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NR 324 Adult Health Test 3 (ch 39, 41, 42, 43, 12, 13, 14, 15, 65, 62, 63, 64, 65)

Pataasin ang iyong marka sa homework at exams ngayon gamit ang Quizwiz!

When teaching a client with acquired immunodeficiency virus (AIDS) about drug therapy, the nurse emphasizes that the drugs must be taken exactly as prescribed, without missing doses. Which of the following statements is the most important reason for adhering to the treatment regimen? A. Missed doses can promote drug resistance, lowering the effectiveness of the drugs. B. Missed doses allow for the development of opportunistic infections. C. An increased chance of allergic reaction to the drug may occur. D. Viral replication decreases when doses are missed.

A. Missed doses can promote drug resistance, lowering the effectiveness of the drugs.

The nurse is caring for a client who may have been infected with HIV. Which of the following are acute clinical manifestations of HIV infection? A. Opportunistic infections B. Fever, night sweats, and muscle aches C. Lymphocytopenia (decreased lymphocyte count) D. Reduced numbers of CD4+ T-cells

B. Fever, night sweats, and muscle aches

Subluxation

partial or incomplete displacement of the joint surface

understand, analyze, evaluate, and be able to apply etiology, clinical manifestations, diagnostic tests, nursing management/collaborative, interventions, treatments, medications, complications, patient education for the following disorders: Appendicitis (from the study guide)

DEF: Inflammation of the appendix Appendix is located in the right lower abdominal quadrant attached to the cecum Pathophysiology Most common cause is obstruction Obstruction causes distention, venous engorgement and accumulation of mucous and bacteria which leads to gangrene and perforation Clinical Manifestations: Symptoms are sometimes vague McBurney's point http://www.youtube.com/watch?v=06MzHSFf0DM http://www.youtube.com/watch?v=FOQTkz57u2I Rovsing's sign - referred pain left → right Periumbilical pain Rebound tenderness Guarding Patient lies still with right leg flexed Low-grade fever Anorexia, nausea and vomiting The pain can begin in the periumbilical region. The pain is persistent and continuous eventually shifting to the right lower quadrant and localizing at Mc Burney's point which is halfway between the right umbilicus and the right iliac crest. Rovsing's sign is pain in the right lower quadrant when the left lower quadrant is palpated. Complications: Perforation Rupture Peritonitis Abscesses Diagnosis: Elevated WBC count Ultrasound CT scan Neutro Spec imaging - tag neutrophils Neutro-spec imaging is a new technique that uses technetium-labeled anti-CD-15 monoclonal antibodies. When injected into the blood the technetium binds with neutrophils. This can be seen with a gamma camera. Medical Management: Appendectomy Post op care? Antibiotics If the appendix ruptures, antibiotics are given 6-8 hours prior to removal of the appendix in order to prevent sepsis and dehydration. Nursing Management: Encourage patients with abdominal pain to see a provider Do not self treat Avoid laxatives NPO Ice pack to right lower quadrant Post-op care

Effects of Aging on the Immune System

Decline in immune system ↑ Incidences of tumors Greater susceptibility to infections Thymic involution ↓ Cell-mediated immunity ↓ Delayed hypersensitivity reaction ↓ IL-1 and IL-2 synthesis Decline in immune system ↓ Proliferation response of T and B cells ↓ Primary and secondary antibody responses

Gerontological Considerations Musculoskeletal

Decreased number and diameter of muscle cells Loss of elasticity in ligaments and cartilage Increased risk for cartilage erosion Loss of fluid from disks between vertebrae Narrowing of intervertebral spaces Decrease in bone density

What 3 functions does immunity serve?

Defense - protects from invasion Homeostasis - damaged cells are removed Surveillance - foreign cells are destroyed

Deglutition

Deglutition (swallowing) is the mechanical component of ingestion

Diagnostic Studies Collaborative Management Drug therapy Nursing Management Chronicity of condition, nutritional therapy, education, support of joints, periodic lab draws, and avoidance of precipitating factors

B lymphocytes

Differentiate into plasma cells when activated Plasma cells produce antibodies (immunoglobulins)

Dilated tortuous veins in lower portion of esophagus Result of portal hypertension Common complication of liver cirrhosis Can cause death

Disruption or break in continuity of the structure of bone Majority from traumatic injuries Some secondary to disease process Cancer or osteoporosis Fractures are described and classified according to Type Communication or noncommunication with external environment Anatomic location of fracture on involved bone Fractures can also be classified as Closed (simple) Open Compound fracture Communication of fracture through skin with external environment Clinical Manifestations: Mechanism of injury associated with numerous signs and symptoms Immediate localized pain Decreased function Inability to bear weight on or use affected part Patient guards and protects extremity Nursing Assessment/Management: Initial treatment Treat life threatening injuries first Check neurovascular status distal to injury before and after splinting Elevate injured limb if possible Do not attempt to straighten fractured or dislocated joint Do not manipulate protruding bone ends Apply ice packs to affected area Obtain x-rays of affected area Administer tetanus diptheria prophylaxis Mark location of pulses to facilitate repeat assessment Splint fracture site Ongoing monitoring Vital signs, level of consciousness, oxygen saturation, neurovascular status, and pain Compartment syndrome Characterized by excessive pain, pallor, paresthesia, paralysis, and pulselessness Monitor for fat embolism Complications of Fractures Indirect complications Blood vessels and nerve damage Compartment syndrome Deep vein thrombosis Fat embolism Traumatic or hypovolemic shock Elevated intracompartmental pressure within a confined myofascial compartment compromises neurovascular function of tissues within that space Early recognition & treatment crucial p. 1650

Billroth II (Gastrojejunostomy)

Distal 2/3 of the stomach is removed and attached to the jejunum The duodenum remains oversewn

Diverticulum- outpouching of the mucosa of the intestinal wall Asymptomatic diverticulosis- the outpouching is there but symptoms are not present Diverticulitis- inflammation of the diverticulum from stool and food becoming trapped in the outpouchings Risk Factors: Age Occurs in 5% of people over 40 Occurs in 50% of people over 80 Associated with diets low in fiber Obesity Clinical Manifestations: Changes in bowel habits Abdominal pain Fever Leukocytosis Perforation and Peritonitis Abscess formation Bowel obstruction Bleeding- most common cause of lower GI hemorrhage Diagnosis: CBC Physical Exam Lower GI Colonoscopy Patients with acute diverticulitis should not have a barium scan or a colonoscopy because of the possibility of perforation or perotinitis Medical Management: Antibiotics NPO status NGT suction IV fluids Colon resection Nursing Management: High fiber diet Decreased intake of fat and red meat Weight reduction Stool softeners Bulk laxatives Avoid seeds and nuts - controversial; still recommended The whole goal of diverticulitis is to prevent inflammation of the diverticulum. Avoid things that can block the diverticulum.

