drug o Heat to the perineum o Drink plenty of fluids o Urinary irritants should be avoided (coffee, tea, colas, citrus) o Frequent voiding (every 2-3 hours) o 2 Monitoring and managing potential complications o Note: gram-negative sepsis - most common complications o Monitor VS and LOC o Antibiotic o Increased fluid intake. UROLITHIASIS ● stones (calculi) in the urinary tract and kidney. ● concentrations of substances (calcium oxalate, calcium phosphate and uric acid). Contributing factors: o Infection o Urinary stasis o Immobility o Alter calcium metabolism or increased calcium formation of stones. Causes. o Renal tubular acidosis o Excessive intake of vit. D o Excessive intake of milk and alkali Clinical Manifestations:
- Infection (fever, chills and urinary frequency)
- Excruciating pain and discomfort
- Intense, deep ache and tenderness in the cost vertebral region (stones in renal pelvis)
- Hematuria
- Nausea and vomiting
- Ureteral colic
- Oxalate stones Assessment and Diagnostic Findings:
- C1 scan
- Blood chemistries test (calcium, uric acid, creatinine, sodium pH) Interventional Procedures:
- Ureteroscopy
- Electrohydraulic lithotripsy- The probe delivers an electric current that creates shock waves, which break up the stone.
- ESWL- Extracorporeal ShockWave Lithotripsy- non-invasive procedure to breakdown stones in part of the urinary system *** Surgical management** - nephrolithotomy Medical Management
- Opioid analgesics
- NSAID'S
- Increased fluid intake
- Limit oxalate intake (spinach, chocolate, peanuts) REPRODUCTIVE SYSTEM PELVIC INFLAMMATORY DSE ● Is an inflammatory condition of the pelvic cavity that may begin with cervicitis and uterus (endometritis), fallopian tubes (salpingitis), ovaries (oophoritis), pelvic peritoneum, or pelvic vascular system. Causes: o Virus o Fungus o Parasite
o Smoking o Heavy alcohol consumption o Obesity o Reduced activity level o Hypertension Heart disease and CHON and refined 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:
- Voiding diary
- Urinalysis
- PSA level
- UTZ Urethrocystoscopy Diagnostic Evaluation: I. History collection II. Physical Examination III. Rectal Examination (Digital) - It shows the smooth, firm, symmetric enlargement of the prostate IV. Urine Analysis V. Serum creatinine and blood urea nitrogen VI. Serum prostate and specific Antigen - It is a blood test to estimate the volume of the prostate VII. Urodynamic Flow Studies (Cystourethrography) - Measures peak urine flow rate, voiding time and volume, status of the bladder's ability to effectively contract. Medical Management:
- Cystostomy - incision in the bladder o 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 (Dihydrotestosterone) and decrease the prostate size. Side effects:
- Dizziness
- Headache
- Asthenia/fatigue
- Orthostatic hypotension
- Rhinitis
- Sexual dysfunction 5-alpha-reductase inhibitors (finasteride)-prevent the conversion of testosterone to DHT (Dihydrotestosterone) and decrease the prostate size. Side effects: a. Decreased libido b. Ejaculatory/ erectile dysfunction c. Gynecomastia d. Flushing Surgical Management:
ü Transurethral resection of the prostate (TURP) SKIN HYPERSENSITIVITY/ ALLERGY ● A disorder of the immune system often also referred to as atopy ● Allery is one of four forms of hypersensitivity and is called type 1 (or immediate) hypersensitivity ● Allergic occurs to normally harmless environment substances known as allergens ● Reactions are acquired, predictable, and rapid include eczema, hives, hay fever, asthma attacks, food allergy, and reactions to drug and the venom of stinging insect such as wasp and bees ● 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 dse- dse in which an autoimmune response plays a pathogenic Hypersensitivity Reactions ● Excessive, undesirable (damaging, discomfort-producing and sometimes fatal) reactions produced by normal immune system ● Require a pre-sensitized (immune) state of the host ● Gell-Coombs classified by the reactions into four types based on the mechanisms involved and time taken for the reaction ● Type 1, type 11, type 111, type IV ● Produce tissue injury Four Types of Hypersensitivity Reactions ● Type 1 (Anaphylactic) Reactions ● Type II (Cytotoxic) Reactions ● Types III (Immune Complex) Reactions ● Type IV (Cell-Mediated) Reactions Type 1 (Anaphylactic) Reactions ● Most severe and rapid hypersensitivity reactions ● Characteristics o Edema (larynx) o Hypotension o Bronchospasm o Cardiovascular collapse ● Primary chemical mediators- responsible for the symptoms (skin, lungs and GIT) ● Occurs within mins of exposure to antigen ● Antigens combine with IgE antibodies ● IgE binds to mast cells and basophils, causing them to undergo degranulation and release several mediators: o Histamine: dilates and increases permeability of blood vessels (swelling and redness), increases mucus secretion (runny nose), smooth muscle contraction (bronchi) o Prostaglandins: contraction of smooth muscle of respiratory system and increased mucus secretion o Leukotrienes: bronchial spasms ● Anaphylactic shock: massive drop in blood pressure. Can be fatal in mins. Treatment for HS-I Disorder ●^ Immunological treatment o Hypersensitization- rpt injections of allergens- may work by shifting from IgE to IgG production o MAB anti-IgE that binds mIgE on B cells- if binds IgE on mas cells lead to degranulation Cytotoxic (Type 11) Hypersensitivity ●^ Occurs when antibodies are directed against on cells or basement membranes of tissue ● Lead to cell lysis and tissue damage ● E.g. hemolytic transfusion ● Involve activation of complement by IgG or IgM binding to antigen cell. ● Antigenic cell is lysed ● Transfusion reactions: o ABO Blood group system: type O is universal donor.
