Scheduled maintenance: Saturday, March 6 from 3–4 PM PST
Upgrade to remove ads
Med Surg I University of Colorado Summer 2012
Terms in this set (65)
Purpose of GI system
digest, absorb, eliminate
Secretions of the GI system
acids, hormones, digestive enzymes, mucous
- gall bladder
How do the nervous systems control the GI system?
- Controlled by ANS
- PNS stimulates (vagus nerve)
- SNS slows
What is first, ingestion or digestion?
Ingestion, then digestion
What are the main arteries and veins in the stomach?
- Celiac artery
- Splenic and gastric veins
What is secreted in the stomach and what do they do?
- Parietal cells secrete:
> Pepsinogen (protein digestion)
> HCl (activation of pepsinogen, prevents infections)
> Intrinsic factor (absorption of B12)
What are the parts of the small intestine?
- Ligament of Treitz
- Mesenteric artery and vein
What is absorbed in the small intestine and where?
- Duodeum: fats, Fe, sugars, protein, M, Na, Ca
- jejunum: sugars, protein
- ileum: B12, salts
What are the parts of the large intestine?
- anal canal
What does the large intestine absorb?
Where do the intestinal bacteria live?
How much of cardiac output does the hepatic artery get?
What goes through the portal vein?
70-80% of blood, deoxygenated, but rich in nutrients
What are the key functions of the liver?
- clotting factors
- drug catabolism/metabolism (and alcohol)
- blood resevoir
- breaks down RBCs (biliruben)
- stores iron
- sinuses are lined with macrophages
- makes albumin
What are the risk factors for gall bladder problems?
Fair, fat, forty, female
What does the gall bladder do?
- Stores and concentrates bile
- Secretes bile, bicarb, enzymes (trypsin, amylase, lipase) into the duodenum
What is the sphincter of Oddi?
controls flow of bile into duodenum
When is the bile released?
- 30 minutes after ingestion of fatty foods
- gall bladder is stimulated by the chyme in the duodenum
What changes occur in the GI system with aging?
Starting at 50:
- dentation changes
- taste bud atrophy
- smell diminishes
- decr salivation
- decr gastric motility leading to incr reflux
- decr iron and vit b12 absorption
- decr intestinal villi leading to malabsorption
- constipation from decr exercise and water
- decr liver size
- decr drug detoxification
Stop HCl from entering cell
- esomeprazole (Nexium)
- lansoprazole (Prevacid)
- omeprazole (Prilosec)
- pantoproazole (Protinix)
- raberazole (Aciphex)
Common H2 blockers
Blocks histamine and HCl secretion
- cimetidine (Tagamet)
- famotidine (Pepcid)
- nizatidine (Axid)
- ranitidine (Zantac)
- ondansetron (Zofran) Most common
- metoclopramide (Reglan) Careful of extrapyramidal effects
- promethazine (Phenergan) Watch for sedation, neuraleptic syndrome: high fever, disorientation
- prochlorperazine (Compazine)
- droperidol (Inaspine)
- dolansetron (Ansemet)
Meds that have adverse GI effects
- NSAIDs: ASA, ibuprophen, ketorolac (Toradol), indomethacin (Indocin), naproxen (Naprosyn, Aleve)
- Contain ASA: Alka-seltzer, pepto-bismol, Maalox, Excedrin, Midol, oxycodone/ASA (Percodan)
Common problems with GI
- nutritional compromise
- bowel elimination dysfunction
- risk for fluid volume deficit
- impaired skin integrity
- ineffective coping
- knowledge deficit (self-health management)
- disturbed body image
- sexual dysfunction
GI system disorders
- vague s/sx
- disrupt multiple functions of the GI system
- Pt presentation is non specific
- diagnosis by process of elimination
- Nursing goals focus on addressing s/sx relief, nutrition, fluid and electrolyte imbalances, education/teaching points
What is constipation and what causes it?
- difficult or infrequent defecation
- can caused by lifestyle habits and drugs
What is diarrhea and what causes it?