Osteocytes

MATURE BONE

Bone

framework to body that facilitates weight bearing..., serve as protection; points of attachment for muscles - connected to bones and tendons; levers for movement; storage for calcium and phosphorus

Dislocation

severe injury to the ligamentous structures that surround a joint

Types of Hypersensitivity Reactions: Type II: IgG-Mediated Cytotoxic Hypersensitivity

Ab directed against cell surface antigens mediates cell destruction via complement activation or ADCC Typical manifestations include blood transfusion reactions, erythroblastosis fetalis, and autoimmunt hemolytic anemia

Types of Hypersensitivity Reactions: Type I: IgE-Mediated Hypersensitivity

Ag induces crosslinking of IgE bound to mast cells and basophils with release of vasoactive mediators Typical manifestations include systemic anaphylaxis such as hay fever, asthma, hives, food allergies, and eczema

Types of Hypersensitivity Reactions: Type III: Immune Complex-Mediated Hypersensititivy

Ag-Ab complexes deposited in various tissues induce complement activation and an ensuing inflammatory response mediated by massive infiltration of neutrophils Typical manifestations include localized Arthus reaction and generalized reactions such as serum sickness, necrotozing vasculitis, glomerulnephritis, rheumatoid arthritis, and systemic lupus erythematosus

Pyloroplasty

An incision is made in the pyloric sphincter to enlarge the outlet and relax the muscle Usually accompanies vagotomy

Allergic Disorders: Drug therapy

Antihistamines Sympathomimetic/decongestant drugs Corticosteroids Antipruritic drugs Mast cell-stabilizing drugs Leukotriene receptor antagonists

Bariatric surgery criteria

BMI greater than 40 or BMI greater than 35 with one or more severe obesity-related complication Understands risks and benefits of surgery Has been obese for greater than 5 years Tried other methods of weight loss No endocrine disorders Psychiatric and social stability Vertical banded gastroplasty partitions a pouch in the lesser curvature of the stomach. It delays gastric emptying and reduces stomach capacity. Gastric banding. The stomach size is reduced with an inflatable band placed around the fundus of the stomach. Also called lap band procedure. Biliopancreatic Diversion involves removing ¾ of the stomach. The remaining portion of the stomach is connected to the small intestine. Pancreatic and bile enter the final segment of the small intestine. Nutrients pass without being digested. Roux-en Y is the most commonly used because it is well tolerated and sustains long term weight loss. The stomach size is decreased and enters directly into the jejunum. Complications: Malabsorption Dumping Syndrome Anemia Bleeding Suture rupture Discharge: Weight loss is considerable for first 6-12 months High protein low carb, low fat diet Fluids should not be ingested with meals 6 small feedings Stress follow-up care Psychosocial support

Osteoclasts

BONE DESTROYERS - REMODELING; help to remove old bone; helps to maintain mineral composition

Osteoblasts

BONE forming cells

Bile Reflux Gastritis

Bile Reflux Gastritis occurs in surgeries in which the pyloric sphincter is removed. Alkaline bile salts is irritating to the gastric mucosa. Questran which is cholestyramine binds with bile salts preventing irritation. Pernicious anemia occurs as a result of the loss or parietal cells that produces intrinsic factor. Intrinsic factor is responsible for the absorption of Vitamin B12.

Fracture Healing

Bone goes through a remarkable reparative process of self-healing Fracture hematoma Granulation tissue Callus formation Ossification Consolidation Remodeling

GI bleed

Clinical Manifestations: Hematemesis Melena Nausea/Vomiting Dizziness Syncope Tachycardia Hypotension Medical Management: IV fluids Blood products Endoscopy Surgery Endoscopy is the primary tool for visualization and diagnosis of upper GI bleed Important to administer IV fluids as first line therapy to correct/prevent hypovolemic shock, however, make sure to monitor closely for signs of fluid overload such as crackles in lungs! Nursing Management: Insert NGT to distinguish fresh blood from coffee ground ----rationale? Vital signs Insert IV line ? Insert an indwelling urinary catheter ? Monitor hemoglobin and hematocrit NG lavage Others/ Important to assess vital signs first and frequently to monitor for hypovolemia

Minerals: Calcium

Calcium - adds rigidity and strength

Caused by compression of median nerve Hobbies or occupations that require continuous wrist movement Numbness and tingling Phalen's test Tinel's test Splint, Cortisone injection,surgery

T lymphocytes

Cells that migrate from bone marrow to thymus differentiate into T lymphocytes Compose 70% to 80% of circulating lymphocytes Responsible for immunity to intracellular viruses, tumor cells, and fungi T cytotoxic cells or CD8 cells- attack antigens on the cell membrane of foreign cells T helper cells or CD4 cells- release cytokines that stimulate the production of B cells and T Cells

Chronic multisystem inflammatory disease Associated with abnormalities of immune system Results from interactions among genetic, hormonal, environmental, and immunologic factors Autoimmune reactions directed against constituents of cell nucleus, DNA Affects the Skin Joints Serous membranes Renal system Hematologic system Neurologic system Ranges from a relatively mild disorder to rapidly progressing, affecting many body systems Most commonly affects the skin/muscles, lining of lungs, heart, nervous tissue, and kidneys Clinical Manifestations: Cardiopulmonary: Tachypnea Pleurisy Dysrhythmias Accelerated CAD Pericarditis Dermatologic: Cutaneous vascular lesions Butterfly rash Oral/nasopharyngeal ulcers Alopecia Hematologic: Antibody formation against blood cells Anemia Leukopenia Trombocytopenia Coagulopathy Anti-phospholipid antibody syndrome Musculoskeletal: Polyarthralgia with morning stiffness Arthritis Swan neck fingers Ulnar deviation Subluxation with hyperlaxity of joints Nervous system: Generalized/focal seizures Peripheral neuropathy Cognitive dysfunction Disorientation Memory deficits Psychiatric symptoms Renal: Lupus nephritis Ranging from mild proteinuria to glomerulonephritis Primary goal in treatment is slowing the progression Diagnostic Studies: No specific test ANA SLE is diagnosed primarily on criteria relating to patient history, physical examination, and laboratory findings Drug therapy and Nursing Implications: NSAIDs Antimalarial drugs Steroid-sparing drugs Corticosteroids Immunosuppressive drugs

