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NURS 428: Evolution > Gastrointestinal Tract > Flashcards

Gastrointestinal Tract Flashcards

Exam 4 (Final)

1
Q

Functions of the Gastrointestinal System

A

Ingestion

Motility

Digestion

Absorption

Elimination

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2
Q

Functions of the Gastrointestinal System

Ingestion: What is it?

A

Ingestion—taking in food

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3
Q

Functions of the Gastrointestinal System

Motility: What is it?

A

Motility—mixing and propelling food through the GI tract

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4
Q

Functions of the Gastrointestinal System

Digestion—What is it?

A

Digestion—breaking down food

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5
Q

Functions of the Gastrointestinal System

Absorption—What is it?

A

Absorption—movement of food particles into the bloodstream

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6
Q

Functions of the Gastrointestinal System

Elimination—What is it?

A

Elimination—waste eliminated from the body

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7
Q

Stomach:

What does it do?

A

Control of gastric secretions

Motility

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8
Q

Stomach:

Control of gastric secretions: What influences secretions? What stimulates secretions?

A

emotions influence secretions.

stretch receptors stimulate secretions.

acidity in the chyme stimulates secretions.

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9
Q

Stomach:

Motility: How does the stomach act to receive food?

A

Stomach reflexively relaxes to receive food.

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10
Q

Stomach:

Motility: When full, how is the stomach?

A

When full, peristaltic contractions mix and propel contents into duodenum.

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11
Q

Pancreas:

What are the two functions?

A

Exocrine

Endocrine

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12
Q

Pancreas:

Exocrine: What happens to secretions?

A

Acinar cells empty secretions into pancreatic ductal system, which eventually join the common bile duct.

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13
Q

Pancreas:

Exocrine: What happens to bile and pancreatic secretions?

A

Bile and pacreatic secretions are carried into the duodenum.

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14
Q

Pancreas:

Exocrine: What is digested?

A

Digests proteins, fat, and starch

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15
Q

Pancreas:

Endocrine: What is secreted?

A

Secretes insulin, glucagon, and pancreatic polypeptide hormones to aid digestion.

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16
Q

Gallbladder:

What does it do?

A

Emulsifies fat into small globules that can be absorbed across the intestinal lumen

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17
Q

Gallbladder:

What does it prevent?

A

Prevents precipitation and deposition of cholesterol, triglycerides, and multiple-density lipoproteins in the vasculature

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18
Q

Gallbladder:

What does the gallbladder store?

A

Bile is stored and concentrated in the gallbladder.

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19
Q

Gallbladder:

What causes gallbladder contraction and relaxation?

A

Cholecystokinin (CCK) causes gallbladder contraction and relaxation allowing bile into the duodenum via the sphincter of Oddi.

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20
Q

Skipped slides 6-14

A
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21
Q

Common Gastrointestinal Disorders

What are they?

A

Acute Gastrointestinal Bleeding

Small bowel obstruction

Colonic obstruction

Ileus

Acute pancreatitis

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22
Q

Acute Gastrointestinal Bleeding

Upper gastrointestinal bleeding includes stuff like?

A

Peptic ulcer disease

Stress-related erosive syndrome

Esophageal varices (enlarged veins in the esophagus)

Mallory–Weiss tears

Dieulafoy’s lesions

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23
Q

Acute Gastrointestinal Bleeding

Upper gastrointestinal bleeding

Peptic ulcer disease

A

Primary factor is H. pylori, ingestion of ASA, NSAIDs, smoking

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24
Q

Acute Gastrointestinal Bleeding

Upper gastrointestinal bleeding

Stress-related erosive syndrome

A

Decreased perfusion of stomach mucosa, related to physiologic stress

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25
Q

Acute Gastrointestinal Bleeding

Upper gastrointestinal bleeding
Esophageal varices: What is this?

A

(enlarged veins in the esophagus)

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26
Q

Acute Gastrointestinal Bleeding

Upper gastrointestinal bleeding
Esophageal varices: (enlarged veins in the esophagus)

What is it caused by?

A

Caused by portal hypertension which develops from cirrhosis, impeding blood flow to and from the liver.

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27
Q

Acute Gastrointestinal Bleeding

Upper gastrointestinal bleeding
Esophageal varices: (enlarged veins in the esophagus)- What happens in response to portal hypertension?

