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N130 Exam 4 Assignment
Systemic Lupus Erythematosus
an inflammatory, autoimmune disorder that affects every organ & redness of skin
# 3 types- discoid lupus, systemic, drug-induced
1.Pathphysiology
a.immune system(B-cell) begin to overproduce antibodies with the help of B-lymphocyte stimulator(BLyS). Antibodies and antigen get trapped in the capillaries of visceral structures
2.Clinical Manifestations
– Cutaneous lesion (malar-cheek, discoid rash) consisting of a butterfly-shaped
– possibly are provoked by sunlight or artificial ultraviolet light(photosensitivity).
– Oral ulcer, alopecia(Bold), Raynaud’s phenomenon
valve incompetence, Atherosclerosis, MI, stroke in women,
3.Assessment & Diagnostic findings
positive ANA (antinuclear antibody), urine protein, elevated BUN
-Belimumab (Benlysta); monoclonal antibodies which binds to BLyS (stimulate B cell to produce antibodies)-Ă No live vaccines while taking it !!!
-Corticosteroids(Prednisone); topically for cutaneous manifestations, Risk Factor “osteoporosis and fracture, weight gain ;taper off,  check renal function(intake & output), take it with food.
-Antimalarials(hydroxychloroquine-Plaquenil)-to treat skin, joint  à check retinal toxicity
-DX; fatigue, impaired skin integrity, body image disturbance, deficient knowledge for self-management decisions, depression, anxiety, difficulty coping disease
-Pt. should avoid exposure or to protect themselves with sunscreen and clothing,stop tobacco,
–Pt needs Bone mineral density test every 2yrs& teach Pt to take calcium ,Vitamin D
-Check Pt. Tem!!
N130 Exam 4 Assignment
Multiple Sclerosis (MS)
;Â an immune-mediated, progressive demyelinating disease of the CNS which causes impaired and worsening function of voluntary muscles. The fatty and protein surrounds damaged nerve fibers in the brain and spinal cord, it results in impaired transmission of nerve impulses.
1.pathophysiology
; sensitized T and B lymphocytes cross the blood-brain, remain in the CNS, promote the infiltration of other agents that damage the immune system. permanent/irreversible damage
-relapsing-remitting(RR), primary progressive, secondary progressive, progressive relapsing
-Risk age-20-40yrs old women.
-main symptoms-fatigue, dysphagia, muscle weakness(flaccidity), numbness, pain, anemia
– visual disturbances (blurring of vision, diplopia, scotoma, blindness),dysphagia,ataxia
-Lhemittes’s Sign-Electric shock sensation/ uhthoff’s sign (over heat symptom)
-Premenopausal women- osteoporosis, estrogen loss, immobility (corticosteroid needed)
-Spasticity (muscle hypertonicity)- LE, loss of the abdominal reflexes (RISK of aspiration), memory  loss, decreased concentration, dementia
-Ataxia(impaired coordination of movements)- tremor, emotional lability, euphoria.
-neurogenic bladder-Â spastic bladder (frequency, urgency, UTI), bowel, sexual dysfunction
3.Gerontologic Considerations
; Toxic effects of MS medications, osteoporosis, Risk for aspiration, increasing disability, immobility, spasticity, pain, bladder dysfunction, impaired sleep & ADLs,
4.diagnostic findings  ;check S/S, MRI (brain, spinal cord)
5.medical management
NO cure exists., Just to relieve symptom/pain, to delay the progression of the disease
–muscle relaxant,
-Pt. needs daily analgesic medications. (opioid, anticonvulsant, antidepressant)
-Disease-modifying therapies- to reduce the frequency of relapse
Beta-Interferon ( Rebif,Betaseron) (subQ every other day),
Avonex(IM)—decreasing immune system   à  check liver damage
corticosteroid(Methylprednisolone)-short time, Check blood glucose, taking it with food
SE*Euphoria, infection
cholinergic(Bethanechol)-to treat bladder emptying
Copaxone(SubQ)( Tcell attack??)- reduce RRcourse—takes 6months to work
Novantrone (IV) –immune suppressing. For secondary progressive RR SE* cardiac toxicity
-Symptom Management–Baclofen,Diazepam(valium) for spasticity SE*jaundice(impaired liver)
6.Nursing process
;Nursing DX-impaired mobility & urinary elimination & verbal communication& skin integrity
Risk for aspiration & injury, Chronic confusion, powerlessness
;NI-Promoting physical mobility
-measure Tem. For risk of infection
If spasticity-warm packs beneficial but no hot bath. Swimming is useful. Take a rest period.