Chronic, systemic autoimmune disease Inflammation of connective tissue in diarthrodial (synovial) joints Periods of remission and exacerbation Frequently accompanied by extra-articular manifestations Occurs globally, affecting all ethnic groups Etiology and Pathophysiology: Pathogenesis of RA is more clearly understood than its etiology If unarrested, RA progresses in four stages Stage 1: Early No destructive changes on x-ray, possible x-ray evidence of osteoporosis Stage 2: Moderate X-ray evidence of osteoporosis, with or without slight bone or cartilage destruction No joint deformities, adjacent muscle atrophy, possibly presence of extra-articular soft tissue lesions Stage 3: Severe X-ray evidence of cartilage and bone destruction in addition to osteoporosis; joint deformity; extensive muscle atrophy; possible presence of extra-articular soft tissue lesions Stage 4: Terminal Fibrous or bony ankylosis, stage III criteria Clinical Manifestations: Joints Specific articular involvement Pain, stiffness, limitation of motion, and signs of inflammation Symptoms occur symmetrically Frequently affect small joints of hands and feet Larger peripheral joints may also be involved Tenosynovitis Produces manifestations of carpal tunnel syndrome Makes grasping objects difficult As RA progresses, inflammation and fibrosis of joint capsule and supporting structures may lead to deformity and disability Extraarticular Manifestations: Three most common Rheumatoid nodules Sjögren's syndrome Felty syndrome Rheumatoid nodules develop in up to 25% of all patients with RA Those affected usually have high titers of rheumatoid factor (RF) Rheumatoid nodules Appear subcutaneously as firm, nontender, granuloma-type masses Usually located over extensor surfaces of joints Nodules at base of spine or back of head are common in older adults Develop insidiously and can persist or regress spontaneously Sjögren's syndrome Seen in 10% to 15% of patients with RA Occurs as a disease itself or in conjunction with an arthritic disorder (RA & SLE) Patients have diminished lacrimal and salivary gland secretion Complaints of burning, gritty, itchy eyes ↓ Tearing and photosensitivity Felty's syndrome Most commonly in patients with severe, nodule-forming RA Characterized by Inflammatory eye disorder Splenomegaly Lymphadenopathy Pulmonary disease Blood dyscrasias This syndrome is a potentially serious condition that is associated with seropositive (rheumatoid factor [RF]-positive) rheumatoid arthritis (RA).[1] Felty syndrome is characterized by the triad of RA, splenomegaly, and granulocytopenia. Although many patients with Felty syndrome are asymptomatic, some develop serious and life-threatening infections secondary to granulocytopenia (http://emedicine.medscape.com/article/329734-overview). Complications: Joint destruction begins as early as first year of disease without treatment Flexion contractures and hand deformities Cardiopulmonary effects may occur later in RA Pleurisy, pleural effusion, pericarditis, pericardial effusion, cardiomyopathy Carpal tunnel syndrome can result from swelling of synovial membrane Diagnostic Studies: Positive rheumatoid factor (RF) occurs in ~80% of patients Titers rise during active disease Antinuclear antibody (ANA) titers Indicators of active inflammation ESR C-reactive protein (CRP) Synovial fluid analysis in early disease shows a straw-colored fluid with many fibrin flecks White blood cell (WBC) count of synovial fluid is elevated (↑ to 25,000/μl) Inflammatory changes in synovium can be confirmed by tissue biopsy Diagnostic Criteria for RA (T65-7) RA is defined as having at least a score or 6 or more of the following criteria A. Joint Involvement B. Serology C. Acute Phase Reactants D. Duration of Symptoms Drug Therapy Drugs remain cornerstone of treatment Disease-modifying antirheumatic drugs (DMARDs) can lessen permanent effects of RA Choice of drug is based on Disease activity Patient's level of function Lifestyle considerations Corticosteroid therapy can aid in symptom control Intraarticular injections may relieve pain and inflammation associated with flare-ups Long-term use should not be a mainstay Risk osteoporosis, avascular necrosis Low-dose prednisone for a limited time to decrease disease activity until DMARD effect is seen

Clostridium Difficile: Gram positive spore forming rod Occurs after use of broad spectrum antibiotic use Antibiotics kills the normal intestinal flora C. diff invades the intestine causing inflammation Responsible for 15-20% of antibiotic-related causes of diarrhea Primary cause of pseudomembranous colitis Responsible for 1.1 billion in health care costs each year Can be fatal Clinical Manifestations: Watery foul smelling diarrhea Abdominal pain and cramping Fever Hypotension Bloody stools Risk Factors: ICU Admission Advanced age Antibiotic therapy Immunosuppressive therapy Multiple and underlying diseases NGT placement Prolonged hospital stay Nursing home resident Sharing a room with a someone with C. diff Use of antacids Diagnosis: History and physical Stool for C-diff toxin Treatment: Discontinue antibiotic Fluid and electrolyte replacement Metronidazole (Flagyl) 500 mg- oral is preferred route (10-14 days) Vancomycin 125-500 mg 10-14 days Nursing Management: Maintain adequate hydration Vital signs Monitor bowel movements GI assessment Disinfect all surfaces Hand washing Contact precautions Highly contagious so contact precautions and isolation in private room Prevention: Antibiotic selection Probiotics- Lactobacillus Hand washing Disinfecting all surfaces

