Clinical Manifestations, Diagnosis, and Treatment of Fractures and Bone Diseases | Exams Nursing | Docsity (2024)

Download Clinical Manifestations, Diagnosis, and Treatment of Fractures and Bone Diseases and more Exams Nursing in PDF only on Docsity! 1 COLLEGE OF NEW ROCHELLE NUR 333 FINAL EXAM STUDY GUIDE ATTAINED GRADE A+ LATEST UPDATE 2022 ASSURED SUCCESS. Chronic Neuromuscular Disorders Guillain-Barre Syndrome Etiology and Pathophysiology • ASCENDING PARALYSIS • Autoimmune disorder preceded by infection, trauma or surgery • Acute, rapidly progressing, and potentially fatal form of polyneuritis Clinical Manifestations • Symptoms appear SYMMETRICAL and develop in days to weeks • Paresthesia (numbness and tingling) in the extremities • Hypotonic (reduced muscle tone) and areflexia (lack of reflexes – in arms and legs) • Orthostatic hypotension, hypertension, and vagal responses (bradycardia, heart block, asystole) • Bowel and bladder dysfunction, diaphoresis, facial flushing • Pain –paresthesias, muscular aches and cramps, and hyperesthesia (increased sensitivity) • Respiratory failure as paralysis progresses upwards • Disease does not affect level of consciousness, cognition or pupillary constriction/dilation – mind is intact Collaborative Care • During acute phase: – Monitor the ascending paralysis; assess respiratory function; monitor arterial blood gases (ABGs); and assess the gag, corneal, and swallowing reflexes. Reflexes are usually decreased or absent. • Carefully assess swallowing and gag reflex and take measures to prevent aspiration – HOB 2 elevated • Plasma exchange (plasmapheresis): removes circulating antibodies thought to be responsible for the disease – monitor for hypovolemia, hypokalemia – is only useful during first 2 weeks – Plasma is separated from the whole blood and blood cells are returned to the patient without the plasma – Interventions: weighing the patient before and after procedure, caring for the shunt or venous access site and preventing complications, provide information and reassurance – Cannot go back to corticosteroids after plasmapheresis • High dose immunoglobin therapy (Sand globulin) – ADE: chills, mild fever, myalgia, headache, anaphylaxis, aseptic meningitis, retinal necrosis Myasthenia Gravis Etiology and Pathophysiology • FACIAL/MUSCLE WEAKNESS – eyes, eyelids, swallowing, speaking, breathing • Alterations/blockage of acetylcholine at neuromuscular junction prevents muscle contraction • Autoimmune disease with fluctuating weakness of certain skeletal muscle groups Clinical Manifestations • Muscles are generally the strongest in the morning and become exhausted with continued activity – periods of rest are necessary • Difficulty breathing (weakness to chest wall muscles), impaired speech and swallow, eyelid drooping (ptosis), double Vision, fatigue, weakness • Exacerbations can be caused by emotional stress, trauma, temperature extremes, hypokalemia 5 • To be diagnosed with MS patient must have: – Evidence of at least two inflammatory demyelinating lesions in at least two different locations in CNS – Damage or an attack occurring at different times (usually 1 month or more apart) – All other possible diagnoses ruled out Collaborative Care • No cure for MS, care is aimed at treating the disease process and providing systematic relief • Drug Therapy: Medications used to slow the progression of MS are taken on a long-term basis – Immunosuppressant’s (methotrexate), and adrenocorticotropic hormone – Corticosteroids: used to reduce the inflammation that spikes during a relapse – Immunomodulation (Copa one, β-interferon): used to prevent relapses and modify progression ▪ ADE may include flushing and SOB after injection ▪ β-interferon (Atone, Betaseron): rotate injection site with each dose, assess for depression and suicidal ideation, wear sunscreen, flu-like symptoms common after initiation of therapy. Blood tests to monitor liver enzymes. – Galena: prevents lymphocytes from damaging CNS, need to have chicken pox before taking drug, monitor BP regularly, avoid pregnancy – monitor for bradycardia Nursing Management • During an acute exacerbation the patient may be immobile and confined to bed – prevent major complications such as respiratory infection, UTI and pressure ulcers • Patient teaching should be focused on building general resistance to illness, including avoiding fatigue, extremes of hot or cold Musculoskeletal Disorders Osteoporosis (fragile bone disease)  calcium in bones,  calcium in blood 6 • Chronic, progressive metabolic bone disease marked by: low bone mass, deterioration of bone tissue • Leads to increased bone fragility – falls  fractures • Known as “silent thief” – slowly robs you of skeletal resources • More common in women because they have lower calcium intake, less bone mass, bone desorption begins earlier and becomes more rapid at menopause, pregnancy and breastfeeding, and live longer than men • Additional risks for fractures: smoking, low body weight, prior fractures • Risk factors: >65 yrs. old, female, low body weight, family history, calcium/Vat D deficiency Etiology and Pathophysiology • Risk factors: excessive use of alcohol (>2 a day), low testosterone in men, diet low in calcium/vitamin D deficiency, specific diseases (malabsorption disease), certain drugs (long use of corticosteroids), thyroid replacement, heparin • Peak bone mass (by age 20) determined by heredity, nutrition, exercise and hormone function. Bone loss after 35- 40 years is inevitable • Osteoblast – bone deposit/ formation – bone building • Osteoclast – resorb bone (remodeling) – osteoclasts exceed osteoblasts in osteoporosis - breaks down bone tissue • Long term corticosteroid use is a major contributor to osteoporosis • Calcium and phosphorus abnormalities – porous brittle bones and  fractures Clinical Manifestations • Occurs in spine, hips, and wrists • First manifestations are back pain or spontaneous fractures • Gradual loss of height leading to kyphosis or “dowager’s hump” Diagnostic Studies • Bone mineral density (BMD) – determined by peak bone mass and amount of bone loss 7 – Quantitative ultrasound (QUS): measures bone density with sound waves in kneecap, heel, and shin – Dual-energy x-ray absorptiometry (DXA): measures bone density in spine, hips and forearm • T-scores – T score above -1.0 = normal bone density – T score between -1.0 and -2.5 = osteopenia – T score of -2.5 or lower = osteoporosis • Z score: compares with someone own age and ethnicity: anything less than -2.0 Collaborative Care • Care focuses on proper nutrition, calcium supplementation, exercise, prevention of falls and fractures, and drugs • Proper nutrition – 1000 mg/day of calcium in women 19-50, men 19-70 years – 1200 mg/day of calcium for women 51+, men 71+ years – Milk, cheese, yogurts, salmon, oysters, broccoli, almonds, turnip greens, ice cream, sardines, spinach • Calcium supplements – take in divided doses with food (easier to absorb) – Calcium carbonate (Tums) – take with meals, 40% elemental calcium – Calcium citrate – less dependent on stomach acid, 20% elemental calcium – Vitamin D necessary for calcium absorption/function; bone formation. Sunlight for 20 minutes, supplemental (800-1000IU/day) for postmenopausal, older adults, homebound, minimal sun exposure • Exercise – Weight-bearing exercise: buildup and maintain bone mass,  strength, coordination (walking, hiking) – Walking 30 minutes, 3x a week is recommended 10 • An infection of the bone, bone marrow, and surrounding soft tissue that results in in inflammation, necrosis, and formation of new bone • Hematogenous osteomyelitis: due to blood borne spread of infection – Caused by pathogens carried in the blood from other sites of infection • Contiguous-focus osteomyelitis from contamination from bone surgery, open fracture, or traumatic injury (GSW) • Osteomyelitis with vascular insufficiency, seen most commonly among patients with diabetes and peripheral vascular disease, most commonly affecting the feet • Patients can become septic Etiology and Pathophysiology • Exogenous: infection enters from outside as in an open fracture • Endogenous (hematogenous): organisms travel by blood