Gi Exam

Front 1

is present in more than 70% to 75% of duodenal ulcers; it occurs at a lower rate with gastric ulcers but is found in most gastric ulcers in which NSAIDs cannot be implicated.

Back 1

Helicobacter pylori

Front 2

is a loss of enteric surface epithelium that extends deeply enough to penetrate the muscularis mucosae.

Back 2

gastrointestinal ulcer

Front 3

refers to a chronic disorder in which the patient has a lifelong underlying tendency to develop mucosal ulcers at sites that are exposed to peptic juice (i.e., acid and pepsin).

Back 3

PUD

Front 4

2 main etiologies of PUD?

Back 4

1. H. pylori
2. Imbalance b/w mucosal protective factors and aggressive facotrs.

Front 5

Protective Factors for PUD

Back 5

1. Mucosal barrier (bicarbonate and gastric mucus)
2. Competent sphinctters (pyloric and LES)
3. Certan medications: H2 blockers, Antacids, Sucralfate, Colloidal bismuth sus. Anticholinergic, Cytotec, prilosec.

Front 6

Prevent bile salt reflux into the stomach and the esophogus.

Back 6

competent sphincters :
pyloric sphincter and lower esophageal sphincter (LES)

Front 7

Aggressive factors that are medications

Back 7

Aspirin
NSAIDS
Gluccocorticoids

Front 8

Aggressive factors in PUD disease

Back 8

a. Gastric acid
b. Pepsin
c. Bile acids
d. Decreased blood flow to gastric mucosa
e. Incompetent sphincters
f. Various medications
H. pylori infection
Cigarette smoking
h. Gastrinoma
Stress,
ETOH,
Impaired proximal duodenal bicarbonate secretion

Front 9

Highly associated risk factors for PUD

Back 9

1. Smoking more than than ½ pack of cigarettes per day
2. Drugs (NSAIDs)
3. Family history
4. Zollinger-Ellison syndrome

Front 10

. Possibly associated with PUD
.

Back 10

1. Corticosteroids
2. Stress

Front 11

(condition caused by non–insulin-secreting tumors of the pancreas, which secrete excess amounts of gastrin)

.

Back 11

Zollinger-Ellison syndrome

Front 12

Types of PUD

Back 12

1. Duodenal ulcers
2. Gastric ulcers

Front 13

In all, 90% to 95% occur in the first portion of the duodenum. 2. Four times more common than gastric ulcers 3. For men, 10% lifetime prevalence; 5% for women 4. New cases annually: 200,000 to 400,000 5. Most common age range is 25 to 55 years.

Back 13

Duodenal ulcers

Front 14

1. Most commonly seen in the lesser curvature of the stomach near the incisura angularis
2. Three to four times more prevalent than duodenal ulcers in NSAID users 4. Peak age of incidence: 55 to 65 years (rare before age 40)

Back 14

Gastric Ulcer

Front 15

Ulcer most commonly seen in ages 55 to 65, rarely before age 40.

Back 15

Gastric Ulcer

Front 16

What type of ulcer is seen in ages 25 to 55.

Back 16

Duodenal Ulcers

Front 17

Epigastric pain (“gnawing,” “aching,” “hunger-like”) occurs 1 to 3 hours after eating. The pain is rhythmic and periodic.

Back 17

Duodenal Ulcers

Front 18

2. Nocturnal pain that awakens a patient from sleep Heartburn (suggests reflux disease)

Back 18

Duodenal Ulcers

Front 19

. Usually relieved by antacid or food ingestion

Back 19

Duodenal Ulcers

Front 20

Epigastric tenderness: usually midline or right of midline

Back 20

Duodenal Ulcers

Front 21

Epigastric pain similar to that associated with duodenal ulcers and also rhythmic and periodic

Back 21

Gastric Ulcer

Front 22

2. Pain is not usually relieved by food in this type of ulcer

Back 22

Gastric Ulcer

Front 23

Food may precipitate symptoms.

