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GI II Final > CLMD: Esophagus, Stomach, Pancreas > Flashcards

CLMD: Esophagus, Stomach, Pancreas Flashcards

1
Q

Upper endoscopy (EGD) is the study of choice for what conditions?

A

Evaluating persistent heartburn

Dysphagia

Odynophagia

Structural abnormalities detected on barium esophagography

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2
Q

What makes EGD both diagnostic and therapeutic?

A

Direct visualization + ability to take biopsies + allows dilation of strictures

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3
Q

Video esophagography (rapid-sequence videofluoroscopy) is the study of choice to evaluate what condition?

A

Oropharyngeal dysphagia

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4
Q

What diagnostic study differentiates between mechanical lesions and motility disorders of the esophagus?

A

Barium esophagography

[barium study more sensitive for detecting subtle esophageal narrowing d/t rings, achalasia, and proximal esophageal lesions]

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5
Q

What diagnostic study should be done to establish the etiology of dysphagia in pts in whom a mechanical obstruction cannot be found, especially if a dx of achalasia is suspected based on previous endoscopy or barium study?

A

Esophageal manometry — assesses esophageal motility

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6
Q

2 types of esophageal pH recording and impedance testing

A

Catheter-based (trans-nasal)

Wireless (capsule attaches directly to esophageal mucosa)

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7
Q

What clues indicate mechanical obstruction vs. motility disorder as the cause of esophageal dysphagia?

A

Mechanical obstruction = solid foods worse than liquids

Motility = solid and liquid difficulty

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8
Q

Types of mechanical obstruction

A

Schatzki ring
Peptic stricture
Esophageal cancer
Eosinophilic esophagitis

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9
Q

Clinical clues associated with schatzki ring as the cause of esophageal dysphagia

A

Intermittent dysphagia, not progressive

[note that Schatzki ring is not progressive while peptic stricture is progressive]

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10
Q

Clinical clues associated with peptic stricture as the cause of esophageal dysphagia

A

Chronic heartburn + progressive dysphagia

[patient may exhibit improving heartburn but worsening dysphagia because the stricture creates a scar that blocks acid from causing irritation]

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11
Q

Clinical clues associated with esophageal cancer as the cause of esophageal dysphagia

A

Progressive dysphagia

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12
Q

Clinical clues associated with eosinophilic esophagitis as the cause of esophageal dysphagia

A

Young adults, small-caliber lumen, proximal stricture, corrugated rings, or white papules

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13
Q

Clinical clues associated with achalasia as the cause of esophageal dysphagia

A

Progressive dysphagia

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14
Q

Clinical clues associated with diffuse esophageal spasm as the cause of esophageal dysphagia

A

Intermittent, not progressive — may have chest pain

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15
Q

Clinical clues associated with scleroderma as the cause of esophageal dysphagia

A

Chronic heartburn + Raynaud phenomenon

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16
Q

Clinical clues associated with ineffective esophageal motility as the cause of esophageal dysphagia

A

Intermittent, not progressive, commonly associated with GERD

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17
Q

What conditions cause progressive dysphagia?

A

Mechanical: peptic stricture, esophageal cancer

Motility disorders: achalasia

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18
Q

Do esophageal webs cause progressive or non-progressive dysphagia?

A

Non-progressive

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19
Q

Alarm features of GERD

A 
Weight loss
Persistent vomiting
Constant/severe pain
Dysphagia/odynophagia
Hematemesis
Melena
Anemia (iron deficiency)

[needs endoscopy or abdominal imaging]

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20
Q

Patients with typical symptoms of heartburn and regurgitation should be treated empirically with what?

A

Once daily PPI for 4-8 weeks

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21
Q

T/F: severity of GERD is correlated with degree of tissue damage

A

False: some pts with severe esophagitis are only mildly symptomatic

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22
Q

Extraesophageal reflux manifestations and recommended tx

A

Asthma, hoarseness (possible laryngopharyngeal reflux), cough, sleep disturbance

Trial of PPI BID x2-3 months

Esophageal impedance pH testing may be performed in pts whose esophageal sxs persist after 3 months of PPI BID

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23
Q

If a pt presents with hx of GERD, pyrosis, and chest discomfort and an air-fluid level is seen on CXR, what is the likely dx?