A

In response to portal hypertension, collateral veins develop to bypass the increased portal resistance in an attempt to return blood to systemic circulation

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28
Q

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?

A

As pressure rises in these veins, they become tortuous and distended, forming varicose veins or varices.

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29
Q

Acute Gastrointestinal Bleeding

Upper gastrointestinal bleeding
Mallory–Weiss tears: What is it?

A

Laceration of the distal esophagus, gastroesophageal junction, and cardia of the stomach

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30
Q

Acute Gastrointestinal Bleeding

Upper gastrointestinal bleeding
Mallory–Weiss tears: How does it occur?

A

Heavy alcohol use, binge drinking, forceful vomiting/retching, or violent coughing

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31
Q

Acute Gastrointestinal Bleeding

Upper gastrointestinal bleeding
Dieulafoy’s lesions: What is it?

A

Vascular malformations, usually in the proximal stomach

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32
Q

Acute Gastrointestinal Bleeding
Upper gastrointestinal bleeding

Clinical Presentation: What does presentation depend on?

A

Presentation depends on the amount of blood loss.

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33
Q

Acute Gastrointestinal Bleeding
Upper gastrointestinal bleeding

Clinical Presentation: What can occur?

A

Slight anemia to shock

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34
Q

Acute Gastrointestinal Bleeding
Upper gastrointestinal bleeding

Clinical Presentation: What can orthostatic changes imply?

A

Orthostatic changes imply volume depletion of 15% or more.

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35
Q

Acute Gastrointestinal Bleeding
Upper gastrointestinal bleeding

Clinical Presentation: What is the hallmark of GIB?

A

Hallmark of GIB is hematemesis, hematochezia, and melena.

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36
Q

Acute Gastrointestinal Bleeding
Upper gastrointestinal bleeding

Clinical Presentation: What specifically occurs in Upper GIB?

A

Upper GIB—hematemesis, “coffee ground,” melena

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37
Q

Acute Gastrointestinal Bleeding
Upper gastrointestinal bleeding

Laboratory studies

A

Decreased H & H;

Mild leukocytosis and hyperglycemia;

Elevated BUN;

Hypernatremia, hypokalemia;

Prolonged PT/PTT;

Thrombocytopenia;

Hypoxemia

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38
Q

Acute Gastrointestinal Bleeding
Upper gastrointestinal bleeding

Definitive Diagnosis:

A

Endoscopy

Angiography

Barium studies

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39
Q

Acute Gastrointestinal Bleeding
Upper gastrointestinal bleeding

Definitive Diagnosis: Endoscopy- When is it done? Where is it done?

A

Endoscopy within 12 to 24 hours to identify the site

Can be done at bedside

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40
Q

Acute Gastrointestinal Bleeding
Upper gastrointestinal bleeding

Definitive Diagnosis: Angiography- What does it do?

A

Locates the site or abnormal vasculature

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41
Q

Acute Gastrointestinal Bleeding
Upper gastrointestinal bleeding

Definitive Diagnosis: Barium studies -how are they viewed?

A

Barium studies are often inconclusive, and risk of retained barium.

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42
Q

Acute Gastrointestinal Bleeding
Upper gastrointestinal bleeding

Management: What should be stopped?

A

Eradication of H. pylori, stop NSAIDs

Alcohol cessation

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43
Q

Acute Gastrointestinal Bleeding
Upper gastrointestinal bleeding

Management: What should be done?

A

Volume resuscitation with blood products,

Oxygen

Prophylactic antibiotics

Acid-suppressive therapy

Beta-blockers

Vasopressin with nitroglycerin, somatostatin

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44
Q

Acute Gastrointestinal Bleeding
Upper gastrointestinal bleeding

Management: Acid-suppressive therapy- includes what?

A

PPIs or H2 antagonistic drugs

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45
Q

Acute Gastrointestinal Bleeding
Upper gastrointestinal bleeding

Management: What are beta blockers for?

A

Beta-blockers for decreasing portal hypertension

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46
Q

Acute Gastrointestinal Bleeding
Upper gastrointestinal bleeding

Management: What is vasopressin with nitroglycerin, somatostatin for?

