Clinical Approach to GI Patients Week 1 Flashcards

1
Q

What is the difference between Latrogenic and Spontaneous Esophageal Perforation?

A

L: trauma, caused by endoscopy/nasogastric tube

S: forceful retching/vomiting, history of alcohol use

  • Boerhaave’s Syndrome: transmural rupture
    • at gastroesophageal junction

Pneumomediastinum and SubQ emphysema

  • emphysema in neck/precordial area
  • Hamman Sign: crunching synchronous w/heartbeat
    • systole, left lateral decubitus position
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2
Q

Peptic Ulcer Disease

What does the pain feel like, how can it be diagnosed (3), and how is it treated?

A
  • gnawing, dull, aching, “hunger-like” atypical chest pain (epigastric) with “coffee ground” emesis

D: EGD w/biopsy (exclude malignancy), detection of H. pylori, Fecal Antigen Test, Urea Breath Test (eradicate)
- stop PPI x 14 days before fecal or breath tests

T: acid suppression (PPI), remove offending agent

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3
Q

What is the difference between Nutcracker Esophagus and Diffuse Esophageal Spasm?

A

NE: hypertensive peristalsis (too powerful w/greater amplitude and duration)

  • elevated LES pressure at baseline
  • diagnose with mamometry

DES: multiple spastic contractions disrupting coordinated peristalsis

  • “corkscrew” or “rosary bead” esophagus
  • LES function is normal
  • diagnose with mamometry/barium swallow

atypical chest pain and dysphagia to solids/liquids

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4
Q

What is “waterbrash” and what is it associated with? What are 3 atypical symptoms of this condition?

A
  • bad taste in mouth from refluxed acid (associated with GERD)

atypical symptoms: asthma, chronic cough, hoarseness

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5
Q

What is a Hiatal Hernia and what is the difference between Sliding vs Paraesophageal?

A
  • stomach herniation into mediastinum through esophageal hiatus of diaphragm

Sliding: inc. intraabdominal pressure from obesity, pregnancy, etc (GERD)

Para: includes visceral structure other than cardia, commonly the colon –> “upside down stomach”
- gastric volvulus and stomach strangulation

barium x-ray and surgical repair if symptoms

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6
Q

What is a common symptom associated with Foreign Body or Food impaction?

A

HYPERSALIVATION

  • inability to swallow liquids including own saliva (drooling, frothing, foaming of the mouth)
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7
Q

How are Oropharyngeal and Esophageal dysphagia diagnosed?

A

O: video fluoroscopy of swallowing

E: mechanical (barium swallow/EGD w/biopsy) or motility (barium swallow/mamometry)

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8
Q

What are two structural and one rheumatologic causes of Oropharyngeal Dysphagia?

A

S: Esophageal Web and Zenker Diverticulum

R: Sjogren’s Syndrome

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9
Q

Esophageal Web

What is it and what condition is it associated with, how is it diagnosed, and how is it treated?

A
  • thin, mucosa membrane located at proximal or mid esophagus and is associated with Plummer-Vison Syndrome and Eosinophilic Esophagitis

D: Barium Swallow (EGD less sensitive)

T: dilation (bougie dilator) and PPI long term (if needing repeat dilation)

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10
Q

What are 4 symptoms of Plummer-Vinson Syndrome, who is it commonly seen in, and what is it a complication of?

A

S: angular chelitis, glossitis, spoon nails (koilonychia), symptomatic proximal esophageal webs

Middle-aged females

C: iron-deficiency anemia (weakness and fatigue)

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11
Q

Zenker Diverticulum

What is it and where does it commonly occur, what are 4 symptoms it causes, and how is it diagnosed? (2)

A
  • false diverticula with herniation of mucosa/submucosa through muscular layer of esophagus posteriorly (proximal to Killian’s Triangle = loss of UES elasticity)
  • can retain food, halitosis, regurgitation, nocturnal choking

D: video esophagography/Barium Swallow BEFORE EGD (risk of perforation) –> SURGERY

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12
Q

Esophageal Stricture

What is it caused by, what problem actually gets better because of it, and how is it diagnosed?