A

Hiatal hernia

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24
Q

____ is a motility d/o that causes dysphagia to mainly solids but some liquids, affects women>men between ages 30-50 (more severe in african americans), and exhibits the hallmark of thickening and hardening of skin

A

Scleroderma

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25
Q

Pt presents with dysphagia, regurgitation, choking, aspiration, voice changes, halitosis, and weight loss. What is the dx study of choice to confirm your dx?

A

Barium swallow (likely Zenker diverticulum) — tx is surgery

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26
Q

Which potential cause of oropharyngeal dysphagia has a strong association with B cell non-hodgkin lymphoma?

A

Sjogrens

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27
Q

Characteristics of sjogrens

A

Rheumatologic condition affecting F>M in mid-50s, usually postmenopausal

Sicca sxs: dry eyes, dry mouth —> oropharyngeal dysphagia, vaginal dryness, tracheo-bronchial dryness, increased incidence of oral infections and dental caries

Parotic or other major salivary gland enlargement

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28
Q

What epithelial changes occur with Barrett esophagus?

A

Squamous epithelium of esophagus is replaced by metaplastic columnar epithelium containing goblet and columnar cells (specialized intestinal metaplasia)

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29
Q

Risk factors for Barrett vs. peptic stricture

A

Risk factors for Barrett: chronic reflux, truncal obesity

Risk factors for peptic stricture: reduction in heartburn because stricture acts as barrier to reflux

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30
Q

If endoscopy shows presence of orange, gastric type epithelium that extends upward from stomach into distal 1/3 tubular esophagus in tongue-like or circumferential fashion, what might your dx be?

A

Barrett esophagus

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31
Q

Purpose of PPI therapy to tx barrett esophagus

A

PPIs do not cause regression of Barrett esophagus but may reduce risk of esophageal adenocarcinoma

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32
Q

2011 clinical guidelines recommend against endoscopic screening for Barrett esophagus in adults with GERD except in those with multiple risk factors for adenocarcinoma. What are the risk factors?

A 
Chronic GERD
Hiatal hernia
Obesity
White race
Male gender
Age 50+

Endoscopy every 3-5 years is recommended to look for low- or high-grade dysplasia or adenocarcinoma in these pts

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33
Q

SCC of the esophagus is the most common type of esophageal cancer in the world. What are the risk factors?

A

Males > females and AA > caucasians

Age 50+

Heavy smoking, alcohol use, achalasia, Plummer-Vinson syndrome, Tylosis, lye ingestion, hot beverages

[note that adenocarcinoma of the esophagus has higher incidence in caucasians than AA]

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34
Q

Truly refractory (unresponsive) reflux disease with esophagitis may be caused by what conditions?

A

ZE syndrome
Pill-induced esophagitis
Resitance to PPIs
Medical noncompliance

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35
Q

Most commonly implicated pills that cause pill-induced esophagitis

A

NSAIDs, potassium chloride pills, alendronate and risedronate, antibiotics

[others not highlighted in her slide: quinidine, zalcitabine, zidovudine, bisphosphonates, emepronium bromide, iron, vitamin C]

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36
Q

Dx and possible complications of pill-induced esophagitis

A

Endoscopy may reveal one to several discrete ulcers that may be shallow or deep

Complications: chronic injury may result in severe esophagitis with stricture, hemorrhage, or perforation

[note that healing occurs rapidly when offending agent is eliminated]

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37
Q

Most common pathogens implicated in infectious esophagitis

A

Candida albicans
HSV
CMV

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38
Q

Risk factors for infectious esophagitis

A

Immunosuppression (AIDS, solid organ transplants, leukemia, lymphoma)

Uncontrolled diabetes, tx with systemic corticosteroids, radiation therapy, systemic abx therapy

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39
Q

Dx of infectious esophagitis is done by endoscopy with brushings, biopsy, and culture. Which pathogen is characterized by one to several large, shallow, superficial ulcerations and may be compounded with infection at other sites such as the colon and retina?