from other sites of infection (bacteremia) • The pelvis, tibia, and vertebrae, which are vascular-rich sites of bone, are the most common sites of infection • Osteomyelitis may also occur in the presence of a foreign object in the body (implant, orthopedic prosthetic device – total joint replacement) • Microorganism grows and ultimately results in ischemia and bone dies 11 • Pus, edema and vascular congestion can occur Clinical Manifestations • Acute osteomyelitis: initial infection or infection lasting <1 month – Local manifestations: constant bone pain unrelieved by rest, swelling, tenderness, warmth at the infection site, and restricted movement – Systemic manifestations: fever, night sweats, chills, restlessness, nausea and malaise – Later signs include drainage from site • Chronic osteomyelitis: bone infection lasting longer than 1-month duration. Can be a continuous problem or a problem of remission and exacerbations - foot ulcers – Constant bone pain and swelling, warmth at the infection site Diagnostic Studies • Bone or soft tissue biopsy to determine causative microorganism • Elevated WBC and erythrocyte sedimentation rate (ESR) • Radionuclide bone scans Collaborative Care • IV antibiotic therapy treatment of choice – mostly caused by staph aureus • NSAIDS, analgesics to help manage pain • Control infection already in the body (respiratory infection, pressure ulcers) to help prevent osteomyelitis • Immobilization of affected limb (splint) can help decrease pain • Patient is frequently on bed rest, frequent body alignment/turn and positioning is important Osteoarthritis • OVERUSE of joints 12 • Most common arthritis – slowly progressive, non-inflammatory disorder = cartilage destruction • Characteristics: synovitis, joint pain, stiffness, loss of joint motion • Risk factors:  age, female, genetics, excessive or  body weight, inactivity, repetitive joint use (sports participants, textile mill workers) Etiology and Pathophysiology • Slow onset with symptoms worsening over time = non-reversible • Causes of OA: dislocations/fractures, repetitive physical activity (causes cartilage to break down), neurologic disorders, skeletal deformities Clinical Manifestations • Systemic manifestations such as fatigue, fever, and organ involvement are NOT present in OA (difference between OA and RA) • Symptoms worse at night from being used all day • ASYMEMETRICAL SYMPTOMS • Pain and stiffness in joints, sciatic nerve pain, decreased ROM, paresthesias, crepitus, joint enlargement, pain may increase with weather changes (barometric pressure) • Crepitation: grating feeling caused by loose particles of cartilage in the joint cavity • Deformity is specific to the involved joint (Heberden’s nodes, Bouchard’s nodes (PIP)– both red, swollen and tender) Diagnostic Studies • MRI/CT to detect early joint changes • H&P, x-ray, examination of synovial fluid Collaborative Care • Lifestyle =  weight • Care focuses on managing pain and inflammation, preventing disability, and maintaining and improving joint function, maintain functional position • Rest and joint protection: affected joint should be rested during acute inflammation 15 toes, co*ck-up toes • Fatigue, weakness, anorexia, anemia, weight loss, low-grade fever, skeletal muscle atrophy, rheumatoid nodules, pleural effusion, vasculitis, pericarditis, splenomegaly • Rheumatoid nodules: masses that can develop over joints of fingers and elbows, base of spine and back • Sjögren’s syndrome: can occur with RA or lupus, patients have decreased lacrimal and salivary gland secretion leading to dry mouth, burning/itchy eyes, • Complications MI, stroke, death,  risk of infection, lymphoma Drug therapy • NSAIDS, mild analgesics, corticosteroids for physical comfort • Disease-Modifying Anti-Rheumatic Drugs (DMARDS): have the potential to lessen the permanent effects of RA – Methotrexate: reduces clinical symptoms in days to weeks, lower toxicity, side effects include bone marrow suppression and hepatotoxicity (frequently monitor labs)  risk of infection – Azulfidine, Plaquenil – used for mild to moderate disease, eye exam because causes blindness • Biologic Response Modifiers (BRMs): slow progression, used to treat severe disease not responsive to DMARDS. Tumor necrosis factors— bind with TNF inhibiting inflammation: – Enbrel: increased risk of heart failure and infection; report fever, bruising, bleeding – Humira: given subq, avoid live vaccine while taking, administer TB test and chest xray prior to beginning treatment Collaborative Care • Rest/exercise during times of pain and inflammation, assistive devices/splints • Maintain joint in neutral position to minimize deformity – press water from a sponge instead of wringing) 16 • Use strongest joint available for any task. – When rising from chair, push with palms rather than fingers • Distribute weight over many joints instead of stressing a few – Slide objects instead of lifting them • Change positions frequently – do not hold book or grip steering wheel for long periods without resting, avoid grasping pencil or cutting vegetables with knife for extended periods. • Avoid repetitious movements – do not knit for long periods, rest between rooms when vacuuming, modify home environment to include faucets and doorknobs that are pushed rather than turned. • Modify chores to avoid stress on joints – avoid heavy lifting, sit on stool instead of standing while cooking Endocrine Disorders Hyperthyroidism Etiology and Pathophysiology 17 • Excessive thyroid hormone secretion from the thyroid gland • Occurs more often in women between ages 20 – 40 • Most common form: Graves’ disease aka toxic diffuse goiter Clinical Manifestations • Fine straight hair, bulging eyes, tachycardia, facial flushing,  systolic BP, breast enlargement (in males), weight loss due to hypermetabolism, muscle wasting, localized edema, finger clubbing, tremors, menstrual changing (amenorrhea), diarrhea Diagnosis: Thyroid panel (T3, T4 – sometimes higher than T3, TSH levels) Graves’ Disease – type of hyperthyroidism Etiology and Pathophysiology • Autoimmune disease – diffuse thyroid enlargement, excess thyroid hormone secretion • Insufficient iodine supply, infection, stressful life events can be precipitating factors • Excessive release of T3, T4 or both leads to thyroxicosis (hyper metabolism from excess circulating levels) Clinical Manifestations •  Metabolism,  tissue sensitivity to stimulation by sympathetic nervous system • Goiter: inspection, auscultation (bruits – increased blood supply to area) • Ophthalmopathy: abnormal eye appearance or functions – Exophthalmos: fat deposits develop behind chamber of the eye and eyes protrude out – Vision loss, muscle weakness, double vision • Hypertension, cardiac hypertrophy (swelling), angina (due to oxygen demand from  metabolic demand) •  Appetite/thirst, weight loss • Thin brittle nails, hair loss/fine, silk hair, clubbing of fingers, diaphoretic, vitiligo (skin disorder), premature graying (more commonly seen in men) • Muscle wasting, osteoporosis (due to  calcium) 20 – Inhibits synthesis of T3 and T4,  vascularity of thyroid gland, maximal effect within 1-2 weeks – Used to prepare patient for thyroidectomy or thyrotoxicosis – Can stain teeth read, teach to use with a straw • B-Blockers : symptomatic relief of thyrotoxicosis – treat the HR and  stimulation of nervousness, tremors – Propranolol – Atenolol for patients with asthma or heart disease • PTU: propulthiouracil – blocks synthesis of hormones, given three times a day, used for rapid reduction of symptoms • Dexamethazone : suppresses release of thyroid hormones, steroid – usually given in high dose IV 2. Radioactive Iodine Therapy (RAI) • Treatment of choice in nonpregnant adults – pregnancy test done prior to treatment • Damages or destroys thyroid tissue • Treatment with antithyroid drugs and propranolol for 3 months before and after the start of RAI treatment • Patient teaching: oral care for thyroiditis/parotidits (can give oral solution to diminish pain in mouth, ice chips or small sips of water), radiation precautions, symptoms of hypothyroidism • Can result in hypothyroidism requiring lifelong hormone therapy • Precautions