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127 Cards in this Set

  • Front
  • Back
GI tract

Supplies nutrients to body by ingestion, digestion and absorption

Enteric nervous system has receptors for pressure and movement

Venous blood drains from GI tract to liver


Parietal layer covers abdominal cavity wall & visceral layer covers organs

Ingestion
Appetite stimulated by ghrelin and suppressed by leptin

Mastication and saliva in mouth


Deglutition (swallowing) by mouth, pharynx and esophagus


Upper esophagus striated skeletal muscle and distal is smooth muscle with an upper and lower esophageal sphincter



Digestion
Stomach mixes food with gastric secretions

Parietal cells secrete HCl to create acidic environment, chief cells secrete pepsinogen to break down proteins, and intrinsic factor promotes B12 absorption


Small intestine continues digestion and absorbs nutrients with villi


Carbohydrates broken down to monosaccharides, fats to glycerol & fatty acids

Elimination
Large intestine absorbs water and electrolytes

Microorganisms break down proteins & synthesize vitamin K & some B vitamins


Valsalva maneuver increase intra-abdominal pressure, contraindicated cardiac problems due to decrease BP

Liver
Lobule is functional unit

Rows of hepatocytes around central vein and Kupffer cells between


Blood enters liver from portal vein

Pancreas
Endocrine and exocrine functions
Consists of head, body and tail
Secretes enzymes for digestion: trypsinogen, chymotrypsin, amylase and lypase
Makes hormones in the Islets of Langerhans
: beta cells secrete insulin and amylin, alpha cells secrete glucagon

Subjective assessment of GI
History: pain, n/v/d, constipation, last BM, weight loss

Diet history: 24 hour recall


Recent travel: exposure to hepatitis or parasite


Allergies


Past medical history of GI problems


Medications: may effect n/v or liver problems

Objective assessment of GI

Start at oral cavity: moist and pink mucosa, lesions, teeth, protrusion of tongue in midline, swallowing


Abdomen: masses, scars, bowel sounds in 4 quadrants, tenderness, nonpalpable liver or spleen, tympany


Anus: lesions or hemorrhoids, sphincter tone, stool soft, brown, heme negative





Diseases that cause constipation/diarrhea
Ulcerative colitis

Cancer


Diverticulitis


Anxiety disorders


Parasitic infections


Food allergies


Celiac disease

Electrolyte imbalance
In acute situation, imbalance can happen rapidly
Vomiting & gastric suctioning

Loss of H+, Cl-, K+


Metabolic alkalosis & hypokalemia (<3.5meq/L)


Diarrhea


Loss of K+, Na+, Mg+


Metabolic acidosis, hypokalemia & hypomagnesemia (<1.5meq/L)

Blood Tests
Amylase and Lipase: diagnoses acute pancreatitis
Gastrin: secreted by stomach antrum & duodenum to produce gastric acid, diagnose tumor or reason for gastric ulcers

Radiology

Upper GI and small bowel series: fluoroscopic x-ray study w contrast to diagnose structural abnormalities, NPO 8-12 hr, stool may be white

Ultrasound: show size & configuration of organ, NPO 8-12 hr


Barium enema: fluoroscopic x-ray to test motility and function, contrast medium administered rectally, bowel prep pre-op, cramping and laxative after


Cholangiography: images of biliary, hepatic and pancreatic ducts


CT scan: may use oral or IV contrast medium

Liver Biopsy
Percutaneous procedure

Check coagulation status and explain holding breath after expiration when need is inserted


After procedure, keep patient lying on right side for 2hr and flat for 12 hr, check vital signs

Endoscopy

Gold standard for diagnosis: uses flexible fiber-optic scope

Esophagogastroduodenoscopy (EGD): visualize esophagus to duodenum, conscious sedation, NPO for 8 hr before & until gag reflex returns, warm saline gargle for sore throat, vitals & temp

Colonoscopy: visualize colon up to ileocecal valve for polyps and routine screening, bowel prep (Golytely or enema) with clear liquid diet 1-2 days, may cause cramping due to air inflation, observe for rectal bleeding & vitals

Fecal tests
Fecal analysis: examined for mucus, blood, parasites and fat content, must keep diet free of red meat for 24-48 hr before occult blood test
Stool culture: presence of bacteria i.e. C. diff

Obesity
Weight gain in adulthood characterized by adipocyte hypertrophy: cell volume increases several thousandfold to accommodate lipid storage

Epidemic proportions: in US most common nutritional problem affecting 1/3 of the population


2nd leading cause of preventable death & 3rd reason for liver transplant

Body mass index
BMI = weight (kg) / height (m) squared

< 18.5 underweight


18.5 - 24.9 normal


25 - 29.9 overweight


> 30 obese


> 40 severely obese





Bariatric surgery
Restrictive bariatric surgery reduces the size of the stomach or the amount allowed to enter the stomach

Malabsorptive procedures decrease the length of the intestine so less food is absorbed