Back 23

Gastric Ulcer

Front 24

Ulcer with subjective findings of Nausea and anorexia

Back 24

Gastric Ulcer

Front 25

Epigastric tenderness at or to the left of midline

Back 25

Gastric Ulcer

Front 26

Epigastric tenderness 1 inch or farther to the right of midline

Back 26

duodenal ulcer

Front 27

S/S of shock with PUD ....think?

Back 27

Acute or chronic blood loss

Front 28

Nausea or Vomitting in PUD is a sign of ?

Back 28

Pyloric channel obstruction

Front 29

Boardlike abdomen and rebound tenderness.

Back 29

Physical findings in PUD with perforation.

Front 30

Hematemis or melena in PUD

Back 30

Ulcer is bleeding

Front 31

For detection of H. pylori:

Back 31

1. Histopathology (endoscopic biopsy)—gold standard
2. Urea breath test
3. Serum H. Pylori antibody test.
4. Stool antigen for H. pylori

Front 32

a. Positive tests implies active infection. b. More expensive than serum and stool tests c. Proton pump inhibitors (PPIs) may cause false-negative results and should be withheld for at least 7 days before testing is done.

Back 32

Urea breath test

Front 33

a. Positive test does not necessarily imply an active infection; it may reflect previous infection.

Back 33

Serum H Pylori antibody test

Front 34

a. Detects active infection by measuring fecal excretion of H. pylori antigens
b. Good test to use to assess whether
treatment has been successful c. PPIs may cause false-negative results and should be withheld for at least 7 days before testing is done.

Back 34

Stool antigen for H. pylori

Front 35

Postitive urea breath test indicates what?

Back 35

H. pylori infection

Front 36

Leukocytosis suggests

Back 36

ulcer penetration or perforation

Front 37

Elevated serum amylase level with severe epigastric pain suggests:

Back 37

possible ulcer penetration into the pancreas.

Front 38

Fasting serum gastrin levels are used to identify what syndrome

Back 38

Zollinger- Ellison syndrom

Front 39

Rec. diagnostic exam for uncomplicated dyspepsia.

Back 39

Upper GI barium studies

Front 40

Complications of PUD

Back 40

GI bleeding
Perforation
Gastric outlet obstruction

Front 41

2. Physical examination
a. Pallor b. Tachycardia c. Hypotension d. Diaphoresis 3. Laboratory findings
a. Decreased hematocrit due to bleeding or hemodilution from IV fluids b. BUN may rise owing to absorption of blood nitrogen from the small intestine and as the result of prerenal azotemia.

.

Back 41

GI bleeding

Front 42

Tx for GI bleeding

Back 42

b. IV hydration with normal saline
c. Blood transfusion as required d. Continuous IV infusion of H2 blockers at a dose adequate to maintain gastric pH above 4 e. Vasopressin (Pitressin) and IV octreotide (Sandostatin) should not be used for bleeding ulcers. f. Surgery if bleeding persists

Front 43

1. Subjective data a. Severe abdominal pain b. Epigastric pain that radiates to back or right upper quadrant 2. Physical examination a. Ill appearance b. Boardlike abdomen c. Severe epigastric tenderness d. Absent bowel sounds e. Knee-to-chest position f. Patient may have symptoms of hypovolemia, fever.

Back 43

Perforation

Front 44

3. Laboratory findings a. Leukocytosis is almost always present. b. Amylase levels may be mildly elevated.

Back 44

Perforation

Front 45

4. Diagnostics
a. Abdominal x-rays may reveal free air in the peritoneal cavity.
b. Upper GI radiography with water-soluble contrast may be useful.
c. Barium studies are contraindicated.

.

Back 45

Perforation

Front 46

Therapy for perforation

Back 46

a. Surgery
b. Patients who are considered poor candidates for surgery or who present more than 24 hours after perforation and are stable may be followed closely while on IV fluids, nasogastric suction, and broad-spectrum antibiotics.
c. If their condition deteriorates, they should be taken to surgery.