at home: – Using private toilet facilities if possible and flushing two or three times after each use – Separately laundering towels, bed linens, and clothes daily at home – Not preparing food for others that requires prolonged handling with bare hands – Avoiding being close to pregnant women or children for 7 days after therapy • Postoperative complications 21 – Hemorrhage, respiratory distress, hypocalcemia and tetany, laryngeal nerve damage, thyroid storm or thyroid crisis, eye and vision problems of Graves’ disease – Airway obstruction after thyroid surgery is an emergency – Oxygen, suction equipment, tracheostomy tray should be readily available in the patient’s room – Assess the patient every 2 hours for 24 hours for signs of hemorrhage or tracheal compression (irregular breathing, neck swelling, frequent swallowing, sensations of fullness at the incision site, choking, and blood on dressings) – Place in semi fowlers position – avoid flexion of the neck – Monitor vital and calcium levels, check for signs of tetany secondary to hyperparathyroidism (tingling in toes, fingers, around the mouth; muscular twitching; apprehension), monitor Trousseau’s sign and Chvostek sign – hypocalcemia – Report temp change of 1 degree = may indicate impending thyroid crisis Hypothyroidism • Deficiency of thyroid hormone = slow metabolic rate • Subclinical hypothyroidism: TSH >4.5 maul/L, T4 levels are normal • Nonthyrodial illness syndrome: critically ill patients, Low T3, T4 and TSH levels Etiology and Pathophysiology • Primary hypothyroidism: destruction of thyroid tissue or defective hormone synthesis – caused by atrophy of the gland and is the end stage of Grave’s disease • Secondary hypothyroidism: pituitary disease with TSH secretion or hypothalamic dysfunction with TRH • Causes: Iodine deficiency (most common), treatment for hyperthyroidism, drugs, hypothyroidism that occurs in infancy (cretinism) 22 Clinical Manifestations • Slow HR (look at HR to see if medications are working), cold intolerance, fatigue, weight gain, constipation, muscle aches • Slowing of body processes, slow onset • HR,  serum cholesterol and triglycerides (because metabolism is slow and don’t excrete), • Anemia = because metabolic rate is low, oxygen demand is low = HgB • Shortness of breath on exertion, low exercise intolerance because always tired • Fatigue and lethargy, personality and mood changes, impaired memory, slowed speech 25 • Round face (moon face) • Ecchymosis (bruise easily), elevated BP • Purple striate on the extremities/abdomen from stretching of skin 26 • Sugar extremely high (hyperglycemia) • Excessive body hair especially in women “hirutism” • Dorsocervical fat pad (buffalo hump), depression • Mood swings and psychosis from excess cortisol • Hypernatremia, hypertension, hypervolemia, hypokalemia, hyperglycemia Diagnostic Studies • 24 hour urine test for free cortisol (<80 to 120 mcg/ 24 hr) – peak for cortisol is between 6am- 8am • Dexamethasone suppression test – give steroids to see if patient is able to clear them – False-positive results in patients with depression and those taking Dilantin or Rifampin • Plasma ACTH levels may be measured (high levels = Cushing’s, low levels = medication or adrenal etiology) Collaborative Care • Primary goal of treatment is to normalize hormone levels • Prep patient for hypophysectomy to remove pituitary • Adrenalectomy: indicated for Cushing’s caused by adrenal tumors or hyperplasia therapy for hormonal cortisol treatment • If Cushing’s is caused by exogenous corticosteroid use: 1. Gradual discontinuation of steroid therapy 2. Reduction of the corticosteroid therapy 3. Conversion to an alternate-day regimen (twice the daily dosage of a shorter- acting corticosteroid is given every other morning) – Gradual taping off is necessary to avoid life-threating adrenal insufficiency • Drug Therapy – Ketoconazole (Nizoral), aminoglutethimide (Cytadren), and mitotane (Lysodren). – Used cautiously because they are often toxic at the dosages needed to reduce cortisol secretion. 27 – Hydrocortisone or prednisone may be needed to avoid adrenal insufficiency. • Monitor for blood sugars • S/S infection – monitor for purulent drainage (can indicate infection) • Emotional support – due to appearance of face and buffalo hump • Postop care: – High doses of corticosteroids are administered during and a few days after surgery to ensure adequate responses to the procedure have been met –  Levels of corticosteroids increase the susceptibility to infection and delay wound healing – 24-48 hours postop is most critical for circulatory instability – monitor for changes in respirations, BP and HR – Vomiting, increased weakness, dehydration, and hypotension may indicate hypocortisolism. Nursing Diagnosis • Impaired skin integrity: excess corticosteroids, immobility • Risk for infection: low resistance to stress and suppression of immune system • Imbalanced nutrition: more than body requirement, high caloric content of foods • Self-care deficits: weakness, fatigue, muscle wasting, altered sleep patterns Patient Teaching • Teach dietary modifications – heart healthy foods (fruits, vegetables) • Teach the patient to avoid exposure to extreme temperatures, infections, and emotional disturbances. • Teach patients to adjust their corticosteroid replacement therapy in accordance with their stress levels. • Surgical removal of the tumor by trans-spheroidal Hypophysectomy – post surgery not allowed to sneeze • Contact PCP if: gain more weight than desired, symptoms worsen • Return to ER: trouble staying awake or are confused, blurred vision • Patient Outcomes Free from infection, normal fluid and electrolyte balance, adequate 30 cortisol Collaborative Care • Hydrocortisone (Solu-crotef) has glucocorticoid and mineralocorticoid properties • Glucocorticoid (cortisol) dose must be  during stressful situations – Homecare: administer 2/3 in the morning and 1/3 in the afternoon • Mineralocorticoid (aldosterone) replacement with fludrocortisone (Florinef) is administered daily in morning • Cortisol replacement: Prednisone or Hydrocortisone treatment: if sick, stress, will need to increase dosage, take regularly do not abruptly stop •  Salt must be added to diet • Protect patient from noise, light, and environmental temperature • Monitor sugar and sodium levels, fluid/electrolyte balance Patient Teaching • Chronic and requiring ongoing treatment – medication is not a cure • Medical alert bracelet • Teach how to administer hydrocortisone 100 mg IM – carry medication with you at all time • Increase dosage of steroid before additional stress is caused (surgery, procedures, stressful situations) • Importance of preventing infections, adjusting medication dosage •  Glucocorticoid dosage when taking: phenytoin, barbiturates, rifampin, antacids • Treat minor flare ups with extra salt and fluids Care of Patients with Skin Problems Common Skin Disorders Pruritus • Itching sensation, with or without rash • Triggered by heat (vasodilation), prostaglandins, dry skin, insect bites or drugs • Increased by release of histamine and chemical mediators 31 • Stimulation or irritation of receptors in the junction between the epidermis and dermis 32 • Treatment: cool environment (vasoconstriction and  itching), antihistamines, wet dressings, topical steroids, antibiotics , therapeutic baths Dry Skin • Decreased activity of sebaceous and sweat glands =  skin lubrication • More common in older adults – aging process less sebaceous glands, not enough moisture • Exposure to environmental heat and low humidity, sunlight, excess bathing, and d fluid intake • Pruritis and flaking of skin Psoriasis • Chronic, noninfectious skin disorder • Raised, reddened, round circ*mscribed plaques covered by silvery white scale (plaques shed gray scales), itching, burning, pain – NO ecchymosis or striae is present • Triggers: sunlight, stress, hormone fluctuations, steroid withdrawal seasonal changes, and drugs may make condition worse • Family history, may be autoimmune • Check cholesterol, triglycerides for early identification of cardiovascular disease • Treatment: topical corticosteroids, tar preparations, retinoids to