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Results from inadequate intake of nutrients

Lack of major nutrients or micronutrients

loss of nutrients due to diarrhea, hemorrhage, or renal failure;

impaired absorption and use of nutrients; increased metabolic needs

Widespread cause of disease and mortality; Young, poor, elderly, homeless, low-income women, and ethnic minorities

PATHO

When dietary intake of nutrients does not meet the body’s energy demands, the body uses glycogen, body proteins, and lipids to support metabolism

Acute illness and stress produces a state of hypermetabolism and catabolism

Surgery or illness may promote Protein-Calorie Malnutriton, a deficiency of proteins and calorie

SIGNS & SYMPTOMS:

Weight loss Body mass reduction Wasted appearance;

Weakness Dry and brittle hair Pale mucous membranes Peripheral or abdominal

edema May be indicative of a

particular nutrient deficit

Diagnostics & Treatment

Nutritional screening tool Serum albumin level&Prealbumin level Serum electrolyte Total lymphocyte count Total daily energy expenditure

Meds: Supplemental vitamins/minerals


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SIGNS & SYMPTOMS:

Weight loss Body mass reduction Wasted appearance;

Weakness Dry and brittle hair Pale mucous membranes Peripheral or abdominal

edema May be indicative of a

particular nutrient deficit

Diagnostics & Treatment

Nutritional screening tool Serum albumin level&Prealbumin level Serum electrolyte Total lymphocyte count Total daily energy expenditure

Meds: Supplemental vitamins/minerals

Nursing Care: Health history and physical examination Provide environment and nursing measures to promote eating Monitor temperature and po intake. Teach S/S of infection and hand washing Weigh daily I& O; Skin turgor; LOC; urine specific gravity Turn Q 2 hours; Turn Clock; Draw sheet Assess skin integrity q shift

PATHO:

Excessive calories are stored as fat & adipose tissue Results from excess energy intake, decreased energy expenditure, or a combination of both Upper body obesity: waist-to-hip ratio of greater than

1 in men and 0.8 in women Associated with a greater risk of complications such

as HTN, lipid levels, heart disease, stroke, and elevated Insulin levels

Lower body obesity: waist-to-hip ratio is less than 0.8; more common in women

More difficult to treat BMI 25-29.9kg/m2 overweight; above 30 obese

RISKS

1. Genetics2. Physiologic3. Psychological4. Environmental5. Sociocultural

*most preventable health problems in US

Diagnostics:

BMI Waist circumference Thyroid profile Glucose, cholesterol,

EKG

Treatment: Medications (appetite suppressants; fat absorption

inhibitors) Exercise & Nutrition Behavior Modification Surgery

NURSING CARE: Establish realistic weight loss goals Discuss behavior modification techniques Assess current activity level Regular, gradually increasing exercise plan (after medical

clearance) Encourage discussion of feelings Encourage decision making in plan of care Establish rapport

MEDICATIONS:

*Phentermine*Meridia*Xenical

PATHO:* Inflammation and ulcers of the oral mucosa from persistent damage to oral mucosal cells. * Release of inflammatory mediators cause tissue damage, progresses from superficial to ulceration to involvement of the entire epithelium (Healing begins in within 2-4 weeks; mucosa does not fully recover

Commonly seen in immunocompromised people, elderly, people with cancer, end of life(renal failure, O2 therapy), poor oral hygiene, tobacco, alcohol use

Causes:1. Viral (most com)

Herpes simplex2. Fungal (Candida

albicans)3. Mechanical trauma

(cheek biting)4. Nutritional deficit5. Irritants (tobacco,

non fit dentures)

MANIFESTATIONS:

Vary according to the cause. May include:

Vesicular lesions (fungal- creamy white curd like patches)

Red, erythematous mucosa Bleeding, tissue necrosis Halitosis Pain (viral irritantant) Tissue necrosis

May lead to malnutrition, F/E imbalances, sepsis, bacterial endocarditis

DIAGNOSTICS Physical exam Cultures, smears (as ordered) Oral lesion don’t respond to therapy 1-