A
  • structural problem caused by GERD, usually at gastroesophageal junction
  • starts as trouble swallowing solids but progresses to solids AND liquids; heartburn/reflux actually improves because the stricture acts as a barrier to it

D: endoscopy (mandatory in all cases) –> helps to differentiate from stricture caused by esophageal carcinoma

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13
Q

Barrett Esophagus D and T

A

inc. risk: obese white males > 50 who smoke

D: EGD w/biopsy (orange, gastric type epi. that extends upward from stomach in a tongue-like fashion; GOBLET CELLS)

T: PPIs and Endoscopic Ablation
- DO NOT SURGICALLY RESECT (not recommended)

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14
Q

Esophageal Squamous Cell Carcinoma vs Adenocarcinoma

Who does it affect, what is it caused by, and how is it diagnosed/treated?

A

SCC: most common, African Americans > Caucasians

  • heavy smoking and alcohol use = synergistic
  • weight loss, cough, hoarseness, dysphagia
  • Dx: EGD w/biopsy
  • Tx: surgery (esophagectomy)

AC: Caucasians > African Americans, distal esophagus

  • GERD, Barrett metaplasia
  • Dx: EGD w/biopsy
  • Tx: endoscopic therapy (ablation)
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15
Q

Esophageal Ring (Schatzki)

What is it and where it is located, what syndrome is associated with it, and how is it diagnosed/treated?

A
  • smooth, circumferential, thin mucosal structure of DISTAL esophagus; associated with hiatal hernia
  • “Steakhouse Syndrome” = poorly chewed food bolus is usually instigator (not progressive)

Dx: barium swallow
Tx: dilation (bougie dilator) and PPI use if heartburn

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16
Q

What is Achalasia and what is the difference between Primary, Secondary, and Pseudoachalasia?

A
  • motility disorder that is progressive (solids and liquids) due to propulsion problem in distal 2/3 of esophagus and failure of LES relaxation

P: loss of ganglion cells in myenteric plexus
S: CHAGAS (Trypanosoma cruzi); endemic areas
- destruction of ganglion THROUGHOUT the body
PC: tumors invade gastroesophageal junction

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17
Q

Achalasia

What are three common findings associated with it (R/B/S), what are three diagnostics that can be performed, and how can it be treated?

A

Findings: Romana Sign (unilateral swelling around eye - Chagas), “Bird Beak” distal esophagus, Sigmoid Esophagus (markedly dilated)

D: Peripheral smear for parasites, Barium Esophagram (“Birds Beak”), and Esophageal Mamometry (CONFIRMS DIAGNOSIS)

18
Q

What is Pill-induced Esophagitis?

How is it diagnosed and how can it be treated?

A
  • medications (usually taken without water or while supine) lead to esophageal dysphagia, odynophagia, and severe retrosternal chest pain due to breakdown in esophagus
  • can use endoscopy to see shallow/deep lesions
  • remove offending agent or take with water and remain upright during ingestion
19
Q

What are 5 common causes of Pill-induced esophagitis? (N/PC/AR/I/A)

A

NSAIDS, potassium chloride, alendronate/risedronate (osteoporosis), iron, antibiotics

20
Q

Infectious Esophagitis

What is the difference in presentation and treatment of CMV, Candida, and Herpes Simplex associated esophagitis?

A

CMV: one to several large, shallow, superficial ulcerations (immune restoration with antiretroviral therapy)

Candida: diffuse, linear, yellow-white plaques adherent to mucosa (systemic treatment: fluconazole)

HSV: multiple small, deep ulcer and oral ulcers (immunosuppressed: oral acyclovir; immunocompetent: symptomatically)

21
Q

What is “Feline Esophagus” or “Tracheal Esophagus” and what is it associated with?

A
  • multiple circular esophageal rings creating corrugated appearance (seen on EGD of pt. with Eosinophilic Esophagitis)
  • pts. with history of allergies or atopic conditions; MALES; history of food bolus impaction
22
Q

What are common symptoms of Caustic Esophagitis and what are two diagnostic tests that should be performed?