Weight loss can be considerable during first 6-12 months

Bariatric surgery criteria

BMI > 40 with 1+ obesity related complication


18 years or older


Understands risks and benefits


Has been obese for >5 years and tried and failed to lose weight


No serious endocrine problems


Psychiatric and social stability


Availability of team of health care providers


Surgery would decrease or eradicate high-risk conditions

Bariatric Surgery Pre and Post-Op
Preoperative ensure that over-sized equipment is available

Postoperative keep HOB 40 degrees to reduce abdominal pressure, assess for re-sedation due to storage of anesthetics in adipose tissue, delayed wound healing and pain


Diet is sugar-free clear liquids, high-protein liquid diet by discharge followed by high protein, low carb/fat/fiber in 6 small meals



Bariatric long-term complications
Overeating leads to gaining back weight
Malnutrition i.e. anemia, chronic diarrhea, malabsorption
Guilt
Flabby skin after weight loss
Pain associated with eating
Postpone pregnancy for at least 12 months due to malnutrition
Health risks associated with obesity
High LDL & triglycerides

HTN & chronic inflammation


Type 2 diabetes


GERD, gallstones & non-alcoholic steatohepatitis


Decreased total lung capacity & sleep apnea


Osteoarthritis & gout


Cancer i.e. breast, colorectal, pancreatic


Metabolic syndrome


Psychosocial problems i.e. low self-esteem and major depression

Metabolic syndrome (syndrome X)
Characterized by 3 or more of the following conditions:

Waist circumference >40 men and >35 women


Triglycerides > 150


HDL <40 men or <50 women


Blood pressure >130/85


Fasting blood glucose >110

Upper GI bleeding Symptoms

Above junction of duodenum and jejunum

Hematemesis: bloody vomitus, appears bright red if active or like coffee grounds if slow due to interaction with HCl in stomach

Melena: black tarry stools caused by digestion of blood in GI tract due to iron, metallic smell, color change may be caused by diet i.e. beets or iron supplements



Bleeding: esophageal origin
Chronic esophagitis r/t GERD, mucosa-irritating drugs (NSAIDs), alcohol, cigarettes

Mallory-weiss tear (tear in mucosa near esophago-gastric junction) r/t severe retching/vomiting, emergency


Esophageal varices dilated tortuous veins in lower esophagus as a result of portal hypertension, anything increasing pressure (cough, sneeze) or irritation (vomit) may cause massive bleeding

Bleeding: stomach and duodenal origin
Gastric cancer

Hemorrhagic gastritis


Peptic ulcer disease


Polyps


Stress-related mucosal disease


Risk factors: NSAIDS, GERD, steroids, alcoholism

Upper GI bleeding: assessment

Keep in Bed, emergency until diagnosed

VS every 15-30 min

Assess shock sxs i.e. decreased urine, pallor, hypotension, tachycardia, weak pulse, cool extremities, prolonged cap refill


Assess respiratory status and apply O2


Assess abdomen including bowel sounds, rigid & board-like may indicate perforation and peritonitis


Treatment ASAP

Upper GI bleeding: management
2 IV lines 16 or 18 gauge established for fluid and blood replacement, check if patent by flushing
Begin with isotonic (lactated Ringer's solution)
Packed RBC and fresh frozen plasma if massive hemorrhage (orthostatic hypotension with 10 mmHg drop in DBP denotes 1,000 mL loss)
Insert indwelling urinary catheter to monitor urine output

Endoscopic cauterization to thrombose bleeding vessel
Drugs to decrease bleeding and HCl secretion or neutralize

Lower GI bleeding

Large and small intestine


Causes: diverticulosis, radiation therapy, cancer, inflammatory conditions, infection


SXS: melana, maroon or blood in stools, fever, dehydration, hematochezia, abdominal pain or distention

Hiatal hernia
Protrusion of stomach through esophageal hiatus of diaphragm into thorax due to weakening muscles of diaphragm and increased abdominal pressure i.e. obesity, pregnancy, ascites, heavy lifting

Sliding hernia: most common, occurring when esophago-gastric junction and portion of fundus slide upward, usually only when supine


Rolling hernia: fundus and greater curvature of stomach rolls into thorax forming a pocket, acute version is a medical emergency


Conservative treatment similar to GERD, surgery if unresponsive

Abdominal Hernia

Displacement or protrusion of a segment of the bowel through an area of weakness in the abdominal wall i.e. umbilicus or inguinal


Reversible (positioned with gentle pressure) or irreversible


Strangulated: leads to small bowel obstruction


Manifestations: visible protrusion, diffuse pain, diagnosis by CT or US


Risk factors: male gender, advanced age, pregnancy, obesity, genetics


Treatment: surgery if strangulated, no lifting, prevent constipation

Esophagitis

Inflammation of the mucosal lining


Causes: GERD, infection (Candida, CMV, HIV, herpes), chemo or radiation


Symptoms: heartburn, dyspepsia, dysphagia, retrosternal chest pain


Diagnosis: CBC, fecal occult blood, barium studies and endoscopy, ECG


Complications: anorexia, weight loss, Barrett's esophagus, perforation (rare)


Tx: Pain management, H2RB, PPI, lifestyle changes (GERD), corticosteroids (IBD)