Complications of Fractures... Compartment Syndrome levated intracompartmental pressure within a confined myofascial compartment compromises neurovascular function of tissues within that space Early recognition & treatment crucial p. 1650 Clinical Manifestations: Ischemia can occur within 4 to 12 hours after onset May occur initially or may be delayed for several days Large amounts of myoglobinemia may result in acute tubular necrosis Common signs of myoglobinuria Dark reddish brown urine Clinical manifestations associated with acute renal failure Collaborative Care: Early recognition & treatment essential Extremity should NOT be elevated above heart level Application of cold compresses may result in vasoconstriction and exacerbate compartment syndrome May be necessary to remove or loosen bandage or bivalve cast Reduction in traction weight may ↓ external circumferential pressures Surgical decompression may be necessary

Surgical Complications

Dumping Syndrome -Fluid shift from intravascular space to intestinal lumen Postprandial Hypoglycemia - ↑ insulin secretion 2° carbohydrate load Bile Reflux Gastritis - irritation from bile Pernicious Anemia (why?) Rupture of sutures Leakage of gastric contents Hemorrhage Abscess formation/Infection Dumping syndrome is the direct result of removing of a large portion of the stomach and the pyloric sphincter. Dumping syndrome is associated with having foods with high osmolarity. Normally after meals a small amount of gastric chyme enters the small intestine and shifts from the extracellular space is minimal. After surgery, there is no control of the amount of gastric chyme that enters the small intestine. Therefore a large amount of hypertonic fluid enters the small intestine and draws fluid into the bowel lumen. Lying down for 30 minutes after eating will reduce the symptoms Postprandial hypoglycemia is considered a variant of dumping syndrome because is the result of uncontrolled gastric emptying of a bolus of fluid high in carbohydrate in the small intestine. The bolus is high in concentrated carbohydrates causing hyperglycemia and the release of large amounts of insulin. As a result a secondary hypoglycemia occurs 2 hours after the meal. The symptoms are the same as the usual hypoglycemia: sweating, weakness, mental confusion, palpitations, tachycardia and anxiety. Bile Reflux Gastritis occurs in surgeries in which the pyloric sphincter is removed. Alkaline bile salts is irritating to the gastric mucosa. Questran which is cholestyramine binds with bile salts preventing irritation. Pernicious anemia occurs as a result of the loss or parietal cells that produces intrinsic factor. Intrinsic factor is responsible for the absorption of Vitamin B12. *****Post-op hemorrhage requires MD notification****************** Prevention of Surgical Complications: Slow passage of food into the small intestine to control symptoms of dumping syndrome Small frequent meals Fluids to be taken 30 minutes after meals Concentrated sweets are avoided Increase protein and fats Postoperative Care DVT prophylaxis Atelectasis/pneumonia prevention Vital signs Pain management Antibiotics NGT care GI assessment Nutrition modifications

Dumping syndrome

Dumping syndrome is the direct result of removing of a large portion of the stomach and the pyloric sphincter. Dumping syndrome is associated with having foods with high osmolarity. Normally after meals a small amount of gastric chyme enters the small intestine and shifts from the extracellular space is minimal. After surgery, there is no control of the amount of gastric chyme that enters the small intestine. Therefore a large amount of hypertonic fluid enters the small intestine and draws fluid into the bowel lumen. Lying down for 30 minutes after eating will reduce the symptoms

Peptic Ulcer Disease (PUD)

Erosion of the gastric mucosa Occurs with any portion of the GI tract coming into contact with gastric secretions Lower esophagus Stomach Duodenum Gastrojejunal anastamosis (after surgical procedures) Pathophysiology: There is a breakdown of the gastric mucosal area Acids can diffuse through the mucosal layer Destruction of mucosal cells Increase pepsin release Inflammatory Process Release histamine Increased vascular permeability Increased vasodilation Erosion and destruction of blood vessels Risk Factors: H. pylori- (60-80%) NSAIDS Nicotine Genetics Clinical Manifestations: Sometimes asymptomatic Burning pain May become symptomatic after blood loss Diagnosis: Endoscopy Serum tests for IgG - sensitive for H Pylori Urea Breath Test -indicates infection Barium Studies CBC - anemia Stool Guiac Endoscopy allows for direct viewing of the ulcer. During endoscopy tissue samples can be taken to rule out the discovery of H. pylori. Complications: Hemorrhage Perforation Gastric outlet obstruction Hypertrophy of stomach & delayed emptying Treatment: Rest stomach Insert NG Replace fluids Hemorrhage is the most common complication. Occurs from erosion of the granulation tissue during the healing process or from erosion through a major blood vessel. Perforation can occur if the ulcer penetrates the surface. Risk for hypovolemic shock, so monitor VS closely Gastric outlet syndrome occurs when the there is edema, inflammation and scaring around the ulcer that causes narrowing in the pylorus. In the beginning the gastric emptying maybe normal or slowed but towards the end, the gastric force needed to empty the stomach results in hypertrophy of the stomach wall. The stomach becomes dilated and atonic. Medical Management: Lifestyle Modifications Nutritional Modifications IV Therapy Blood products Medications Antibiotics-10-14 days Proton Pump Inhibitors & H2 Receptor Blockers Prokinetic Drug Therapy Cholinergic Medications Antacids Surgical Therapy Perforation Gastric Outlet Obstruction Pyroplasty Vagotomy Ulcer Removal/reduction Billroth I Billroth II Vagotomy Pyloroplasty Lifestyle modifications include smoking cessation and rest. Nutritional modifications bland diet, six small meals a day. IV therapy and blood products if bleeding is a concern. The recommended medical therapy includes what is called triple therapy with two antibiotics and a proton pump inhibitor. ***carafate needs acidic environment so do not give with antacid or after meals Nursing Diagnosis: Acute pain Nausea Risk for vomiting Imbalanced nutrition: less than body requirements Ineffective self-health management Others?