.

Front 47

1. Caused by edema or narrowing of the pylorus or duodenal bulb

Back 47

Gastric outlet obstruction

Front 48

Subjective findings: a. Early satiety b. Nausea c. Vomiting of undigested food d. Epigastric pain unrelieved by food or antacids e. Weight loss

.

Back 48

Gastric outlet obstruction

Front 49

Physical examination findings: a. “Succussion splash” may be audible on physical examination, caused by large amounts of air and fluid in the stomach. b. Nasogastric aspiration may return a large amount (more than 200 ml) of foul-smelling fluid.

Back 49

Gastric outlet obstruction

Front 50

Diagnostics and labs for gastric outlet obstruction.

Back 50

Diagnostics
a. Upper GI endoscopy should be performed after 24 to 72 hours to determine the source of obstruction.
b. At 72 hours, all patients should be given the saline load test, accomplished by instilling 750 ml of normal saline into the stomach and checking the residual in 30 minutes.
c. Residual volume greater than 400 ml is considered positive.
d. Patient should remain on nasogastric suction for 5 to 7 additional days.
Laboratory:
Metabolic alkalosis and hypokalemia may be present.

Front 51

Epigastric pain or burning, early satiety, or postprandial fullness.
Endoscopy is warranted in patients with alarm features or in those older than 55 years.
All other patients should first undergo testing for Helicobacter pylori or a trial of empiric proton pump inhibitor.

Back 51

dyspepsia

Front 52

the chewing and swallowing of food that is regurgitated volitionally after meals.

Back 52

rumination

Front 53

Acute symptoms of N and V without abdominal pain are typically caused by

Back 53

food poisoning,
infectious gastroenteritis, drugs,
systemic illness

Front 54

The acute onset of nausea and vomiting with severe pain suggests

Back 54

peritoneal irritation,
acute gastric
intestinal obstruction, pancreaticobiliary disease.

Front 55

Persistent vomiting suggests:

Back 55

pregnancy, gastric outlet obstruction, gastroparesis, intestinal dysmotility, psychogenic disorders, and central nervous system or systemic disorders.

Front 56

Vomiting that occurs in the morning before breakfast is common with:

Back 56

pregnancy, uremia, alcohol intake, and increased intracranial pressure.

Front 57

Vomiting immediately after meals strongly suggests

Back 57

bulimia or psychogenic causes.

Front 58

Vomiting of undigested food one to several hours after meals is characteristic of

Back 58

gastroparesis or a gastric outlet obstruction; physical examination may reveal a succussion splash.

Front 59

The cause of gastric outlet obstruction is best demonstrated by

Back 59

upper endoscopy

Front 60

the cause of small intestinal obstruction is best demonstrated with

Back 60

abdominal CT imaging.

Front 61

What condition is confirmed by nuclear scintigraphic studies or 13C-octanoic acid breath tests, which show delayed gastric emptying and either upper endoscopy or barium upper gastrointestinal series showing no evidence of mechanical gastric outlet obstruction.

Back 61

Gastroparesis

Front 62

Abnormal liver function tests or elevated amylase or lipase suggest

Back 62

pancreaticobiliary disease

Front 63

pancreaticobiliary disease, which may be investigated with an

Back 63

abdominal sonogram or CT scan.

Front 64

Complications of nausea and vomittingh include:

Back 64

dehydration, hypokalemia, metabolic alkalosis, aspiration, rupture of the esophagus (Boerhaave syndrome), and bleeding secondary to a mucosal tear at the gastroesophageal junction (Mallory-Weiss syndrome).

Front 65

For patient with more severe acute vomiting,unable to eat and losing gastric fluids has become dehydrated, resulting in hypokalemia with metabolic alkalosis. Treat with?

Back 65

Intravenous 0.45% saline solution with 20 mEq/L of potassium chloride is given in most cases to maintain hydration.

