Gastrointestinal Tract Flashcards
Exam 4 (Final)
Functions of the Gastrointestinal System
Ingestion
Motility
Digestion
Absorption
Elimination
Functions of the Gastrointestinal System
Ingestion: What is it?
Ingestion—taking in food
Functions of the Gastrointestinal System
Motility: What is it?
Motility—mixing and propelling food through the GI tract
Functions of the Gastrointestinal System
Digestion—What is it?
Digestion—breaking down food
Functions of the Gastrointestinal System
Absorption—What is it?
Absorption—movement of food particles into the bloodstream
Functions of the Gastrointestinal System
Elimination—What is it?
Elimination—waste eliminated from the body
Stomach:
What does it do?
Control of gastric secretions
Motility
Stomach:
Control of gastric secretions: What influences secretions? What stimulates secretions?
emotions influence secretions.
stretch receptors stimulate secretions.
acidity in the chyme stimulates secretions.
Stomach:
Motility: How does the stomach act to receive food?
Stomach reflexively relaxes to receive food.
Stomach:
Motility: When full, how is the stomach?
When full, peristaltic contractions mix and propel contents into duodenum.
Pancreas:
What are the two functions?
Exocrine
Endocrine
Pancreas:
Exocrine: What happens to secretions?
Acinar cells empty secretions into pancreatic ductal system, which eventually join the common bile duct.
Pancreas:
Exocrine: What happens to bile and pancreatic secretions?
Bile and pacreatic secretions are carried into the duodenum.
Pancreas:
Exocrine: What is digested?
Digests proteins, fat, and starch
Pancreas:
Endocrine: What is secreted?
Secretes insulin, glucagon, and pancreatic polypeptide hormones to aid digestion.
Gallbladder:
What does it do?
Emulsifies fat into small globules that can be absorbed across the intestinal lumen
Gallbladder:
What does it prevent?
Prevents precipitation and deposition of cholesterol, triglycerides, and multiple-density lipoproteins in the vasculature
Gallbladder:
What does the gallbladder store?
Bile is stored and concentrated in the gallbladder.
Gallbladder:
What causes gallbladder contraction and relaxation?
Cholecystokinin (CCK) causes gallbladder contraction and relaxation allowing bile into the duodenum via the sphincter of Oddi.
Skipped slides 6-14
Common Gastrointestinal Disorders
What are they?
Acute Gastrointestinal Bleeding
Small bowel obstruction
Colonic obstruction
Ileus
Acute pancreatitis
Acute Gastrointestinal Bleeding
Upper gastrointestinal bleeding includes stuff like?
Peptic ulcer disease
Stress-related erosive syndrome
Esophageal varices (enlarged veins in the esophagus)
Mallory–Weiss tears
Dieulafoy’s lesions
Acute Gastrointestinal Bleeding
Upper gastrointestinal bleeding
Peptic ulcer disease
Primary factor is H. pylori, ingestion of ASA, NSAIDs, smoking
Acute Gastrointestinal Bleeding
Upper gastrointestinal bleeding
Stress-related erosive syndrome
Decreased perfusion of stomach mucosa, related to physiologic stress
Acute Gastrointestinal Bleeding
Upper gastrointestinal bleeding
Esophageal varices: What is this?
(enlarged veins in the esophagus)
Acute Gastrointestinal Bleeding
Upper gastrointestinal bleeding
Esophageal varices: (enlarged veins in the esophagus)
What is it caused by?
Caused by portal hypertension which develops from cirrhosis, impeding blood flow to and from the liver.
Acute Gastrointestinal Bleeding
Upper gastrointestinal bleeding
Esophageal varices: (enlarged veins in the esophagus)- What happens in response to portal hypertension?
In response to portal hypertension, collateral veins develop to bypass the increased portal resistance in an attempt to return blood to systemic circulation
Acute Gastrointestinal Bleeding
Upper gastrointestinal bleeding
Esophageal varices: (enlarged veins in the esophagus)-
In response to portal hypertension, collateral veins develop to bypass the increased portal resistance in an attempt to return blood to systemic circulation.
As pressure rises in these veins, what happens?
As pressure rises in these veins, they become tortuous and distended, forming varicose veins or varices.