Gastroesophageal reflux disease (GERD)
Backward flow GI contents into esophagus

Reflux esophagitis characterized by acute symptoms of inflammation


Due to elevated gastric volume or intra-abdominal pressure, decreased tone or inappropriate relaxation of lower esophageal sphincter (LES)


Risk factors: Alcohol, asthma or BP meds, obesity, tobacco


Complications: esophagitis, Barrett's esophagus (metaplastic changes and risk of adenocarcinoma), respiratory problems

GERD clinical manifestations

Dyspepsia (heart burn)


Regurgitation (acid in mouth)


Hypersalivation or water brash


Dysphagia (difficulty) or odynophagia (painful swallowing)


Chronic cough, asthma


Atypical chest pain


Eructation, flatulence or bloating after eating


Nausea and vomiting

GERD collaborative care
Decrease high-fat foods

Fluids between rather than with meals


Avoid milk products and snacking 3 hours before bed


Avoid triggers i.e. alcohol, chocolate, peppermint, caffeine, tomatoes, orange juice, colas


Elevate HOB with 6 inch blocks


Weight reduction


Decrease HCl with proton pump inhibitors and H2 receptor blockers

Gastritis
Inflammation of the gastric mucosa due to breakdown of gastric mucosal barrier

Acute or chronic


Risk factors: NSAIDs & corticosteroids inhibit prostaglandin synthesis, alcohol abuse, irritating spicy foods, H. pylori and E. coli


Most common cause is bacterial


Autoimmune gastritis related to intrinsic factor deficiency (B-12)


Hyperplasia may lead to esophageal or gastric cancer



Gastritis clinical manifestations
Acute: abdominal tenderness, bloating, n/v, anorexia
If bleeding, hematemesis
, melena, intravascular depletion and shock
Chronic: same symptoms or asymptomatic, loss of intrinsic factor may lead to pernicious anemia and neurologic complications, associated with gastric adenocarcinoma and MALT lymphoma

Gastritis treatment

Acute: fluid and electrolyte balance, discontinue causative agents i.e. NSAIDs and corticosteroids, H2 blockers and PPI, antibiotics for H. pylori


Chronic: specific to causative agents (3 antibiotic course for H. pylori and long-term surveillance), assess hemorrhage

Peptic ulcer disease (PUD)
Mucosal lesion of stomach (gastric) or duodenum (most common) due to impaired gastric mucosal defenses

Use endoscopy to differentiate
HCl acid & pepsin causes cellular destruction, inflammation and histamine release, resulting in vasodilation and further HCl acid release


H . Pylori may alter gastric secretion and produce tissue damage


NSAIDs inhibit prostaglandins


Smoking, high stress, alcohol and coffee stimulates acid secretion

Stress ulcer
Acute gastric mucosa lesion occurring after an acute medical crisis or trauma

Associated with head injury, major surgery, burns, respiratory failure, shock and sepsis


Principle manifestation: bleeding caused by gastric erosion

PUD complications
Hemorrhage causing hematemesis

Perforation emergency requiring immediate surgical closure, sudden severe abdominal pain, rigid abdominal muscles, weak pulse/tachycardia


Pyloric obstruction causes vomiting due to stasis and gastric dilation


Intractable disease no longer responds to conservative treatment or recurrences interfere with ADLs

PUD clinical manifestations
Epigastric tenderness at mid-line between umbilicus & xiphoid process

Dyspepsia


Sharp, burning or gnawing pain, often 30 minutes-2 hours after meals if gastric or 2-5 hours if duodenal


Sensation of abdominal pressure, fullness or hunger

PUD pain management
Discontinue NSAIDS

May give Tylenol or narcotics if severe pain


Promoting healing of gastric mucosa: H2 receptor blockers, PPI (long-term)


Eradicate H. pylori infection: amoxicillin and clarithromycin for 1-2 weeks with subsequent testing

PUD diet therapy
Directed toward neutralizing acid and reducing hyper-motility

Bland, nonirritating diet is recommended during acute symptomatic phase


Avoid bedtime snacks, carbonated beverages, alcohol and tobacco

PUD complications: perforation
Monitoring and early recognition of complications is critical

If small may heal itself, if larger sudden cramping abdomen or back, rigid and board-like, shallow/rapid respirations, weak pulse, no bowel sounds
NG tube inserted for aspiration and gastric decompression


Blood volume replaced with Lactated Ringer's, albumin solution, packed RBC


Monitor urine output, NPO, give antibiotics and pain medications


Open or laparoscopic procedure to repair

PUD complications: hemorrhage
Acute exacerbation: managed as an upper GI bleed

Acid suppressive agents used to stabilize clot by raising gastric pH

PUD complications: gastric outlet obstruction

Pyloric obstruction related to edema, spasm and fibrous tissue


Generally responds to medical therapy


Decompress stomach with NG tube suction


Clamped after several days to measure gastric residual volume, when < 200 mL, start oral fluids gradually


IV fluids and electrolytes administered according to electrolyte and fluid imbalances



PUD surgical therapy
Excision of lower stomach if complications are unresponsive to treatment: Billroth I (connected to duodenum) or Billroth II (to jejunum)
Monitor for acute upper GI bleeding
Delayed gastric emptying for 1 week: use NG tube suctioning to let bowel rest
Recurrent ulceration in about 5% of clients

