Adult 1 Exam 4 Review

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Adult 1 Exam 4 Review
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Adult 1 Exam 4 Review
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  1. Stomach
    • (food stays 4 hours)
    • Liquefies food into chyme (creamy, semi-fluidmaterial) as it mixes with gastric enzymes, HCL, &pepsin (Protein digestion begins)

    • Mechanical Digestion churning of the food to help break into smaller particles
    • Absorbs small quantities of food (water, glucose);

    • Intrinsic factor synthesized by cells of stomach combines with Vit. B12 so it can be absorbed in the ileum
    • If no Vit. B12=pernicious anemia;
    • Pyloric sphincter allows a small amount of chyme to enter duodenum at a time
  2. Liver Functions:
    • (largest organ)
    • Carb, Protein & FatMetabolism
    • Detoxification
    • Synthesize clottingfactors
    • Bile production & excretion
    • Glucose (Glycogen) storage
    • Breakdown old RBC, WBC, hemoglobin &bacteria (Kupffer cells)
  3. Recommended Balance of Carbohydrates, Proteins and Fats
    • Carbohydrates (50-55% of caloric intake)
    • Proteins (15-20% of caloric intake)
    • Fats (30% or less of caloric intake with< 10% saturated)

    Total Dietary intake of all 3 should be20-35 calories / kg of body wt for average adults
  4. GI Gerontologic Considerations
    • GI Gerontologic Considerations:
    • Teeth wear down, periodontal disease, lose teeth (no appetite)
    • Decrease in:
    • Taste buds, smell, salivary secretions,GI motility, & HCL acid
    • Delayed emptying of stomach
    • Increase in gallstones
    • Decrease in dietary fiber/fluid
    • Increased constipation

    Decrease in weight is not normal even in elderly clients
  5. G.I. assessment
    • inspection
    • auscultation
    • percussion
    • palpation
  6. Upper GI/Barium Swallow
    detects ulcers,varices, regional enteritis, malabsorption, spasms, pyloric valve, anatomy- may find enlarged R atrium pushes on esophagus can be seen by pressure defect in esophagus

    • pre exam care:
    • Low Residue Diet 2-3 days,
    • no smoking (stimulates gastric motility),
    • NPO 8-12hours
    • don't take any medications for eight hours pretest

    • procedure:
    • swallow barium & look at underfluoroscope
    • Double contrast=barium + CO2 releasing pills will show fine details

    • posttest
    • administer laxatives
    • make sure barium comes out-stools will be white /pink and chalky looking
  7. Lower GI or Barium Enema
    • used to detect polyps, tumors, lesions, anatomy, malfunction of bowel
    • pre exam:
    • Low Residue Diet 1-3 days,
    • clear liquids 24 hours before test
    • NPO 8 hours before test
    • laxative,
    • cleansing enemas until clear

    • procedure:
    • substance instilled rectally,
    • viewed under fluoroscope

    • Post exam:
    • increase fluid intake
    • laxative - stools will be white until barium is expelled
    • barium impaction -digital disempaction requires a doctor's order
  8. ENDOSCOPY
    • EGD esophagogastroduodenoscopy-
    • to show direct visualization of gastric mucosa through a lighted endoscope, flexible , shows on TV,
    • may retrieve bile duct stones also laser for neoplasms
    • looks that esophagus, stomach, small intestine to the duodium

    • pre:
    • clear liquid diet 24 hours before procedure
    • NPO X 8 hr.
    • diazepam- spraying or gargling of local anesthetic, atropine - anticholenergic-reduce secretions

    procedure: positioned on left side to facilitate saliva drainage and easy access

    • Post procedure
    • must have gag reflex before resuming PO intake(usually takes 1 hour)

    It is considered a minimally invasive procedure since it does not require an incision into one of the major body cavities and does not require any significant recovery after the procedure

    often used with colonoscopy
  9. Stool exam
    • -for occult blood, parasites,food residue, fat, nitrogen Color-gray or clay= biliary obstruction
    • Consistency- steatorhea, (fat in stools) bulky, greasy, foamy, foul odor = liver or gallbladder
    • gray shiny= (pancreas)
    • mucus or pus (chronic ulcerative colitis)
    • constipation, dry, hard
    • impaction, may leak liquid stool
    • black/tarry - G.I. bleeds
    • red = lower G.I. bleeds

    stool should be S-shaped and golden brown
  10. Total Parental Nutrition/”TPN”
    • Composition:
    • Dextrose/Protein (amino acids), vitamins
    • IV Fat Emulsion-Lipids

    • Indications for:
    • Injury/Trauma
    • Surgery esp. abdominal
    • Burns
    • Long term lack of nutrition (Rule of 5)

    • Administration via:
    • Central catheters (triple lumen)
    • Peripherally inserted central catheters (PICC)
    • Peripheral lines not used