Acute Gastrointestinal Bleeding
Upper gastrointestinal bleeding
Mallory–Weiss tears: What is it?
Laceration of the distal esophagus, gastroesophageal junction, and cardia of the stomach
Acute Gastrointestinal Bleeding
Upper gastrointestinal bleeding
Mallory–Weiss tears: How does it occur?
Heavy alcohol use, binge drinking, forceful vomiting/retching, or violent coughing
Acute Gastrointestinal Bleeding
Upper gastrointestinal bleeding
Dieulafoy’s lesions: What is it?
Vascular malformations, usually in the proximal stomach
Acute Gastrointestinal Bleeding
Upper gastrointestinal bleeding
Clinical Presentation: What does presentation depend on?
Presentation depends on the amount of blood loss.
Acute Gastrointestinal Bleeding
Upper gastrointestinal bleeding
Clinical Presentation: What can occur?
Slight anemia to shock
Acute Gastrointestinal Bleeding
Upper gastrointestinal bleeding
Clinical Presentation: What can orthostatic changes imply?
Orthostatic changes imply volume depletion of 15% or more.
Acute Gastrointestinal Bleeding
Upper gastrointestinal bleeding
Clinical Presentation: What is the hallmark of GIB?
Hallmark of GIB is hematemesis, hematochezia, and melena.
Acute Gastrointestinal Bleeding
Upper gastrointestinal bleeding
Clinical Presentation: What specifically occurs in Upper GIB?
Upper GIB—hematemesis, “coffee ground,” melena
Acute Gastrointestinal Bleeding
Upper gastrointestinal bleeding
Laboratory studies
Decreased H & H;
Mild leukocytosis and hyperglycemia;
Elevated BUN;
Hypernatremia, hypokalemia;
Prolonged PT/PTT;
Thrombocytopenia;
Hypoxemia
Acute Gastrointestinal Bleeding
Upper gastrointestinal bleeding
Definitive Diagnosis:
Endoscopy
Angiography
Barium studies
Acute Gastrointestinal Bleeding
Upper gastrointestinal bleeding
Definitive Diagnosis: Endoscopy- When is it done? Where is it done?
Endoscopy within 12 to 24 hours to identify the site
Can be done at bedside
Acute Gastrointestinal Bleeding
Upper gastrointestinal bleeding
Definitive Diagnosis: Angiography- What does it do?
Locates the site or abnormal vasculature
Acute Gastrointestinal Bleeding
Upper gastrointestinal bleeding
Definitive Diagnosis: Barium studies -how are they viewed?
Barium studies are often inconclusive, and risk of retained barium.
Acute Gastrointestinal Bleeding
Upper gastrointestinal bleeding
Management: What should be stopped?
Eradication of H. pylori, stop NSAIDs
Alcohol cessation
Acute Gastrointestinal Bleeding
Upper gastrointestinal bleeding
Management: What should be done?
Volume resuscitation with blood products,
Oxygen
Prophylactic antibiotics
Acid-suppressive therapy
Beta-blockers
Vasopressin with nitroglycerin, somatostatin
Acute Gastrointestinal Bleeding
Upper gastrointestinal bleeding
Management: Acid-suppressive therapy- includes what?
PPIs or H2 antagonistic drugs
Acute Gastrointestinal Bleeding
Upper gastrointestinal bleeding
Management: What are beta blockers for?
Beta-blockers for decreasing portal hypertension
Acute Gastrointestinal Bleeding
Upper gastrointestinal bleeding
Management: What is vasopressin with nitroglycerin, somatostatin for?
Vasopressin with nitroglycerin, somatostatin to reduce blood flow
Lower Gastrointestinal Bleeding
diseases includes:
Diverticulosis
Angiodysplasia/Arteriovenous (AV) malformation
Lower Gastrointestinal Bleeding
Diverticulosis: What is it?
Sac-like protrusions in the colon; arteries are prone to injury.
Lower Gastrointestinal Bleeding
Diverticulosis: What are risk factors?
Risk factors: diet low in fiber, Aspirin(ASA)/NSAIDs, advanced age, and constipation
Lower Gastrointestinal Bleeding
Angiodysplasia/Arteriovenous (AV) malformation: What is it?