PUD risk for nutritional deficit
Deficiencies of Vit B12, folic acid and iron
Impaired calcium metabolism
Reduced absorption of calcium and vitamin D absorption as result of partial removal of stomach

Caused by shortage of intrinsic factor
Monitor CBC for signs of megaloblastic anemia and leukopenia

Gastric cancer
Adenocarcinoma in the stomach wall
Early cancer may be asymptomatic
Ingestion & abdominal discomfort
Risk factors: gastritis, H. pylori, autoimmune inflammation, exposure to irritants i.e. anti-inflammatory agents, tobacco
Associated w consumption of smoked foods, salted fish/meat, pickled vegetables

Complications of gastric surgery
Hemorrhage
Reflux aspiration
Wound infection
Sepsis
Reflux gastritis
Paralytic ileus
Bowel obstruction
Dumping syndrome

Dumping syndrome
Food rapidly enters jejunum without duodenal processing
Caused by rapid movement of extracellular fluids into bowel
Fluid shift creases circulating blood volume
Usually subsides in 6-12 months

Dumping syndrome: symptoms
Vertigo
Tachycardia
Syncope
Diaphoresis
Pallor
Palpitations
Nausea
Desire to lie down

Dumping syndrome: interventions
High protein, moderate fat, low carb diet
Lie down after meals
Eat little and often
Chew food well
Don't drink with meals

Irritable bowel syndrome (IBS)
Alternating diarrhea and constipation, abdominal pain, bloating
Collection of symptoms, lab tests rule out other disorders

Individualized treatment focused on triggers i.e. stress or diet
Increase fiber slowly, avoid gassy foods (broccoli, cabbage, milk)
Psychologic therapies
Drug therapy for symptoms

Probiotics

Inflammatory bowel disease (IBD)
Autoimmune disease of widespread tissue destruction in intestinal tract: Crohn's disease or Ulcerative colitis

Characterized by periods of remission and exacerbation


SXS: diarrhea, bloody stools, weight loss, abdominal pain, fever, fatigue
Linked to environmental factors (diet, stress, smoking), antibiotic use and genetics (family history IBD or colon cancer)
Increased incidence of colorectal cancer


Diagnosis: r/u infection, endoscopy, imaging, serum and stool studies

Crohn's disease
Regional enteritis: occurs anywhere along GI in skipping lesions (cobblestone appearance), distal ileum and R colon most common
Chronic inflammation with remissions and exacerbations
Usually involves entire thickness of bowel wall (transmural)

RLQ pain and cramping
Complications: fistula, ulcerations, microscopic leaks causing peritonitis, strictures causing bowel obstruction


Associated with other autoimmune diseases (arthritis)


Occurs in younger folks, esp. whites

Ulcerative colitis
Starts in rectum, spreads in a continuous fashion up the colon
Involves only mucosa and sub-mucosa
Ulcerations, thickening, edema, bleeding, abscesses
Occurs in all ages, more common than Crohn's

10 to 20 stools per day, bowel, obstruction, tenesmus, LLQ pain
Complications: water & electrolytes imbalance (malabsorption), protein loss (cell breakdown), rectal hemorrhage, perforation

May be cured by total colectomy

IBD treatment
Start with Aminosalicylates and progress to antibiotics, corticosteroids and immunomodulators

Bowel rest by decreasing food intake
Anti-inflammatory drugs and pain relief


Accurate I&O, # and appearance of stool
Great nutrition because of malabsorption


Quitting smoking (stimulated GI tract), reduction of stress, emotional support


Emergency care: hemorrhage, megacolon or obstruction

Diverticulosis

Diverticula are saccular dilation or out-pouching of mucosa that develop in the colon


Diverticulosis (state of) and diverticulitis (inflammation)


Symptoms: may be asymptomatic, N/V, LLQ pain, fever, chills, palpable mass


Most common >45 and obese


Higher risk of diverticulitis if diagnosed before age 50


Risk factor: low fiber diet, related to pressure of stool staying inside colon

Diverticular disease
Occurs when particles or bacteria are caught in diverticula, becomes irritated and inflamed, congested with blood

May bleed or lead to perforation when trapped mass erodes bowel wall, leading to hemorrhage and peritonitis


Treatment: Bowel rest, IV fluids, antibiotics, nasogastric decompression


Clear liquid to low fiber to high fiber diet


Surgery (colectomy) based on Hinchey classification of inflammatory changes and integrity of bowel wall

Diverticular disease prevention
Primary: high fiber diet, lose weight if obese

Secondary: bulk laxatives, avoid straining, coughing, lifting


Tertiary: surgery (colon resection), prevention of complications

Colorectal cancer (CRC)
Third most common cancer, second cause of death, men>women

Adenomatous polyp grows, invades muscularis mucosa, often metastasizes to liver


Risk factors: genetic, smoking, low fiber/fruits/veg, high red/processed meat, irregular bowel movements, obesity, physical inactivity


Symptoms: often asymptomatic in early stages, abdominal pain, mass, change in bowel habits, anemia, obstruction, bright red blood in stool, rectal discomfort