A

Vasopressin with nitroglycerin, somatostatin to reduce blood flow

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47
Q

Lower Gastrointestinal Bleeding

diseases includes:

A

Diverticulosis

Angiodysplasia/Arteriovenous (AV) malformation

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48
Q

Lower Gastrointestinal Bleeding

Diverticulosis: What is it?

A

Sac-like protrusions in the colon; arteries are prone to injury.

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49
Q

Lower Gastrointestinal Bleeding

Diverticulosis: What are risk factors?

A

Risk factors: diet low in fiber, Aspirin(ASA)/NSAIDs, advanced age, and constipation

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50
Q

Lower Gastrointestinal Bleeding

Angiodysplasia/Arteriovenous (AV) malformation: What is it?

A

Dilated, tortuous submucosal veins, small AV communications, or enlarged arteries

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51
Q

Lower Gastrointestinal Bleeding

Angiodysplasia/Arteriovenous (AV) malformation: Where does it occur?

A

Occurs anywhere in the colon and can be venous or arterial bleed

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52
Q

Lower Gastrointestinal Bleeding

Clinical Presentation:

A

Hemodynamic instability and hematochezia (blood in stool)

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53
Q

Lower Gastrointestinal Bleeding

Clinical Presentation: How is Diverticular bleeding?

A

Diverticular bleeding is often painless, may complain of cramping.

54
Q

Lower Gastrointestinal Bleeding

Clinical Presentation: How does Angiodysplasia present?

A

Angiodysplasia presents with painless hematochezia.

55
Q

Lower Gastrointestinal Bleeding

Clinical Presentation: How does Chronic lower GIB present?

A

Chronic lower GIB presents with iron deficiency anemia.

56
Q

Lower Gastrointestinal Bleeding

Clinical Presentation: How can hemorrhoids present?

A

Hemorrhoids can present with massive bleeding from rectal varices from portal hypertension.

57
Q

Lower Gastrointestinal Bleeding

Management:

A

Fluid resuscitation

Colonoscopy

Upper endoscopy

Radionucleotide imaging

Angiography

Surgical intervention

58
Q

Lower Gastrointestinal Bleeding

Management: What is NG tube for?

A

NG-tube to eliminate an upper GI bleed

59
Q

Lower Gastrointestinal Bleeding

Management: What is done for diagnosis and treatment?

A

Colonoscopy for diagnosis and treatment

60
Q

Lower Gastrointestinal Bleeding

Management: What testing distinguishes the source of lower gastrointestinal bleeding?

A

Upper endoscopy distinguishes the source.

61
Q

Lower Gastrointestinal Bleeding

Management: What locates the site of bleeding?

A

Radionucleotide imaging—locates the site of bleed

62
Q

What is the test of choice for evaluation of lower GIB?

A

Colonoscopy

63
Q

Lower Gastrointestinal Bleeding

Management: What angiography for?

A

Angiography—for diagnosis and embolization

64
Q

Lower Gastrointestinal Bleeding

Management: What is surgical intervention for?

A

Exploratory lap,

segmental bowel resection,

total colectomy

65
Q

Small Bowel Obstruction:

What is the most common cause?

A

Adhesions are the most common cause after laparotomy, radiation, ischemia, infection, or foreign body.

66
Q

Small Bowel Obstruction:

How do adhesions occur?

A

Adhesions are the most common cause after laparotomy, radiation, ischemia, infection, or foreign body.

67
Q

Small Bowel Obstruction:

What is the second most common cause?

A

Hernias—strangulated

68
Q

Small Bowel Obstruction

What is an uncommon cause of SBO?

A

Tumors—uncommon in the small bowel

69
Q

Small Bowel Obstruction

Pathophysiology: What occurs?

A

Fluid and air accumulate proximal to obstruction causing distention.

70
Q

Small Bowel Obstruction

Pathophysiology: What happens to bowel wall?

A

Bowel wall becomes edematous and distended.

71
Q

Small Bowel Obstruction

Pathophysiology: What decreases?

A

Peristalsis decreases and normal function halts.

72
Q

Small Bowel Obstruction

Clinical Presentation: What occurs?

A

Acute onset of intermittent, crampy, periumbilical pain

Fever, constipation

73
Q

Small Bowel Obstruction

Clinical Presentation: What relieves pain?

A

Vomiting often relieves the pain.

74
Q

Small Bowel Obstruction

Clinical Presentation: How is strangulated SBO?