What should NOT be administered to pts. with Caustic Esophagitis?

A

Sx: severe burning, chest pain, gagging, dysphagia, drooling IMMEDIATELY after ingestion of liquid/crystalline alkali or acid

Dxs: Laryngoscopy (need for tracheostomy) and EGD (12-24 hours to assess damage)

DO NOT give nasogastric lavage or oral antidotes –> do not want reexposure to caustic agents

23
Q

What test should ALWAYS be performed in female patients presenting with nausea, vomiting, and abdominal pain?

A

PREGNANCY TEST

24
Q

Gastroperesis

What are two common causes and how does the patient present, what diagnostic test can be used, and how is it treated? (2)

A
  • commonly caused by diabetes mellitus or post-viral infection; present with postprandial fullness (early satiety)

Dx: Gastric Scintigraphy (gastric emptying study)

  • low-fat solid meal (eggs)
  • 60% retention after 2 hrs or 10% after 4 hrs = BAD

Tx: metoclopramide (tardive dyskinesia: involuntary/uncontrollable/unintentional lip-smacking or other twitching movements) and erythromycin

  • DO NOT use agents that reduce GI motility
  • keep blood glucose below 200 mg/dL
25
Q

Acute Paralytic Ileus

What is it, what is it commonly caused by, how is it diagnosed, and how can it be treated? (3)

A
  • loss of peristalsis in intestine in ABSENCE of mechanical obstruction, commonly seen in hospital pts. due to surgery, electrolyte problems, and severe medical illness

Dx: plain radiography or CT scan
- gas/fluid in small or large bowel

Tx: treat precipitating condition, nasgastric suction (SEVERE Ileus), or potential OMM

postoperative ileus reduced by analgesia, gum chewing, clear liquid diet

26
Q

Acute Small Bowel Obstruction (SBO)

What is it, what are its symptoms, how is it diagnosed, and how can it be treated?

A
  • caused by adhesions (Crohns/surgeries) and can present with feculent N/V, obstipation, and dec. bowel sounds (possible TINKLING bowel sounds)

Dx: plain radiography or CT scan
- dilated loops or air/fluid levels

Tx: nasogastric tube for suction and supportive

27
Q

Menetrier Disease

What is it, what are its symptoms, and how can it be diagnosed?

What is the pt. at increased risk for?

A
  • idiopathic; giant thickened gastric folds involving body of the stomach with chronic protein loss (hypoproteinemia and anasarca)

Sx: usually nausea, epigastric pain, WL, and diarrhea

Dx: suspicion and EDG with biopsy

Tx: cetuximab, gastric resection in severe cases

inc. risk of gastric adenocarcinoma

28
Q

What is the top three differentials for dyspepsia/heartburn/indigestion?

A
  1. GERD
  2. Gastritis
  3. PUD and surgical stress ulcers
29
Q

What is the difference between Type B Gastritis and Type A Gastritis?

A

Type B: H. Pylori (ANTRUM) –> inc. adenocarcinoma

  • can lead to B12 deficiency, B cell lymphoma
  • H. pylori eradication if PUD or MALToma

Type A: Autoimmune (FUNDIC) –> inc. adenocarcinoma

  • loss of rugal folds with Abs to parietal cells/IF
  • can cause B12 deficiency or carcinoid tumors
30
Q

Duodenal Ulcers vs Gastric Ulcers

A

D: anterior wall of proximal duodenum

  • gastric acid hypersecretion (90% due to H. pylori)
  • burning (gnawing) pain 60-180 min after meal
  • relieved by eating food

G: lesser curvature of ANTRUM of stomach

  • gastric acid normal or low (75% due to H. pylori)
  • burning pain within 30 min of eating (food adverse)
  • perform endoscopy to rule out malignancy
31
Q

What is a perforated viscus, how is it treated, and what can be seen on imaging that lead to diagnosis?