A

CMV

Tx: in pts with HIV, immune restoration with antiretroviral therapy is most effective means of controlling CMV infection. Initial therapy is with ganiciclovir — although neutropenia is frequent dose-limiting SE

40
Q

Dx of infectious esophagitis is done by endoscopy with brushings, biopsy, and culture. Which pathogen is characterized by multiple small, deep ulcerations as well as possible associated oral ulcers?

A

HSV

Tx: immunocompetent pts treated symptomatically but immunosuppressed pts require tx with acyclovir

41
Q

Dx of infectious esophagitis is done by endoscopy with brushings, biopsy, and culture. What pathogen is implicated with diffuse, linear, yellow-white plaques adherent to esophageal mucosa?

A

Candidal esophagitis

Tx: systemic antifungal like fluconazole

42
Q

Sxs of caustic esophageal injury

A

Almost immediate severe burning and varying degrees of CP, gagging, dysphagia, and drooling

Aspiration results in stridor and wheezing

Other symptoms may include dyspnea and hematemesis

43
Q

Dx of caustic esophageal injury

A

Initial exam directed to circulatory status as well as assessment of airway patency and oropharyngeal mucosa including laryngoscopy

Chest and abdominal radiographs are obtained looking for pneumonitis or free perforation (both potential complications of caustic injury)

44
Q

Why should endoscopic surveillance be considered 15-20 years after caustic ingestion esophageal injury?

A

Risk of esophageal SCC is 2-3% after caustic ingestion

45
Q

T/F: nasogastric lavage and oral antidotes may be dangerous and should NOT be administered following caustic esophageal injury

A

True

46
Q

Risk factors for eosinophilic esophagitis

A

GERD, PPI-responsive eosinophilia, celiac dz, Crohn dz, and pemphigus

Food or environmental Ags thought to stimulate inflammatory response

Children and young-middle-aged adults

Predominantly men and those with hx of allergies or atopic conditions (asthma, eczema, hay fever)

47
Q

Dx of eosinophilic esophagitis

A

Barium swallow studies show small-caliber esophagus with multiple concentric rings

Endoscopy with esophageal biopsy is required to establish dx to demonstrate multiple eosinophils in mucosa [endoscopy also shows white exudates or papules, red furrows, corrugated concentric rings, and strictures]

48
Q

Treatment for eosinophilic esophagitis

A

Topical corticosteroids effective in 70% — budesonide or fluticasone

Dilation of strictures can be done, but beware of high risk of perforation in these pts

49
Q

Dx of esophageal webs

A

Best visualized with barium esophogram (more sensitive test for this than endoscopy)

50
Q

Esophageal rings (Schatzki rings) are associated in nearly all cases with a ____ _____ and are bes visualized using ____ ____

A

Hiatal hernia; barium esophagogram

51
Q

Combination of sxs seen with plummer vinson syndrome

A 
Esophageal webs
Iron-deficiency anemia
Angular cheilitis
Glossitis
Koilonychia (spoon nails)
52
Q

What factors increase the risk of bleeding from esophageal varices?

A
  1. Size > 5 mm
  2. Presence of red wale markings
  3. Severity of liver disease
  4. Active alcohol abuse
53
Q

Tx for bleeding esophageal varices

A

Initial management in ICU: fluid resuscitation, FFP or platelets for possible coagulopathy, IV vitamin K

Antibiotic prophylaxis with fluoroquinolones or IV-3rd gen cephalosporins for possible infection

Somatostatin and octreotide to reduce portal pressures

Lactulose bc encephalopathy may complicate an episode of GIB in pts with severe liver dz

54
Q

What is used to prevent re-bleed from esophageal varices?

