101: GI

General function of the GI tract

-physical breakdown of food into nutrients

-absorption of nutrients, vitamins, water and electrolytes

-elimination of waste via feces

Stomach

-glands in stomach secrete gastric juices (1.5- 2.5, kill bacteria in food)

-infants (secrete rennin, curdles milk in stomach)

-muscular contractions (combine w/ gastric juices = chyme, then it pushes through pyloric sphincter into duodenum)

Small Intestine (majority of digestion occurs here)

-proteins → peptides → amino acids 

-carbohydrates → polysaccharides → monosaccharides 

-10 to 20% absorbed monosaccharides, fatty acids, and glycerol

-80% synthesized into triglycerides and through lacteal (lymph) 

Large intestine (remaining unabsorbed food moves down the GI tract and helps gut bacteria) 

-segmental contraction and peristalsis propel the bolus 

-ascending color absorbs → water, Vit B. Via K and NaCl

-defecation

Achalasia (lower esophageal sphincter cannot relax) 

-aperistalsis (absence of peristalsis) of lower esophagus 

R/F include → nerve degenerative of inhibitory neurons, hypertrophy, idopathetic, esophageal dilation d/t accumulation of food or fluid

Achalasia: Clinical manifestations

-substernal chest pain (behind or below the sternum) 

-dysphagia (difficulty swallowing) 

-coughing, regurgitation of food, weight loss, weakness and poor skin turgor 

Achalasia: Complications 

-megaesophagus, chest pain, nocturnal regurgitation, aspiration, 

-GERD (stomach contents flow back up into esophagus = irritation and discomfort

-Halitosis (bad breathe)

Achalasia: Diagnostic test and Pt education

-upper GI barium x ray (thick white fluid to see how things are being swallowed) 

-esophageal manometry (strength of esophageal) 

Pt. education: diet adjustment, medications, elevate HOB after meals/at night, and procedural teaching 

Achalasia Diagnostic test: Esophagogastroduoedenoscopy (EGD)

-to see if sphincter is working

-has pinchers to take biopsy

-can do injections

-medications/sedation can help relax

Achalasia: Treatment

-medications → anticholinergics, smooth muscle relaxants before meals, botulism (can cause further issues)

-invasive → Heller myotome (a cut) , POEM (internal surgery) 

Hiatal Hernia (weakened diaphragm around esophagus): Sliding and rolling 

sliding → most common, stomach slides above diaphragm and back down

rolling → funds of stomach rolls through diaphragm and stays, forma a pocket next to esophagus (risk for strangulation)

Hiatal Hernia: Diagnostic and Treatments 

diagnostic → upper GI barium study, EGD

tx: prevent problems w/ gastric reflux & Nissan or Toupet fundoplication surgery (can’t throw up bc it makes splinter tighter) 

Hiatal Hernia: Clinical manifestations and Complications 

clinical: heartburn, dyspepsia, regurgitation, pain

complications: esophagitis, hemorrhage, GERD, strangulation, ulcer

Ulcer: Nursing implications

plan of care includes → NPO, IVF, NG tube ofr bowel rest, medications

Ulcer: Complications and Pt education 

complications: Hemorrhage, perforation, gastric outlet obstruction 

pt education: ID cause and eliminate, avoid food that irritate, no smoking, alcohol and stress

Ulcer: H2 receptor block medication

-blocks histamine (which produces stomach acid) receptors on the cells of the stomach lining, decreasing stomach acid production 

Ulcer: Proton pump inhibitor medication 

-decreasing stomach acid producing by inhibiting active enzymes ( which is a building block for hydrogen ions) in some parietal cells 

Ulcer: Surgery

-partial gastrectomy

-vagotomy 

-pyloroplasty

Upper GI bleed (in the esophagus, stomach, duodenum) 

causes → gastritic, ulcer, cancer, med

chronic →difficult to deter, may occur intermittently 

acute → sudden or massive onset 

(can develop into hypovolemic shock, and requires primary hemodynamic stabilization) 

Gastric surgery: Nursing complications

-monitor for bleeding

-monitor for s/sx of decreased peristalsis 

-post prandial hypoglycemia

Gastric surgery: Complications and pt education

complications: 20% dumping syndrome; pernicious or iron deficient anemia, postprandial hypoglycemia, bile reflux 

pt education: pernicious anemia long term complication and dumping syndrome (s/sx diet changes, meds to delay) 

What is Crohn’s disease

a chronic transmural, INCURABLE, inflammatory disease of the bowl 

-often leads to fibrosis and obstruction 

-entire thickness of bowl wall & submucosa layers

-”skipped lesions” → cobble like 

-altered nutrition d/t malabsorption and scarring 

Crohn’s disease: Risk factors 

-environmental (industrial) 

- dietary (high sugars) 

-genetic → heredity, gender, age, familial (women) 

-altered immune system, gut microflora 

Crohn’s disease

-episodes of diarrhea and abdominal pain (Lower right) 

-steatorrhea (excess fat in stool), anorexia, N/V, malabsorption (wt. loss, anemia, fatigue) 