- frequent passage of loose stools
>6 x per day, loose, watery
- can be acute or chronic. Chronic > 4wks
- usually caused by infection
What is the patho of constipation?
- neurogenic disorders (MS, spinal cord)
- decr abdominal muscle strength
- colon/anal lesion causing stretching and hypertonicity of anal sphincter and decreasing ability to defecate
- low residue diet
- hypothyroid, diabetes
- abdominal surgery
- sedentary lifestyle
What is patho of diarrhea?
- decreased fluid absorption
- increased fluid secretion
- increased or decreased motility
What are clinical manifestations of constipation?
- History and subjective complaints
- Distended abdomen, SOB
What are the clinical manifestations of diarrhea?
- incr frequency, volume, and consistency
- subjective complaints
What are some collaborative cares for constipation?
- dietary habits exercise, bowel training
- Avoid enemas
- stool softeners while in hospital
- gut decompression
What are some collaborative cares for diarrhea?
- F/E replacement
- Watch use of antidiarrheals, laxatives
- dietary habits
- antibiotics while in hospital
What are s/sx of a GI bleed?
- associate with blood volume loss:
> hypotension, incr/decr HR, dizziness
- bloody vomit, melena stools, hematochezia, coffee ground emesis
- gut irritation, diarrhea, pain
- increased BUN with normal creatinine
- decreased H/H
What are lab tests done for GI bleed?
- CBC: Hct may not reflect blood loss for 4-6hrs
- Metabolic panel
- Hepatic panel
- Coagulation studies
- Type and crossmatch
- urine specific gravity
What are collaborative cares for a GI bleed?
- frequent VS
- Assess circulation, s/sx of shock, abdomen (tense, rigid and boardlike = perforation and peritonitis)
- Insert 2 16 or 18 guage IVs
- Administer fluids or PRBCs
- Monitor for fluid overload
- Foley to monitor output
- NGT or OGT
- Triple lumen cath to monitor CVP
- Assess vomitus and stool for blood
- Clear liquid diet
- If alcohol related, watch for DTs
- EGD to visualize and stop site of bleed thru heat coagulation, clerotherapy, balloon tamponade (sengstaken blakemore tube), variceal ligation or injection of alcohol or epinephrine (causes edema and pressure that compresses vessels)
What is a lower GI bleed?
Bleed anywhere from duodenum down to anus
What are some drug therapies for a GI bleed?
- vasopressin (Pitressin): vasoconstriction; may decr myocardial contractility or decrease coronary blood flow; monitor for ischemia
- somatostatin (Sandostatin): reduces splanchic blood flow and decr acid secretion
- antacids, H2 blockers, PPIs: neutralize acid; for bleeds cause by GERD and PUD
What are some educational interventions for GI bleed?
- High risk: chronic gastritis, PUD, GERD, cirrhosis
- If you have 1 bleed, higher risk for another
- avoid irritants and certain meds (ASA, NSAIDs, steroids, ETOH, smoking)
What are some upper GI diseases?
- Gastroespohageal Reflux Disease (GERD)
- Peptic Ulcer Disease
What is the definition of GERD?
- Reflux of chyme
- inflammation and erosion of esophageal mucosa
- precancerous lesions can develop
What are pre-disposing conditions of GERD?
- Hiatal hernia
- delayed gastric emptying
- decreased ability to clear food/fluids
What are clinical manifestatoins of GERD?
- pain within 1 hour of eating
- esophageal spasm
- can't eat citric or acidic foods
How is GERD diagnosed?
- esophageal endoscopy
- barium swallow
What are collaborative cares for GERD?
- Hx and nutrition assessment
- Antacids and H2 blockers, PPIs
- HOB >45 after eating
- weight management
- small frequent meals
- stop smoking
- surgical repair of esophageal sphincter
What is gastritis?
- Inflammation of gastric mucosal layers: fundus, antrum or both
What is acute gastritis?
- diffused or localized injury pattern
- heals in weeks to months
What is chronic gastritis?
- patch diffuse inflammation or injury
- seen in the elderly because of degeneration of stomach wall
What are the clinical manifestations of gastritis?