A

Nonselective beta-adrenergic blockers (propranalol, nadolol)

Long term tx with band ligation reduces incidence of rebleeding in about 30%

[other invasive treatments include balloon tube tamponade, transvenous intrahepatic portosystemic shunts (TIPS), liver transplant]

55
Q

Etiology of achalasia

A

Denervation of esophagus resulting primarily from loss of NO-producing inhibitory neurons (ganglion cells) in myenteric plexus

Secondary achalasia caused by Chagas disease — especially in endemic regions of Mexico, Central, and South America [trypanosoma cruzi infection]

56
Q

Diagnostic tests used in series to dx achalasia

A

Barium esophagram (shows “birds beak” distal esophagus)

Then EGD to exclude distal stricture or submucosal infiltrating carcinoma

Esophageal manometry confirms dx

57
Q

If achalasia is not treated, the esophagus may become markedly dilated, known as _____ esophagus

A

Sigmoid

[tx includes once-daily PPI and may include botulinum toxin injection, pneumatic dilation, or surgery]

58
Q

Define and describe Nutcracker esophagus in terms of LES tone, symptoms, dysphagia pattern, and diagnostics

A

Nutcracker esophagus = hypertensive peristalsis; swallowing contractions are too powerful

LES relaxes normally but has elevated pressure at baseline

Sxs = dysphagia to solids and liquids, atypical CP

Dysphagia is intermittent and non-progressive

Dx by manometry and/or video fluoroscopy

59
Q

Define and describe Diffuse Esophageal Spasm in terms of LES tone, symptoms, dysphagia pattern, and diagnostics

A

DES = Uncoordinated esophageal contraction (“corkscrew esophagus” or “rosary bead esophagus” on barium xray)

LES function is normal

Sxs = dysphagia to solids and liquids, atypical CP

Dysphagia is intermittent and nonprogressive

Dx by manometry, EGD, and/or barium swallow

60
Q

Signs suggestive of pneumomediastinum

A

Subcutaneous emphysema (typically detected in neck or precordial area)

Hamman’s sign = crunching sound synchronous with heartbeat, heard over precordium mainly during systole

Dyspnea

61
Q

What factors reduce incidence of stress ulcers or bleeding from those ulcers in ICU pts?

A

The use of enteral nutrition reduces risk of stress-related bleeding

Use of H2 blocker or PPI reduce incidence

62
Q

Most common clinical manifestation of erosive gastritis

A

Upper GI bleeding, which presents as hematemesis, “coffee-ground” emesis, or bloody aspirate in pt receiving NG suction

May also see melena

63
Q

Characteristics of Type A Gastritis (Fundic-type)

A

Body predominant and less common form

Generally asymptomatic and more common in elderly

Autoimmune mechanism may be associated with achlorhydria, pernicious anemia, and increased risk of gastric cancer [Abs to parietal cells present in 90%]

May see carcinoid tumors, decreased IF secretion, vit B12 malabsorption, and loss of rugal folds

64
Q

Characteristics of Type B gastritis (Antral type)

A

Antral-predominant disease caused by H.pylori

Associated with dyspepsia, atrophic gastritis, gastric atrophy, gastric lymphoid follicles, and gastric B cell lymphomas may occur

Eradication of H.pylori not routinely recommended unless PUD or gastric MALT lymphoma is present

65
Q

Idiopathic entity characterized by giant thickened gastric folds involving predominantly the body of the stomach resulting in chronic protein loss — pts may present with severe hypoproteinemia and anasarca

A

Menetrier disease

66
Q

When H.pylori infection is located in the gastric antrum, there is ____ gastric acid secretion. When it is located in the gastric body, there is ____ gastric acid secretion

A

Increased;decreased

67
Q

Risk factors for PUD not associated with H.pylori

A

NSAID use, corticosteroid use, smoking, hypercalcemia, mastocytosis, blood group O, alcohol