Front 66

are effective in preventing chemotherapy- and radiation-induced emesis when initiated prior to treatment. Although 5-HT3-receptor antagonists are effective as single agents for the prevention of chemotherapy-induced nausea and vomiting, their efficacy is enhanced by combination therapy with a corticosteroid (dexamethasone) and NK1-receptor antagonist (see below).

Back 66

Serotonin 5-HT3-receptor antagonists
Ondansetron, granisetron, dolasetron, and palonosetron

Front 67

increasingly are used for the prevention of postoperative nausea and vomiting because of increased restrictions on the use of other antiemetic agents (such as droperidol).

Back 67

Serotonin antagonists

Front 68

have antiemetic properties, but the basis for these effects is unknown. These agents enhance the efficacy of serotonin receptor antagonists for preventing acute and delayed nausea and vomiting in patients receiving moderately to highly emetogenic chemotherapy regimens.

Back 68

Corticosteroids

Corticosteroids (eg, dexamethasone

Front 69

are highly selective antagonists for NK1-receptors in the area postrema. They are used in combination with corticosteroids and serotonin antagonists for the prevention of acute and delayed nausea and vomiting with highly emetogenic chemotherapy regimens. Combined therapy with a neurokinin1 receptor antagonist prevents acute emesis in 80–90% and delayed emesis in > 70% of patients treated with highly emetogenic regimens.

Back 69

AprNeurokinin receptor antagonists

epitant and fosaprepitant

Front 70

have antiemetic properties that are due to dopaminergic blockade as well as to their sedative effects. High doses of these agents are associated with antidopaminergic side effects, including extrapyramidal reactions and depression. These agents are used in a variety of situations. Cases of QT prolongation leading to ventricular tachycardia (torsades de pointes) have been reported in several patients receiving droperidol, hence it is no longer recommended as an antiemetic agent.

Back 70

Dopamine antagonists

The phenothiazines, butyrophenones, and substituted benzamides

Front 71

may be valuable in the prevention of vomiting arising from stimulation of the labyrinth, ie, motion sickness, vertigo, and migraines. They may induce drowsiness. A combination of oral vitamin B6 and doxylamine is recommended by the American College of Obstetricians and Gynecologists as first-line therapy for nausea and vomiting during pregnancy.

Back 71

Antihistamines and anticholinergics

These drugs (eg, meclizine, dimenhydrinate, transdermal scopolamine)

Front 72

are used in psychogenic and anticipatory vomiting

Back 72

Sedatives
Benzodiazepines

Front 73

has been used widely as an appetite stimulant and antiemetic. Pure 9-tetrahydrocannabinol (THC) is the major active ingredient in marijuana and is available by prescription as dronabinol. In doses of 5–15 mg/m2, oral dronabinol is effective in treating nausea associated with chemotherapy, but it is associated with central nervous system side effects in most patients.

Back 73

Cannabinoids

Marijuana

Front 74

In patients on mechanical ventilation, _____ can trigger a full respiratory cycle and result in respiratory alkalosis.

Back 74

hiccups

Front 75

Evaluation of the patient with persistent hiccups should include

Back 75

a detailed neurologic examination, serum creatinine, liver chemistry tests, and a chest radiograph. When the cause remains unclear, CT of the head, chest, and abdomen, echocardiography, bronchoscopy, and upper endoscopy may help. On occasion, hiccups may be unilateral; chest fluoroscopy will make the diagnosis.

Front 76

A number of drugs have been promoted as being useful in the treatment of hiccups, what is the most commonly used.

Back 76

Chlorpromazine, 25–50 mg orally or intramuscularly

Front 77

A number of simple remedies may be helpful in patients with acute benign hiccups.

Back 77

(1) Irritation of the nasopharynx by tongue traction, lifting the uvula with a spoon, catheter stimulation of the nasopharynx, or eating 1 tsp of dry granulated sugar. (2) Interruption of the respiratory cycle by breath holding, Valsalva maneuver, sneezing, gasping (fright stimulus), or rebreathing into a bag. (3) Stimulation of the vagus by carotid massage. (4) Irritation of the diaphragm by holding knees to chest or by continuous positive airway pressure during mechanical ventilation. (5) Relief of gastric distention by belching or insertion of a nasogastric tube.