Colon cancer prevention
Primary: low fat & high fiber diet, limited ingestion of refined food, 2-3 L fluid intake

Secondary: early detection by annual fecal occult blood test (yearly) and rectal exam if > 50 or >40 if high risk, regular flexible sigmoidoscopy (every 5 years), colonoscopy (gold standard, every 10 years)


Tertiary: surgery, chemotherapy, radiation



Colon cancer diagnostic tests
Digital rectal exam

Fecal occult blood test (FOBT)


Sigmoidoscopy and colonscopy: visualize and remove polyp to test for cancer


Clear liquid diet for 24-48 hours and 4L of polyethylene glycol (PEG) the evening before, stools should be clear or yellow

Colon cancer treatment
Surgery: tumor resection with margins, removal of lymph nodes and exploration of abdomen to determine spread

A temporary and permanent ostomy may be placed


Chemotherapy if stage II+


Radiation as adjunct post-op or palliation

Colon surgery pre-op care
Assess knowledge

Provide information: ostomy, NG tube, changes in bowel function, pain


Assist to verbalize feelings about treatment


Prep for surgery: reduction of colonic bacteria w polyethylene glycol lavage (GoLytley or MiraLax) and oral antibiotics

Bowel surgery nursing diagnosis
Risk for infection

Anxiety


Risk for body image disturbance


Alteration in nutrition less than body requirements


Risk for ineffective management of therapeutic regimen

Bowel surgery post-op care
Pain management

Pulmonary care


Assess bowel function and provide bowel rest (NG tube suction), progress to clear liquids to normal diet


Wound care, often drains (Jackson-Pratt, Hemovac)


Ostomy care


Nutritional needs


Sexual dysfunction due to cutting nerves


Monitor for infection: edema, erythema & drainage, WBC count, fever

Ileostomy
Ileum is brought to abdominal wall and stoma is created

Indications: ulcerative colitis, Crohn's, cancer, trauma


Fecal material is more liquid, larger volume and electrolyte malabsorption

Ostomy
Surgical procedure that allows intestinal contents to pass from bowel to opening on abdomen, permanent or temporary

Assess stoma every 4 hours: dark pink to beefy red, blue indicates ischemia & black-brown necrosis, no excessive bleeding, may be swollen for 2-3 weeks


Keep skin clean, dry, odor free, assist to visualize and do self-care


Skin barrier, ensure adhesion, empty when 1/3 full, clear pouch post-op

Colostomy
Colon is brought to abdominal wall and stoma is created

The more distal the ostomy, the more fecal resemblance


May use irrigation and have regular bowel movements if sigmoid


Indications: rectal cancer, trauma, perforating diverticulum

Ileostomy
Ileostomy is liquid and drains continuously

Pouch is worn at all times: drainable pouch changed every 4-7 days


Monitor post-op for Na, K and fluid deficit


2-3L minimum intake, low-fiber diet and well-chewed food at first to prevent obstruction


Indications: Ulcerative colitis, Crohn's disease, trauma, cancer





GI Emergencies
Hemorrhage, dehiscence, evisceration, perforation of ulcer, peritonitis, obstruction

ABCs: Airway, oxygen, IV access (2 16/18 gauge) and BP management


NPO


Vital signs

Wound dehiscence and evisceration
Due to infection, edema, pressure

Common abdominal surgery due to pressure of movement


Use moist sterile dressing and prepare for surgery

Bowel obstruction

Content cannot pass through GI at pylorus (gastric outlet), small intestine or bowel, may be partial or complete

Mechanical: adhesion, tumor, volvulus (twisting), intussusception (telescoping), hernia

Non-mechanical: decreased peristalsis, neurogenic disorder


Symptoms: N/V, abdominal distention and cramping, anorexia, metabolic acidosis, severe electrolyte and fluid loss, no gas or BM


Caution with inserting any tubes

Special nutrition
NG tube: for short term feeding

HOB >30 during feeding and 2 hours after, may be NPO, suction or feeding, assess placement & residual prior to feeding, flush, oral and nasal care, site care, prevention of infection


Percutaneous endoscopic gastrostomy (PEG): long-term (>3 weeks)


Regurgitation less likely because cardiac sphincter remains intact

Functions of liver
Metabolic functions: carbohydrate, protein and fat metabolism, synthesis of plasma proteins & clotting factors, detoxification, makes corticosteroid hormones

Bile synthesis: bile salts, cholesterol & bilirubin, stored in gallbladder


Storage: glucose (glycogen), vitamins, fatty acids, amino acids (albumin)


Mononuclear phagocyte system: breakdown old RBCs, WBCs & bacteria into billirubin

Bilirubin cycle
RBCs destroyed by macrophages: hemoglobin to heme & globin

Globin & iron are recycled, heme becomes unconjugated bilirubin (insoluble) & is attached to albumin


Bilirubin is conjugated in liver, excreted in bile to intestines, reduced by intestinal bacterial


Excreted in feces (stercobilin) & urine (urobilin): causes fecal matter to be dark brown and urine to be yellow