● Itching ● Sneezing ● Runny nose ● Headache ● Red and watery eyes ● Hives or rash Common symptoms (^) ● Sneezing ● Coughing ● Runny nose ● Sore throat Food allergy symptoms ●^ Stomach pain ● Vomiting ● Hives ● Swollen tongue Environmental symptoms ●^ Rash ● Congestion ● Watery or burning eyes ● Itchy nose, mouth or throat IMMUNOLOGIC DISORDER SYSTEMIC LUPUS ERYTHEMATOUS ● Chronic multisystem 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, 15-40 yrs old ● 50%- 10 yrs survival rate ● Raynaud’s phenomenon- fingers bcome white due to lack of blood flow, then blue as vessels dilate to keep blood in tissues, finally red as blood flow returns. Causes (^) ● Unknown ● Autoimmune ● Drugs ● Viral infection ● Genetic susceptibility ● Drug induced (phenergan, apresoline, dilantin, quinidine, isoniazid, pronesty Prognosis (^) ● The prognosis improve with early detection and treatment but as poor for patient who develops CV, Renal, or neurologic complications or severe bacterial infection Clinical manifestation (^) ● Fever ● Fatigue ● Skin rashes ● Joint pain and swelling Systemic Involve (^) ● Mucocutaneous- o Papulo squamous or annular polycyclic lesions, discold rash, erythematous papules or plaques and scaling causing scarring and pigmentation. o Lesions worsens- during exacerbations and provoked by sunlight or artificial ultra violet light. o Oral ulcers, splinter hemorrhage, alopecia, Raynaud’s phenomenon ● Musculoskeletal system o Joint pain and swelling o Morning stiffness ● Renal system o Nephritis ● Nervous system o Psychosis, cognitive impairment, seizures, peripheral and cranial neuropathies transverse myelitis, strokes ● Cardiovascular system o Chest pain, myocarditis, hypertension, cardiac arrhythmias, valvular incompetence o Pleural effusion Diagnostic Test (^) ● CBC- pancytopenia ● Elevated ESR (erythrocyte sedimentation rate)
● ANA (Anti- nuclear antibodies) ● Anti-DNA (most specific)- antibody that develops against the patient’s own DNA ● LE factor (Lupus erythematosus cells) Nursing Assessment (^) ● Weakness ● Anorexia ● Malaise ● Fatigue ● Joint pains ● Fever ● Oral/ Nasopharyneal ulcerations ● Alopecia ● Photosensitivity ● Butterfly rash over nose and cheeks (malar rash) ● Neuropathy ● Seizures ● Psychosis ● Renal/CNS/ Cardiopulmonary involvement (pleural effusion) Factors that may increase the risk of SLE exacerbation ● Genetic predisposing ● Stress ● Streptococcal or viral infection ● Exposure to sunlight or UV light ● Immunization ● Pregnancy ● Abnormal estrogen ● Metabolism ● Med that increase the risk SLE: procainamide, hydralazine, anticonvulsant, less commonly, penicillin, sulfa drugs, and hormonal contraceptives Nursing Interventions (^) ● Rest- relieve muscle and joints pains ● ROM exercises ● Avoid exposure to sunlight o Sunblock o Long- sleeved clothing o Hats o Sunglasses ● High calorie, high protein diet Pharmacotherapy (^) ● Acetylsalicylic acid (Aspirin) ● Steroids ● NSAIDS ● Anti-malarial drugs ● Cytotoxic agents (Cyclophosphamide/ Methotrexate) ● Plasmapheresis MULTIPLE SCLEROSIS ● Immune- mediated progressive demyelinating dse of the CNS characterized as a chronic, progressive and non- contagious dse. ● Is a major cause of chronic disability in young adults ● Results from progressive demyelination of the white matter of the brain and spinal cord and is characterized by remission and exacerbation ● It progress rapidly, disabling patients by early adulthood or causing death within months of onset. ● Demyelination- destruction of myelin- fatty and protein material that surrounds nerve fibers in the brain and spinal cord resulting in impaired transmission of nerve impulses. Causes (^) ● autoimmune Risk Factors (^) ● Virus ● Environmental- obesity, lack of vit D exposure, high salt diet in teenage yr ● Age- younger adults ● Gender- women ● Geographic area- Europe, New Zealand, Southern Australia, Northern US, South Canada ● Genetic predisposition- presence of human leukocyte antigen on the cell wall. Frequently Affected areas ● Optic nerve chiasm and tracts (??) ● Cerebrum