- vague discomfort
- epigastric tenderness
- more common in elderly
What are collaborative cares for gastritis?
- management of s/sx
- rest gut
- small bland meals
- antacids: H2 blockers, PPIs
- stop offending drugs/chemicals
- I/Os and F/E balance
- Vit B12 if anemic
- Antibiotics for H. pylori infection
- surgical interventions
What is Peptic Ulcer Disease? (PUD)
- break or ulceration in protective mucosal lining of esophagus, stomach, duodenum
- superficial or deep ulcerations
- 4 million people with the disease
- duodenal ulcers are more frequent
What is the patho of PUD?
- increased acidity in the duodenum
- increase in number and function of parietal cells in the gut
- H. pylori infection
What are the clinical manifestations of PUD?
- Intermittent to chronic pain
- onset 30 mini to 2 hours after eating
- bleeding: hematemesis. Vomits bright red or coffee ground blood (upper) or black/dark stool (lower)
- s/sx hypovolemia
- acute confusion
- syncope or orthostasis
What are some collaborative cares of PUD?
- management of s/sx
- antibx for infx
- Antacids: H2 blockers, PPI
- rest gut, decompress gut (NG)
- Bland diet
- small frequent meals
- I/O and F/E balance
- surgical interventions
What are some lower GI diseases?
- intestinal obstruction
- inflammatory bowel disease
- colorectal cancer
What is an intestinal obstruction?
- Any obstruction to flow of chyme
- Can be partial or complete
- intrinsic: inside the lumen; edema, tumor, prior procedures
- extrinsic: outside the lumen compressing it; tumors, adhesions, inflammatory diseases
- perforation can occur within 3 hours of onset of pain
What are the consequences of obstruction?
- sequestration of fluid leading to abd distention and respiratory compromise
- abd pain
- tension on abd wall leading to decreased venous return, ischemia, then inflammation, then fever and peritonitis
- incr capillary permeability causes fluid shifts and hypovolemia
- fluid shifts cause electrolyte and acid/base imbalances
- inschemia causes perforation then overwhelming sepsis
- fluid shift can cause drop in BP (goes into peritoneum)
What are clinical manifestations of an small intestine obstruction?
- n/v, colicky pain to excruciating pain (can vomit bile, then feces)
- pain is intermittent to constant
- abdomen distention
- BS absent to high pitched tinkling
- change in defecation pattern
What are clinical manifestations of a large intestine obstruction?
- vomiting is rare
- pain develops gradually, crampy, constant
- constipation, no bm
- abd distention
- high pitched BS proximal to obstruction
What are diagnostics for an obstruction?
- barium enema
- sigmoid or colonoscopy
- Labs: WBC, H&H, serum amylase, serum osmolality, electrolytes, SCr, BUN, ABGs
What are collaborative cares for intestinal obstruction?
- monitor vital signs
- IV F/E, monitor I/O including NGT output
- Pain and anxiety management
- NGT to low suction to decompress bowel
- NPO, may require TPN
- Oral care if vomitting
When an NGT is not draining, what do you do?
- check placement
- twist or turn
- inject air to equalize pressure or move away from the wall
- change the patients position
- secure to the patients gown so it doesn't get dislodged
- check the nares for pressure points
- humidify if needed
What is peritonitis?
- serious complication associated with abdominal disorders
- complication of obstructions and gastric lesions
- acute inflammation of the peritoneum
- initially see hypermotility progresssing to ileus
- significant fluid and electrolyte shifts
What are the clinical manifestations of peritonitis?
- Severe diffuse abd pain
- diminished or absent BS
- abd distension and/or ascites
- rebound tenderness of involved area
- boardlike abdomen
- muscle spasm
- tachycardia, tachypnea w/shallow respirations
YOU MIGHT ALSO LIKE...
Patho Exam 5
GI disorders and nursing care
Ch 41: Alterations of Digestive Function
RNSG 1341 Test 3: Lower GI
OTHER SETS BY THIS CREATOR
The Older Adult
Fluid and Electrolyte Alterations