    • High risk of infection
    • Monitor glucose - 50 to 70% dextrose
  11. TPN NURSING MANAGEMENT
    • Absolute aseptic technique
    • Chg. dressing frequently according to hosp. protocol (q 2, 3, or 4 days is typical)
    • Observe for S & S of infection (culture if needed)
    • -monitor insertion site and patient's temperature
    • Use of filter & new tubing with each bottle
    • Gradually increase (for 24-48 hr) to desired rate to avoid hyperglycemia
    • Check VS q 2-4 hr
    • Daily wt.
    • Ck blood glucose q 4-6 hr
    • Daily electrolytes,protein, CBC
    • Hospital protocol may require culturing catheter when DC’d
    • Never give meds/blood thru TPN line
  12. Bulimia
    • Binge eating with self-induced vomiting or purging with laxatives 2X/wk. X 3 mons.
    • High calorie, high fat, high sweet diet
    • Depression—over eat to feel better—vomit/purge—more depressed
    • Signs & Symptoms Bulimia:
    • Stays at normal wt,, (not usually emaciated)
    • Dental problems (loss of enamel)
    • Enlarged salivary glands
    • Pharyngitis or esophagitis
    • Rectal bleeding
    • Electrolyte imbalance (loss gastric fluid/diarrhea)
    • Cardiac arrest
  13. stomatitis
    • = inflammation of oral mucosa
    • Due to: Viral (Herpes simplex I)
    • Fungal (Candida albicans)
    • Irritants (smoke, chemo, bite cheek)
    • Signs & Symptoms: (last over week)
    • Swelling & redness
    • Patches (erythroplakia & leukoplakia)
    • Painful oral ulcers

    • Treatments:
    • Lidocaine or Orabase protective paste
    • Mouth care (saline or bicarb. mouthwash)
    • -brushing and flossing
    • Nystatin swish/swallow for fungal infection
    • Acyclovir for viral/oral herpes simplex
    • Antibiotics for bacterial infections
  14. Oral Cancer
    • = squamous cell CA of lips, tongue or mouth
    • Risk factors: ultraviolet light/sun
    • Men over 40
    • Cigarettes, chewing tobacco, marijuana
    • Alcohol
    • Viruses esp. Human papillomavirus/HPV

    • Signs & Symptoms:
    • Painless oral ulcer or sore lasts > 2 wks.
    • Asymmetrical face, neck or jaw
    • Patches (erythroplakia or leukoplakia)
    • Pigmented areas (brown or black)
    • Dysphagia, swollen lymph nodes
    • Blood tinged sputum

    TX: radiation, chemotherapy, surgery
  15. Gastroesophageal Reflux Disease (GERD)
    • = Backward flow of GI contents with exposure of esophagus to gastric/duodenal contents causes inflammatory changes & scarring/fibrosis
    • “Reflux esophagitis”
    • Pathophysiology (due to): - risk factors
    • *Incompetent or relaxed lower esophageal sphincter (LES)
    • * Increased stomach pressures (more volume,positioning supine/bending, or increased pressure from obesity or tight clothes)Gastroesophageal RefluxDisease (GERD)
  16. GERD treatment
    Goal: Improving LES function, increase esophageal clearance, decrease vol. &acidity, protect mucosa

    Diet therapy - avoid acidic foods such as tomatoes, citrus, spicy foods, and coffee. avoid fatty foods, chocolate, peppermint, and alcohol that relax the LES

    • patient education
    • Lifestyle changes-
    • No smoking, no gum, 6 sm meals/day
    • Upright 2 hrs after meals, no eat 3 hrs bedtime, bed blocks (HOB up 6-8 inches)
    • Surgical therapy-antireflux surgery
  17. G.I. medications
    • Antacids
    • Neutralizes acid
    • Maalox, Mylanta, Tumd Gelusil etc.

    • Histamine (H2) receptor blockers
    • Decreases gastric acid production - block histamine from stimulating secretion
    • Ranitidine (Zantac); Cimetidine (Tagamet)

    Proton Pump Inhibitors (Prilosec, prevacid,Protonix, Nexium) Decrease acid & promote healing -

    • Sucralfate (Carafate)
    • Cytoprotective properties (protects against acid)
    • -reacts with gastric acid to form a thick paste that adheres to damaged gastric mucosal tissue and promote healing.
  18. Achalasia/Impaired Motility
    • Lack of peristalsis of lower 2/3 of esophagus (ANS disorder)
    • Increased LES pressures as unable to relax → Enlargement above
  19. Achalasia/Dysphagia
    S&S and treatment
    • S & S:
    • Dysphagia with solid &liquid foods
    • Chest pain or fullnessin chest after eating
    • Nighttime cough
    • Esophageal spasm
    • Wt. loss
    • Vomit undigested food
  20. Treatment:
    • Balloon Dilation(decreases pressure atsphincter)
    • Nifedipine/Procardia
    • Botox (relaxes sphincter)repeat q 6 – 9 mos.
    • Sleep on blocks ↑ HOB
    • Surgery- LaparoscopicMyotomy (incision ofLES)
  21. GASTRITIS
    • =Inflammation of stomach lining from irritation of the gastric mucosa
    • Acute gastritis – disrupts gastric mucosa yet regenerates
    • Erosive gastritis (Curling, Cushing)Chronic gastritis - atrophy of mucosa
    • Type A – autoimmune (No. Europeans)
    • Type B - H. pylori , esp. elderly > 70
    • the rotation the street [pyloric area of stomach that produces gastrin
  22. GASTRITIS SYMPTOMS

    risk factors
    treatments
    • ACUTE(mild)
    • Anorexia, Nausea, vomiting
    • Hematemesis -vomit blood
    • Melena-black tarry stools
    • Abdominal pain
    • Possibly shock

    • CHRONIC
    • Vague discomfort after eating
    • May be asymptomatic
    • Anemia (B12 &intrinsic factor)
    • Fatigue

    • Risk factors
    • elderly
    • chronic alcoholics
    • cigarette smokers

    • Treatment:
    • Meds – histamine2 receptors, proton-pump inhibitors, Carafate, antibiotics for H. pyloric,B12
    • NPO 12 hrs. then slowly introduce liquids &food NG suction/lavage if corrosive substance orblood

  23. Peptic Ulcer Disease (PUD)
    Break in gastrointestinal mucosa with mucosal barrier unable to protect it from damage by hydrochloric acid and pepsin(gastric digestive juices)