2 weeks need to be evaluated for malignancy

TREATMENT:

• Meticulous oral hygiene, with brushing and flossing• Solution of saline/sodium bicarbonate given after and between meals• Topical anesthetic-viscous lidocaine• Orabase-protective paste• Amphojel/Kaopectate- coating agents• Nystatin-“Swish and Swallow” OR “Swish and Spit”-for

TREATMENT:

• Meticulous oral hygiene, with brushing and flossing• Solution of saline/sodium bicarbonate given after and between meals• Topical anesthetic-viscous lidocaine• Orabase-protective paste• Amphojel/Kaopectate- coating agents• Nystatin-“Swish and Swallow” OR “Swish and Spit”-for

NURSING:• HX & physical• ID clients at risk• Assess oral mucosa; Regular performance of mouth care • Regular Dental appointments• 8 oz buttermilk/yogurt if taking antibiotics• Limit spicy, hot, acidic foods, hot beverages• Avoid ETOH and smoking• Weigh daily & High-calorie, high-protein diets• Analgesics for pain

Risk factors

1. smoking2. drinking

ETOH3. chewing

tobacco 4. marijuana 5. occupationl

exposure to chemicals & viruses

Nursing diagnoses1. Impaired Oral Mucous

Membrane2. Imbalance Nutrition: less than

body requirements

MANIFESTATIONS:

Earliest—Painless oral ulceration or lesion White Patches—Leukoplakia Red Patches-Erythroplakia Later—Impaired speaking, swallowing, chewing; swollen lymph nodes; blood tinged sputum pigmented areas (brown or black masses, ulcers, fissures Asymmetry of head, face, neck, jaw

DIAGNOSTICS:

Physical examination Cultures, Smears, as ordered Oral lesion not responding to therapy in 1-2 weeks need to be evaluated for malignancy Biopsy of the lesion CT Scan & MRI

TREATMENT: Eliminate causative factors (tobacco, alcohol) Radiation/Chemotherapy Surgery is generally treatment of choice Remove lesion and potentially cancerous surrounding tissues and lymph nodes Radical neck dissection may be required if advanced (Lymph nodes, muscles of the

neck removed)- A TRACHEOSTOMY IS performed at time of surgery Tracheostomy may be required (Temp or permanent)

NURSING:• Teaching related to causative factors, Early identification and interventions• Assessment of oral mucosa, lips on physical exam• Monitor airway• Semi fowlers position• TCDB every 2 hours• Adequate hydration• Weigh daily• Soft, bland diet high in calories/protein• Feeding tube---interventions??• Establish communication plan• Disturbed body image---interventions

PATHO: (commonly occurring 15-20% adults)

May result from 1. transient relaxation of the lower esophageal

sphincter2. an incompetent lower esophageal sphincter3. increased pressure within the stomach

*Backward flowing of gastric content into the esophagus &May develop inflammatory esophagitis as a result of acidic contents

FACTORS THAT CONTRIBUTE:1. Increased gastric volume(after

meals)2. body positioning3. increased gastric pressure( obesity/

tight clothes)4. hiatal hernia5. Damage to the esophageal mucosa

occurs due to prolonged exposure to

Diagnoses1. Risk for Ineffective AW

Clearance-(Fowler’s position, turn cough deep breath, hydration)

2. Imbalance Nutrition: Less than body Requirements

3. Impaired Verbal Comm.4. Disturbed Body Image

MANIFESTATIONS: Heartburn& indigestion Dysphagia Regurgitation Chest Pain Pain after eating Belching Aspiration may cause hoarseness and

respiratory symptoms

DIAGNOSTICS:

Barium Swallow-assesses esophagus stomach, and upper small intestine.

Upper Endoscopy-directvisualization…tissue may be obtained for a biopsy.

Bernstein test 24 hour ambulatory pH monitoring Esophageal manometry

TREATMENT: Antacids may relieve mild or moderate symptoms by neutralizing stomach acid.