Etiology and Pathophysiology: Risk factors Smoking Excessive alcohol intake Barrett's esophagus - (pre-cancerous lesions Diets low in fruits and vegetables Majority of tumors located in middle and lower portion of esophagus Malignant tumor Usually appears as ulcerated lesion May penetrate muscular layer and outside wall of esophagus Obstruction in later stages Clinical Manifestations: Symptom onset is late - related to what the tumor presses upon Progressive dysphagia is most common Initially with meat, then soft foods and liquids Pain develops late Substernal, epigastric, or back areas Increases with swallowing May radiate Weight loss Regurgitation of blood-flecked esophageal contents Sore throat Choking Hoarseness Complications: Hemorrhage (can be fatal) If erodes into aorta Esophageal perforation with fistula formation Peritonitis Esophageal obstruction Metastasis Liver and lung common Collaborative Care: Treatment depends on location and spread Poor prognosis Usually not diagnosed until advanced ↓20% survival after 5 yrs. Best results with combination therapy Surgical procedures Esophagectomy Removal of part or all of the esophagus Use of Dacron graft to replace resected part Esophagogastrostomy "Esophageal pull up" Resection of a portion of esophagus and anastomosis of remaining portion to stomach Concurrent radiation and chemotherapy Slows progression Sometimes started before surgery Nursing Diagnosis: Imbalanced nutrition: less than body requirements Pain Others?

Musculoskeletal system: Fibers

Fibers White muscle - fast fibers; anaerobic metabolism Red muscle - slow fibers; aerobic metabolism

PUD: Gastric vs. Duodenal Ulcers

GASTRIC Ulcers: gastric secretion: normal to decreased Greater in women Peak age 50-60 yr Smoking, drug use, alcohol, NSAIDS Increased with incompetent sphincter Burning or gaseous pressure Pain 1-2 hours after meals Occasional N/V Weight loss DUODENAL Ulcers: gastric secretion: increased Greater in men Peak age 35-45 yr Smoking, drug use, alcohol, NSAIDS Associated with other diseases Burning cramping, pressure like pain, midepigastric and upper abdomen, back pain Pain 2-4 hours after meals Relieved with food or anatacids

Gastric outlet syndrome

Gastric outlet syndrome occurs when the there is edema, inflammation and scaring around the ulcer that causes narrowing in the pylorus. In the beginning the gastric emptying maybe normal or slowed but towards the end, the gastric force needed to empty the stomach results in hypertrophy of the stomach wall. The stomach becomes dilated and atonic.

Herniation of portion of the stomach into esophagus through an opening or hiatus in diaphragm Also referred to as diaphragmatic hernia and esophageal hernia Etiology and Pathophysiology: Cause is unknown Many factors involved Structural changes Weakening of muscles in diaphragm Increased intra-abdominal pressure Obesity Pregnancy Heavy lifting Clinical Manifestations: May be asymptomatic Symptoms include Heartburn After meal or lying supine Dysphagia Complications: GERD Esophagitis Hemorrhage from erosion Stenosis Ulcerations of herniated portion Strangulation of hernia Regurgitation with tracheal aspiration Diagnostic Studies: Barium swallow May show protrusion of gastric mucosa through esophageal hiatus Endoscopy Visualize lower esophagus Information on degree of inflammation or other problems Conservative Therapy: Lifestyle modifications Eliminate alcohol Elevate HOB Stop smoking Avoiding lifting/straining Weight reduction, if appropriate Surgical Therapy: Reduction of herniated stomach into abdomen Gastropexy - anchor stomach below diaphragm Herniotomy Excision of hernia sac Herniorrhaphy Closure of hiatal defect

Hypersensitivity reactions Type I: IgE-mediated reactions Anaphylaxis Atopic reactions Type II: Cytotoxic and Cytolytic Reactions Type III: Immune-complex reactions - Systemic Lupus Erythematosus (SLE), Rheumatoid arthritis (RA), and Glomerulonephritis IgE antibodies are produced after exposure and bind to mast cells and basophils. After second exposure, the allergens will link to mast cells and basophils coated with IgE causing a release of cytokines like histamine, serotonin, leukotrienes, bradykinin.

Antibodies

Immunoglobulins produced by lymphocytes in response to antigens

Infections: Stomatitis Candidiasis Tumors: Three Types Pre-Malignant-leukoplakia Malignant-squamous cell, basal cell Benign

Gastritis

Inflammation of the gastric mucosa Etiologies: Drugs Diet - alcohol & spicy foods Microorganisms - H Pylori, CMV, Syphilis Physiologic stress NG suction Clinical Manifestations: ACUTE: Rapid onset of pain N/V Hematemesis Gastric Hemmorhage Dyspepsia Anorexia CHRONIC: Vague c/o pain Pain relieved w/ eating Anorexia N/V Intolerance to spicy/fatty foods Pernicious Anemia - loss of factor X Collaborative Management: ACUTE: NPO IV fluids NG tube Remove cause Drugs: Antiemetics Antacids H2R Blockers PPIs CHRONIC: Eliminate cause Dietary education Smoking cessation Drugs: Antibiotics Vitamin B12 replacement Antacids H2R Blockers PPIs

Immunodeficiency Disorders

Involve one or two immune mechanisms Primary immunodeficiency disorders - cells are not adequately formed Secondary immunodeficiency disorders - immune system is activated as a result of illness or injury. Graft vs. Host Disease - an immunocompromised person is transplanted with immunocopetent cells. Targets the skin GI tract and the liver. Usually seen with bone marrow transplants.

What are the signs and symptoms of an anaphylactic reaction?

Laryngeal edema Hives Bronchoconstriction Wheezing Difficulty breathing

Most common form of joint disease in North America Slowly progressive noninflammatory disorder of the diarthrodial joints 20 million Americans affected Expected to greatly increase as population ages Etiology and Pathophysiology: OA occurs as Idiopathic disorder Secondary disorder Trauma, mechanical stress, inflammation, joint instability, neurologic disorder, skeletal deformities, hematologic/endocrine disorders, use of selected drugs OA results from cartilage damage that triggers a metabolic response at level of chondrocytes Cartilage becomes Dull, yellow, and granular Soft and less elastic Less able to resist wear with heavy use Clinical Manifestations: Joint pain Predominant symptom ranging from mild discomfort to significant disability Pain worsens with joint use Early stages: Rest relieves pain Later stages: Pain with rest and sleep is disturbed because of pain and increased joint discomfort Becomes worse as barometric pressure ↓ Increased pain can contribute significantly to disability and loss of function Pain may be referred to groin, buttock, or medial side of thigh or knee Sitting down becomes difficult, as does getting up from a chair when hips are lower than knees Diagnostic Studies: In early OA tests Detect joint changes Bone scan, computed tomography (CT) scan, magnetic resonance imaging (MRI) In progressed OA Detect joint space narrowing, bony sclerosis, osteophyte formation X-rays Collaborative Care: Focuses on Managing pain and inflammation Preventing disability Maintaining and improving joint function Foundation for OA management is nonpharmacologic interventions Drug therapy serves as an adjunct Drug Therapy: Based on severity of patient's symptoms Mild to moderate joint pain Acetaminophen (1000 mg every 6 hours) Topical agent (e.g., capsaicin cream [Zostrix]) Topical salicylates (e.g., Aspercreme) Hyaluronic acid (HA) Based on severity of patient's symptoms (cont'd) Moderate to severe joint pain Nonsteroidal antiinflammatory drug (NSAID) Antibiotics Arthroscopic surgery Debridement is usually not recommended Effective in reducing pain and improving function when it is used to Repair ligament tears Remove bone bits or cartilage