Front 78

Adjunct in the prevention and treatment of portal-systemic encephalopathy; treatment of chronic constipation

Back 78

Lactulose

Front 79

Genitourinary irrigant in transurethral prostatic resection or other transurethral resection or other transurethral surgical procedures; diuretic; humectant; sweetening agent; hyperosmotic laxative; facilitate the passage of sodium polystyrene sulfonate through the intestinal tract

Back 79

Sorbitol

Front 80

Use
Treatment of Paget's disease of bone (osteitis deformans); adjunctive therapy for hypercalcemia; treatment of osteoporosis in women >5 years postmenopause

Back 80

Calcitonis

Front 81

Diarrhea of < 2 weeks duration is most commonly caused by

Back 81

invasive or noninvasive pathogens and their enterotoxins.

Front 82

Watery, nonbloody.
Usually mild, self-limited.
Caused by a virus or noninvasive bacteria.
Diagnostic evaluation is limited to patients with diarrhea that is severe or persists beyond 7 days.

Back 82

Acute noninflammatory diarrhea

Front 83

Blood or pus, fever.
Usually caused by an invasive or toxin-producing bacterium.
Diagnostic evaluation requires routine stool bacterial cultures (including Escherichia coli O157:H7) in all and testing as clinically indicated for Clostridium difficile toxin, and ova and parasites.

Back 83

Acute inflammatory diarrhea

Front 84

Diarrhea present for > 4 weeks.
Before embarking on extensive work-up, common causes should be excluded, including medications, chronic infections, and irritable bowel s

Back 84

Chronic Diarrhea

Front 85

Hyponatremia and nonanion gap metabolic acidosis occur in

Back 85

secretory diarrheas.

Front 86

Increased erythrocyte sedimentation rate or C-reactive protein

Back 86

suggests inflammatory bowel disease.

Front 87

increased osmotic gap suggests an

Back 87

osmotic diarrhea or disorder of malabsorption

Front 88

A positive fecal fat stain suggests

Back 88

a disorder of malabsorption

Front 89

The presence of fecal leukocytes or lactoferrin may suggest

Back 89

inflammatory bowel disease.

Front 90

24-hour stool collection quantification of total weight and fat
A stool weight of < 200–300 g/24 h

Back 90

excludes diarrhea and suggests a functional disorder such as irritable bowel syndrome

Front 91

24-hour stool collection quantification of total weight and fat

A weight > 1000–1500 g suggests

Back 91

a significant secretory process, including neuroendocrine tumors.

Front 92

24-hour stool collection quantification of total weight and fat Fecal elastase < 100 mcg/g may be caused by

Back 92

pancreatic insufficiency.

Front 93

A fecal fat determination in excess of 10 g/24 h confirms a

Back 93

malabsorptive disorder

Front 94

Hematemesis (bright red blood or "coffee grounds").
Melena in most cases; hematochezia in massive upper gastrointestinal bleeds.
Volume status to determine severity of blood loss; hematocrit is a poor early indicator of blood loss.
Endoscopy diagnostic and may be therapeutic.

Back 94

Upper GI bleed

Front 95

Hematochezia usually present.
Ten percent of cases of hematochezia due to upper gastrointestinal source.
Evaluation with colonoscopy in stable patients.
Massive active bleeding calls for evaluation with sigmoidoscopy, upper endoscopy, angiography, or nuclear bleeding scan.

Back 95

Lover GI bleed

Front 96

Total serum bilirubin is normally

Back 96

0.2–1.2 mg/dL
(3.42–20.52 mcmol/L)

Front 97

jaundice may not be recognizable until levels are about

Back 97

3 mg/dL
(51.3 mcmol/L).