Maalox, Mylanta, Gaviscon, Tums Proton pump inhibitors reduce gastric secretions, promote healing, and relieve

symptoms. Nexium, Prevacid, Prilosec, Protonix, Aciphex

Histamine2 –Receptor blockers reduce gastric acid production and treat GERD symptoms.

Tagament, Pepcid, Zantac, Axid Promotility agents may be ordered to enhance clearance of the esophagus and stomach

emptying…Not recommended for long-term useReglan

NURSING: Perform health history and Physical exam Provide small frequent meals, Restrict fat, acidic foods,

coffee, and ETOH Stop smoking Administers meds as ordered Remain upright after meal

Acute Pain

PATHO: Occurs when part of the stomach protrudes through the esophageal hiatus of

the diaphragm into the thoracic cavity, incidence increases with ageSliding hiatal hernia

Gastroesophageal junction and the fundus of the stomach slide upward through the esophageal hiatus (few symptoms)

Paraesophageal hiatal herniaJunction between the esophagus and stomach remains in its normal position below the diaphragm while a part of the stomach herniates through the esophageal hiatus- may develop gastritis or gastrointestinal bleeding.

Strictures lead to dysphagia

Barrett’s esophagus increased cancer risk

Surgery- Laparoscopic fundoplication – gastric fundus wrapped around distal esophagus (increase pressure in the lower esophagus, inhibiting gastric content reflux)

(PEPTIC ULCER DISEASE)

MANIFESTATIONS: most people asymptomatic Reflux, heartburn Feeling of fullness Substernal chest pain Dysphagia Occult bleeding Belching indigestion

DIAGNOSTICS BARIUM SWALLOW UPPER

ENDOSCOPY

TREATMENT:

Often asymptomatic…No treatment required. Treatment measures such as those for clients with GERD may be ordered Surgery may be required

Nissen fundoplication (may be open or laparoscopicall)-prevents gastroesophageal junction from slipping into thoracic cavity

NURSING:

Similar to that of GERD clients If surgery is performed, nursing care is pre-op and post-op interventions and complications.

PATHO

* A break in the mucosal lining of the GI tract where it comes in contact with gastric juice (hydrochloric acid and pepsin of the mucosa).Ulcers may be superficial or deep affecting all layers of the mucosa*Exacerbations may occur with trauma, infection, stress-both physical and psychological

Risks H pylori infection NSAIDs Advanced age Personal/family HX of

ulcers smoking

PATHO

* A break in the mucosal lining of the GI tract where it comes in contact with gastric juice (hydrochloric acid and pepsin of the mucosa).Ulcers may be superficial or deep affecting all layers of the mucosa*Exacerbations may occur with trauma, infection, stress-both physical and psychological

MANIFESTATIONS:

Epigastric Pain (gnawing, burning, aching, or hunger-like) Pain occurs when the stomach is empty (2-3 hours after meals and in the middle of the night) Pain is relieved by eating Heartburn Regurgitation Vomiting Chest pain, Weight loss, Anemia may also occur

DIAGNSOTICS: Upper GI Series- barium contrast used 1st Endoscopy Biopsy Specimens Testing for H Pylor

COMPLICATIONS:• Hemorrhage

1. Slow & insidious blood loss, with occult blood in stool.

2. Anemia, weakness, dizziness, hypotension may occur if bleeding continues.

3. If large vessel is affected, hematememsis, blood in the stool, signs of hypovolemic shock occur.

• Obstruction- gradual process1. Edema, smooth muscle spasms, or scar tissue2. Epigastric fullness, N/V, F/E imbalances

• Perforation1. Most lethal; causes peritonitis- immediate, severe upper

abdominal pain, shock• Zollinger-Ellison Syndrome- Caused by a gastrinoma

TREATMENT: H Pylori Eradication increases ulcer healing & reduces recurrence Triple therapy (7-14 days twice daily) (1.) Full dose PPI (2.) Amoxicilin (3.) Clarithromycin/