Most common manifestations of GI disease May occur in unrelated conditions Identify and treat underlying cause Complications include fluid and electrolyte imbalance

Occurs when blockage prevents flow of contents through the intestine Types Small Large Mechanical: Adhesions Herniation Strictures Intussusception Tumors/Cancer Non mechanical (functional): Neuromuscular or vascular disorder Functional causes a decrease and slowing of peristalsis in the bowel. It can be caused by medications namely opiods. It can also be caused by muscular dystrophy, diabetes, amyloidosis, parkingson's disease. They can also be caused from lack of nerve innervation, namely from spinal cord injuries and electrolyte imbalances that slow nerve conduction. Clinical Manifestations: Small Bowel Crampy abdominal pain Constipation/Distention Vomiting Fecal-smelling breath Dehydration Hyperactive bowel sounds above the blockage, absent or hypoactive below the blockage Large Bowel Can occur over months Constipation Weakness Weight loss Anorexia Bloody stool Pain Distention Rebound tenderness Diagnosis: Physical Assessment Serum Electrolytes Stool FOBT X-ray of abdomen Barium test CT MRI Medical Management: NGT NPO IV fluids Electrolyte replacement Antibiotics Pain management Surgical Management

Pathophysiology of HIV RNA virus (retrovirus) discovered in 1983 Binds to specific CD4 and chemokine receptors to enter cell HIV likes certain receptors. A particular receptor is the gp 120 receptor. This happens to be the receptor on the CD4 cells which are the helper T cells. Helper T cells release cytokines that stimulate the production of B cells and T Cells that will fight infection. Once in the cell, reverse transcriptase assists to make viral DNA Viral DNA enters cell nucleus and splices itself into genome permanently HIV produces reverse transcriptase which helps the viral RNA to be transcribed into viral DNA. It enters the nucleus and uses the enzyme integrase to splice itself into the DNA of the cell. Now all genetic material will be replicated during cell division and viral DNA will tell the cells to replicate the virus. Viral RNA is made using the enzyme protease Immune dysfunction results mostly from destruction of CD+ 4 T cells Key cells for immune recognition and defense against pathogens These cells recognize pathogens and defends against them. Normal T cell life span is 100 days, whereas infected cells live only 2 days Viral activity destroys 1 billion T cells daily Immune problems start when CD4+ T cell counts drop below 500 cells/μl Normal range is 800 to 1200 cells/μl Initial infection Viremia (large viral levels in blood) for 2 to 3 weeks Transmission is more likely when viral load is high Followed by prolonged period (years) of low viral load If low viral load and CD4 cell counts within normal range, then early stage of chronic infection Acute infection Flulike symptoms Fever, swollen lymph glands, sore throat, headache, malaise, nausea, muscle and joint pain, diarrhea, or a diffuse rash Occurs about 1 to 3 weeks after infection Most people think that they have a bad case of the flu and symptoms are often dismissed as such. Early chronic infection Generally asymptomatic Fatigue, headache, low-grade fever and night sweats often occur Most are not aware of infected status CD4 cells are still above 500. Intermediate chronic symptoms Thrush Oral hairy leukoplakia Drenching night sweats Severe fatigue Localized infections Late chronic or AIDS Immune system severely compromised Great risk for opportunistic disease Possible wasting and dementia Common opportunistic diseases Pneumocystis jiroveci pneumonia Cryptococcal meningitis Cytomegalovirus retinitis Development of pneumocystis pneumonia is a diagnostic criteria for AIDS Pneumocyctitis jiroveci- symptoms much like pneumonia and is treated with antibiotics Cryptococcal meningitis- cognitive impairment, motor dysfunction seizures, nuccal rigidity- treated with antibiotics. CMV- antiviral are given. Common opportunistic diseases Mycobacterium avium complex Kaposi sarcoma Influenza virus MAC- GI symptoms- antibiotics given Kaposi sarcoma- vascular lesions on the skin- chemo and radiation. Influenza- need vaccinations for prevention Acquired Immunodeficiency Syndrome (AIDS): Diagnostic CDC criteria CD4+ T cell count below 200 cells/μl Specific opportunistic infection or cancer Wasting syndrome - loss of 10% or more of ideal body mass. AIDS dementia complex (ADC) Assessment Ask at-risk patients Received blood transfusion or clotting factors before 1985? Shared needles, syringes, or other injection equipment with another person? Had a sexual experience with your penis, vagina, rectum, or mouth or in contact with these areas of another person? Had a sexually transmitted disease (STD)? Diagnosit Studies: Most useful screening tests detect HIV-specific antibodies May take 2 months (window period) to detect antibodies Rapid testing strongly recommended by CDC After an initial positive EIA test, the EIA is repeated Western blot is more specific test, done if repeat EIA is positive After an initial positive EIA test, the EIA is repeated. If negative risk factors are assessed and repeat testing is recommended if said risk factors are found Western blot is more specific test, done if repeat EIA is positive EIA= enzyme immunoassays. Progression monitored by CD4+ T cell counts and viral load Abnormal blood tests common Neutropenia, thrombocytopenia, and anemia Collaborative Care Focus: Monitoring HIV disease progression and immune function Initiating and monitoring antiretroviral therapy (ART) Drug Therapy: Main goals Decrease viral load Maintain/raise CD4+ counts Delay HIV-related symptoms and opportunistic infections Drug therapy for HIV positive patients is individualized and based on CD4 counts viral load and patient's wishes Also need to take into consideration patient compliance Drug Therapy/Antiretroviral (ATR) ART drugs work in various ways to decrease viral replication Nucleoside, non-nucleoside, and nucleotide reverse transcriptase inhibitors Inhibit the ability of HIV to make a DNA copy early in replication ART is appropriate for patients exhibiting AIDS defining illness. If the DNA copies can not be made then the virus can not replicate. Drug Therapy: Protease inhibitors Interfere with activity of enzyme protease Remember protease allows for replication of the virus Fusion inhibitors Interfere with HIV CD4 receptor site binding and entry into cells Prevents HIV entry into the CD4 cell so that it does not get infected Combination antiretroviral therapy Three or more drugs from different groups are prescribed at full strength Major advantage of combination antiretroviral therapy Attacks viral replication in several ways Drug resistance is reduced ART effectiveness is evaluated by viral load testing Health Promotion: Major goal: Prevention Four CDC strategies Use testing as routine health care Use rapid testing Work to modify risky behaviors Offer tests universally to pregnant women Testing is only sure method to determine infection Negative results: Opportunity for prevention education Positive results: Treatment and education to protect sexual and drug-using partners Terminal Care Focus of nursing intervention Patient comfort Promoting acceptance of finite nature of life Help significant others deal with loss Maintain safe environment