A
  • any hollow organ that perforates (can happen in PUD)
  • NPO, IV antibiotics, preoperative labs, surgery consult and EMERGENCY SURGERY

Dx: free air under diaphragm or in mediastinum (CT or plain X-Ray)

32
Q

Stress Ulcers

What is the difference between Curling’s Ulcers and Cushing’s Ulcers?

Which stress ulcer is the most common?

A

Curling: peptic ulcer of duodenum in pts. with extensive BURNS

Cushing: peptic ulcer occuring from severe head/brain injury or with other lesions of the CNS

most common stress ulcer is caused by severe medical or surgical illness

33
Q

What is the landmark that separates an Upper GI bleed from a Lower GI bleed?

A

Ligament of Treitz

  • can see with and EGD (endoscopy)
34
Q

How should a pt. with an Acute UGIB be stabilized?

How much should hemoglobin rise for each unit of transfused PRBC’s?

A
  • two large bore “18-gauge or larger” intravenous lines prior to further diagnostic testing
  • give intravenous fluids: 0.9% sodium chloride or Lactated Ringer
  • assess and manage their ABC’s (airway, breathing, circulation)

hemoglobin should rise by 1 g/dL for each unit of transfused PRBC’s

35
Q

What should each pt with an upper GI bleed undergo withing 24 hours of arriving to the emergency department?

What are two pharmacologic therapies for Acute UGIB? (AIT/O)

A
  • should undergo UPPER ENDOSCOPY
    • both diagnostic and therapeutic
    • ID bleeding, determine risk of rebleed, therapy

Pharmacologic therapy: Acid Inhibitory Therapy (oral/IV PPIs) and Octreotide (dec. splanchnic blood flow and portal blood pressure)

36
Q

What are the top 6 differentials for Upper Gastrointestinal Bleeds? (PS/EV/HG/MB/DL/GS)

A
  1. PUD/stress ulcers
  2. Esophageal varices
  3. hemorrhagic gastritis/gastropathy (Zollinger-Ellison)
  4. Mallory-Weiss Tear/Boerhaave Syndrome
  5. Dieulafoy lesion
  6. GAVE syndrome
37
Q

What 4 things increase the risk of bleeding from esophageal varices?

What are two things that can help prevent rebleeding?

A
  1. size of varices (> 5 mm)
  2. red wale markings
  3. severity of liver disease
  4. active alcohol abuse

Prevention: nonselective beta-adrenergic blockers and long-term treatment with band ligation (dec. by 30%)

38
Q

Zollinger Ellison Syndrome

What is it and what genetics are it associated with, how does it present, how is it diagnosed (MF/SFG/SST), and how is it treated?

A
  • primary gastrinoma found in the proximal duodenum, then pancreas (2/3 are malignant); associated with MEN1 (multiple endocrine neoplasia type 1 –> tumor often multifocal and unresectable)
  • presents as PUD that doesn’t respond to tx and is severe, atypical, and recurrent

Dx: large mucosal folds; Serum Fasting Gastrin (>1000 ng/L is confirmatory), Secreting Stimulation Test (+)

Tx: PPIs

39
Q

What are 4 levels that are drawn to exclude MEN1 in Zollinger Ellison? (P/P/L/G)

A

PTH, prolactin, LH-FSH, and GH

40
Q

GAVE (Gastic Antral Vascular Ectasia) Syndrome

What is it, how is it diagnosed, and what are treatment options?

A
  • multiple superficial telangiectasias in gastric antrum (Watermelon Stomach) associated with diffuse scleroderma and cirrhosis

Dx: EGD (“watermelon stripes”) and can be confused with portal HTN gastropathy (more changes in fundus than antrum)

Tx: transfusion (if needed) and endoluminal therapies

41
Q

Dieulafoy Lesion

A
  • obscure GI bleeding lesion that can be treacherous and life-threatening; large diameter vessel that protrude through mucosal defect in STOMACH
  • presents with MASSIVE, OBSCURE GI bleeding and can cause iron-deficiency anemia

Dx: clinical suspicion and careful EGD

Tx: transfusion (if needed), EGD therapy, angiographic interventions (if inaccessible), surgery (if all else fails)