Metronidazole (works in 80-85%) H2 receptor antagonists Proton pump inhibitors, antacids, sucralfate (binds to proteins in ulcer base form protective barrier)

NURSING: HX & physical *Asses Ab., girth, bowel sounds, tenderness Pain management & relaxation techniques *IV therapy, NG tube maintenance Nutritional & dietary consult *discontinue NSAIDS, STOP SMOKING

PATHO: common (acute or chronic) Inflammation of the stomach lining, results from irritation of the gastric mucosa

ACUTE:

• Characterized by disruption of the mucosal barrier by a local irritant; hydrochloric acid and pepsin come in contact with the gastric tissue causing irritation, inflammation, and superficial erosions.

CHRONIC:

• Progressive disorder that begins with superficial inflammation and gradually lead to atrophy of gastric tissues. Classified as Type A and Type B

Acute Pain Disturbed Sleep Pattern Imbalanced Nutrition: Less Risk for bleeding

ACUTE:

• Characterized by disruption of the mucosal barrier by a local irritant; hydrochloric acid and pepsin come in contact with the gastric tissue causing irritation, inflammation, and superficial erosions.

CHRONIC:

• Progressive disorder that begins with superficial inflammation and gradually lead to atrophy of gastric tissues. Classified as Type A and Type B

DIAGNOSTICS Hx & clinical presentation Gastric analysis- decreased

hydrochloric acid secretion H&H , RBC (elevated if anemia) Vitamin B12 levels Upper endoscopy Test for H pylori

TREATMENT:*PPI, H2-Receptor blockers, Sucrlfate may be given to prevent or treat stress gastritis.* If H. pylori is present, combination therapy of two antibiotics and a PPI are used.Metronidazole (Flagyl), Clarithromycin (Biaxin), or Tetracycline (Sumycin

NURSING:• GI tract rest (NPO for 6-12 hours)• Clear liquids-full liquids-soft (bland) diet- regular diet• Monitor for F/E imbalance, N/V• Gastric lavage may be ordered- washing out stomach contents • Weigh daily & I/O• Assess skin turgor• Increase fluid if not contraindicated

PATHO:• Increase in frequency, volume, & fluid content of stool, water content in stool increased• May result from either osmotic or secretory processes• Water may be pulled into the bowel by osmosis– Laxatives, Stool softeners, E. coli infections, lactose intolerance, unabsorbed dietary fat• Secretory may include inflammation or disease of the colon– IBS, Bowel resection, Gastric bypass• Increase in the frequency, volume, and fluid content of stool• Manifestation rather than a disorder• May be acute or chronic– Acute lasts less than a week, due to infection

Complimentary therapy:Aromatherapy- chamomile tea, garlic, ginger, mint oil

PATHO:• Increase in frequency, volume, & fluid content of stool, water content in stool increased• May result from either osmotic or secretory processes• Water may be pulled into the bowel by osmosis– Laxatives, Stool softeners, E. coli infections, lactose intolerance, unabsorbed dietary fat• Secretory may include inflammation or disease of the colon– IBS, Bowel resection, Gastric bypass• Increase in the frequency, volume, and fluid content of stool• Manifestation rather than a disorder• May be acute or chronic– Acute lasts less than a week, due to infection

MANIFESTATIONS:

• Depend on cause, duration, and severity as well as the area of the bowel affected• Several, large watery stools daily• Very frequent, small stools containing fat,mucous, blood or exudates•Loss of bicarbonate can lead to METABOLIC ACIDOSIS

DIAGNOSTICS:• Stool culture• Sigmoidoscopy• Serum electrolytes- potassium & magnesium lost• Serum osmolality

TREATMENT:Antidiarrheal Medications– NOT used until the cause has been identified– Examples: Pepto-Bismol, Kaopectate, Lomotil• Anticholinergics may also be used– Examples: Atropine, Donnatal• Antibiotics• Fluid/Electrolyte replacement & nutrition– Hold solid food/milk/milk products first 24 hours– Avoid raw fruits, veggies, fried foods, bran, whole grain cereals, spices, coffee, ETO- foods with fructose, lactose, sucrose, caffeine