    • Risk factors associated with PUD:
    • H. pylori infection
    • Use of NSAID and/or glucocorticoids esp. with age
    • Cigarette smoking, ETOH, caffeine
    • Family history (suggestive of genetic factor)
    • Possible stress factorPeptic Ulcer Disease (PUD)
  24. Peptic Ulcers (3 areas) -
    • 1. Esophageal ulcers
    • 2. Gastric ulcers
    • Deep and penetrating
    • Occur on lesser curvature of stomach
    • Esp. ages 55 –70 with NSAID
    • Chronic pain immediately after eating
    • Associated with cancer
    • 3. Duodenal ulcers (most common)
    • 95% occur in first portion of duodenum
    • Deep, sharply demarcated lesions
    • Penetrate through mucosa and submucosa into muscle layer
    • 95% to 100% due to H. pylori infection
    • Esp. ages 30 –55 and males > females
    • Intermittent pain 3 hrs. after eating
  25. PUD Signs & Symptoms:
    • Epigastric tenderness/pain 2-3 hrs. after eating & in middle of night (“pain-food-relief”pattern)
    • Dyspepsia (heartburn/indigestion)
    • Vomiting (BRB or coffee-ground)
    • Melena
    • Elderly with vague symptoms of chest pain,weight loss or occult bleed
  26. PUD Treatment
    • Diet management – balanced meals at regular intervals (not bland), mild ETOH
    • 􀂄 Lifestyle changes/stress management
    • 􀂄 No smoking as slows healing
    • 􀂄 Surgery usually not needed for PUD due to H. pyloric
    • 􀂄 Manage complications
  27. Peptic Ulcer Disease Complications
    • Hemorrhage (10-20%)
    • Serious complication; erodes into blood vessel of mucosa
    • Hematemesis, hematochezia, dizziness, ortho BP, shock
    • Treat with fluids, RBC’s, sclerosing agents or laser photocoagulation (endoscopy with heater probe)

    • Perforation (lethal/med. emergency)
    • Ulcer perforates into mucosa wall with chemical then bacterial peritonitis
    • Sudden severe upper abd. pain, quickly spreads entire abd.; BS hyperactive then absent; rigid board-like abdomen; rebound tenderness—open laparotomy

    • Gastric Outlet (Pyloric) Obstruction
    • Due to repeated inflammation & scarring
    • N/V, hypokalemia
    • Treat with NG decompression or balloon dilation
  28. nursing diagnoses for peptic ulcer disease
    • acute pain
    • disturbed sleep patterns
    • imbalanced nutrition: less than body requirements
    • risk for bleeding
  29. total gastrectomy
    remove entire stomach and connect esophagus to duodenum or jejunum

    • postop concerns
    • anemia-rapid gastric emptying interferes with absorption
    • B12 deficiency-B 12 is only absorbed in the presence of intrinsic factor which is produced in the stomach
    • postop teaching
    • small frequent meals
    • liquid and solid eat separately
    • increase protein and fat diet
    • reduced carbohydrate especially sugars
    • rest in a recumbent position 30 to 60 min. after eating
  30. abdominal perforation
    S & S and nursing care
    caused by peptic ulcer that perforates into mucosa wallwith chemical then bacterial peritonitis

    • S & S
    • sudden severe upper abdominal pain that quickly spreads to the entire abdomen
    • bowel sounds hyperactive that absent
    • rigid boardlike abdomen
    • rebound tenderness

    • Treatment
    • IV fluids to maintain fluid and electrolyte balance
    • NGT suction removes gastric contents and minimizes peritoneal contamination
    • Fowlers or semi-Fowlers position to allow peritoneal contaminants to pool in the pelvis
    • IV antibiotics
    • laparotomy to close the perforation
  31. Cholecystitis/Cholelithiasis
    inflamed gallbladder/gallstones
    • cholecystitis -inflammation of the gallbladder caused by a stone blocking the cystic duct. Blockage causes pressure within the gallbladder leading to ischemia. bile trapped inside causes chemical irritation and bacterial inflammation follows
    • Common Signs/Symptoms-
    • Abrupt onset with severe steady pain
    • Radiates to back, R scapula & shoulder
    • Nausea & vomiting
    • Cholelithiasis- localized pain in epigastrium & RUQ Lasts 30 min. – 5 hrs.
    • Jaundice
    • Complications of liver disease & pancreatitis
    • Cholecystitis- generalized pain to RUQ
    • Lasts 12 – 18 hrs.
    • Fever/chills
    • RUQ guarding/tenderness
    • Complications of gangrene & ileus/obstruction

    • Risk Factors -
    • Familial history of gallstones
    • Women, over 40, mulitparous(pregnancy)
    • Dietary habits (fasting; yo-yo diets)
    • Sedentary lifestyle (obesity)
    • Ethnic: Native American & No. Europe
    • Increased cholesterol(hyperlipidemia)
    • (Female, Fair, Fat, Forty & Fertile…)
  32. Cholelithiasis/Cholecystitis Treatments
    • Nonsurgical Management
    • Diet therapy- low fat, low carb., low calorie & low cholesterol advance when flatulence; fat soluble vitamins (A,D,E & K)

    • Drug therapy-
    • Actigall or Chenix
    • reduce cholesterol in stones → dissolves stones Analgesics for pain- Demerol is preferable over opiates-causes less spasms (? New research)
    • Questran to bind bile salts and decrease itching Antibiotics if infection/cholecystitis
  33. non-viral causes of hepatitis -toxic hepatitus
    • CHEMICALS
    • carbon tetrachloride
    • phosphorus
    • chloroform