Immobility Pt- pressure ulcer check, perform coughing and deep breathing exercise
Inability to store, empty urine Pt-set voiding time, med for bladder spasticity
Swallowing difficulties—risk aspiration. Check suction, position, liquid
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N130 Exam 4 Assignment
Rheumatoid Arthritis
;an autoimmune disease, females, 20-60yrs old. The incidence of RA increases after the
60yrs    Risk factor: pollution, smoking, family history, bacterial and viral illness.
1.Pathophysiology
-the autoimmune reaction originates in the synovial tissue. Produce inflammatory and destructive synovial fluid.
-The consequence is the loss of articular surfaces and joint motion. Muscle fibers degenerated. Tendon and ligament elasticity and contractile power are lost.
-The synovial inflammation compress the nerve, causing neuropathies and paresthesia.
-classic symptom: symmetric joint pain, morning joint stiffness last longer than 1hr, swelling,
fatigue, feverĂ Pt. tends to immobilize them
-fluid, when palpated, spongy or boggy tissue “Heberden’s nodes
-small area(hands, wrists and feet) to big area joint (shoulder,hips,elbow,ankle..)
-soft tissue deformity-swan neck, heberden’s and Bouchards’s nodes
-weight loss, anemia, lymph node enlargement, Raynard’s phenomenon
-RA inflammatory processes make arterial wall stiffnessĂ cardiovascular risks with diabetes.
-palpation, X-ray, MRIÂ -BC(blood count)Â Â Â Â –Arthrocentesis- show synovial fluid
-80% presents Rheumatoid factor, Anti-CCP 95%Â Â Â Â Â Â -Increased ESR, CRP, platelets, anemia
-Check liver, kidney (elevated liver enzymes)
4.Medical Management
;to decrease joint pain and swelling, achieve remission
a.Early RA: to prevent inflammation and joint damage.
#Nonbiologic DMARDs-sulfasalazine,hydroxycholrotquine
Work within 6 weeksĂ check liver, kidney function & CBC(anemia), (normal hgb 12-15)
hydro…eye examination(due to retinal damage)
b.moderate RA; Cyclosporine(immunosuppressant)
c.persistent RA; surgery & corticosteroids-for unremitting inflammation and pain
d.Advanced RA; high dose methotrexate, cyclophosphamide(Cytoxan)& azathioprine(Imuran)
Ă high toxic, bone marrow suppression, anemia, GI disturbances, rashes.
; vitamin, protein, iron
5.Nursing Management
; -Pain, fatigue, depression, sleep disturbance, stiffness, impaired skin integrity & mobility /
-complication-cardiovascular disease, RA medication’s SE
N130 Exam 4 Assignment
Peptic Ulcer Disease
; ulcerations at gastric(after meal), duodenum(at night), pylorus, or esophagus
1.Pathophysiology
-Damage of mucosa barrier by H.plyori or NSAIDsà release Histamineà more HCLà worsen…
2.Clinical Manifestations
-Silent peptic ulcers most commonly occur in older adults and those taking aspirin
-Risk factor-H.plyori(spiral shape, produce urease,spread via oral-fecal), NSAIDs usage,
Zollinger-Ellison Syndrome (tumor formation which secrete gastrin)
Stress and food NOT causing!!!
-Pain after eating(gastric ulcer), pain at night(duodenal ulcer), dull, burning sensation.
Pyrosis, vomiting, constipation, diarrhea, bleeding, sour eructation, weight loss
-GI bleeding(hematemesis, melena) Ă see a doctor!!!
-Severe-extreme tenderness,hypotension, tachycardia.
3.Assessment, Diagnostic Findings
-tenderness, distention, low serum albumin (normal 3.8-4.5g/dL), EGD, Endoscopy—NPO
4.Medical Management
a.Medication- Antibiotics(metronidazole(Flagyl), amoxicillinĂ keep 14 days!!)
bismuth salts-subsalicylates(suppress H.pylori & cover ulcer),
                   PPI(_prazole)& H2 blockers(_tidine,Zantac)à ; reduce HCLà ->keep 4-8 weeks
Mucosal healing- Carafate- with an empty stomach, no with H2 blocker
-acute pain, anxiety, imbalanced nutrition
-monitoring hemorrhage,Ă faintness, dizziness, nausea,tachycardia,hypotension, tachypnea due to GI bleedingĂ Risk of hemorrhagic shock
-monitor bowel sound, tenderness, stools/vomit
-penetration and perforationĂ severe abdominal pain, tender, vomiting, high Tem & HR
-Gastric outlet obstructionĂ nausea, vomiting, distended abdomen, pain
-Pt. eat freq. small meals, lie down for 30 mins. No drink fluids w/meals.