Hepatitis
Inflammation of liver

Acute viral hepatitis is most common (Hepatitis A through G, CMV, Epstein-Barr, adenovirus)


Non-infectious hepatitis may be caused by drugs (recreational and prescription), autoimmune disease, metabolic disorders, alcohol abuse

Hepatitis etiology
Viral hepatitis caused by one of 5 major viruses, A-E

A, B & C are most common in US


90% of post-transfusion and community acquired hepatitis are caused by viruses


Viruses identified by presence of antigens in blood


Symptoms: mild-flu like symptoms (nasuea, fatigue, malaise, RUQ pain) or acute hepatitis with jaundice


Phases: Asymptomatic infection (1), mild symptoms (2), progressive liver dysfunction (3), recovery (4)

Hepatitis A
Fecal-oral route: small outbreaks r/t fecal contamination of food, water, poor hygiene, crowded conditions, poor sanitation, institutions, raw fish or shellfish from contaminated water

Prevent by vaccine & immune globulin (IG) post-exposure, hand-washing & private room if stool incontinent

Hepatitis B
IV or SQ exposure to blood & body fluids, perinatal (high risk), sexual activity (considered 100x more infectious than HIV)


May cause acute or chronic disease: carrier if presence of HBsAg (HBV antigen) in blood for >6 months


Treatment: antivirals to decrease adenocarcinoma incidence


Vaccine for Hep B (3 IM injections)

Hepatitis C
Parenteral or mucosal exposure to blood or blood products, sexual contact, perinatal


Majority develop chronic infection, leading to liver disease & cirrhosis


Leading need for a liver transplant


Associated w HIV infection

Hepatitis D
Transmitted with or after HBV infection (co-infection)

Causes more virulent strain of hepatitis


Endemic in Mediterranean & Middle East

Hepatitis E
Fecal-oral route, often transmitted by contaminated water

Rare in US, epidemic in India

Hepatitis G
Transmitted by blood transfusion

Recently discovered

Hepatitis pathophysiology
Acute infection: liver damage due to cytotoxic cytokines & NK cells that lyse infected hepatocytes & inflammation, cells can regenerate if not complications

Chronic infection: chronic inflammation leading to fibrosis & cirrhosis


Inflammation can interferes with bile production, causing cholestasis & increased pressure around portal vein


Body's immune response to clear virus & damaged liver cells associated w lab changes

Hepatitis lab values
Elevated serum transaminase (AST) (10-40 IU/L) may be 3 times normal

Elevated ALT (6-50 IU/L)


Elevated alkaline phosphatase (ALP)


Elevated total bilirubin (0.3 to 2 mg/dL)


Prolonged PT (<20 sec)


Low serum albumin (made only in liver)


Thrombocytopenia

Hepatitis: preicteric phase sxs
Inflammatory process

Elevated temp & chills


N/V, fatigue, loss of appetite


Dyspepsia


Joint pain


Enlarged lymph nodes


Viral antibodies present


Elevated AST & ALT

Hepatitis: icteric phase sxs
Impaired bilirubin metabolism

Jaundice (sclera, hard palate, or skin if light-colored)


Pruritus due to bile salts under skin


Elevated total bilirubin


Dark, amber urine


Light brown to gray stools


RUQ tenderness

Hepatitis: posticteric phase
Lab values return to normal

Decreased jaundice


Improved appetite


Fatigue may last a long time

Hepatitis: nursing diagnosis
Fatigue: rest in bed and slowly increase activity

Fluid volume deficit: due to vomiting


Risk for infection


Altered nutrition: anorexia, pain while eating, impaired fat breakdown


Pain (right upper quadrant)


Impaired skin integrity r/t pruritus & itching, avoid harsh soap


Risk for injury r/t bleeding

Hepatitis treatment

Acute disease: nutrition (small, frequent meals, esp. morning), 2-3L fluid, physical & psychological rest


Chronic B&C: drug therapy using interferon & nucleoside analogs to prevent viral replication, diet of adequate calories to maintain weight & low fat if not tolerated, maintain fluid & electrolyte balance

Cirrhosis of the liver pathology

Chronic disease of the liver, characterized by diffuse inflammation & fibrosis (scar tissue) resulting in drastic structural changes and significant loss of liver function


Fatty infiltration leads to acute inflammation to cirrhosis


3/4 liver can be destroyed due to fibrotic changes prior to symptoms


Increased pressure on portal veins affects spleen, gallbladder & liver function



Cirrhosis of the liver risk factors

Viral Hepatitis (C is most common cause)


Non-alcoholic fatty liver disease (NAFLD) related to diabetes, obesity and HLD

Alcoholic liver disease (Laennec's Cirrhosis)

Sarcoidosis


Primary biliary cirrhosis


Right-sided heart failure


Alpha 1 antitrypsin deficiency

Cirrhosis of the liver symptoms
Early symptom is fatigue, often asymptomatic until advanced

Ascites with portal hypertension


Anorexia, n/v, GI distress, malnutrition


Weight loss masked by water retention


Jaundice


Anemia, leukopenia, thrombocytopenia


Coagulation disorders: Spider angiomas and increased bleeding


Encephalopathy

Portal hypertension
Pressure is elevated as liver damage (disorganized regeneration) results in abnormal blood vessels and impedes blood flow