decrease inflammation, photochemotherapy, ultraviolet –B Dermatitis • Acute or chronic inflammation of the skin • Erythema (redness), and pain or pruritis, vesicles, scales • Progresses to edema, serous discharge and crusting • Skin can become thick, leather looking • Types: contact (poison ivy, poison oak, detergent, hair dye, latex allergy), atopic (eczema), seborrheic (common in kids, plaque on kids), exfoliative (find in patients who are immunocompromised – workup for hematological cancer) Acne 35 • Can develop as a result of earrings • Results of deposits of excessive amounts of collagen during scar formation Nevi (moles): rounded, well-defined borders = CAN BECOME MALIGNANT Animas (hemangiomas) • Benign vascular tumors • Types include nevus flammeus, cherry, spider, telangiectasis, venous lake Bacterial infections • Arise from the hair follicle where bacteria accumulate and grow • Localized infection, systemic if invade into deeper tissue Folliculitis • Staphylococcus aureus • Skin surface and extends into hair follicle – inflammation • Scalp and extremities – face of bearded men, legs of women who shave legs, eyelids (stye) • May be caused by poor hygiene, nutrition, prolonged moisture, trauma Furuncle (boil) • Infection of the hair follicle, usually staphylococcus aureus • Carbuncle: group of infected hair follicles • Deep red nodule that gets larger and cystic • May cause fever, chills, or malaise Cellulitis • Infection of dermis and underlying hypodermis • Spreads as a result of spreading factor hyaluronidase • Breakdown of fibrin network and other barriers – infectious process • Red swollen, painful, fever, chills, malaise, headache, swollen lymph glands • The skin is erythematous, edematous, tender, and sometimes nodular • Cephalosporins are good choice 36 for treatment Impetigo • Seen mostly in children • Bacterial skin infection, contagious • Topical, antibiotics (systemic if bad infection – augmentin, keflex) • Crusted corners of mouth, around the nose Fungal Infections • Organism that live in soil, on animals, on humans • Dermatotypes live on stratum corneum, hair, and nails • Superficial infections: ringworm, tine • Mycoses: fungal disorders Dermatophyte (tinea) infections • Tinea pedis: athlete’s foot • Tinea curis: groin infection Candidiasis Infections • Yeastlike infections on skin, vagin*, GI tract • Mouth: white, cheesy plaque, resembles milk curds • vagin*: vaginitis with red, edematous, painful vagin*l wall, white patches, pruritus, pain on urination and intercourse. • Skin: diffuse papular erythematous rash with pinpoint satellite lesions around edgesof affected area Viral Infections Warts • Human papillomavirus • Transmitted via skin and mucous membranes 37 • Nongenital warts are benign lesions, genital warts are precancerous 40 • This skin cancer is highly metastatic, and a person's survival depends on early diagnosis and treatment. 41 • Pathophysiology and manifestations – Lesions can be benign until they infiltrate the dermis and mingle with blood and lymph – Precursor lesions are congenital or dysplastic nevi (moles) and lentigo meligna – Melanomas are not painful or accompanied by sign of inflammation • ABCDE method to assess lesions: – Asymmetry – Border irregularity – Color variation – Diameter is greater than 6 mm – Evolution of skin lesion change • Vertical growth phase: rapid growth and color change Collaborative Care • Treatment focuses on removal of malignant tissue • Diagnosis: microscopic exam and tissue biopsies, liver function tests, chest x-rays (to see if it metastasizes) • Surgery: Mosh surgery (remove one skin layer at a time), wide surgical excision for melanoma (full thickness of skin, subcutaneous tissue, take out one big chunk) • Curettage and electrodessication or cryosurgery – Radiation therapy: for lesions that are inoperable (location or patient age), may itself cause cancer – Biologic therapy: enhance, restore immune system to fight cancer – BCG (slows the cancer growth), interferon, interleukin, monoclonal antibodies Nursing Care • Patient anxiety, feelings of hopelessness, impaired skin integrity, provide teaching • Health promotion: early detection, self-examination, dermatologist appointments • Risk factors: familial history, blonde, fair skin, blue eyes • Assessing: present health status – change in mole, wart, birthmark scar, 42 exposure; PMH: skin cancer or family history Patient Teaching • Avoid sun exposure between the hours of brightest sunlight (10 a.m. and 4 p.m.) • Sunscreen, a hat, thick clothing, and sunglasses should be worn for outdoor activities • The client should be instructed to examine the body monthly for the appearance of any cancerous or any precancerous lesions • Sunscreen should be reapplied every 2 to 3 hours and after swimming or sweating Skin Trauma Pathophysiology and Manifestations • Impairment of flow of blood and lymph causing ischemia from distortion of capillaries • If pressure continues, platelets clump and form micro thrombi (block blood flow  ischemia, hypoxia) • Cells and tissue die and become necrotic, secondary bacterial invasion common • Types: – Superficial trauma: red or blister – Deep tissue injury: deep structures where tissue becomes necrotic and dies • Shearing forces – Result when one tissue layer slides over another – Stretching and bending of blood vessels – Head of bed elevated and torso slides down toward foot of bed, pulling patient up in bed – Increased risk with immobility • Older adult is at increased risk Collaborative Care • Goal is prevention • Treatment: topical and systemic antibiotics, surgical debridement, specialty dressings and 45 Headaches • Also known as cephalic • Primary headaches are not caused by disease or another medical condition (tension-type, cluster and migraine) • Secondary headache are caused by another condition or disorder: sinus infection, neck injury, brain tumor Migraine • More common in women, family history of migraine headaches, onset between 20-30 years • Triggered by stress, rapid changes in glucose levels, foods, menstrual cycle • May last hours to days with aura usually lasts less than an hour • Unilateral pulsating or throbbing headache (synchronous with pulse, may last 4-72 hours) on one side of the head. Accompanied by n/v, sensitivity to light and sound • Aura: trigger point (foods, smells), individualized to the patient Risk factors • Familial history, low level education, low socioeconomic status (don’t have resources to seek treatment), high workload • Frequent tension-type headaches: without aura – common migraine, with aura – classic migraine Etiology and Pathophysiology • Genetic factors • May or may not have known precipitating events or factors • Associated with seizure disorders, ischemic stroke, asthma, depression, anxiety, myocardial infarction, Raynaud’s syndrome, and irritable bowel syndrome • May be triggered by foods: chocolate, cheese, oranges, tomatoes, onions, smoked meats and alcohol (red wine) Clinical Manifestations • The prodromal may include neurologic (photophobia), psychological 46 (hyperactivity, irritability), and other (food craving) manifestations. • Aura: visual (bright lights, patchy blindness, visual distortions, zigzag lines), sensory (voices or sounds that do not exist, strange smells), and motor (weakness, paralysis, feeling that limbs are moving) phenomena – Aura lasts 10-30 minutes before headache starts • Patients with migraine may tend to “hibernate.” Hide from noise, light, odors, people, and problems 47 • Unilateral pulsating or throbbing headache (synchronous with pulse, may last 4-72 hours) Diagnostic Studies • History, no specific lab or radiologic tests, other diagnostic exams often have normal results Drug Therapy • Goal is terminating or decreasing symptoms • Mild to moderate headache can obtain relief with NSAID, aspirin, or caffeine-containing combination analgesics. • For moderate to severe headaches, Sumatririptan (Imitrex) (mindful of patients with history of heart disease, stroke, and HTN because causes vasoconstriction – putting additional workload on the heart) have been first line of therapy – Excess dosage may produce tremor and decrease respirations – Reduce