68
Q

Detection of H.pylori infection

A

Tell pt to stop PPI 14 days prior to fecal and breath tests

Fecal Ag test sensitive, specific, and inexpensive for detection (can also do EGD with biopsy stained with warthin-starry silver stain)

Urea breath test typically used to confirm eradication

69
Q

Possible lab findings with symptomatic H.pylori infection

A

Anemia - may occur with acute or chronic blood loss (hematocrit may also fall)

Leukocytosis - suggests ulcer penetration or perforation

Increased serum amylase + severe pain suggests ulcer penetration into pancreas

BUN may rise as result of absorption of blood nitrogen from small intestine and prerenal azotemia

70
Q

Dietary and other risk factors for gastric adenocarcinoma

A

Dietary factors: smoked fish and meats, pickled vegetables, nitrosamines, benzpyrene, reduced intake of fruits and veggies

Others: H.pylori, smoking, blood type A, menetrier disease, more common in Japan

71
Q

Histological and PE findings associated with gastric adenocarcinomas

A

Histology: Signet-ring cells and linitis plastica

PE: Virchow sentinel node and Krukenberg tumor

72
Q

ZE syndrome is associated 25% of the time with what other syndrome?

A

MEN 1

[gastrinoma, hyperparathyroidism, hypercalcemia, pituitary neoplasm]

73
Q

Dx of ZE syndrome

A

Suggestive = large mucosal folds on endoscopy or upper GI radiograph

Confirmatory = serum gastrin >1000 ng/L; secretin stimulation test +

74
Q

What labs must be drawn in all pts with ZE syndrome to exclude MEN 1?

A

Serum PTH
Prolactin
LH-FSH
GH

75
Q

Gastric scintigraphy imaging following a low-fat solid meal is used to dx what condition?

A

Gastroparesis

76
Q

____ and _____ are each of benefit in tx of gastroparesis

A

Metoclopramide; erythromycin

[note that metoclopramide use x3+months —> slightly increased risk of tardive dyskinesia]

77
Q

Diagnosis of pancreatitis is established by 2 out of what 3 criteria?

A
  1. Typical abdominal pain in epigastrium that may radiate to back
  2. Threefold or greater elevation in serum lipase and/or amylase (lipase more accurate than amylase)
  3. Confirmatory findings of acute pancreatitis on cross-sectional abdominal imaging
78
Q

Most common causes of pancreatitis in US

A

Cholelithiasis

Alcohol

[other common causes: hypertriglyceridemia, ERCP after biliary manometry, drugs, trauma, or post op]

79
Q

Possible PE findings in pt with pancreatitis

A

Low-grade fever, tachycardia, hypotension

Erythematous skin nodules d/t subcutaneous fat necrosis

Basilar rales, pleural effusion, edema (3rd spacing — possible anasarca)

Abdominal tenderness and rigidity

Cullen’s sign

Grey Turner sign

80
Q

Besides lipase/amylase, other labs found in acute pancreatitis

A 
Proteinuria
Granular casts in urine
Glycosuria
Leukocytosis
Hyperglycemia
Hyperbilirubinemia
Increased alkaline phosphatase
Abnormal coag studies
Increased BUN
Elevated creatinine
Elevated ALT (suggest biliary etiology)
Hypocalcemia (possible tetany)
Elevated Hct (panc.necrosis)
Increased CRP (severe)
Hypoalbuminemia and increased LDH (increased mortality rate)
81
Q

Imaging findings with acute pancreatitis

A

Xray may show sentinel loop (segment of air-filled small intestine in LUQ), colon cut-off sign, calcified gallstones, focal linear atelectasis of lower lobe of lungs with/without pleural effusion

US may identify gallstones, pseudocysts, mass lesions, or edema/enlargement of pancreas

CT can confirm clinical impression of acute pancreatitis and its complications

Rapid bolus IV contrast enhanced CT, MRI, endoscopic US

Perfusion CT (PCT) may show fluid collection in pancreas, which correlates with increased mortality rate

82
Q

Pancreatitis is a possible complication of what imaging procedure?