-the importance of adherence with prescribed medication regimen
-Avoid sugary foods, no too hot or cold. EAT high fiber, protein, &low cab.
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N130 Exam 4 Assignment
Diverticular Disease
;a saclike herniation anywhere in GI tractĂ becomes inflamedĂ Diverticulitis
-prevalence increases with increasing age; over 65yrs 50%
1.Pathophysiology
-Bowel contents can accumulate e in the diverticulum and decompose, causing inflammation and infection. most common in the sigmoid colon(LLQ)
-The inflammation can cause it to perforate, giving rise to irritability and spasticity of the colonĂ Diverticultitis
-Risk Factor-Low intake of FIBER!!, obesity, cigarette, NSAIDs, family history
2.Clinical Manifestations
-S/S unrelenting cramping pain(LLQ), blood in stool, fever, constipation, bloating
-Acute complication- abscess formation, bleeding, peritonitis, leukocytosis(increased WBC)
3.Diagnostic findings -Colonoscopy, CT, elevated WBC, blood in stool
4.Medication
-Stage #1 Rest, oral fluids, and analgesic medication are recommended -High fiber, low fat diet
-Stage #2 diverticulitis- require hospitalization-withhold oral intake, administer IV fluids, NG suctioning, Antibiotics(ampicillin,sulbactam(Unasyn), Opioid for pain relief No PO,
-Stage #3,4 need surgical managements. (Hartmann procedure), ileostomy, colostomy
5.Nursing Management
-Rest, oral fluids, analgesic medications
-NI- GI assessment and diet regime, check risk of peritonitis(fever, Pain)
-Drain abscess of infected pouch, IV antibiotics, bowel rest(NPO)
-During recovery-clear liquids food, and then low-fiber food, no fresh food
Healed- high fiber to promoting defecation /Â fresh food, plenty of fluids(2-3L)
-Higher stage- NPO, IVÂ fluids, NG suction if vomit, low fiber diet.
-Risk of perforations!
-pt’s family and counseling important for pt.
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N130 Exam 4 Assignment – Cholecystitis
; Stones in a Gallbladder cause pain, tenderness, and rigidity of  RUQ that radiate to right shoulder and is associated with nausea, vomiting and the usual signs of an acute inflammation
-stone obstructs bile outflow-> edema->blood vessels comprssedĂ Gangrene,perforationĂ bacteria,infection
1.Pathophysiology -Cholesterol stones -more over 40yrs old women than men
2.Clinical Manifestations
-abdominal distention, RUQ pain, -Due to a meal rich in fatty foods.
-Pain but NO using Morphine(cause spasm), use meperidine(Demerol)
-Jaundice, very dark color urine, clay or grayish fecesĂ affects kindey and skin(discoloration)
-Risk of Vitamin K deficitsĂ bleeding
-, skin itching(pruritus)
3.Diagnostic Findings
; Abdominal ultrasound- NPO midnight
–Lab result– ????, liver enxzyme increased// bleeding long time(due to miss vitamin K)
-ERCP-NPO, after administrate glucagon or anticholinergicĂ check respiratory, hypotension
-Percutaneous Transhepatic Cholangiography(PTC) Ă check bleeding, pain
-abdominal rebound tenderness, positive murphy sign.
-removal of the gallbladder-cholecystectomy
-due to no bile-digest lipid ->No fatty food
-Ursodeoxycholic &che nodeoxycholic acid-dissolve cholesterol-
After surgeryĂ bleeding, infection watch out
N130 Exam 4 Assignment
Inflammatory Bowel Disease (IBD)- Crohn’s Disease(Regional Enteritis??)
; characterized by periods of remission and exacerbation. It is a subacute and chronic inflammation of the GI tract wall that extends through all layers. It most occurs in the distal ileum and the ascending colon.