neurogenic inflammation of cerebral blood vessels • Preventive: Topiramate (Topamax) taken prophylactically to prevent migraines – Side effects: hypoglycemia, paresthesia, weight loss, and cognitive changes – Do not abruptly discontinue, may cause seizures – Adequate fluid intake to prevent renal stones • Several different classes of medications are used: antiseizure drugs, botox, SSRIs Tension-type (stress headaches) • More common in women • May be triggered by stress, eyestrain, or poor posture. These triggers can cause muscle contraction in neck, face and scalp • Bilateral pain, tightness, pressure, or viselike feeling; pain is most common on awakening • Episodic or chronic Clinical Manifestations • Bilateral frontal-occipital headache described as a constant, squeezing 50 • Symptomatic: triptans – contraindicated for patients with vascular risk factors, heart failure • 100% oxygen at 6-8 L/min for 10 min, can be repeated after 5 minute rest • Patient must have continuous access to O2 • Preventive: high-dose verapamil • Invasive nerve blocks, DBS, and ablative neurosurgical procedures Nursing Management of Headaches Assessment • Health history: location, type, onset, frequency, duration, time of day, relation to outside events (headaches when it’s extremely hot) • Personality, life adjustment, environment, neurologic and physical status, family situation • Seizures, cancer, stroke, trauma, asthma or allergies, mental illness, stress, menstruation, exercise, food, bright lights, noxious stimuli Implementation • Effective therapy may be to help patients: to examine their lifestyle, recognize stressful situations, learn to cope more appropriately • Daily exercise, relaxation periods, and socializing help reduce recurrence and should be encouraged • Alternative pain management: relaxation, meditation, yoga, self-hypnosis • Encourage a quiet, dim environment • Massage and heat packs can help with tension-type • Patient should make a written note of medications to prevent accidental overdose • Watch out for – Medication Overuse Headache (MOH) is an analgesic rebound headache – Acetaminophen, aspirin, NSAIDS, butalbital, triptans, ergotamine, opioids Seizure Disorders • Transient, uncontrolled electrical discharge of neurons in brain, interrupting normal function • May accompany other disorders or occur spontaneously without apparent cause 51 – Patients going through alcohol withdrawal may experience seizures • Seizures resulting from metabolic disturbances are not considered epilepsy if seizures cease when underlying condition is corrected (acidosis, electrolyte imbalance, hypoglycemia, hypoxemia, alcohol or barbiturate withdrawal, dehydration or water intoxication) • Extracranial disorders associated with seizures: HTN, systemic lupus erythematosus, DM, septicemia Etiology and Pathophysiology • Many possible causes, most common causes vary by age (children may experience seizures from fever) • Common causes birth to 6 months: severe birth injury, congenital birth defects of CNS, infections, inborn errors of metabolism • Common causes 2yrs – 20yrs: birth injury, trauma (car accidents), infection, genetic factors • Common causes 20yrs – 30yrs: structural lesions, brain tumor, trauma, vascular disease • Common causes after 50yrs: stroke, metastatic brain tumors • 1/3 of cases are idiopathic (unknown cause): idiopathic generalized epilepsy (IGE), not attributable to specific cause • Classification of seizure: – Partial seizures: begins in one part of the brain – Simple partial: consciousness remains intact – Complex partial: impairment in consciousness – Generalized seizures: involve the whole brain Phases of Seizures • Prodromal Phase: signs of activity that precede the seizure • Aural Phase: a sensory warning • Ictal Phase: full seizure • Postictal Phase: period of recovery after the seizure 52 Generalized Seizures: involve both sides of the brain; patient loses consciousness for few seconds to several minutes • Tonic-clinic seizure (grand mal seizure) – Loss of consciousness and falling from upright position 55 socially disadvantaged populations, history of Alzheimer’s disease or stroke • Status epileptics – continuous seizure Etiology and Pathophysiology 56 • Abnormal neurons undergo spontaneous firing, firing spreads to adjacent or distant areas of brain – cause of abnormal firing is unclear • Locating seizure focus is critical for successful surgical intervention • Gliosis (scar tissue) often found in area of brain from which seizure activity arises • Thought to interfere with normal chemical and structural environment of neurons • This makes them more likely to abnormally fire • Changes in function of astrocytes ma play several key roles in recurring seizures – Activation of astrocytes by hyperactive neurons is one of crucial factors that predisposes nearby neurons to generate an epileptic discharge/firing Genetic Link between Seizures and Epilepsy • Genetic abnormalities may be the most important factors contributing to IGE • Some types of epilepsy run in families • Other times are related to abnormalities in specific genes • Genetic link: difficult to determine role of genetics due to problem of separating genetic from environmental or acquired influences Complications of Seizures • Status epileptics (SE): continuous seizure activity without return to consciousness between seizures – Any seizure lasting > 5 minutes – can occur with any type of seizure = neurologic emergency!! – Causes brain to use more energy than is supplied – Neurons become exhausted and cease to function, permanent brain damage can result – Tonic-clinic/convulsive status epileptics is the most dangerous because it can cause ventilator insufficiency, hypoxemia, cardiac dysrhythmias, and hyperthermia 57 – Always give Ativan first for immediate treatment!! Load with a long acting anticonvulsant Dilantin or Luminal (or said in class Keera??) • Severe injury and death from trauma during a seizure • Patients who lose consciousness are at greatest risk • Sudden Unexplained Death in Epilepsy (SUDEP) –related to respiratory dysfunction, dysrhythmias, cerebral depression • Effect on lifestyle is most common complication of seizure disorder: depression, social stigma still exists, discrimination in employment and education, driving sanctions Diagnostic Studies • EEG – may help determine type of seizure and focus • CBC, serum chemistries, liver and kidney function, UA to rule out metabolic disorders • CT, MRI in new-onset to rule out structural lesions • Diagnosing seizure type is necessary to determine appropriate treatment Interprofessional Care • Nursing actions during a seizure include providing for privacy, loosening restrictive clothing, removing the pillow and raising padded side rails in the bed, and placing the client on one side with the head flexed forward, if possible, to allow the tongue to fall forward and facilitate drainage • The limbs are never restrained because the strong muscle contractions could cause the client harm • If the client is not in bed when seizure activity begins, the nurse lowers the client to the floor, if possible; protects the head from injury; and moves furniture that may injure the client. • Most seizures do not require emergency medical care because they are self-limiting • Patient teaching: importance of following drug regimen, what to do if dose is missed, lifetime treatment 60 effective for multiple seizure types • Gabapentin (Neurontin), Topiramate (Topamax), Lamictal Focal seizures • Pregabalin (Lyrica): additional treatment for focal seizures that are not successfully controlled with a single medication Status epilepticus: always give Ativan first for immediate treatment!! Load with a long acting anticonvulsant Dilantin or Luminal Surgical Management: confirmed diagnosis of epilepsy, adequate trial of drug therapy without satisfactory results Acute Care During Seizure • Maintain patent airway, support head, turn to side, loosen constrictive clothing, east to floor • Do not restrain patient or place any objects in their mouth • May require positioning, suctioning or oxygen after seizure Disorders of the Eye and Ear Cataracts • A cataract is clouding of