    • ALCOHOL
    • DRUGS
    • Isoniazid
    • Halothane
    • Acetaminophen
    • antibiotics
    • antimetabolites
    • anesthetics

    HEPATOBILIARY
  34. HEPATITIS VIRAL TYPES
    • 5 major categories of viruses (A,B,C,D,E)
    • Enteral forms
    • 1. Hepatitis A and E
    • 2. Transmitted by fecal-oral route, personto-person by contact with virus in feces,saliva, contaminated food or water

    • Parenteral forms
    • 1. Hepatitis B, C, D
    • 2. Transmitted through venous blood/sexual contact
    • Acute or chronic
  35. 3 Phases of Acute Hepatitis
    • Preicteric/Prodromal Phase
    • 2 wks after exposure; highly transmittable
    • Flu like symptoms

    • Icteric Phase
    • 2 wks after prodromal & lasts 2 – 6 wks
    • Jaundice, itching, clay-colored stools,dark urine, hepatomegaly

    • Posticteric/Convalescent Phase
    • 6 – 8 wks after exposure
    • Bilirubin & liver enzymes return to normal
  36. Hepatitis Symptoms
    • PREICTERIC
    • fever
    • anorexia
    • dyspepsia
    • abdominal pain
    • general aching
    • malaise
    • weakness

    • ICTERIC
    • •jaundiced if bilirubin > 2.5
    • •light colored stools
    • •dark urine
    • •liver tender &enlarged
    • •enlarged posterior cervical lymph nodes
  37. Hepatitis Preventative Care-Vaccines
    • Hepatitis A vaccine (Havrix)
    • Vaccine 2 doses 6 –12 mos. apart
    • Post exposure – single dose Immune Globulin IG within 2 wks of exposure

    • Hepatitis B vaccine (Recombivax)
    • Vaccine 3 doses (initial, 4 wks, then 5 mos.)
    • Post exposure - vaccine (long term) plus Hepatitis B Immune Globulin (HBIG) for shortterm

    CAN NEVER BE BLOOD DONOR
  38. ABGs of N & V versus diarrhea
    diarrhea = metabolic acidosis due to loss of HCO3

    • vomiting = metabolic alkalosis due to loss of hydrochloric acid from the stomach
  39. Constipation
    = Abnormal infrequency of defecation with abnormally hardened stools that pass painfully and with difficulty(normal 3 x wk- every third day)

    Pathology: interference in the colon with mucosal transport (slowed)

    • Etiology:
    • 􀂄 Aging
    • 􀂄 Emotional stress
    • 􀂄 Ignoring urge to defecate
    • 􀂄 Insufficient dietary fiber or fluids
    • 􀂄 Change in routine (shy bowel)
    • 􀂄 Decrease activity
    • 􀂄 Drugs (narcotics, calcium, aluminum)
    • 􀂄 Chronic overuse of laxatives or enemas
    • 􀂄 Barium Impaction (post UGI or BariumEnema)
    • 􀂄 Hypothyroidism
  40. Constipation Treatments
    • 􀂄 Diet – high fiber (fruits, veggies, bran) & 8 glasses water per day
    • 􀂄 Enemas – in acute situation (NS, soap suds, oilretention; tap water & phosphate/Fleets); cancause electrolyte imbalances & impaired bowelfunction

    • 􀂄 Medications-
    • laxatives = mild effects
    • cathartics= strong effects

    • 􀂄 Bulk-forming agents (Bran, Metamucil) draw in water with indigestible veg. fiber-
    • *only laxatives safe for long-term use
    • -mix with a full glass of liquid and administer immediately
    • -drink 6 to 8 glasses of water per day
    • -may be next with water,milk, or fruit juice
    • -take in the morning with meals
    • -do not take at bedtime-risk of impaction

    • 􀂄 Wetting agents (docusate, Colace, Surfak) reduce stool surface tension with emulsion of fat &water;
    • -don’t crush
    • -administer with ample fluids
    • -do not take within one hour of other PO meds

    • 􀂄 Osmotic & saline laxatives (Sorbitol, MOM,Lactulose) increase osmotic pressure & draw in water; short-term use as irritate bowel
    • -works rapidly-3 to 6 hours-do not take before bed

    • Irritant or stimulant laxatives (Ducolax ,Senna, Caster oil) stimulate motility &secretion;
    • -don’t crush
    • -less than 1 wk. use -habit forming and suppresses bowel reflexes
    • -discourage use of OTC preparations of this type of laxative
    • in
    • 􀂄 Lubricants (Mineral oil) forms oily coat on fecal mass preventing water absorption;interferes with fat soluble vitamin absorption (A, D, E & K); watch for aspiration
  41. Acute Appendicitis
    • Due to: Obstruction of the appendix lumen by:
    • 􀂄 Feces (“Fecalith”)
    • 􀂄 Foreign body
    • 􀂄 Tumors
    • 􀂄 Increased pressure, infection,necrosis, gangrene, & perforation with peritoniti

    • 􀂄 Assess (Signs & Symptoms):
    • + McBurney’s point - Midway between the umbilicus and the anterior iliac crest in the RLQ-localized pain and rebound tenderness with appendicitis
    • 􀂄 Guarding, rebound tenderness RLQ
    • 􀂄 N/V
    • 􀂄 Low-grade fever (high if perforated)
    • 􀂄 Elderly

    • 􀂄 Diagnosis:
    • 􀂄 Palpation, WBC, U/A to rule out other dx;Abd. X-ray, Ultrasound
    • 􀂄 Surgery:
    • 􀂄 Laparoscopic
    • 􀂄 Laparotomy (open)