Phases of the tissues response to injury: Vascular response - blood flow changes, chemical mediators, and clotting Cellular response - white blood cell responses and chemical mediators Exudate formation - types of inflammatory exudate (p. 175, Table 12-2) Healing - regeneration and repair

Minerals: Phosphate

Phosphate - regulate Vitamin D; mineralization

Postprandial hypoglycemia

Postprandial hypoglycemia is considered a variant of dumping syndrome because is the result of uncontrolled gastric emptying of a bolus of fluid high in carbohydrate in the small intestine. The bolus is high in concentrated carbohydrates causing hyperglycemia and the release of large amounts of insulin. As a result a secondary hypoglycemia occurs 2 hours after the meal. The symptoms are the same as the usual hypoglycemia: sweating, weakness, mental confusion, palpitations, tachycardia and anxiety.

Cells of Immune Response: Lymphocytes

Produced in the bone marrow Eventually migrate to peripheral organs Differentiate into B and T lymphocytes

Lymphoid Organs: Central (primary) lymphoid organs: Bone marrow

Produces red blood cells, white blood cells, and platelets

Gastroesophageal Reflux Disease (GERD)

Reflux of gastric contents into the lower esophagus Most common upper GI complaint in adults Pathophysiology: The lower parts of the esophagus come into contact with gastric contents The acidic gastric contents are corrosive to the esophageal mucosa Predisposing factors Hiatal hernia Incompetent Lower Esophageal Sphincter Impaired esophageal clearance Decreased gastric emptying The lower esophageal sphincter is the main sphincter to prevent gastric reflux. The degree of inflammation depends on the amount and constitution of gastric contents. One of the primary factors of GERD is an incompetent LES. Decreased pressure in the distal portion of the esophagus. The increased gastric pressure compared to the lower esophageal pressure. Fluids travel from an area of greater pressure to an area of lower pressure resulting in reflux. Risk Factors: Foods Medications Alcohol Obesity Pregnancy Smoking Hiatal Hernia Foods include fatty foods, chocolate, caffeine, peppermint. Medications include anticholinergics because they delay gastric emptying, beta blockers, calcium channel blockers, nitrates, morphine, progesterone, theophylline and valium. Clinical Manifestations: Pyrosis (Heartburn) Dyspepsia/ indigestion Chest Pain Sore throat Globulus sensation (lump in the throat) Regurgitation Respiratory Complications Respiratory complications occur due to aspiration of regurgitated stomach contents when supine. Especially important to note in an unconscious patient to prevent aspiration Complications: Esophagitis Esophageal stricture Barrett's Esophagus - pre cancerous cells Respiratory Complications Esophageal cancer Diagnosis: Barium Swallow Endoscopy Manometric Studies - movement of peristalsis Will first try PPIs when diagnosing due to cost of these procedures Medical Management: Phased Approach: General measures - Phase I Medication Management - Phase II Surgical intervention - Phase III Avoid late evening meals and late night snacking KNOW MEDS!!!!! Antacids neutralize gastric acids. H2R blockers are antisecretory agents PPIs inhibit proton pump mechanism responsible for secretion of H ions, also promote esophageal healing-will try PPIs before diagnostic testing in order to save money Prokinetics promote gastric emptying and reduce risk of reflux Cholinergics increase LES pressures and improve esophageal emptying and increase gastric emptying Phase I: General Measures Lifestyle Modifications - exercising, sitting up 2-3 hours several hours after meals Nutritional Therapy - types of foods, portion control, Phase II: Medications - see pg. 934, Table 42-10 Antacids Antisecretory H2 Receptor Blockers Proton Pump Inhibitors Cholinergic Medications Facilitate gastric emptying; parasympathetic effects Increase lower esophageal pressure Cytoprotective Phase III: Fundoplication - see pg. 935, Figure 42-4 Endoscopic and other procedures Nursing Management: HOB elevated Do not lie down for 2-3 hours after eating Small frequent meals Avoid alcohol, caffeine, and quit smoking Avoid eating within 3 hours of bedtime Weight loss Others?