accumulate quietly, which eventually leads to gout attack. Pain, swelling and redness ● Chronic Tophaceous Gout ○ This is the final stage of gout, which is a form of chronic arthritis characterized by permanent damage to the cartilage and bone in the joint Diagnostic Test ● Elevated levels of uric acid in the blood ● Uric acid stones in the kidney positive urate crystal in the synovial fluid Medical Mgt ● Colchicine- prevents urate crystal formation. Used for acute attacks ● Allupurinol (ZYLOPRIM)- rash signifies reaction. Reduce uric acid formation. Take with food ● Probenecid (BENEMID)- increase uric acid excretion ● Febuxostat tablet Nursing Intervention ● Provide a diet with LOW purine. Avoid Organ meats, aged and processed foods. STRICT dietary restriction is NOT necessary ● Encourage an increased fluid intake (203L/day) ● Instruct the pt to avoid alcohol ● Provide alkaline ash diet to increase urinary ph (cranberry/ prune juice, meat, eggs, poultry products and vit. c) ● Provide bed rest during early attack of gout ● Elevate the affected joint and hot or cold compresses for comfort ● A liberal fluid itake ( 3 or more LPD) ● Sodium bicarbonate or K citrate to minimize uric acid renal stones ● Administer anti- gout med and analgesic (NSAIDs) ASA is C/I cause interfere uric acid excretion Factors ● Genetic ● Auto-immune connective tissue disorders with unknown cause ● Fatigue, emotional stress, cold, infection Assessment ● Joint: ● PAIN, swelling, tenderness; usually PIP and MCP joints of fingers, wrists, knees, ankles and toes ● Limited range of motion ● Morning stiffness lasting more than 1h ● Joint destruction and deformity ● Swan neck deformity: hyperextension of DIP joint with flexion of PIP joint ● Ulnar deviation and subluxation of Metacarpophalangeal joints ● Carpal tunnel syndrome ● Hallux valgus/ bunion (foot deformity) and hammertoe deformities of the foot systemic ● Fatigue, weakness ● Anorexia, weight loss ● Low-grade fever ● Anemia ● Rheumatoid nodules: firm SQ tissue nodules over elbow, MCP joints, toes Stages of Rheumatoid Arthritis
● STAGE 1
○ The body mistakenly attacks its own joint tissue. ● STAGE 2 ○ The body makes the antibodies and theJoints start swelling up ● STAGE 3 ○ The joints start becoming bent and deformed,the fingers become crooked. These misshapen joints can press on the nerves and can cause nerve pain aw well ● STAGE 4 ○ If not treated the dse will progress to the last stage, in which there's no joint remaining at and the joints essentially fused Medical MGT ● Therapeutic dose of NSAIDS and Aspirin to reduce inflammation ● Chemotherapy with methotrexate,antimalarials, gold therapy and steroid ● For advanced cases- arthroplasty, synovectomy 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 Intervention ● 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 ● Increase Mobility and prevent deformity: ○ Lie FLAT on a firm 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 flexion contractures OSTEOARTHRITIS ● The most common form of degenerative joint disorder 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 fingers to severe disability in people with hip or knee involvement ● Chronic,NON-systemic disorder of joints Assessment Findings
- Joint pain ● Caused by: ● Inflamed cartilage and synovium ● Stretching of the joint capsule ● Initiation of nerve endings
- 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 activity ● Crepitation may be elicited