    • nursing care
    • icepack to abdomen-never use heat
  42. Peritonitis
    • = inflammation of the peritoneum due to chemical or bacterial irritant
    • 􀂄 Signs/Symptoms:
    • 􀂄 Pain, guarding with rebound tenderness
    • 􀂄 Paralytic ileus - no peristalsis
    • 􀂄 Abd. Distension/rigid
    • 􀂄 Decreased BS orabsent
    • 􀂄 Fever
    • 􀂄 Tachycardia
    • 􀂄 Restless/confused
    • 􀂄 Oliguria-low urine output

    • 􀂄 Treatment:
    • 􀂄 NG decompression
    • 􀂄 Broad spectrum antibiotics
    • 􀂄 Surgery
    • 􀂄 Peritoneal lavage
    • 􀂄 Drains

    • 􀂄 Complications:
    • 􀂄 Abscess
    • 􀂄 Fibrous adhesions &obstruction
    • 􀂄 Hypovolemic shock
  43. Gastroenteritis
    • =􀂄 Inflammation of stomach & small intestine due to bacteria, virus, parasite or toxins
    • -also called enteritis and food poisoning

    • 􀂄 Signs & Symptoms:
    • 􀂄 N & V
    • 􀂄 Diarrhea
    • 􀂄 Fever
    • 􀂄 Metabolic alkalosis or acidosis
    • 􀂄 Abd. cramping/pain
    • 􀂄 Borborygmi-rumbling or gurgling noise
    • 􀂄 May have blood or mucus in stool
    • 􀂄 Dry skin & mucous membranes
    • 􀂄 Orthostatic BP & tachycardia

    • 􀂄 DX: Stool for ova & parasites
    • 􀂄 Serum toxin levels for botulism
    • 􀂄 Sigmoidoscope
  44. GASTROENTERITIS
    types and treatments
    • Traveler’s diarrhea
    • 􀂄 Staphylococcal food poisoning-
    • 􀂄 Botulism foodpoisoning
    • 􀂄 Cholera
    • 􀂄 Hemorrhagic colitis
    • 􀂄 Salmonellosis
    • 􀂄 Shigellosis

    • 􀂄 Most resolve quickly
    • -antidiarrheals are contraindicated
    • 􀂄 Antibiotics for cholera, shigellosis& salmonellosis
    • 􀂄 Botulism antitoxin
    • 􀂄 Fluid & electrolytes
    • 􀂄 Gastric lavage
    • 􀂄 Plasmapheresis
    • 􀂄 Renal dialysis

    complications-most complications revolve around fluid and electrolyte imbalance
  45. Ulcerative Colitis
    • Affects mucosal & submucosal lining of rectum & sigmoid colon resulting in:
    • Multiple loose stools with blood/mucus
    • Poor absorption of nutrients (wt. loss)
    • Anemia
    • LLQ abdominal cramping
    • Extra-intestinal manifestations(erythema nodosum and/or uveitis)
    • Complications:
    • Ulceration with abscess & hemorrhage
    • Perforation and peritonitis (15% mortality)
    • Toxic Megacolon (motor paralysis &dilated colon)
  46. Crohn's Disease(Regional Enteritis)
    • Cobblestone patchy ulcerations affecting entire bowel wall (transmural) of terminal ileum & ascending colon resulting in:
    • Diarrhea without blood
    • Malabsorption with weight loss
    • Anemia
    • RLQ abdominal pain and/or mass
    • Fever
    • Fatigue/malaise
    • Thicken wall with rubber hose appearance
    • Complications-
    • Intestinal obstruction
    • Abscess
    • Fistulas (bowel, bladder, & skin)
  47. IBD Medication
    IBD = Inflammatory BowelDisease: ulcerative colitis and Crohn's disease

    • Medications:
    • Anti-inflammatories that inhibit prostaglandin production in the bowel-prostaglandin is a mediator in inflammation process-blocking at reduces inflammation
    • (sulfasalazine (Azulfidine), Asacol,Dipentum)
    • -anaphylactic responses may occur
    • -use sunscreen-med increases sensitivity to sound
    • -may interfere with the effectiveness of oral contraceptives
    • -do not take with asked burn or vitamin C
    • -take after meals to decreased gastric distress
    • -drink two quarts of fluid per day to prevent kidney damage

    • Steroids (Prednisone, Solu-Medrol)
    • Immunosuppressive drugs (Imuran,Cyclosporine)
    • Antibiotics (Flagyl, Cipro)
    • Anti-diarrhea agents if not acute attack(Lomotil & Imodium)
  48. IBD treatments
    • Inflammatory Bowel Disease:
    • Diet-Elemental (Ensure): high-calorie, high nitrogen, fat-free, no residue, absorbed in the proximal small bowel
    • TPN for Crohn’s to rest bowel
    • Supplemental vitamins & iron
  49. Surgery (not a cure, recurrence)
    • Resection for bowel obstruction
    • Total colectomy with ileal pouch-anal anastomosis
    • Ostomy (Ileostomy, Continent/Kock’s ileostomy)
  50. Ileostomy
    • Ileostomy–stool is always liquid (green to yellow-brown)
    • Pt must always wear bag
    • Empty when 1/3 full
    • Should avoid gas-producingfoods
    • Good skin care
    • Use elec. Razor to shave hair
    • Use protective ointment
    • Assessment
    • Cuts
    • Stenosis
    • Separation from abdominal surface
  51. Ostomies
    • Ostomy surgery terms
    • Ostomy= surgical incision/fistula
    • Stoma = artificial body cavity opening
    • Stoma should be pink or red & raised 2 cm
    • dusky blue = ischemia,
    • brown/black = necrosis
    • Edema, sm. amt. bleeding, oozing when touched is normal initially