A

In strangulated SBO, the pain is localized, steady, severe.

75
Q

Small Bowel Obstruction

Assessment:

A

History of abdominal surgery/trauma, inflammatory bowel disease, diverticulitis, radiation, PUD, pancreatitis

76
Q

Small Bowel Obstruction

Assessment: History of abdominal surgery/trauma, inflammatory bowel disease, diverticulitis, radiation, PUD, pancreatitis

A

Medication history, psychiatric history

77
Q

Small Bowel Obstruction

Assessment: Physical examination
What is present?

A

Visible peristalsis and distention, epigastric/periumbilical/diffuse abdominal tenderness, hyperactive BS early then high-pitched tinkling

78
Q

Small Bowel Obstruction

Assessment: Physical examination
What are signs and symptoms?

A

S & S of dehydration, palpable mass; palpate for inguinal hernia.

79
Q

Small Bowel Obstruction

Diagnostic Studies include:

A

Radiography

Computed tomography

Endoscopy

80
Q

Small Bowel Obstruction

Diagnostic Studies: Radiography
What could it diagnose?

A

Dx of obstruction, perforation

81
Q

Small Bowel Obstruction

Diagnostic Studies: Computed tomography

What could it diagnose?

A

Obstructive lesions,

neoplasms (tumors),

hernias,

and ischemia

82
Q

Small Bowel Obstruction

Diagnostic Studies: Endoscopy

What could it diagnose?

A

Direct visualization of obstruction in colon or proximal SB

83
Q

Small Bowel Obstruction

Management: Two types

A

Medical management

Surgical management

84
Q

Small Bowel Obstruction

Management: When possible, how are SBOs treated?

A

When possible, obstructions, especially incomplete obstructions, are treated medically rather than surgically.

85
Q

Small Bowel Obstruction

Management: Medical Management- What procedure occurs?

A

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.

86
Q

Small Bowel Obstruction

Management: Medical Management- What should be monitored?

A

Monitor for S & S of sepsis, perforation, ischemia, necrosis

Closely watch all patients with intestinal obstructions for signs and symptoms

87
Q

Small Bowel Obstruction

Management: Surgical management
What is a surgical emergency?

A

Acute complete SBO is a surgical emergency.

88
Q

Small Bowel Obstruction

Management: Surgical management
What patients require immediate surgery?

A

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.

89
Q

Small Bowel Obstruction

Management: Surgical management
Surgical procedures include?

A

Lysis of adhesions,

resection,

ostomy,

bowel decompression

90
Q

Acute Pancreatitis:

What is responsible for most cases?

A

Gallstones are responsible for 40% of cases.

91
Q

Acute Pancreatitis:

What is the second leading cause of pancreatitis? What percent does it account for?

A

Alcoholism is the second leading cause of pancreatitis and accounts for 35% of the cases.

92
Q

Acute Pancreatitis:

What are metabolic causes of acute pancreatitis?

A

Hypercalcemia and hypertriglyceridemia, medications, infectious processes

93
Q

Acute Pancreatitis:

Pathophysiology

A

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.

94
Q

Acute Pancreatitis:

Clinical Presentation: What kind of pain occurs?

A

Deep, boring midepigastric or periumbilical pain

95
Q

Acute Pancreatitis:

Clinical Presentation: What signs and symptoms?

A

Nausea/vomiting without pain relief,

tachycardia,

hypotension,

abdominal distention,

low-grade fever

96
Q

Acute Pancreatitis:

Clinical Presentation: What kind of history may they have?

A

History of biliary disease, alcohol use, diabetes, medications, location of pain, weight loss, N/V

97
Q

Acute Pancreatitis:

Physical examination: When examining patient what may present?

A

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

98
Q

Acute Pancreatitis

Diagnostic Studies:

A

Labs

Imaging studies

99
Q

Acute Pancreatitis

Diagnostic Studies: Labs

A

Elevated serum amylase and lipase,

electrolyte imbalance,

hyperglycemia,

LFTs elevated with concurrent liver disease,

elevated ALT and alkaline phosphatase with biliary disease

100
Q

Acute Pancreatitis

Diagnostic Studies: Imaging studies
What are they for? What is the preferred test?

A

Radiographs exclude other causes.