- Functional joint impair -ment 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 Diagnostic findings ● X-ray ○ Narrowing of joint space ○ Loss of cartilage ○ Osteophytes ● Blood tests will show no evidence of systemic inflammation and are not useful Medical MGT ● Weight reduction ● Use of splinting devices to support joints ● Occupational and physical therapy Pharmacologic management ● Use of PARACETAMOL,NSAIDS ● Use of Glucosamine and chondroitin ● Topical analgesics ● Intra-articular steroid to decrease inflammation Nursing Intervention ● Provide relief of PAIN ○ Administer prescribed analgesics ○ Application of Reat modalities. ICE PACKS may be used in the earty acute stage!!! ○ Plan daily activities when pain is less severe ○ Pain meds before exercising ● Advise patient to reduce weight ○ Aerobic exercise ○ Walking ○ Administer prescribed medications ○ NSAIDS ● Position the client to prevent flexion deformity ○ Use of foot board, splints, wedges and pillows RA (Rheumatoid Arthritis) OA (Osteoarthritis) Onset is early Onset is late Chronic systemic dse Degenerative dse Involves the synovium Involves the cartilage Involved joints are symmetrical- fingers, cervical spine Involved joints are unilateral- weight bearing knee, hips spine Malaise, fever, anemia No other s/sx systemic TRANSPLANT REJECTION ● Occurs when transplant tissue is rejected by the recipient’s immune system, which destroys the transplant tissue ● Can be lessened by determining the molecular similitude between donor and recipient and by use of immunosuppressant drugs after transplant What causes transplant rejection? ● Hyperacute rejection- caused by specific antibodies against
is a syndrome of impaired carbohydrate, fat, & protein metabolism caused by either lack of insulin secretion or decreased sensitivity of the tissues to insulin Two major Types Type 1 diabetes
- 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: o OBESITY o HISTORY OF GESTATIONAL DIABETES OR STRONG FAMILY HISTORY OF DM o GLYCOSURIA o ETHNIC GROUPS (HISPANIC AMERICANS, ASIAN AMERICANS) MANAGEMENT: o DIETARY MODIFICATION o BLOOD GLUCOSE MONITORING TYPE 1 DM o Lack of insulin production by beta cells of the Pancreas o Occurs at about 14 years of age o Juvenile DM o Plasma glucose of 300-1200 mg/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 depletion of the body's proteins
- Weight loss & asthenia (lack of energy) despite eating large amounts of food (polyphagia) Type 2 DM o Onset at 30 years old o Known as adult-onset diabetes o Causes o Obesity o Insulin resistance o Cushing's syndrome General Assessment o POLYPHAGIA o POLYDIPSIA o POLYURIA o HYPERGLYCEMIA o WEIGHT LOSS o BLURRED VISION o SLOW WOUND HEALING o VAGINAL INFECTIONS o WEAKNESS & PARESTHESIAS
o SIGNS OF INADEQUATE FEET CIRCULATION Methods of Insulin Delivery:
- Insulin Pen
- Jet injectors
- Insulin pumps
- Transplantation of Pancreatic Cells Providing Patient Education o Develop a diabetes education plan o Organizing information o Assessing the readiness to leam o Educating experienced patients o Determining education methods o Educating patients to self-administer insulin 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. 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 absorption. D. Don't use the exact same site more than once in 2- weeks E. Insulin should not be injected into the limb that will be exercised – drug absorbed faster resulting to hypoglycemia. OHA Sulfonylureas (stimulate pancreas to produce insulin) o Chorpropamide (Diabinase) o Tolbutamide (Orinase) o glyburide (DIA BETA), Glimipiride (Amara) BIGUANIDES (improves glucose use in skeletal muscles) o metformin (GLUCOPHAGE) ALPHA-GLUCOSIDE INHIBITORS (slows digestion & absorption of carbohydrates) o Acarbose (PRECOSE) MEGLITINIDES (stimulates pancreas to secrete insulin) o repaglinide (PRANDIN) THIOZOLIDINEDIONES (increases insulin sensitivity at receptor sites on liver, muscle, & fat cells) o Rosiglitazone (Avandia) Treatment o Increase fluid intake o Insulin to reduce hyperglycemia & acidosis) o Electrolyte replacement (PNSS to correct Na loss); after 3 hours changed to half-saline to prevent hypernatremia o Potassium may be added to IVF o Regular insulin o Check VS, monitor LOC, monitoring IV o infusions, monitor 180 Hyperglycemic Hyperosmolar Nonketotic Coma - Similar to DKA but without Kussmaul respirations and acetone breath.
- Treatment correcting F&E imbalances, insulin to lower hyperglycemia, PNSS followed by half-saline
- Check VS, monitor LOC, monitoring V infusions, monitor I&O Micro vascular complications o Diabetic retinopathy: retinal ischemia & possible retinal hemorrhage or detachment