    • diet
    • -low residue diet is recommended
    • -avoid foods that cause odor for gas
    • -fluid and salt intake port to prevent dehydration
  52. POLYPS
    • = tissue mass from the mucosal surface protrudes into the lumen
    • Adenomas
    • Neo-plastic changes in the epithelium
    • Familial adenomatous polyposis (FAP), very rare yet life time risk of developing colorectal CA 100%
    • Indication-total colectomy; q 6 mo. colonoscopy

    • Types of adenoma polyps:
    • Tubular (pedunculated)=globe like with ones > 2cm having 35% CA rate
    • Villous (sessile)=broad base & larger > 5cm having 25-40% CA rate
    • Tubulovillous=both tubular & villous
  53. celiac disease
    avoid gluten
  54. POLYPS
    S & S and treatment
    • Signs/Symptoms:
    • Asymptomatic, found on exam
    • Intermittent painless rectal bleeding
    • Abdominal cramping
    • Diarrhea & mucus discharge if villous

    • Treatment – remove as high malignancy rate
    • Colonoscopy with electrocautery
    • Total colectomy with ileo-rectal anastomosis if multiple polyps in different parts of colon
    • Preventative: screen with sigmoidoscope q 5 yrs.after age 50 (q 3 yrs. if + polyps)
  55. Hernia
    • =defect in adb. wall allows contents to protrude out of cavity
    • Types of Hernias:
    • Inguinal most common (80%)
    • Indirect/congenital - improper closure of testes tract
    • Direct/acquired – weakness in femoral ring(pregnancy, obesity)
    • Ventral/incisional from previous abd. surgery
    • Umbilical – congenital or due to pregnancy or obesity; strangulation common

    • Reducible - abdominal contents move into the sack when intra-abdominal pressure increases and moves back into the abdomen when pressure decreases
    • irreducible-incarcerated-contents of the hernia cannot return to the abdominal cavity
    • strangulated-blood supply to hernia sac is compromised leading to necrosis. Bowel can infarct leading to perforation and contamination of peritoneal cavity
    • (severe pain, N&V, distention, fever,tachycardia)
  56. Diverticular Disease:
    • Diverticula=saclike projections of mucosa thru muscular layer of colon esp. sigmoid area (90-95%) Diverticulosis=presence of diverticula
    • May be asymptomatic (2/3)
    • Diverticulitis = inflammation & perforated diverticulum with formation of local abscess
    • Minor bleeding to massive hemorrhage
    • Retained undigested food = bacterial invasion of sac with abscess & peritonitis
  57. Diverticular Disease Treatments:
    • High fiber diet with bran (avoid seeds, nuts, corn, berries, popcorn); progress from liquids to low roughage to high fiber
    • Medications- Broad antibiotics (Flagyl, Cipro, Septra, Mefoxin)
    • Pain meds (Talwin over Demerol or MSO4)
    • Stool Softener (Colace)-usually contraindicated
    • Surgery if hemorrhage, abscess or peritonitis (Hartmann with temp. ostomy
  58. hemorrhoridectomy
    postop care
    • apply ice packs over rectal dressing
    • sits bath 3 to 4 times a day
    • sideline position
    • flotation pad for use when sitting

    • Stool softener's as prescribed
    • analgesics before first postop bowel movement and PRN
  59. colonoscopy
    visual exam of entire colon to the ileocecal valve to identify tumors, polyps, and IBS

    beginning at age 50, men and women should get a colonoscopy every 10 years
  60. G tubes and PEG tubes
    • G tube =gastrostomy
    • PEG tube = percutaneous endoscopic gastrostomy

    • Checking placement
    • 1. Aspirate GI secretions - should be tan or grain
    • 2. measure the pH -
    • pH of 1-6 =gastric-placement in stomach
    • pH of 6 to 10 was signed placement and small intestine or in lungs - x-ray needed to confirm tube location
    • 3. Osco take the stomach while injecting air-should here wooshing, gurgling, or bubbling sound and the ULQ

    • care
    • care of new placement requires surgical asepsis
    • regularly clean around insertion point and watch for signs of infection
  61. G.I. bleed and treatment
    • coffee grounds appearance = partially digested blood from stomach or upper G.I.
    • black tarry stools = melena
    • bloody stools = lower G.I. bleed
    • occult bleeding = hidden-detected by chemical means

    Bleeding is irritating to the stomach and causes nausea and vomiting. Blood and the G.I. tract stimulates peristalsis leading to diarrhea.

    G.I. hemorrhage-loss of significant amount of blood can cause shock, tachycardia, hypotension, pallor, and decreased urine output.

    • Fresh whole blood is used in acute hemorrhage.
    • packed red cells are used as last acute situations
    • gastric lavage may be used to prevent vomiting and prepare for upper endoscopy
  62. differences between type I and type II DM
    • Type 1 Diabetes (5-10%)
    • -IDDM
    • - Destruction of beta cells leading to an absolute deficiency of insulin. Must be treated with insulin therapy
    • Juvenile onset-12yrs.
    • Insulin dependent
    • Autoimmune destruction of beta cells
    • DKA (ketones)
    • Normal or under wt.
    • Whites > nonwhites esp. Finland
    • Abrupt onset s/s
    • Tx with insulin