the lens of the eye that impairs vision • Affect most people over 65 • Risk factors: exposure to sunlight (UV), cigarette smoking, heavy alcohol use, congenital conditions, eye trauma, DM, and drugs such as corticosteroids and chlorpromazine (Thorazine) • Vision loss can be restored with surgery Etiology and Pathophysiology • Immature cataract: when only a portion of the lens is affected • Mature cataract involves the entire lens, both near and distance vision are affected – Details become obscured – Clouded lens scatters light rays, causing problems with glare and difficulty 61 adjusting between light and dark environments – Pupil appears cloudy gray or white rather than black Collaborative Care 62 • Ophthalmoscopic exam: lens changes, loss of red reflex • Elective surgery: lens removal, intraocular lens implant • Teaching, learning needs in pre- and postoperative periods – Post-op: avoid bending, stooping, coughing or lifting ( intraocular pressure) • Cycloplegics and Mydriatics: pupillary dilation, paralysis of accommodation – Instruct patient to wear dark glasses to minimize photophobia – Monitor for signs of systemic toxicity (e.g., tachycardia, central nervous system [CNS] effects) • Suggest wearing sunglasses, adequate intake of vitamin C and E Glaucoma • Characterized by  intraocular pressure and gradual loss of vision. Peripheral vision is lost so slowly that it often is not noticed until late in the disease. Vision loss is permanent. Pathophysiology and Manifestations • Open-angle glaucoma : aqueous humor drainage is obstructed, fluid in the eye increases =  intraocular pressure – Increased pressure damages retinal neurons and the optic nerve – Peripheral vision is gradually lost, and the visual field narrows, both eyes are usually affected – untreated glaucoma eventually leads to blindness. – Painlessness, gradual loss of peripheral vision, difficulty adapting from light to dark, blurred vision, halos around lights, and difficulty focusing on near objects. • Angle-closure glaucoma : angle between the cornea and iris closes, completely blocking drainage of aqueous humor from the eye. The intraocular pressure rises abruptly, damaging the retina and the optic nerve = emergency !! 65 • When giving the carbonic anhydrase inhibitor dorzolamide, the nurse instills the drug 10 minutes apart from other topical ophthalmic drugs. The nurse reports ADE such as conjunctivitis or redness/itching of the lid. • When giving the carbonic anhydrase inhibitor acetazolamide, the nurse monitors the patient’s weight daily, as well as intake and output and vital signs, and reports serum electrolyte values to the physician. Detached Retina • Trauma: hole, tear in retina • Separation of the retina from the choroids, the vascular layer of the eye. Retinal detachment can occur spontaneously or result from trauma. The vitreous humor shrinks with aging, increasing the risk for detached retina. The retina can remain intact but separate from the choroids or tear and fold back on itself. Pathophysiology and Manifestations • A break or tear in the retina allows fluid to seep between the retina and choroid, separating these layers. If the layers remain separated, the neurons of the retina become ischemic and die, causing permanent vision loss. Retinal detachment is a medical emergency!! • Manifestations: painless, sense that a curtain or veil is being drawn across the vision (affected area of vision relates to the area of detachment), floaters and flashes of light, “cobweb” or “hairnet” in visual field Collaborative Care • Position with detached portion lower than rest of eye until treatment available • Gas into vitreous cavity to press detached portion against choroid Otitis Media Pathophysiology and Manifestations 66 • Middle ear infection • Serous otitis media: occurs with prolonged obstruction of Eustachian tube – Negative pressure draws fluid – "Snapping”, “popping", retracted, bulging ear drum – Changes in atmospheric pressure can cause acute pain, bleeding into the middle ear, rupture of the eardrum, or rupture of the round window • Acute otitis media – Follows upper respiratory infection due to impaired tube drainage – The eardrum is red and inflamed or dull and bulging – Collection of fluid, pus and mucus or bacterial growth ( pressure and rupture eardrum) – Severe pain, fever, malaise, and reduced hearing indicate infection – Hearing loss, vertigo, tinnitus Collaborative Care • Medications – Acute otitis media is treated with antibiotics for 5 to 10 days sometimes combined with decongestants – Mild analgesics such as acetaminophen are recommended to relieve pain and reduce fever • Surgery: tympanocentesis, myringotomy, ventilation tubes • Complementary therapies: lavender oil, warm cloth or chamomile tea bag • When instilling eardrops, place the patient on the unaffected side or tilts the head toward the unaffected side, straighten ear canal by pulling the pinna of the ear up and back, keeps the patient on the side for about 5 minutes after putting in the drops, and loosely places a small piece of cotton in the opening to the ear canal for 15 to 20 minutes. Gastrointestinal Disorders 67 Gastroesophageal Reflux Disease (GERD) • GERD is chronic symptom of mucosal damage caused by reflux of stomach acid into the lower esophagus. Etiology and Pathophysiology • Backflow of GI contents and enzymes into esophagus • Caused by incompetent lower esophageal sphincter. Under normal conditions, the LES acts as an anti- reflux barrier. An incompetent LES lets gastric contents move from the stomach to the esophagus when the patient is 70 (digested blood) • Melena – dark tarry stools indicating slow bleeding from an upper GI source • The longer the passage of blood through the intestines, the darker the stool color because of the breakdown of hemoglobin and the release of iron. • Patients with chronic gastritis or PUD are at a higher risk of GI bleed Collaborative Management: • Establish large IV, if upper GI (critical care)- fluid (lactic ringers solution) and blood replacement. Oxygen therapy to  blood oxygen saturation, PPI’s and H2 receptor blockers to stop bleeding 71 • Varices: variceal band ligation – causes thrombosis and fibrosis of bleeder, vasopressin +/- IV nitro • Esophagastroduodenoscopy: Patient NPO, remove dentures, post-procedure do not feed until gag reflex returns Nasogastric Tubes • Decompression of stomach, lavage, gastric analysis, tube feeding • Place patient in high-fowlers position Care of NG tube • Skin care for external nares to prevent irritation and ulcers • Frequent oral care • Post-op do not irrigate or reposition tube Liver Disorders Hepatic Portal-System Encephalopathy and Coma • Is caused by neurotoxic effects of ammonia. The liver is unable to convert ammonia to urea and it crosses the BBB • Portal-systemic encephalopathy (PSE) is a complex cognitive syndrome that results from liver failure and cirrhosis • Life threatening complications accumulation of ammonia and other toxic metabolites in the blood • Causes: high-protein diet, infection, hypovolemia, hypokalemia, constipation, GI bleeding, drugs (opioids, sedatives, illicit drugs) Clinical Manifestations • Changes in neurologic and mental responsiveness; impaired consciousness; and inappropriate behavior, ranging from sleep disturbances to lethargy to deep coma. • Asterixis: flapping hand tremors, cannot keep hands in dorsiflexion 72 • Apraxia: inability to construct simple figures, handwriting analysis • Fetor hepaticus: musty, sweet odor of patients breath • Monitor: EEG, changes in LOC, potential seizures, fetor hepaticus (fecal breath), monitor fluid, electrolyte, and ammonia levels Stages of Hepatic Portal-System Encephalopathy: • Stage 0: insomnia, sleep disturbance, impaired handwriting, tremor • Stage 1: personality changes, lack of awareness, mild confusion, short attention span, asterixis • Stage 2: lethargy, inappropriate behavior, disorientation to time, place or person, asterixis (hand flapping) • Stage 3: asleep, arousable, lack of meaningful conversation, progressive deterioration – marked mental confusion, muscle twitching, asterixis • Stage 4: unarousable, unresponsiveness, absent intellectual