-may have rectal bleeding

-may have remissions, exacerbation and systemic problems

What is Ulcerative Colitis

inflammatory disease of the colon, with unknown cause

-autoimmune disese, increased risk of colon cancer

-3x more common than Crohn’s 

Ulcerative Colitis: Clinical manifestations

-4 to 20 stool/ dal → with pus, blood

-abd pain, involuntary leakage, wt. loss, remissions, exacerbations

Crohn’s and Colitis: Diagnostic test 

-colonoscopy (can differentiate) 

-biopsy of inflamed or normal tissue 

-CT, MRI, Labs 

CROHN’S ONLY → CAPSULE ENDOSCOPY

Crohn’s and Colitis: Treatment

-nutrition → diet changes, mangage wt. loss, dehydration (colitis) 

-surgery indications → for Crohn’s 75% will have it at one point

for colitis, connection of ileum to rectum 

Crohn’s and Colitis: Tx via Medications

-anti inflammatory, immunosuppressants, steroids, ATBs, anti diarrheal agents, pain relievers, correct anemia and fluid volume deficit if necessary

Crohn’s and Colitis: Nursing implications and complications

-bowel rest, control inflammation, teach to avoid triggers, provide symptom relief, improve quality of life

complications → toxic megacolon, bowel obstruction

What is colorectal cancer

malignant neoplasm, invades the epithelium and surrounds tissue of the colon and rectum → can extend through bowel wall and metastasize (preventable w/ screening, age 50)

Colorectal cancer: Diagnostic test

-colonoscopy, CT, MRI, barium enema, stool test for occult blood, biopsy for diagnosis or staging

Colorectal cancer: Clinical manifestations 

-vague in early disease, insidious (no symptoms) or asymptotic for years

-rectal bleeding, abd pain, wt. loss

Colorectal cancer: Warning signs for Assessment

-change in bowel elimination habits, blood in stool, rectal or abd pain

-change in character or the still, sensation of incomplete emptying

Colorectal cancer: treatments

-surgery → bowel prep, colectomy, colostomy, colon or rectum removal

-radiation for some pts, chemo, recurrence, quality of life

Post op bowel surgery care

-surgical site care and dressing changes, stoma care

-ambulate, fluid volume status, strict I&O, drain care if indicated, prevent complications

Liver functions

-Bilirubin metabolism, fat and protein metabolism

-carbohydrate metabolism, hematological role, endocrine role

-detoxification

Risk factors for liver disease

-alcohol abuse, some medications, gastric bypass surgery,

-elevated cholesterol, iron overload, and obesity/ metabolic syndrome 

-rapid weight loss

Classic signs of liver disease

-anorexia, dark urine, hepatomegaly, jaundice  

-ascities (fluid in abd) and steatorrhea (mucous fat in urine) 

-RUQ tenderness

General treatment for liver disease

-control of symptoms, supportive care, rest

-small, high calories, high protein meals 

-avoid alcohol and consider liver transplant 

-surveillance for infection, bleeding 

Liver disorder: Diagnostic test

-Ultrasound, Ct scan abdomen, Radioisotope liver scan 

-liver biopsy 

-lab → clotting studies, CBC, liver function test 

What is Cirrhosis

chronic, progressive disease of the liver characterized by the generation and destruction of hepatocytes

diagnostic test → CT, biopsy, U/S

Cirrhosis: Clinical manifestations → EARLY SIGNS

loss of appetite, generalized malaise, wt. losss, jaundice, itching, nausea, nosebleeds, easy bruising

Cirrhosis: Clinical manifestations → LATE SIGNS

-ascites, peripheral edema, vomiting of blood, black stools

-dilated blood vessels and muscle wasting

Cirrhosis: Treatment

-REST, nutritional changes/ support

-management of ascites, ammonia levels

-upper respiratory infections treated promptly

-monitory bleeding status and correct electrolyte/ acid base imbalances

Transjugular intrahepatic portosystemic shut → TIPS

-treatment of portal hypertension and gastric varices 

-intervantional radiology procedure that puts a stent between portal vein and the hepatic vein = relies pressure 

Liver cancer: Hepatocellular caner 

-symptoms are similar to liver failure 

-diagnostic test  → alpha- fetoprotein which is 60% accuracy and CT, MRI, liver biopsy 

-liver transplant may be possible 

Liver transplant

-MELD score, screen for hepatic transplant qualification → age + bilirubin + sodium +INR + creatine and alcohol abstention for 6 months

POST OP CARE → monitor neuro status, signs of hemorrhage, prevent pulmonary complication, monitor for renal failure, signs of rejection

Bilirubin

yellow colored compound, produced when hemoglobin is broken down (by spleen)

-unconjugated → water insoluble (cannot be stirred up w/ ), transported to liver by albumin

-conjugated → changed to soluble by liver, a component of bile and excreted in stool/urine

Bile

-formed in hepatocytes → aids in fat digestion in the small intestine

-some excreted in stool, some reabsorbed in portal vein

-contains conjugated bilirubin and stored in gallbladder

Grey turner sign

-bluish flank discoloration

Cullen signs

-bluish peri umbilical discoloration

Choledocholithiasis

gallstones occluding the common bile duct

Cholecysitis

gallbladder inflammation , obstruction, infection

Cholelithiasis

presence of gallstones in gallbladder