Billroth I (Gastroduodenostomy)

Removal of the lower part of the stomach where the cells that secrete gastrin are located Removal of duodenum and pylorus Remaining is anastamosed to the duodenum

Types of Hypersensitivity Reactions: Cell Mediated Hypersensitivity

Sensitized TH1 cells release cytokines that activate macrophages or TC cells which mediate direct cellular damage Typical manifestations include contact dermatitis, tubecular lesions, and graft rejections

Vagotomy

Severing of the vagus nerve Partial of Complete

Lymphoid Organs: Peripheral lymphoid organs:

Skin-associated lymphoid tissues Tonsils GI tract; Genitourinary; Bronchial Lymph nodes Spleen

Antigens

Substances the body recognizes as foreign that elicit an immune response Most are composed of protein

Third most common form of cancer Second leading cause of cancer-related deaths 85% of colorectal cancers arise from adenomatous polyps Etiology and Pathophysiology: More common in men Risk factors Family or personal history of colorectal cancer Increased age Colorectal polyps Risk factors (cont'd) Inflammatory bowel disease (IBD) Lifestyle factors Obesity Smoking Alcohol Large amounts of red meat Clinical Manifestations: Usually nonspecific, do not appear until advanced Symptoms include Hematochezia Passage of blood through rectum Melena Black, tarry stools Diagnosis: Family history Physical examination Digital rectal examination Colonoscopy Colorectal CancerDiagnostic Studies Colonoscopy Gold standard Entire colon is examined Biopsies can be obtained Polyps can be immediately removed and sent to laboratory for examination Colorectal CancerDiagnostic Studies Fecal occult blood tests Cancerous tumors bleed intermittently into colon Used to detect very small quantities of blood Does not detect nonbleeding tumors Colorectal CancerDiagnostic Studies Fecal occult blood tests (cont'd) Guaiac-based tests (FOBT) Avoid NSAIDs, vitamin C, citrus juices, red meat for 3 days before test Six samples from three consecutive bowel movements Fecal immunochemical test (FIT) No special restrictions Two stool specimens Colorectal CancerDiagnostic Studies Stool DNA test DNA markers are shed from premalignant adenomas and cancer cells in stool and not degraded Stools collected and analyzed Not yet sensitive enough to replace other screening methods Colorectal CancerDiagnostic Studies Colonoscopy and tissue biopsies confirm diagnosis Additional laboratory studies must be done CBC Coagulation studies Liver function tests Colorectal CancerDiagnostic Studies Carcinoembryonic antigen (CEA) Complex glycoprotein Produced by 90% of colorectal cancers Helpful in monitoring disease recurrence Colorectal CancerDiagnostic Studies CT scan or MRI Helpful in detecting Liver metastases Retroperitoneal and pelvic disease Depth of penetration of tumor in bowel wall Medical Management: Chemotherapy Radiation Polypectomy Tumor resection Colon resection Colectomy Post-op care includes ambulation to improve peristalsis and facilitate gas elimination If perineal incision, monitor closely for S/S of infection due to incision location Stoma appearnce post-operatively should be red, moist, and possibly some edema

Lymphoid Organs: Central (primary) lymphoid organs: Thymus gland

Thymus gland shrinks with age Important in the differentiation and maturation of T lymphocytes

Inflammatory Bowel Disease

Ulcerative Colitis & Crohn's Disease Both: Periods of chronic inflammation with exacerbations and remissions Exact cause is unknown Strong family history No cure Commonly occurs in early teenage years and adulthood More prevalent in the Caucasian population More common in industrialized nations ULCERATIVE COLITIS: Onset: teens to mid 30's Diarrhea, abdominal cramping, rectal bleeding, tenesmus Bloody stools in ulcerative colitis Usually begins in the rectum and spreads upward Involves the mucosa and submucosa Continuous areas of inflammation Perforation Toxic Megacolon Carcinoma Cures with colostomy CROHN'S DISEASE: Onset: teens to mid 30's Diarrhea, abdominal cramping, pain, weight loss, malabsorption Occurs anywhere along the GI tract Involves the entire thickness of the GI tract Cobblestoning of mucosa Fistulas and strictures Anal abscesses Carcinoma Perforation IBD Clinical Manifestations: Diarrhea Colicky abdominal pain Weight loss - more so with Crohn's disease Diarrhea GI Bleeding Malabsorption Ectraintestinal Manifestations: Arthritis Ankylosing Spondilitis Sacroilitis Finger clubbing Erythema Nodulum Pyoderma gangrenosun Thromboembolism Apthous ulcers Conjunctivitis Gallstones Primary schlerosing cholangitis Osteoporosis Complications: Hemorrhage Abscesses Strictures Toxic Megacolon - dilated colon; more common in Ulcerative Colitis Perforation - with both IBDs Nutritional problems Cancer Diagnosis: History & physical Stool cultures CBC Electrolyte panel Erythrocyte Sedimentation Rate (ESR) Colonoscopy Capsule endoscopy Ultrasound Double contrast barium enema - air and barium CT, MRI Management: Medication therapy Surgical therapy Colectomy Nutritional Therapy provide adequate nutrition Correct and prevention malnutrition Replace fluid and electrolyte losses Prevent weight loss The goals of therapy is to reduce the number exacerbations, maintain normal fluid and electrolyte balance. Initially, bowel rest by NPO Sulfasalazine suppresses the inflammatory process Postoperative Care: Atelectasis prevention DVT prophylaxis Vital signs Pain management Patient teaching GI assessment Nutrition modifications Ostomy assessment Ostomy care NGT care Antibiotics Nursing Diagnosis: Deficient fluid volume related to loose stools Pain related to inflammation of the colon Imbalanced nutrition: less than body requirements Body image disturbance related to portion of colon pulled to surface of skin for fecal drainage into external collection device Anxiety Ineffective coping Activity intolerance Risk for impaired skin integrity related to drainage from ostomy site Nursing Intervention: Diarrhea management Anxiety Reduction Coping enhancement Pt education Nutritional therapy Teaching the disease process Record color, volume, frequency, and consistency of stool. Perform actions to rest the bowel (NPO), stress reduction techniques, encourage small frequent feedings and gradually add bulk forming agents, high protein diet, low in fiber, eliminate gas forming foods from the diet. Avoid spicy foods. Encourage patient to verbalize feelings, perceptions and fears, provide factual information about diagnosis, stay with the patient to promote safety and reduce fear, foster constructive outlets for anger and hostility, allow patient to verbalize their feelings, provide an atmosphere of acceptance. Assist the patient to solve problems in a constructive manner. Monitor weights, albumin, total protein. Monitor caloric intake, encourage nutritional substances, Instruct the patient about the prescribed diet. Assess the patient's current level of knowledge. Describe the rationale behind the therapy, discuss lifestyle changes.

NR 324 Adult Health Test 3 (ch 39, 41, 42, 43, 12, 13, 14, 15, 65, 62, 63, 64, 65)

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