Dilated, tortuous submucosal veins, small AV communications, or enlarged arteries
Lower Gastrointestinal Bleeding
Angiodysplasia/Arteriovenous (AV) malformation: Where does it occur?
Occurs anywhere in the colon and can be venous or arterial bleed
Lower Gastrointestinal Bleeding
Clinical Presentation:
Hemodynamic instability and hematochezia (blood in stool)
Lower Gastrointestinal Bleeding
Clinical Presentation: How is Diverticular bleeding?
Diverticular bleeding is often painless, may complain of cramping.
Lower Gastrointestinal Bleeding
Clinical Presentation: How does Angiodysplasia present?
Angiodysplasia presents with painless hematochezia.
Lower Gastrointestinal Bleeding
Clinical Presentation: How does Chronic lower GIB present?
Chronic lower GIB presents with iron deficiency anemia.
Lower Gastrointestinal Bleeding
Clinical Presentation: How can hemorrhoids present?
Hemorrhoids can present with massive bleeding from rectal varices from portal hypertension.
Lower Gastrointestinal Bleeding
Management:
Fluid resuscitation
Colonoscopy
Upper endoscopy
Radionucleotide imaging
Angiography
Surgical intervention
Lower Gastrointestinal Bleeding
Management: What is NG tube for?
NG-tube to eliminate an upper GI bleed
Lower Gastrointestinal Bleeding
Management: What is done for diagnosis and treatment?
Colonoscopy for diagnosis and treatment
Lower Gastrointestinal Bleeding
Management: What testing distinguishes the source of lower gastrointestinal bleeding?
Upper endoscopy distinguishes the source.
Lower Gastrointestinal Bleeding
Management: What locates the site of bleeding?
Radionucleotide imaging—locates the site of bleed
What is the test of choice for evaluation of lower GIB?
Colonoscopy
Lower Gastrointestinal Bleeding
Management: What angiography for?
Angiography—for diagnosis and embolization
Lower Gastrointestinal Bleeding
Management: What is surgical intervention for?
Exploratory lap,
segmental bowel resection,
total colectomy
Small Bowel Obstruction:
What is the most common cause?
Adhesions are the most common cause after laparotomy, radiation, ischemia, infection, or foreign body.
Small Bowel Obstruction:
How do adhesions occur?
Adhesions are the most common cause after laparotomy, radiation, ischemia, infection, or foreign body.
Small Bowel Obstruction:
What is the second most common cause?
Hernias—strangulated
Small Bowel Obstruction
What is an uncommon cause of SBO?
Tumors—uncommon in the small bowel
Small Bowel Obstruction
Pathophysiology: What occurs?
Fluid and air accumulate proximal to obstruction causing distention.
Small Bowel Obstruction
Pathophysiology: What happens to bowel wall?
Bowel wall becomes edematous and distended.
Small Bowel Obstruction
Pathophysiology: What decreases?
Peristalsis decreases and normal function halts.
Small Bowel Obstruction
Clinical Presentation: What occurs?
Acute onset of intermittent, crampy, periumbilical pain
Fever, constipation
Small Bowel Obstruction
Clinical Presentation: What relieves pain?
Vomiting often relieves the pain.
Small Bowel Obstruction
Clinical Presentation: How is strangulated SBO?
In strangulated SBO, the pain is localized, steady, severe.
Small Bowel Obstruction
Assessment:
History of abdominal surgery/trauma, inflammatory bowel disease, diverticulitis, radiation, PUD, pancreatitis
Small Bowel Obstruction
Assessment: History of abdominal surgery/trauma, inflammatory bowel disease, diverticulitis, radiation, PUD, pancreatitis
Medication history, psychiatric history
Small Bowel Obstruction
Assessment: Physical examination
What is present?
Visible peristalsis and distention, epigastric/periumbilical/diffuse abdominal tenderness, hyperactive BS early then high-pitched tinkling
Small Bowel Obstruction
Assessment: Physical examination
What are signs and symptoms?
S & S of dehydration, palpable mass; palpate for inguinal hernia.
Small Bowel Obstruction
Diagnostic Studies include:
Radiography
Computed tomography
Endoscopy
Small Bowel Obstruction
Diagnostic Studies: Radiography
What could it diagnose?