    • Type 2 Diabetes (90-95%)
    • -NIDDM
    • - Disorder with a combination of insulin resistance and a defect in insulin secretion. May be treated with diet, exercise, oral agents,and/or insulin 40%
    • -a decrease in the body's ability to respond to insulin-resistance
    • Adult onset > 40yrs.
    • Non-insulindependent
    • Resistance to insulin
    • HHNK (no ketonesusually)
    • Obese
    • Native Amer.,Hispanic & Afr. Amer
    • Gradual onset s/s
    • Tx with diet, exercise& oral agents
  63. diagnostic tests for DM
    • Fasting plasma glucose
    • Normal < 100
    • goal 70-110 mg/dL
    • action needed at >or = 126mg/dL
    • impaired fasting glucose o pre-DM for glucose 100-126

    >Random plasma glucose 200 mg/dLwith symptoms of diabetes

    • OGTT - “oral glucose tolerance test”
    • (normal< 140)
    • –impaired glucose tolerance 140-200
    • action needed>200 mg/dL

    • HbA1c ,
    • normal < 6%,
    • goal <7%
    • action suggested > 8%

    UA normal = nope glucose, key tones, or albumin
  64. TYPE I - IDDM Signs & Symptoms
    Polyuria/freq. urine - hyperglycemia causes serum hyper osmolality and draws water from intracellular spaces into general circulation

    • Polydipsia/thirst- dehydration caused by decrease in intracellular volume and increase in urinary output
    • Polyphagia/appetite- because glucose cannot enter cell, energy production decreases leading to hunger

    Weight loss - body loses water and break down proteins and fats in an attempt to restore energy sources

    Fatigue - caused by decrease in energy

    Blurred vision - caused by osmotic effects that cause swelling of the lenses of the eyes

    • Infections - immune response and healing are impaired by lack of energy in the cells
    • Rapid, early onset
    • Insulin dependent
  65. Type II - NIDDM Clinical Manifestations
    D rowsiness - insulin resistance causes lack of glucose in cells =lack of energy for cells

    • I tching/dry skin from dehydration - caused by hyper osmolality
    • A family history of diabetes
    • B lurred vision
    • E xcessive weight - leads to insulin resistance by the cells and DM
    • T ingling, numbness, pain in extremities
    • E xcessive serum glucose level- low glucose up. Take due to insulin resistance by the cells
    • S kin infections, slow healing cuts
  66. DIABETES MANAGEMENT ADA REQUIREMENTS
    Type I
    • Carbohydrates:45 –65% (1u R insuling per 10-15gms)
    • Saturated Fats:< 10%
    • Proteins: 15 - 20%
    • Cholesterol:< 300mg/day
    • Fiber: 20 – 35 gms/d
  67. DIET PLAN FOR TYPE 2 DIABETES
    • Variety of fruits, vegetables, whole grains,beans, nuts, and low-fat dairy products - every color on the plate - white, red, green, yellow
    • Portion = size of a fist or computer mouse
    • Animal protein low in saturated fat and high in omega 3 fatty acids
    • Fat calories from monounsaturated or polyunsaturated vegetable fat
    • Trans fatty acids should be avoided
    • Consult with a registered dietician fortailored medical nutrition therapy (MNT)
  68. TYPES OF INSULIN
    Know this
    • Rapid acting-- Humalog or Novolog(Lispro or Aspart)
    • onset 15 min. peak 60-90mins. duration 3-4 hrs.

    • Short-acting– Regular (Humulin orNovolin)
    • onset 30-60 min. peak 2-3 duration hrs. 4-6 hrs.

    • Intermediate-acting-- NPH or Lente
    • onset 2 hrs. peak 6-8 hrs. duration 12-16 hrs.

    • Long-acting-- Ultralente
    • onset 2 hrs. peak 16-20 hrs. duration 24-36 hrs.

    • Basal insulin-- Glargine (Lantus orLevemir)
    • onset 2 hrs. peak None duration 22-24 hrs

    Combinations– NPH/Regular 75/25,70/30 or 50/50

    open insulin is good for one month at room temperature and three months in the refrigerator
  69. ORAL ANTIDIABETIC AGENTS
    • SULFONYLUREA AGENTS (8-24 hrs.)
    • Exs. DiaBeta, Glucotrol, Amaryl, Tolinase
    • -type 2
    • Stimulate the pancreas to secrete insulin
    • Improve peripheral sensitivity to insulin
    • Side effects of hypoglycemia, weight gain &multi-drug interactions

    • BIGUANIDES (12-24 hrs.) -Type 2
    • Glucophage (Metformin)
    • Increases sensitivity to insulin
    • Decreases liver’s overproduction of glucose
    • Side effects of renal, liver & heart problems,GI problems, lactic acidosis & no ETOH

    • THIAZOLIDINEDIONES/GLITAZONES (12-24 hrs.)
    • Exs. Avandia, Actose
    • Sensitize peripheral tissue to insulin
    • Alone or in combo with Sulf., Metformin, or insulin
    • Use cautiously in CHF (liver damage); take with food

    • MEGLITINIDES (6-8 hrs.) - Type 2
    • Exs. Prandin, Starlix
    • Stimulates release of insulin from pancreas
    • Side effect of hypoglycemia (take before meal);