Ascites


Esophageal & gastric varices (most dangerous complication)


Hemorrhoids

Ascites

Decreased synthesis of albumin (allowing movement of fluid out of blood vessels) and poor hepatic lymph flow


Increased nitric oxide leads to vasodilation, sodium retention of kidneys


Sodium restriction (<2g/day) & diuretics


Paracentesis may be required for respiratory distress: sterile procedure, complications include peritonitis & bleeding, monitor for hypovolemia & shock

Esophageal varices: pathology
High risk for hemorrhage

Small, tortuous veins that are enlarged and swollen due to portal hypertension


Increased abdominal pressure (cough, sneeze, Valsalva) cause bleeding


Screening every 2-3 years (may be asymptomatic until rupture)

Esophageal Varices: treatment

Risk of rupture: constipation, vomiting, coughing, alcohol


Stool softeners


Beta blockers


Prophylactic surgery if >5mm: endoscopic band ligation


Active bleeding is emergency: endoscopy with ligation, vasopressin, intra-hepatic porto-systemic shunt, balloon tamponade (keep scissors at bedside to cut if obstructs airway) with crystalloid and colloid fluids

Portal systemic encephalopathy
Major complication of cirrhosis

High levels of toxic substances, can occur quickly or over several days


Change in LOC, intellect, behavior, neuromuscular


Characteristic manifestation: flapping tremors of arms & hands


Due to elevated serum ammonia, hemorrhage, hypoxia

Portal systemic encephalopathy: nursing interventions
Decrease ammonia: restrict protein, increase CHO, enemas, neomycin to kill bacteria in GI, lactulose as laxative, hemodialysis

Skin integrity r/t malnutrition, pruritus, ascites, frequent stools


Prevent infection, careful drug admin, nutrition, good oral hygiene, small frequent meals (20-40g/day protein)

Cirrhosis of the liver: nursing diagnosis
Ineffective breathing patterns r/t ascites: high fowlers

Fatigue: rest


Excess fluid volume


Risk for infection: spleen inflammation


Risk for injury: bleeding, falls


Imbalanced nutrition: high calorie, low fat, normal protein


Pain


Skin integrity r/t pruritus & edema


Body image r/t jaundice

Cirrhosis: treatments

Antivirals (Viral Hepatitis)


Diuretics, beta-blockers, digoxin (Cardiac conditions)


Immunosuppressants (autoimmune disorder)


Symptomatic: treatment of pruiritis, zinc deficiency and osteoporosis


Liver Transplant

Galbladder

Problems of the biliary system and pancreas extends to other organs i.e. gallstones interfere or obstruct normal bile flow to duodenum, causes vascular congestions (decrease venous flow, edema & congestion contribute to initial inflammatory response)

Cholelithiasis

Gallstones develop when cholesterol, bile salts & calcium precipitate


Associated w disturbance in cholesterol metabolism & infection


Supersaturation of bile with cholesterol (most common type of stone), bile stasis, delayed emptying or change in bile concentration


Risk factors: genetics, sedentary lifestyle, female, obesity (fat), middle-aged women (40), estrogen therapy, oral contraceptives & pregnancy (changes cholesterol production or delays emptying of gallbladder)


Diagnosis: LFT and abd ultrasound

Acute cholecystitis
Inflammation of the gallbladder

Calculous cholecystitis (associated w gallstones or biliary sludge) is most common


Acalculous cholecystitis r/t immobility, fasting, infection


Symptoms: Colicky severe epigastric pain radiating RUQ, indigestion & N/V, children and elderly may have vague tenderness or jaundice


C/B perforation or gangrene

Chronic cholecystitis
Repeated episodes of cystic duct obstruction result in chronic inflammation may lead to pancreatitis, jaundice & pruritus

Flatulence, fat intolerance, dyspepsia, eructation, anorexia, n/v, abdominal pain


Biliary colic or steady pain: RUQ to R shoulder


Murphy's sign (deep breath while palpated R subcostal area illicits pain)


Steatorrhea

Cholelithiasis: nonsurgical
Low-fat diet, fat-soluble vitamin supplements, bile salts

Opioid analgesia w meperidine hydrochloride, antispasmodic or anticholinergic drugs, antiemetics


Percutaneous transhepatic biliary catheter insertion


Bowel rest, IV fluids


Antibiotics

Cholelithiasis: surgical
Laparoscopic cholecystectomy (preferred treatment)

Post-op: shoulder pain due to carbon dioxide retention in abdomen, use Sim's position (L side with L leg flexed), deep breathing & ambulation, return to activities in 1-3 weeks


Traditional cholecystectomy


Post-op: patient-controlled analgesia pump, antiemetics, prevent respiratory complications, wound care, T-tube care placed in common bile duct, NPO, diet is liquids to light meals avoiding excessive fat

Acute pancreatitis pathophysiology


Rapid onset and progression


Excessive pancreatic enzymes resulting in inflammation, increased pancreatic vascular permeability, edema, hemorrhage and eventually necrosis and shock