1.Pathophysiology
-Fistulas, fissures, and abscesses as the inflammationà all the GI layers “mouth to the anus”
-the bowel wall thickens and becomes fibrotic and the intestinal lumen narrows
2.Clinical Manifestations
-prominent RLQ pain ,fever, leukocytosis and diarrhea unrelieved by defecation
-crampy abdominal pain, tenderness and spasm after meal
– Pt. limit food intake, reduce the amounts and types of food
-Risk of malnutrition, weight loss, secondary anemia, fluid loss  -steatorrhea (fat in stool)
-manifestations- joint disorders, skin lesions, ocular & liver disorder, and oral ulcer
3.Assessment and diagnostic Findings     -MRI, CT
-CBC, Albumin & protein decreased, increased WBC & ESR(erythrocyte sedimentation)
4.Complications
-No cure , surgery may help         -Risk of colon cancer
-fluid and electrolyte imbalances, malnutrition
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N130 Exam 4 Assignment – Inflammatory Bowel Disease (IBD)- Ulcerative Colitis
; a chronic ulcerative and inflammatory disease of the mucosal and submucosal layers of the colon and rectum that is characterized by unpredictable periods of remission and exacerbation with bouts of abdominal cramps and bloody or purulent diarrhea
1.Pathophysiology
-affects ONLY the superficial mucosa of colon, by multiple ulcerations, diffuse inflammations
-bleeding by ulcerations. Stool+blood         -the mucosa becomes edematous and inflamed
-bowel narrows, shortens, and thickens because of muscular hypertrophy and fat deposits.
2.Clinical Manifestations
-Urgent/frq. Bowel movement, low RBCs(anemia), rectal bleeding, severe diarrhea
LLQ pain, intermittent tenesmus, diarrhea
-pallor, fatigue, anorexia, weight loss, fever, vomiting, dehydration, cramping
-Colonoscopy, CT, MRI , Bariem enema (Xray)Â -low hmt, hgb, albumin /Â high WBC, CRP
4.Complications
-flare ups and period of remission-> narrowing colon,
–toxic megacolonĂ colonic distention, perforation, bleedingĂ nasogastric suction!!!
-If colonostomyĂ check Pt. anxiety for imulsing surgery.. and infection around the stomy area
5.Medication
-to reduce inflammation(flare up), suppress inappropriate immune responses, provide rest
-MED – Anti-inflammatory-sulfasalazine-first line tx for mild
-Corticostroids-predisone-no use long term, tapered off, osteoporosis, high glucose
-Immunosuppresseors-Azathioprine, Immuron- risk infection(No live vaccine)
-Modulaters- adalimumab,humria
-Sedatives, antidiarrheal and antiperstaltic medications are used to minimize peristalsis
-surgical-colectomy w/ileostomy
if Pt. with megacolon no responds within 72hrs, IV fluid needed with electrolytes
-Moniter VS, BM
-Diet education-Avoid high fiber fat /hard to digest. Eat low fiber, high protein, stay hydrated
-Nutrition- oral fluids, high protein, high calorie diet with vitamin & iron
-No cold food or smoking (it causes increasing intestinal motility)
-IV fluids
– diarrhea RT inflammation, acute pain, deficit fluid volume, imbalanced nutrition,
ineffective coping RT, impaired skin integrity, deficient knowledge
-Postoperative(ostomy) Care- IV fluid for 4-5 days to replace lost fluids, NG suction
Manage diets.
Appendicitis(???????)
;a small appendage that is attached to the cecum below the ileocecal valve.
The appendix is prone to obstruction and to infection (inflammation) Ă appendicitis
-McBurney’s point- pain around umbilicus, right lower quadrant. Between superior iliac spine and umbilicus one-third distance. with anorexia, nausea, fever
-If the appendix has ruptured, the pain consistent with peritonitis (abdominal distention develops, Pt’s condition worsens)
-constipation- BUT no enema, laxative, it may result perforation of the inflamed appendix
-Risk factor- fecalith, lymph node enlargement (due to infection)
2.Assessment and Diagnostic Findings -elevated WBC,CRPÂ Â -abdominal rebound tenderness
3.Complications-Gangrene or perforation of the appendix within 6 to 24 hours after the onset of pain and leads to peritonitis
4.Medical Management -Immediate surgery “appendectomy”
-To correct or prevent fluid /electrolyte imbalance, dehydrationĂ &IV fluids
-Risk of infectionĂ antibiotic
-goal-relieving pain, preventing fluid volume deficit, reducing anxiety, preventing surgical site
infection, maintaining skin integrity, attaining optimal nutrition
-Before S-monitor VS,peritonitis;aute relief of pain,high HR,RR,Temp,abd. Distention/bloating
-After surgery- High Fowler positionà reduce abdominal organs’ tension
-Pts uses incentive spirometer to prevent atelectasis, ambulate(VTE)
-2weeks after surgery, check with MD.
-Resume normal activity within 2-4 weeks