function, leading to death in most patients, no response to painful stimuli, seizures Medical Management • Lactulose to reduce serum ammonia levels – drug effectiveness is not measured by number of bowl movements, but by mental status change (if mental status isn’t improving, drug is not working, ammonia is still in blood and not decreasing) • Protein restriction because buildup of protein • Discontinue sedatives analgesics and tranquilizers because change in mental status Collaborative Care • Goal of management is reduction of ammonia formation. • Lactulose: traps ammonia in the gut – Can be given orally, enema, or through NG tube – The laxative effect of the drug expels the ammonia from the colon • Rifaximin antibiotic: decrease in bacterial flora, decreased formation of ammonia • Prevent constipation 75 hepatocellular cancer – Risk factors for the progression of HCV to cirrhosis: male gender, alcohol consumption,  cholesterol and triglycerides, obesity and diabetes. • There is no vaccination for HCV Hepatitis D: (delta virus) is a defective single stranded RNA virus that cannot survive on its own – requires HepB to replicate (can either get HBV and HDV at the same time or acquire HDV later) • Is transmitted percutaneously • No vaccine available Hepatitis E: RNA virus transmitted via fecal-oral route • Mode of transmission is contaminated drinking water Clinical Manifestations • Classified as acute and chronic, many patients asymptomatic • The acute phase usually lasts 1-6 months and is the time of maximal infectivity – Generally don’t feel well – anorexia, lethargic, n/v/ RUQ pain, distaste of cigarettes –  Sense of smell, low grade fever, skin rashes, myalgia, arthralgia, skin rashes – Can be icteric (jaundice), or anicteric ▪ The urine may darken because of excess bilirubin being excreted by the kidneys. If conjugated bilirubin cannot flow out of the liver because of obstruction or inflammation of the bile ducts, the stools will be light or clay colored. ▪ Pruritus (chronic itching) sometimes occurs with jaundice as a result of bile salts beneath the skin • The convalescent phase begins with jaundice is disappearing, lasts weeks to months (2-4 months) – Major complaints are general malaise and easily fatigability – Hepatomegaly remains during this time, but 76 splenomegaly subsides Collaborative Care • Acute viral hepatitis: adequate nutrition and rest, vitamin supplements, avoid alcohol • Chronic HBV: standard interferon, pegylated interferon *What do you offer your patient first who has been diagnosed with hepatitis – Immunoglobin should always be given first before vaccination to develop immunity. You can offer both if an option. Stages of Hepatitis (C) 77 1. Acute: The first six months following infection is the acute phase of the disease. Early symptoms may include fatigue, loss of appetite, or mild yellowing of the skin and eyes (jaundice). 2. Chronic: Progression begins with inflammation of the liver, followed by the death of liver cells = scarring of tissue 3. Cirrhosis • Irreversible scarring of the liver – end stage liver damage, chronic reaction to inflammation and necrosis • In compensated cirrhosis, the liver has scarring but is still able to perform essential functions • In decompensated cirrhosis, liver function is impaired with manifestations of failure Clinical Manifestations • Early Manifestations: the onset of cirrhosis develops in a gradual, subtle way, but with harmful effects – Fatigue and enlarged liver • Late manifestations: result from liver failure and portal hypertension – Jaundice, peripheral edema, ascites – Skin lesions, hematologic disorders, endocrine disturbances, peripheral neuropathies • Jaundice : decreased ability to conjugate and excrete bilirubin, overgrowth of connective tissue in liver compresses bile ducts = mild or severely ill, lack of appetite, n/v, weight loss, malaise, fatigue, weakness, headache, chills, fever, infection, dark orange-brown urine, clay colored stools, dyspepsia and intolerance of fats, impaired digestion, • Skin lesions: due to  in circulating estrogen caused by inability of liver to metabolize steroid hormones. Spider angiomas (telangiectasia), palmar erythema • Hematologic disorders : thrombocytopenia, leukopenia, anemia, coagulation disorders – Thrombocytopenia, leukopenia, and anemia are probably caused by the splenomegaly that results from backup of blood from the portal vein into the 80 Diagnostic Studies: • Ultrasound is used to diagnose gallstones – is useful in jaundice patients because it doesn’t affect the liver or those allergic to contrast medium • ERCP (visualize gallbladder, hepatic duct) • Percutaneous trans hepatic cholangiography: needle inserted into gallbladder duct and contrast medium is injected, ultrasound is done to view blockage Laboratory Testing: •  amylase (increased if pancreas is involved) WBC from inflammation,  bilirubin levels Collaborative Care • During an acute episode of cholecystitis, treatment focuses on pain control, control of possible infection with antibiotics, and maintenance of fluid and electrolyte balance • If n/v severe an NG tube may be placed to prevent further stimulation of gallbladder • Surgical therapy: Laparoscopic cholecystectomy is the treatment of choice for symptomatic cholelithiasis. – A common postoperative problem is referred pain to the shoulder because of the carbon dioxide that is used to inflate the abdominal cavity during surgery. • Drug therapy: fat soluble vitamins, bile salts, analgesics, NSAIDS • Nutritional therapy: smaller more frequent meals with some fat, high fiber and calcium Cirrhosis • Irreversible scarring of the liver – end stage liver damage, chronic reaction to inflammation and necrosis • After cirrhosis occurs a patient needs a new liver • Causes: alcohol abuse, hepatitis B and C, bile duct disease, and genetic diseases • In compensated cirrhosis, the liver has scarring but is still able to perform essential functions • In decompensated cirrhosis, liver function is impaired with manifestations of failure Clinical Manifestations 81 • Early Manifestations: the onset of cirrhosis develops in a gradual, subtle way, but with harmful effects – Fatigue and enlarged liver • Late manifestations: result from liver failure and portal hypertension – Jaundice, peripheral edema, ascites – Skin lesions, hematologic disorders, endocrine disturbances, peripheral neuropathies • Jaundice : decreased ability to conjugate and excrete bilirubin, overgrowth of connective tissue in liver compresses bile ducts – Leads to obstruction,  bilirubin in vascular system Hepatocellular and Obstructive Jaundice: – Hepatocellular: mild or severely ill, lack of appetite, nausea or vomiting, weight loss, malaise, fatigue, weakness, headache, chills, fever, infection – Obstructive: dark orange-brown urine, clay colored stools, dyspepsia and intolerance of fats, impaired digestion, pruritus • Skin lesions: due to  in circulating estrogen caused by inability of liver to metabolize steroid hormones. Spider angiomas (telangiectasia), palmar erythema • Hematologic disorders : thrombocytopenia, leukopenia, anemia, coagulation disorders – Thrombocytopenia, leukopenia, and anemia are probably caused by the splenomegaly that results from backup of blood from the portal vein into the spleen (portal hypertension). – The coagulation problems result from the liver’s inability to produce prothrombin and other factors essential for blood clotting. • Endocrine disorders: secondary to  metabolism of hormones, gynecomastia, loss of axillary and pubic hair, impotence and loss of libido (in men), amenorrhea, vagin*l bleeding, hyperaldosteronism in both sexes • Peripheral neuropathy: Common finding in alcoholic cirrhosis and is probably due to a dietary deficiency of 82 thiamine, folic acid, and Cobalamin (vitamin B12). Diagnostic Studies • Liver enzyme tests, protein, serum albumin, CBC 85 1. Bone Marrow • Soft substance in core of bones • Blood cell production (Hematopoiesis): the production of all types of blood cells (RBCs, WBCs, Platelets) 86 2. Liver • Liver synthesis plasma proteins including clotting factors and albumin • Liver clears damaged and non-functioning