    • ALPHA-GLUCOSE INHIBITORS (6-8 hrs.)
    • Exs. Glyset, Procose
    • Slow carbohydrate digestion, delay glucose intestine absorption - used in diabetic candy
    • Side effects of gas, bloating, abdominal pain &diarrhea; – take with food
  70. DEEPS: MANAGEMENT OPTIONS
    • Diet (medical nutrition therapy)
    • Exercise (physical activity plan)
    • Education (diabetes self-managementeducation) Pharmacotherapy (drug education)
    • Monotherapy
    • Combination therapy
    • Insulin therapy
    • Self-monitoring of blood glucose (SMBG)
  71. BLOOD SUGAR MNEMONIC
    • Hyperglycemia HOT & DRY=SUGAR HIGH
    • Hypoglycemia COLD & CLAMMY=NEED SOME CANDY
  72. GLYCOSYLATED Hgb HEMOGLOBIN A1C
    • BLOOD SUGAR LEVEL ABOVE 180 SUGAR ATTACHES TO HEMOGLOBIN
    • BLOOD SUGAR LEVEL BELOW 180 NO SUGAR ATTACHES TO THE HEMOGLOBIN
    • HEMOGLOBIN A1C(HbA1C) IS A COMBINATION OF SUGAR AND HEMOGLOBIN
    • REFLECTS AVERAGE SUGAR LEVELS FOR THE PAST 3 MONTHS

    goal is <7%

    • 6 =135 average
    • 7 =170
    • 8 you= 205
  73. DIABETES Acute Complications
    Hypoglycemia = glucose less than 50

    • Diabetic Ketoacidosis (DKA)
    • elevated glucose and elevated ketones

    • Hyperosmolar Hyperglycemic State(HHS) AKA Hyperglycemic
    • elevated glucose, but no ketones

    Hyperosmolar Non- Ketonic (HHNK)Syndrome
  74. HYPOGLYCEMIA
    • Signs / Symptoms
    • diaphoresis
    • tremors
    • tachycardia
    • palpitation
    • nervousness
    • hunger

    • Treatment
    • 15/15 rule
    • check blood sugar
    • normal blood sugar wait 15 minutes and repeat
    • low blood sugar give15 Gm rapid acting carbohydrate and repeat blood sugar in15 min.
    • blood sugar remains low repeat treatment

    • 15 g of carbs =
    • three glucose tabs
    • 4 ounces juice
    • three Graham cracker squares
    • 4 ounces soda
    • 1 cup milk
    • six saltine crackers
    • 1/2 cup pudding

    irritability is the main symptom of moderate hypoglycemia

    • severe hypoglycemia
    • disorientation
    • unconsciousness
    • seizures
    • glucose less than 50
  75. DIABETIC KETOACIDOSIS
    • Insufficient insulin with fat stores breaking down leading to ketosis & loss of bicarb.
    • Metabolic acidosis from ketones
    • Hyperosmolarity leads to dehydration & electrolyte imbalance
    • Glucose > 250 mg/dL
    • pH < 7.3
    • Bicarb. < 15 mEq./L
    • + Urine ketones & glucose

    • SIGNS / SYMPTOMS
    • Polyuria
    • Polydipsia
    • Polyphagia
    • Kussmauls respirations- confident shallow
    • Fruity breath
    • Anorexia, nausea,vomiting
    • Abdominal pain
    • Blurred vision
    • Decreasing LOC

    • TREATMENT AIMED AT
    • Dehydration
    • Electrolyte loss
    • Acidosis
    • Correct glucose
  76. DIABETIC KETOACIDOSIS
    nursing interventions
    • Fluid replacement
    • 0.9% normal saline rapid infusion (500 then 200 cc)
    • 0.45% if hypertension, hypernatremia, CHF
    • Vital signs, Lung assessment
    • Intake & Output
    • Monitor K+ closely, frequent EKG’s (flat T, Uwave)
    • Acidosis reversed with insulin (Regular)
    • Prevent rapid decrease in glucose level,hypoglycemia can result in fatal cerebral edema
  77. SICK DAY RULES for DM
    • Take Insulin or oral hypoglycemic agent as usual
    • Test blood glucose every 3 - 4 hours (and urine ketones if Type I, glucose> 240 mg/dl)
    • Report elevated glucose levels > 300)or ketones to the physician
    • May need supplemental doses of Insulin every 3 - 4 hours
    • If usual meal plan cannot befollowed, substitute soft foods 6 - 8 times per day
    • If vomiting, diarrhea, or fever persists take liquids every 1/2 - 1 hr to prevent dehydration & provide calories
    • Report nausea, vomiting & diarrhea
    • Type I - inable to retain oral fluids may warrant hospitalization to prevent DKA
  78. diabetes drug therapy
    • insulin
    • oral anti-diabetes agents

    aspirin therapy-81 to 325 mg of enteric-coated aspirin is primary prevention for heart disease
  79. chronic complications of diabetes mellitus
    -macro circulation (large blood vessels) changes due to atherosclerosis. Also, hypertension, hyperlipidemia, cigarette smoking, and obesity

    • -Microcirculation-structural defects in the basement membrane of smaller blood vessels or capillaries
    • -this defect causes the capillary basement membrane to thicken which results in decreased tissue perfusion
    • -this alteration in microcirculation affects all body tissues, but is seen primarily and I've and kidney

    Diabetes mellitus puts client at risk for CAD, hypertension, and stroke
  80. diabetic neuropathy
    • -vascular changes in the lower extremities result in arteriosclerosis (hardened vessels)-usually below the knee
    • -blockages form due to loss of compliance of the vessels in the lower lakes, and feet
    • -multiple blockages and decreased blood flow result in:
    • loss of hair on lower lake, feet, and toes
    • shininess and thinning skin
    • cold feet
    • feet and ankles starker than Lake
    • thick toenails
    • diminished or absence pulses
    • nocturnal pain
    • intermittent claudication-pain caused by exercise and relieved by rest
    • patchy areas of gangrene on feet and toes
  81. diabetic foot care
    • inspect feet daily
    • cut nail straight across and smooth edges with emery board
    • never go barefoot-wear slippers when leaving the that night
    • do not put heating pads or ice packs on feet
    • do not set with the legs crossed at the knees or ankles
    • do not wear open toed shoes
    • make sure shoes fit properly
    • buy shoes made of natural fibers

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