Dx of obstruction, perforation
Small Bowel Obstruction
Diagnostic Studies: Computed tomography
What could it diagnose?
Obstructive lesions,
neoplasms (tumors),
hernias,
and ischemia
Small Bowel Obstruction
Diagnostic Studies: Endoscopy
What could it diagnose?
Direct visualization of obstruction in colon or proximal SB
Small Bowel Obstruction
Management: Two types
Medical management
Surgical management
Small Bowel Obstruction
Management: When possible, how are SBOs treated?
When possible, obstructions, especially incomplete obstructions, are treated medically rather than surgically.
Small Bowel Obstruction
Management: Medical Management- What procedure occurs?
NPO, NG-tube, IV fluids, electrolyte repletion, I & Os, TPN
Oral food and fluid are withheld (i.e., the patient is put on NPO status), and a nasogastric tube is placed to decompress the stomach or duodenum.
Fluid and electrolytes are aggressively supplied via IV with lactated Ringer’s or saline solution.
When possible, the underlying causes are treated. Total parenteral nutrition (TPN) may be required to provide nutritional support.
Small Bowel Obstruction
Management: Medical Management- What should be monitored?
Monitor for S & S of sepsis, perforation, ischemia, necrosis
Closely watch all patients with intestinal obstructions for signs and symptoms
Small Bowel Obstruction
Management: Surgical management
What is a surgical emergency?
Acute complete SBO is a surgical emergency.
Small Bowel Obstruction
Management: Surgical management
What patients require immediate surgery?
An acute complete SBO is accompanied by the risk for bowel strangulation.
Patients with strangulated bowel, volvulus, and incarceration of bowel loop in a hernia or a closed-loop obstruction require immediate surgery.
Small Bowel Obstruction
Management: Surgical management
Surgical procedures include?
Lysis of adhesions,
resection,
ostomy,
bowel decompression
Acute Pancreatitis:
What is responsible for most cases?
Gallstones are responsible for 40% of cases.
Acute Pancreatitis:
What is the second leading cause of pancreatitis? What percent does it account for?
Alcoholism is the second leading cause of pancreatitis and accounts for 35% of the cases.
Acute Pancreatitis:
What are metabolic causes of acute pancreatitis?
Hypercalcemia and hypertriglyceridemia, medications, infectious processes
Acute Pancreatitis:
Pathophysiology
Pancreatic enzymes become prematurely activated.
This premature activation results in autodigestion of the pancreas and the peripancreatic tissue.
Pancreatic enzymes, vasoactive substances, hormones, and cytokines released from the injured pancreas cause a cascade of events that can lead to edema, vascular damage, hemorrhage, and necrosis.
Acute Pancreatitis:
Clinical Presentation: What kind of pain occurs?
Deep, boring midepigastric or periumbilical pain
Acute Pancreatitis:
Clinical Presentation: What signs and symptoms?
Nausea/vomiting without pain relief,
tachycardia,
hypotension,
abdominal distention,
low-grade fever
Acute Pancreatitis:
Clinical Presentation: What kind of history may they have?
History of biliary disease, alcohol use, diabetes, medications, location of pain, weight loss, N/V
Acute Pancreatitis:
Physical examination: When examining patient what may present?
Diffuse abdominal tenderness and guarding, tympanic to percussion
Hypoactive or absent bowel sounds, jaundice, ascites
Assess for S & S of dehydrations or hypovolemic shock which may indicate severe acute hemorrhagic pancreatitis
Grey Turner’s or Cullen’s sign
Acute Pancreatitis
Diagnostic Studies:
Labs
Imaging studies
Acute Pancreatitis
Diagnostic Studies: Labs
Elevated serum amylase and lipase,
electrolyte imbalance,
hyperglycemia,
LFTs elevated with concurrent liver disease,
elevated ALT and alkaline phosphatase with biliary disease
Acute Pancreatitis
Diagnostic Studies: Imaging studies
What are they for? What is the preferred test?
Radiographs exclude other causes.
CT is the preferred test.
What is an assessment tool to measure the severity of Acute Pancreatitis?
Ranson’s Criteria
Acute Pancreatitis:
Ranson’s Criteria:
When are the two times this tool is used?
- Evaluate on admission or on diagnosis
- Evaluate during initial 48 hours
Acute Pancreatitis:
Ranson’s Criteria: What is predictive of severe AP?