Front 98

refers to bleeding that is not apparent to the patient. It is manifested by recurrent positive FOBTs or FITs or recurrent iron deficiency anemia, or both in the absence of visible blood loss (as described below).

Back 98

Obscure-occult bleeding

Front 99

bleeding refers to bleeding of unknown origin that persists or recurs after initial endoscopic evaluation with upper endoscopy and colonoscopy.

Back 99

Obscure gastrointestinal

Front 100

is manifested by persistent or recurrent visible evidence of gastrointestinal bleeding (hematemesis, hematochezia, or melena). Up

Back 100

Obscure-overt bleeding

Front 101

2 major causes of peptic ulcer disease.

Back 101

NSAIDS
Chronic H. pylori infection

Front 102

is the feeling of substernal burning, often radiating to the neck. Caused by the reflux of acidic (or, rarely, alkaline) material into the esophagus, it is highly specific for GERD

Back 102

Heartburn (pyrosis)

Front 103

is an intraesophageal acid perfusion study that can be used to confirm that the patient's symptoms are acid related.

Jr.Barkley, Thomas W. (2007). Practice Guidelines for Acute Care Nurse Practitioners (Kindle Locations 11330-11331). A Saunders Title. Kindle Edition.

Back 103

The Bernstein test

Front 104

is an excellent study for the diagnosis and evaluation of reflux esophagitis and other complications of GERD (strictures, Barrett's esophagus).

Jr.Barkley, Thomas W. (2007). Practice Guidelines for Acute Care Nurse Practitioners (Kindle Locations 11326-11327). A Saunders Title. Kindle Edition.

Back 104

Endoscopy

Front 105

The test requires an alternating infusion of 0.1 N hydrochloric acid and normal saline into the esophagus. 2. With reflux esophagitis, symptoms of heartburn occur with infusion of acid but not with infusion of saline.

Back 105

Bernstein test

Front 106

measures esophageal pressure.
1. Identifies abnormalities of the LES
2. Identifies esophageal muscle contraction abnormalities

Jr.Barkley, Thomas W. (2007). Practice Guidelines for Acute Care Nurse Practitioners (Kindle Locations 11340-11342). A Saunders Title. Kindle Edition.

Back 106

Esophogeal manometry

Front 107

The most sensitive diagnostic test used to detect the presence of abnormal acid reflux is?

Back 107

24 hour ambulatory ph monitoring
Gold standard for many practitioners

Front 108

normal serum bilirubin

Back 108

0.2-1.2mg/dl

Front 109

cholestasis

Back 109

retention of bile in the liver

Front 110

Cholestatic jaundice

Back 110

conjugated hyperbilirubinemia results from impaired bile flow

Front 111

Splenomegaly occurs in hemolytic disorders except in ?

Back 111

Sickle cell anemia

Front 112

occult blood in the stool suggests what ?

Back 112

cancer of the ampulla

Front 113

courvoisier sign

Back 113

hepatomegaly and a palpable gallbladder

Front 114

elevated ALT and AST levels result from ?

Back 114

hepatocellular necrosis or inflammation

Front 115

unvaccinated person exposed to HAV is advised to recieve post exposure prophylaxis. Which consist of?

Back 115

Single dose HAV vaccine or
Immune globulin 0.02ml/kg
Vaccine: healthy 1-40
Immune globulin:
older than 40
younger than 1
immunocomprimised
chronic liver disease.

Front 116

Causes of esophageal varices

Back 116

Cirrhosis-most common cause
High Portal Venous Pressure

Front 117

Normal portal venous pressure

Back 117

2-6

Front 118

Portal venous pressure associated with esophageal varices bleeding

Back 118

at least 12

Front 119

bleeding from esophageal varices usually occurs where?

Back 119

distal 5cm of esophagus
upper portion of stomach

Front 120

Associated with 1st variceal bleeding episode?

Back 120

ASA / NSAID use alone or in combo. in pt with cirrhosis