NURSING:Hx & physical

• Monitor frequency, characteristics of bowel movements• Assess bowel sounds• Measure abd girth• Standard precautions• Limit food intake if acute (limit fiber, milk, caffeine)• Monitor lab values• I&O, Weigh Daily, Vital Signs• Assess perineal areaTeach hand washing

PATHO:• May be a primary problem or a manifestation of another disease or condition• Acute constipation– Definite change in bowel patterns that persists or becomes more frequent or severe• Chronic constipation– Functional causes that impair storage, transport, or evacuation mechanisms• Infrequent or difficulty passage of stool– Two or fewer bowel movements frequentlyCAUSES

1. Decreased activity/mobility status

MANIFESTATIONS:

• Having decreased bowel movements than usual pattern• Frequent flatus• Abd discomfort• Anorexia• Straining to have a BM• Passage of hard, dry stools• *Fecal Impaction may develop

DiarrheaRisk for Deficient Fluid VolumeRisk for Impaired Skin Integrity

PATHO:• May be a primary problem or a manifestation of another disease or condition• Acute constipation– Definite change in bowel patterns that persists or becomes more frequent or severe• Chronic constipation– Functional causes that impair storage, transport, or evacuation mechanisms• Infrequent or difficulty passage of stool– Two or fewer bowel movements frequentlyCAUSES

1. Decreased activity/mobility status

MANIFESTATIONS:

• Having decreased bowel movements than usual pattern• Frequent flatus• Abd discomfort• Anorexia• Straining to have a BM• Passage of hard, dry stools• *Fecal Impaction may develop

DIAGNOSTICS:

• Barium enema•Sigmoidoscopy/

TREATMENT:1. Laxative- Used to promote stool evacuation, short term use, do not administer if client has an

undiagnosed obstruction, Abdpain, impaction, fissures, hemorrhoids• May cause mechanical damage or perforate the bowels

2. Bulking Agents- Only laxatives appropriate and safe for long term use– Examples: Psyllium seed (Metamucil), methylcellulose (Citucel), calcium polycarbophil(Fibercon)

3. Cathartics and enema- Interfere with normal bowel reflexes, should not be used for simple constipation (Saline 500-2000mL) (tap water- 500-1000mL) (Soap-suds enemas)

4. Increase fiber- raw veggies, bran, fruits, flaxseed5. Increase fluid- 6-8 glasses a day, exercise6. Enemas- only use short term (acute situations), continued use leads to F/E imbalance &

impaired bowel function, may cause perforation or ulcers

NURSING:• Perform health history, PE• Monitor stool consistency/pattern of defecation• Increase intake of fluid• Consult dietician• Frequent ROM, Ambulation• Administer laxatives, stool softeners, enemas as ordered• Provide time and privacy for bowel elimination

PATHO:• Motility disorder of the lower GI tract- no identifiable cause• Commonly occurring; 20% of people; Younger people; (Women more than men)

• CNS regulation of the motor & sensory functions of the bowel is altered• Increased motor reactivity of the small intestine & bowel in response to

food intake, hormonal influences, physiologic or psychological stress• Characterized with visceral hyperactivity and hyperactivity of the GI tract,

including mucus production

MANIFESTATIONS:• Abdominal pain– May be relieved by defecation– May be intermittent and colicky/dull & continuous• Altered bowel elimination– Constipation– Diarrhea– Mucous stools• Abdominal bloating, flatulence, tenderness (esp over sigmoid colon)• N/V

DIAGNOSTICS:

• Based on the presence of abdominal pain or discomfort atleast 3 days per month in the last 3 months that has two of the three following characteristics– Relieved by defecation– Associated with changes in frequency of elimination– Associated with a change in stool form• Stools for occult blood, O&P, WBCs