CT is the preferred test.

101
Q

What is an assessment tool to measure the severity of Acute Pancreatitis?

A

Ranson’s Criteria

102
Q

Acute Pancreatitis:

Ranson’s Criteria:

When are the two times this tool is used?

A
  1. Evaluate on admission or on diagnosis
  2. Evaluate during initial 48 hours
103
Q

Acute Pancreatitis:

Ranson’s Criteria: What is predictive of severe AP?

A

Three or more signs identified at the time of admission or during the initial 48 hours are predictive of severe AP.

104
Q

Acute Pancreatitis:

Ranson’s Criteria: How accurate is this tool?

A

Ranson criteria have a greater than 90% accuracy rate and are useful clinically in identifying high-risk patients.

105
Q

Acute Pancreatitis:

Ranson’s Criteria: What is the primary disadvantage of this tool?

A

The primary disadvantage to Ranson criteria is the 48-hour delay before the assessment is completed.

106
Q

Acute Pancreatitis:

Ranson’s Criteria: Evaluate on admission or diagnosis?

A

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

107
Q

Acute Pancreatitis:

Ranson’s Criteria: Evaluate during initial 48 hours?

A

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

108
Q

Acute Pancreatitis:

Complications include what types?

A

Local

Pulmonary

Cardiovascular

Renal

Hematologic

Metabolic

Gastrointestinal

109
Q

Acute Pancreatitis:

Complications: Local

A

pancreatic necrosis,

pseudocyst,

abscess

110
Q

Acute Pancreatitis:

Complications: Pulmonary

A

Pulmonary—atelectasis, ARDS, pleural effusion

111
Q

Acute Pancreatitis:

Complications: Cardiovascular

A

shock states

112
Q

Acute Pancreatitis:

Complications: Renal—

A

ARF

113
Q

Acute Pancreatitis:

Complications: Hematologic

A

Disseminated intravascular coagulation DIC

114
Q

Acute Pancreatitis:

Complications: Metabolic—

A

hyperglycemia, hypertriglyceridemia, hypocalcemia, metabolic acidosis

115
Q

Acute Pancreatitis:

Complications: Gastrointestinal—

A

GIB

116
Q

Acute Pancreatitis:

Management:

A

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

117
Q

Acute Pancreatitis:

Management: Surgical management

A

With massive necrosis, pancreatic resection is done.

Broad-spectrum antibiotics

118
Q

Cirrhosis:

What is it?

A

Complication of liver disease

119
Q

Cirrhosis:

What is it caused by?

A

Caused by chronic HCV,

alcohol abuse,

nonalcoholic steatohepatitis,

hereditary hemochromatosis,

Wilson’s disease,

and alpha1-antitrypsin deficiency

120
Q

Cirrhosis:

Pathophysiology

A

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

121
Q

Cirrhosis:

Pathophysiology: What does it result in?

A

Results in splenomegaly,

varices,

hemorrhoids,

cardiac dysfunction

122
Q

Cirrhosis:

Assessment: What would H and P reveal?

A

H & P reveals altered liver function.

123
Q

Cirrhosis:

Assessment: What is altered?

A

Altered glucose, carbohydrate, fat, and protein metabolism

124
Q

Cirrhosis:

Assessment: What is there a decrease of?

A

Decreased synthesis of albumin leads to interstitial edema and decreased plasma volume.

125
Q

Cirrhosis:

Assessment: What dysfunction occurs?

A

Clotting dysfunction

126
Q

Cirrhosis:

Assessment: What else occurs?

A

Ascites,

lower extremity edema,

hypotension

127
Q

Cirrhosis:

Management: What should be monitored?

A

Monitor nutrition, fluid balance, urine output, electrolytes, PT/PTT, platelet function, hematocrit.

Monitor LOC, abdominal girth.

128
Q

Cirrhosis:

Management: What should be managed?

A

Manage ascites—paracentesis or Venous-Peritoneal shunt.

129
Q

Cirrhosis:

Management: How should ascites be managed?

A

Manage ascites—paracentesis or Venous-Peritoneal shunt.

130
Q

Cirrhosis:

Management: What other procedure is done? What does this do?

A

Transjugular intrahepatic portosystemic shunt (TIPS) procedure to decompress portal venous system

NURS 428: Evolution (17 decks)

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