Three or more signs identified at the time of admission or during the initial 48 hours are predictive of severe AP.
Acute Pancreatitis:
Ranson’s Criteria: How accurate is this tool?
Ranson criteria have a greater than 90% accuracy rate and are useful clinically in identifying high-risk patients.
Acute Pancreatitis:
Ranson’s Criteria: What is the primary disadvantage of this tool?
The primary disadvantage to Ranson criteria is the 48-hour delay before the assessment is completed.
Acute Pancreatitis:
Ranson’s Criteria: Evaluate on admission or diagnosis?
Age more than 55 years
Leukocyte count more than 16,000/mL
Serum glucose more than 200 mg/dL
Serum lactate dehydrogenase more than 350 IU/mL
Serum AST more than 250IU/dL
Acute Pancreatitis:
Ranson’s Criteria: Evaluate during initial 48 hours?
Fall in hematocrit more than 10%
BUN level rise more than 5mg/dL
Serum calcium less than 8mg/dL
Base deficit more than 4 mEq/L
Estimated fluid sequestration more than 6L
Arterial PaO2 less than 60 mmHg
Acute Pancreatitis:
Complications include what types?
Local
Pulmonary
Cardiovascular
Renal
Hematologic
Metabolic
Gastrointestinal
Acute Pancreatitis:
Complications: Local
pancreatic necrosis,
pseudocyst,
abscess
Acute Pancreatitis:
Complications: Pulmonary
Pulmonary—atelectasis, ARDS, pleural effusion
Acute Pancreatitis:
Complications: Cardiovascular
shock states
Acute Pancreatitis:
Complications: Renal—
ARF
Acute Pancreatitis:
Complications: Hematologic
Disseminated intravascular coagulation DIC
Acute Pancreatitis:
Complications: Metabolic—
hyperglycemia, hypertriglyceridemia, hypocalcemia, metabolic acidosis
Acute Pancreatitis:
Complications: Gastrointestinal—
GIB
Acute Pancreatitis:
Management:
IVF,
electrolyte repletion,
pain management,
rest pancreas with NGT connected to suction decompress the stomach and decrease stimulation of secretion
NPO,
TPN for nutritional support,
bed rest
Surgical management
Acute Pancreatitis:
Management: Surgical management
With massive necrosis, pancreatic resection is done.
Broad-spectrum antibiotics
Cirrhosis:
What is it?
Complication of liver disease
Cirrhosis:
What is it caused by?
Caused by chronic HCV,
alcohol abuse,
nonalcoholic steatohepatitis,
hereditary hemochromatosis,
Wilson’s disease,
and alpha1-antitrypsin deficiency
Cirrhosis:
Pathophysiology
Inflammation, fibrotic changes, and increased intrahepatic vascular resistance cause compression of the liver lobule, leading to increased resistance or obstruction of normal blood flow through the liver, which is normally a low-pressure system
Cirrhosis:
Pathophysiology: What does it result in?
Results in splenomegaly,
varices,
hemorrhoids,
cardiac dysfunction
Cirrhosis:
Assessment: What would H and P reveal?
H & P reveals altered liver function.
Cirrhosis:
Assessment: What is altered?
Altered glucose, carbohydrate, fat, and protein metabolism
Cirrhosis:
Assessment: What is there a decrease of?
Decreased synthesis of albumin leads to interstitial edema and decreased plasma volume.
Cirrhosis:
Assessment: What dysfunction occurs?
Clotting dysfunction
Cirrhosis:
Assessment: What else occurs?
Ascites,
lower extremity edema,
hypotension
Cirrhosis:
Management: What should be monitored?
Monitor nutrition, fluid balance, urine output, electrolytes, PT/PTT, platelet function, hematocrit.
Monitor LOC, abdominal girth.
Cirrhosis:
Management: What should be managed?
Manage ascites—paracentesis or Venous-Peritoneal shunt.
Cirrhosis:
Management: How should ascites be managed?
Manage ascites—paracentesis or Venous-Peritoneal shunt.
Cirrhosis:
Management: What other procedure is done? What does this do?
Transjugular intrahepatic portosystemic shunt (TIPS) procedure to decompress portal venous system