TREATMENT:Meds for management of manifestations

• Bulk forming laxatives for constipation• Anticholinergic drugs- Bentyl, Anaspaz- inhibit bowel motility ,

relieves postprandial ab pain when taken 30-60 mins before meals• Antidiarrheals for diarrhea- Imodium or Lomotil• Antidepressants- tricyclis or SSRIs (Zoloft, Prozac)

Nutrition support - Additional dietary fiber;Limiting lactose, fructose, sorbitol; reducing gas forming foods; Limiting caffeine intake

NURSING:Health history; Physical examination• Education is the key! Reduce stress & anxiety• Referrals to counselors• Nursing care related to constipation and diarrhea *dietary changes

PATHO:• Inflammation of the vermiform appendix• Common cause of acute abdominal pain, most common emergency surgery (males more than female, young)• Located in the right iliac region…called McBurney’s point• Most common cause is secondary to obstruction– Feces, Stones, Foreign Body, Inflammation, Tumor, Parasites, Edema of lymph tissue• Appendix fills with fluid secreted from mucosa, pressure increases, inflammation, edema, ulceration, & infection may result as well as purulent exudate• Within 24-48 hours, tissue necrosis and gangrene results leading to perforation• Classified

1. Simple Appendicitis2. Gangrenous Appendicitis3. Perforated Appendicitis

MANIFESTATIONS:•Continuous mild generalized or upper abdominal pain with pain intensifying and localizing at McBurney’s point• Aggravated by movement, walking or coughing• Rebound tenderness is noted• Extension/Internal rotation of right hip increases pain• Low grade temp, anorexia, N/V• Perforation, Peritonitis, and Abcess are complication

DIAGNOSTICS:

• Rapid diagnosis and treatment is imperative• Abdominal ultrasound• Abdominal X-rays• IVP• UA• Pelvic exam

TREATMENT:

• IVFs restore or maintain vascular volume, prevent electrolyte imbalance• Antibiotic therapy (Prior to Surgery & Post-Op)– Third generation cephalosporin- Claforan, Fortaz, Rocephin• Appendectomy is performed– Either laproscopic or laparotom

NURSING:• Health History; Physical Examination• Keep NPO Acute Pain• Monitor VS, especially temperature• IVFs as ordered Risk for Infection• Assess wound, Abd girth, Post-op pain• Pain Management

PATHO:

• Inflammation of the stomach and small intestine Bacterial or viral infection, parasites or toxins produces inflammation, tissue damage and manifestations caused from two mechanisms: (1.) the production of exotoxins-impair intestinal absorption & cause secretion of electrolytes & water (Staph, clostridium, E coli)(2.) invasion and ulceration of the mucosa- damage tissue more directly (Shigella, Salmonella)• “food poisoning”• Causes: Bacteria, Virus, Parasites, Toxins• Generally mild and self limited• Debilitating for very young, very old, and immunocompromised

MANIFESTATIONS:

• GI Effects: Anorexia, N/V, Abd pain, Cramping, Boborygm)(loud hyperactive bowel sounds), Diarrhea• General Effects:Malaise, Weakness, Muscle aches, H/A, Dry skin, Dry mucous membranes, Poor skin turgor, Orthostatic hypotension, Tachycardia, Fever

DIAGNOSTICS:

• Labs F/E Balance, ABG• Stool culture• Stools for occult blood, O&P, WBCs• Sigmoidscopy

TREATMENT:

• No drug treatment is required unless severly ill or manifestations are prolonged.• Antibiotic therapy specific to the organism• Antidiarrheal may be prescribed• Replace fluid & electrolytes• Oral/IV rehydration-NS or Ringer’s solution; Lactated Ringer’s if metabolic acidosis present• Gastric Lavage-washing out stomach if Botulism• Plasmapheresis-plasma exchange therapy• Dialysis

NURSING:• Health History; Physical Exam• Monitor frequency, characteristics of bowel movements• Assess bowel sounds• Measure abd girth• Standard precautions• Limit food intake if acute• Monitor lab values• I&O, Weigh Daily, Vital Signs• Education