Etiology: idiopathic, alcoholism, biliary tract disease, infection, antibiotics, chemo post-op GI surgery (ERCP)


Diagnosis by history, labs and physical exam (ECRP if biliary disease)

Acute pancreatitis symptoms

Pain LUQ or middle abdominal, piercing & severe


Abdominal tenderness w rigidity & guarding


Nausea, vomiting, diarrhea


Low-grade fever & tachycardia


Intravascular damage from trypsin: blue ecchymoses on flanks (Turner's sign) or peri-umbilical (Cullen's sign)


Complications: sepsis, RDS, renal failure, GI hemorrhage, jaundice


Labs: elevated serum amylase, lipase & glucose, low calcium

Acute pancreatitis complications

Hemorrhage


Paralytic ileus


Cardiovascular: hypotension, hypovolemic or septic shock, renal failure


Pulmonary: pleural effusion, respiratory distress syndrome, pneumonia


Trypsin can increase clotting: disseminated intravascular coagulation


Diabetes mellitus


Multi-system organ failure

Acute pancreatitis treatment

Analgesics


NPO & TPN or IV fluids early stages


Antiemetics for N/V


Small, frequent moderate to high carbohydrate, high protein, low fat


Avoid foods that cause GI stimulation


Abstain from alcohol


Fat-soluble vitamin supplements


Surgery to repair pancreatic duct or biliary tree

Endoscopic retrograde cholangiopancreatography (ERCP)

Pre-op: NG tube may be inserted


Post-op: monitor drainage tubes, record output, meticulous skin care and dressing changes, maintain skin integrity

Bowel Obstruction treatment

Gastric or enteric decompression


Bowel rest with IV fluids


Tumor excision or colectomy


Emergency treatment for peritonitis or hemorrhage

Chronic pancreatitis
Progressive destructive disease of pancreas, characterized by remission and exacerbations, replaced by fibrotic tissue

Manifestations: gnawing or cramping abdominal pain, mild jaundice, malabsorption, weight loss, steatorrhea, may develop diabetes


Nonsurgical management: drug therapy, analgesics, enzyme replacement (amylase, lipase, trypsin), insulin, small bland meals, low fat, no caffeine, alcohol or smoking

Appendicitis

Inflammation of veriform appendix, from cecum at the terminal end of ileum


Obstruction of lumen by accumulated fecaliths, bacteria or parasites


Surgical emergency: risk of perforation and sepsis


Symptoms: anorexia, periumbilical pain to RLQ, vomiting


Treatment: antibiotics and appendectomy

Barrett's esophagus

Metaplasia from flat to columnar epithelial cells due to GERD


Increases cancer risk due to enzymes


Treatment: corticosteroids, lifestyle changes

Peritonitis

Inflammatory process affecting peritoneum: irritation/pathogens from perforated gallbladder or stomach


Abdominal pain, N/V, fever, chills, altered peristalsis, encephalopathy


Diagnosis: blood cultures, CT, x-ray


Treatment: aggressive antibiotics, control inflammatory process

Foreign Body

Swallowed object lodged in oropharynx, small intestine (>2cm) or pylorus (>6cm)


Symptoms: gagging, dysphagia, respiratory distress, bloating


Diagnosis: radiograph, ultrasound


Treatment: high Fowler's, pro-motility medications


Battery or magnet may be medical emergency due to necrosis, or obstruction

Gastroenteritis

Diarrhea and vomiting with fluid loss, electrolyte deficiency, fever, abdominal pain


Causes: osmotic, inflammatory, secretory, motility


Children and elderly most common


Organisms are spread by contact i.e. Norovirus (#1) and Salmonella (#2)


Treatment: broad spectrum abx, supportive (fluids and electrolytes)


C/B: colitis, toxic megacolon, perforation, sepsis

Intussusception

Abnormal movement of bowel that is folded back


Causes: common in infants due to altered peristalsis and respiratory infections, bariatric surgery, IBD, tumors


Untreated fatal in 5 days


Symptoms: lethargy, vomiting, colicky abdominal pain, palpable mass, diarrhea with blood/mucous


Diagnosis by contrast enema


Treatment: Reducing agent (barium, water-based, air) if no peritonitis/perforation, laparoscopic reduction or surgical resection

GI trauma

Penetrating: Gunshot or stabbing injury


Blunt force: Automobile accidents or domestic violence


Seatbelt may cause Cullen's sign (periumbilical trauma) or abdominal bruit (vascular trauma)


Symptoms: hemorrhage, altered consciousness, tachycardia, hypotension


Treatment: estimate blood loss, restore fluid status with colloids and crystalloids, prevent infection, surgical repair

Malnutrition: lab values and half life

Albumin 3.5-5.5 g/dL, 20 days


Pre-albumin 16-40 mg/dL, 3 days


Retinal binding protein 2.6-7.6mg/dL, 12 hours


Transferrin 200-400 mg/dL


Total Lymphocyte 1,800-3,000



Malnutrition: symptoms

Rapid turnover of epithelial and mucosal cells


Dry flaky skin


Brittle hair and nails


Bleeding gums


Muscle wasting


Ascites and peripheral edema