RBCs/erythrocytes from circulation 3. Spleen • Located in upper left quadrant of abdomen • Functions: produces fetal RBCs, filter and reuse certain cells, 30% platelets stored in spleen Aging on Hematologic System –  Hemoglobin (Hb or Hgb) –  response to infection (WBC) – Platelets = no change –  PTT Diagnostic Studies • WBCs: normal 4,000 -11,000 µ/ℓ – Associated with infection, inflammation, tissue injury or death – Leukopenia--  WBC – Neutropenia --  neutrophil count • RBC: males 4.5 – 5.5 trillion cells/L; females 4.0 – 5.0 trillion cells/L • Hematocrit (Hct): males 40 – 54%; females 36 – 46% – % of whole blood that is composed of red blood cells – measures number of RBC and size of RBC • Hemoglobin: males 13.5 – 18 g/dL; females 12 – 15 g/dL • Platelet Count: 150,000 – 400,000 – Thrombocytopenia –  platelet count – Spontaneous hemorrhage likely when count is below 20,000 • Pantocytopenia:  in RBC, WBC and platelets 87 Anemia • Anemia is a reduction in the number of RBCs, the quantity of hemoglobin, or the volume of RBCs • Because the main function of RBCs is oxygenation, anemia results in varying degrees of hypoxia • Prevalent conditions: blood loss,  production of erythrocytes,  destruction of erythrocytes Clinical Manifestations • Pallor/pale Headache, dizziness, and restlessness – from hypoxia • Fatigue, weakness Slowing of thought • Dyspnea Paresthesia • Palpitations, tachycardia • The client with anemia is likely to experience shortness of breath and complain of fatigue because of the decreased ability of the blood to carry oxygen to the tissues to meet metabolic demands. Nursing Management • Replace blood loss to sustain adequate oxygenation • Reduce activities and stimuli that cause tachycardia and increase cardiac output Nursing Interventions • Administer blood products/erythropoietin/oxygen as prescribed • Allow for rest between periods of activity • Elevate the patients head on pillows during episodes of shortness of breath • Teach the patient/family about underlying pathophysiology and how to manage the symptoms of anemia Iron-Deficiency Anemia • Most at risk: women in reproductive years, very young, poor nutrition • Inadequate dietary intake; malabsorption: absorbed in duodenum, GI surgery 90 • Vitamin B12 (cobalamin) is an important water-soluble vitamin. • Relies on intrinsic factor for absorption • Absence of intrinsic factor (IF) –  cobalamin absorption. Also a  in HCl secretion • Causes of cobalamin deficiency – Gastric mucosa not secreting IF – GI surgery loss of IF-secreting gastric mucosal cells – Long-term use of H2-histamine receptor blockers cause atrophy or loss of gastric mucosa – Nutritional deficiency – Hereditary defects of cobalamine utilization Clinical manifestations • Classic signs of pernicious anemia include weakness, mild diarrhea, and a smooth red tongue that is sore. • Sore, red,beefy,shiny tongue; anorexia; n/v; weakness; parathesias of the feet and hands; altered thought processes (confusion  dementia) • Pallor, tachycardia, and a sore tongue are all characteristic findings in pernicious anemia. Other clinical manifestations include anorexia; weight loss; a smooth, beefy red tongue; a wide pulse pressure ; palpitations; angina; weakness; fatigue; and paresthesia of the hands and feet Diagnostic Studies • RBCs appear large, abnormal shapes – cell membrane is fragile • Structure contributes to erythrocyte destruction • Schilling Test: a medical investigation used for patients with vitamin B12 deficiency. The purpose of the test is to determine if the patient has pernicious anemia Collaborative Care • Parenteral administration of Cobalamin • ↑ Dietary cobalamin does not correct the anemia – important to emphasize adequate dietary 91 intake • Intranasal form of cyanocobalamin (Nascobal) is available • High dose oral cobalamin and SL cobalamin can use be used • In pernicious anemia, the gastric mucosa doesn't secrete intrinsic factor, a protein necessary for vitamin B12 absorption. Without intrinsic factor, vitamin B12 replacements taken orally won't be absorbed; therefore, vitamin B12 92 must be administered through the I.M. or deep subcutaneous routes. Clients must take vitamin B12 each day for 2 weeks initially, then weekly for several months, then for life Nursing Management • Familial disposition: early detection and treatment can lead to reversal of symptoms • Potential for Injury r/t patient’s diminished sensations to heat and pain • Ongoing evaluation of GI and neurologic status: evaluate patient for gastric carcinoma frequently Folic Acid Deficiency • Folic acid deficiency is caused by macrocytic normochromic cells; these are large red blood cells • Folic Acid Deficiency also causes megablastic anemia (RBCs that are large and fewer in number) • Folic Acid required for RBC formation and maturation • Causes: poor dietary intake, malabsorption syndromes, drugs that inhibit absorption, alcohol abuse, hemodialysis Clinical Manifestations • Insidious onset: progress slowly • Absence of neurologic problems • Treated by folate replacement therapy • Encourage patient to eat foods with large amounts of folic acid: – Leafy green vegetables, liver, mushrooms, oatmeal, peanut butter, red beans Sickle Cell Anemia Etiology/ Epidemiology • Genetic malfunction of hemoglobin molecule • "Sickle-shaped" red blood cells (sickled cells) 95 tissues and a reduction of the circulating fluid volume • Sickle cell crisis can begin suddenly and persist for days to weeks • Treatment: – Administer oxygen to control hypoxia – Assess for changes in respiratory status – Rest periods and prophylactic anticoagulants for DVT – Fluids and electrolytes to reduce blood viscosity and maintain renal function Diagnostic Studies • RBC morphology, hemoglobin electrophoresis, peripheral blood samples, hemoglobin values, RBC count, bilirubin level Management • Avoid triggering events: infection and fever, temperature extremes, anxiety or stress, excessive exercise, hypoxia (including sleep apnea), smoking, dehydration • Administer and monitor: • Teach the patient ways to avoid crises = avoid dehydration and hypoxia (avoiding high altitudes) and seeking medical attention quickly to counteract problems such as upper respiratory tract infections. • Teach about pain control Alcohol Related Anemia • Heavy alcohol consumption can cause generalized suppression of blood cell production and the production of structurally abnormal blood cell precursors that 96 cannot mature into functional cells. • Alcoholics frequently have defective red blood cells that are destroyed prematurely, possibly resulting in anemia • In many alcoholic patients, blood loss and subsequent iron deficiency are caused by gastrointestinal bleeding • Nutritional deficiencies also contribute to developing anemia Disseminated Intravascular Coagulation DIC • Abnormally initiated and accelerated clotting • Alternates between clotting and hemorrhaging • Can be a complication of toxic shock syndrome • Syndrome that occurs from a primary disease or condition, sign of an underlying disorder • Triggers may include sepsis, trauma, shock, cancer, abrupto placenta, toxins, and allergic reactions. • Altered hemostasis mechanism causes massive clotting in microcirculation. As clotting factors are consumed, bleeding occurs. Symptoms are related to tissue ischemia and bleeding. • Treatment: treat underlying cause, correct tissue ischemia, replace fluids and electrolytes, maintain blood pressure, replace coagulation factors, use heparin • Syndrome characterized by widespread intravascular clotting and bleeding • Can be severe and life-threatening or very mild • Assess for signs and symptoms and progression of thrombi and bleeding. Diagnosis • The diagnosis of DIC is based on the results of laboratory studies of prothrombin time, 97 platelet count, thrombin time, partial thromboplastin time, and fibrinogen level as well as client history and other assessment factors Potential Complications • Renal failure, gangrene, pulmonary embolism or hemorrhage, acute respiratory distress syndrome, stroke Nursing Care • Stabilize patient with fluids and oxygen, control ongoing thrombosis and bleeding, treat underlying problem