PATHO:• Polyp-Mass of tissue arising from the bowel wall and protrudes into the lumen• Most polyps, result from some form of genetic (DNA) mutation in one of the colon lining cells. • Healthy cells grow and divide in an orderly way — a process that's controlled by two broad groups of genes. • Mutations in any of these genes can cause cells to continue dividing even when new cells aren't needed. In the colon and rectum, this unregulated growth can cause polyps to form, and over a long period of time, some of these polyps may become malignant

• May develop at any portion of the colon• Vary in size; may be single or multiple• Approximately 30% of people over 50 have polyps• Most are benign; Some are malignant

MANIFESTATIONS:

• Most are asymptomatic• Intermittent, painless rectal bleeding, bright or dark red• Larger polyps may cause abdominal cramping, pain or manifestations of obstruction• Diarrhea• Mucous discharge may be present

DIAGNOSTICS:

• Sigmoidoscopy/Colonoscopy

TREATMENT:

• Polypectomy– May be cauterized or completely excised depending on the type of polyp– Some cases a total colectomy may be performed• TX also depends on histologic exam of the tissue removed• Chemo/Radiation may be necessary if the polyp is malignant

NURSING:• Health History• Post-op Care ( Monitor for hemorrhage post-op)• Administer Cathartics/Cleansing enemas as prescribed• Monitor F/E Imbalances• Client education:because polyps tend to reoccur, a colonoscopy is recommended in 3 years and then every 5 years if no polyps are detected.

PATHO:

• Hemorrhoids are swollen veins in the anal canal• Develop when venous return from the anal canal is impaired. • Straining increases venous pressure and is the most common cause of distended hemorrhoids• Classified as internal or external– Veins can swell inside the anal canal to form internal hemorrhoids– Veins can swell near the opening of the anus to form external hemorrhoids– May have both types at the same time– May prolapse or protrude as they enlarge

Risks

Bouts of diarrhea or constipation

pregnancy

Obesity

low fiber diet

prolonged sitting

MANIFESTATIONS:

• “Normally” asymptomatic; painless• Internal Hemorrhoids– Rectal bleeding is possible; may even cause anemia; mucous discharge; feeling of incomplete evacuation• External Hemorrhoids– Anal irritation is possible; feeling of pressure; difficulty cleaning perineal area

DIAGNOSTICS:

• Client’s history and physical • External hemorroids visible• Anoscopic exam

MANIFESTATIONS:

• “Normally” asymptomatic; painless• Internal Hemorrhoids– Rectal bleeding is possible; may even cause anemia; mucous discharge; feeling of incomplete evacuation• External Hemorrhoids– Anal irritation is possible; feeling of pressure; difficulty cleaning perineal area

TREATMENT

• Bulk-forming laxatives• Stool softeners• Suppositories or local ointments• Warm sitz baths• Bed rest• Compresses• High fiber diet; increased water intake• Sclerotherapy-injecting chemical irritant into tissues around hemorrhoid to induce inflammation, fibrosis, & scarring. Minimal pain• Hemorrhoidectomy- hemorrhoids surgically excised, few complications (laxer or conventional)

NURSING:

• Primary prevention of symptomatic hemorrhoids*dietary fiber intake, fluid, exercise• Post-Op Care – monitor V/S q4hrs, urine op, clean with sitz bath after defacation– Assessment?– Pain Control?– Elimination?• Client teaching– Home care? – OTC Meds? – Nutrition

PAHTO:

• Formation of stones within the gallbladder or biliary duct system• Gallstones form when several factors interact: abnormal bile composition, biliary stasis, and gallbladder inflammation. Most composed of cholesterol & migrate into ducts.*CAN LEAD TO CHOLECYSTITIS

MANIFESTATIONS: epigastric fullness after a large or fatty meal distention may cause biliary colic-steady severe pain in the epigastric region (RUQ) radiating to

the back and shoulder blade (lasts 30mins-5hrs) Obstruction can cause jaundice, pain, liver enzymes &

pangreatitis N/V

DIAGNOSTICS:

• Serum Bilirubin (reduced)• CBC (elevated WBC)• Amylase & Lipase (pancreatitis)• Flat plate of abdomen (show gallstone with high calcium)

Acute Pain

Constipation

Risk for Infection

MANIFESTATIONS: epigastric fullness after a large or fatty meal distention may cause biliary colic-steady severe pain in the epigastric region (RUQ) radiating to

the back and shoulder blade (lasts 30mins-5hrs) Obstruction can cause jaundice, pain, liver enzymes &

pangreatitis N/V

DIAGNOSTICS:

• Serum Bilirubin (reduced)• CBC (elevated WBC)• Amylase & Lipase (pancreatitis)• Flat plate of abdomen (show gallstone with high calcium)

TREATMENT:• Ursodiol (Actigall) and Chenodiol (Chenix) reduce cholesterol content of stone thus dissolve stones– Disadvantage-cost, long duration (2 yrs or more), high incidence of reformation, hepatotoxic• Antibiotics may be ordered• Questran (Cholestyramine)-used to treat pruritus (itching)-accumulation of bile salts under the skin-excreted in feces• Pain Management-Narcotic AngalgesicsMorphine• Laparoscopic cholecystectomy• Open cholesystectomy– T-Tube Care• Nutrition– Eliminate food intake during acute attack; NG tube may be inserted; eliminate dietary fat; Fat soluble vitamins if bile flow is obstructed• Lithotripsy

Nursing:

• Health History/Physical Examination• Reduce fat intake• Pain Management• Fowler’s Position• Assess V/S, temp, nutritional status, lab results• Dietary/Nutritional consult• Assess abdomen• TCDB, IS• Ambulate as tolerated/ordered

PATHO:INFLAMMATION of gallbladder

Acute - follows obstruction of cystic duct by a stone*causes ischemia*bacterial/chemical inflammation*leads to necrosis & perforation of gallbladder wallS/S- RUQ pain tender to palpation 12-18 hrs/ anorexia/N & V/ fever & chills

Chronic - by repeated bouts of acute or persistent irritation, may be asymptomatic

Complications:1. Empyema2. Gangrene3. Obstruction4. Perforation

DIAGNOSTICS:

• Serum Bilirubin• CBC• Amylase (0-130 u/L) Lipase (0-160u/L• Flat plate of abdomen• Ultrasound of gallbladder• Gallbladder Scan

MANIFESTATIONS: Abrupt onset, severe &

steady RUQ of abdomen, radiate

to back, last 12-18 hrs Aggravated by movement

& breathing

Review of Anatomy of GI

1. LIVER- Functions-

makes bile (700-1200mL daily), necessary for fat digestion & absorption & stores it in the gallbladder; receives nutrients absorbed by small intestine & metabolize them so can be used by cells of body

stores fat soluble vitamins A,D, E, K

Location- R side of abdomen, inferior to diaphragm, anterior to stomachBile- greenish, watery solution contains bile salts, cholesterol, bilirubin, electrolytes, water & phospholipids

TREATMENT:• Ursodiol (Actigall) and Chenodiol (Chenix) reduce cholesterol content of stone thus dissolve stones– Disadvantage-cost, long duration (2 yrs or more), high incidence of reformation, hepatotoxic• Antibiotics may be ordered• Questran (Cholestyramine)-used to treat pruritus (itching)-accumulation of bile salts under the skin-excreted in feces• Pain Management-Narcotic AngalgesicsMorphine• Laparoscopic cholecystectomy• Open cholesystectomy– T-Tube Care• Nutrition– Eliminate food intake during acute attack; NG tube may be inserted; eliminate dietary fat; Fat soluble vitamins if bile flow is obstructed• Lithotripsy- shock waves by ultrasound break up stones (watch for colic)

MANIFESTATIONS: Abrupt onset, severe &

steady RUQ of abdomen, radiate

to back, last 12-18 hrs Aggravated by movement

& breathing

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