A

ERCP

[however, ERCP can be used to evaluate pancreatitis in certain pts]

Post ERCP prophylaxis includes NSAIDs, indomethacin rectally, and aggressive IV hydration with lactated ringers

83
Q

Most important tx for acute pancreatitis

A

Safe but aggressive IV fluid rescuscitation

Other measures include nothing PO and parenteral analgesics for pain

84
Q

Risk factors for high levels of fluid sequestration in acute pancreatitis (3rd spacing/edema)

A

Younger age, alcohol etiology, higher hematocrit value, higher serum glucose, and SIRS in first 48 hrs of hospital admission

85
Q

In pts with pancreatitis, infusions of FFP or serum albumin may be necessary if coagulopathy or hypoalbuminemia is present. However, with these colloid solutions, there is increased risk of ______

A

ARDS

86
Q

Complications of acute pancreatitis

A 
Necrotizing pancreatitis
Multisystem organ failure
IV volume depletion
Ileus
Fluid collections
Necrotic pancreatic pseudocysts
ARDS (3-7 days after)
Pancreatic abscess

Others include hemorrhage, colonic necrosis, portosplenomesenteric venous thrombosis, chronic pancreatitis, permanent DM and exocrine pancreas insufficiency

87
Q

Ranson Criteria for assessing severity of pancreatitis (number of criteria correlates with increasing mortality rate)

A 
GA-LAW for characteristics at admission: 
Glucose > 200
Age > 55
LDH > 350 
AST > 250
WBC > 16,000
C & Hobbs for characteristics 48 hours after admission:
Calcium <8
Hct drop >10%
Oxygen (PaO2) <60 mmHg
Base deficit >4
BUN increase > 5
Sequestration of fluid > 6L
88
Q

Most frequent cause of clinically apparent chronic pancreatitis

A

Alcoholism

89
Q

The pathogenesis of chronic pancreatitis may be explained by what hypothesis?

A

The SAPE hypothesis: by which the first (sentinel) acute pancreatitis event initiates an inflammatory process that results in injury and later fibrosis

90
Q

Autoimmune pancreatitis is associated with ______, often with autoantibodies and other autoimmune diseases. It is responsive to tx with _____

A

Hypergammaglobulinemia (IgG4); corticosteroids

91
Q

Genes associated with chronic pancreatitis and pancreatic exocrine insufficiency

A 
PRSS1 — AD inheritance
CFTR
CASR
CTRC
SPINK1
92
Q

Useful tests in evaluation of pts with suspected pancreatic steatorrhea (malabsorption/insufficiency)

A

Fecal elastase-1 and small-bowel biopsy

Fecal elastase will be low in pts with pancreatic insufficiency

Plain film imaging also may show pancreatic calcifications

93
Q

Complications of chronic pancreatitis

A

Chronic abdominal pain, gastroparesis, malabsorption/maldigestion, impaired glucose tolerance (Brittle DM)

Nondiabetic retinopathy d/t vitamin A and/or zinc deficiency

GI bleeding, icterus, effusions, subcutaneous fat necrosis, metabolic bone dz

Opioid/narcotic addiction common

Pancreatic pseudocyst or abscess, bile duct stricture, steatorrhea, malnutrition, osteoporosis, peptic ulcer, increased risk of pancreatic cancer

94
Q

Signs of pancreatic adenocarcinoma

A

Painless jaundice, N/V, fatigue, weight loss, steatorrhea, new onset diabetes

Trousseau sign of malignancy (migratory thrombophlebitis)

Courvoisier sign

95
Q

Risk factors for pancreatic cancer

A

Smoking, obesity, male, african american, >65 y/o, DM, chronic pancreatitis, liver cirrhosis, family hx

96
Q

3 P’s with MEN 1 syndrome

A

Parathyroid (hypercalcemia, increased intact PTH)

Pancreas (gastrinoma/ZE, insulinoma w/ hypoglycemia)

Pituitary (possible acromegaly, Cushing dz)

GI II Final (8 decks)

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