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Surgery Clerkship > Upper GI > Flashcards

Upper GI Flashcards

1
Q

What are key items in the differential for upper GI bleed?

A 
Gastritis
Gastric ulcer
Duodenal ulcer
Erosive esophagitis
Mallory-Weiss tear
Esophageal varices
Gastric cancer
Angiodysplasia
Isolated gastric varies
Aortoenteric fistula
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2
Q

What are key lifestyle factors that must be asked about in upper GI bleed?

A

Alcohol use

NSAID use

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3
Q

What does bright-red bloody emesis tell you about location of the bleed?

A

UGI

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4
Q

What does coffee ground emesis tell you about location of the bleed?

A

UGI

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5
Q

What does black, tarry, foul-smelling stool (melon) tell you about location of the bleed?

A

UGI usually, LGI possible

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6
Q

What does bright red bloody stool tell you about the location of the bleed?

A

LGI probably, may be UGI

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7
Q

What does maroon colored stool tell you about the location of the bleed?

A

UGI (probably)

LGI (maybe)

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8
Q

What causes esophageal varies?

A

Cirrhosis: portal vein has more difficulty draining its blood into the scarred liver duh that blood flows retrograde under high pressure back into esophagus

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9
Q

What is acute vs. chronic gastritis?

A

Acute: erosive, superficial inflammation in stomach lining due to dysfunction of mucosal defenses
Chronic: Non erosive inflammation of gastric mucosa: due to inflammation

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10
Q

What is a Dieulafoy’s lesion?

A

rare cause upper GI bleed: vascular malformation: large tortuous artery in the submucosa is eroded by gastric acid

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11
Q

What causes acute gastritis?

A

NSAID abuse
Alcohol
Steroids
Uremia

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12
Q

What causes chronic gastritis?

A

Pernicious anemia, H. pylori

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13
Q

What artery can be behind a gastric ulcer in the posterior wall of stomach?

A

Splenic

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14
Q

What artery can be behind a gastric ulcer in the lesser curvature of the stomach?

A

Left gastric artery

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15
Q

What artery can be behind a duodenal ulcer in the posterior wall of 1st portion of duodenum?

A

Gastroduodenal artery

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16
Q

Where is UGI bleeding coming from?

A

Proximal to ligament of Treitz

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17
Q

Why can Hb or hematocrit be normal in spite of major GI bleed?

A

Because of loss of all portions of blood at same rate: do not see drop until 12-24 hours later once kidney begins to conserve Na and water

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18
Q

What happens to BUN/Cr during UGI bleed?

A

Increases to >36 signifies UGI bleed

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19
Q

How can bloody emesis and bright red blood per rectum present together?

A

UGI bleed: very fast transit through GI tract - no time for digestion

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20
Q

What is difference between obscure and occult GI bleeding?

A

Occult: not known to patient
Obscure: obvious bleeding to patient, but hard to identify source on endoscopy (usually due to bleeding in small bowel)

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21
Q

What are first steps in management of UGI bleed?

A 
2 large bore IVs
IVF resuscitation
NGT
Blood: type and cross
Admit
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22
Q

Why place NGT in UGI bleed?

A

Differentiate between UGI and LGI bleed

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23
Q

What is difference between “type & screen” vs. “type & cross”?

A

Type and screen: no likely blood transfusion.

Type and cross: likelihood of needing blood is high

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24
Q

What does blood typing determine?

A

ABO and Rh status

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25
Q

What does blood screening determine?

A

Presence of alloantibodies in recipient’s blood that may react with donor blood

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26
Q

What does blood crossmatching determine?

A

Recipient blood tested against donor packed cells to determine if there is clinically sig response to antigens on donor cells

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27
Q

After admission for UGI bleed, what is the next step to determine source of bleeding? In what window?

A

Endoscopy w/in 12 hours

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28
Q

After admission for UGI bleed, if endoscopy is negative, what do we do?

A

Look in small bowel: capsule endoscopy, push enteroscopy, angiography, look in LGI

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29
Q

When do we give blood transfusion ?

A

Only when Hb < 7

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30
Q

Where in the hospital do we manage UGI bleed?

A

ICU

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31
Q

How do we position bed in patient who is vomiting blood?

A

Head of bed to 30 degrees unless ongoing hypotension

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32
Q

After resuscitation for UGI bleed, what is next step?

A
  • Correct coagulopathy w/ blood/platelets/FFP if needed
  • Reverse anticoagulants
  • Start PPI
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33
Q

What are endoscopic therapeutic options for UGI bleed?

A

Inject epi
Bipolar electrocoagulation
Endoscopic clips
Plasma coagulator

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34
Q

When do we take UGI bleed patients to surgery?

A
  • Failure of endoscopic therapy (>twice)
  • Persistent hemodynamic instability despite aggressive resuscitation
  • CV dz w poor predictive response to hypotension
  • Hemorrhagic shock
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35
Q

What are surgical options for bleeding ulcer that fails medical management?

A

Duodenal: open duodenum, 3-point ligation of ulcer
Gastric: excise and close for acute vs. distal gastrectomy for chronic history of ulcer dz

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36
Q

If ulcer or gastritis is found on endoscopy, what else do we test for?

A

H. pylori - Tx with PPI, clarithromycin, amoxicillin

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37
Q

How do we test for H. pylori?

A

Urea breath test: test for ammonia labeled with c isotope in breath that the patient eats

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38
Q

How do we manage UGI bleed for esophageal varies?

A
  • Short term AB prophylaxis
  • Esophageal band ligation is best option
  • Repeat endoscopy to band any remaining vessels
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39
Q

What is the best way to prevent recurrent UGI bleed from esophageal varies?

A

beta blockers (propranolol)

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40
Q

How do we manage UGI bleed from Mallory-Weiss tear?

A

Self limited - very rarely need sclerosis therapy or electrocautery

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41
Q

In alcoholic patient, what is important to calculate before surgery?

A

MELD: Model for End Stage Liver Disease which can influence surgical decision making

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42
Q

What do we think of with isolated gastric varies along the greater curve of stomach?

A

Splenic vein thrombosis from prior pancreatitis: splenectomy is curative

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43
Q

For patients with chronic NSAID therapy, what can we use to prevent ulcers?

A

PPIs

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44
Q

What does free air under the diaphragm indicate?

A

Perforated viscus

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45
Q

What are most common causes of free air under diaphragm?

A

Perforated ulcers

Perforated diverticulitis

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46
Q

What are most common symptoms in a patient with PUD?

A

Burning in epigastric region, non radiating

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47
Q

How do patients with perforated peptic ulcers present?

A
  • Acute onset sharp abdominal pain in epigastrium that rapidly becomes diffuse
  • Shoulder pain
  • Peritonitis: exquisite tenderness to palpation, abdominal guarding and rigidity
  • SIRS
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48
Q

What are most common cause of peptic ulcers?

A

H. pylori

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49
Q

How do NSAIDs lead to peptic ulcers?

A

Inhibit production of prostaglandins that regulate inflammation in gastric mucosa and reduce acid production

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50
Q

What factors can lead to peptic ulcers?

A

NSAID use
Smoking
Alcohol
High stress environments

51
Q

What are type I peptic ulcers?

A

Lesser curvature, no acid hypersecretion (disruption in mucosal defense)

52
Q

What are type II peptic ulcers?

A

Lesser curvature/duodenum with acid hypersecretion

53
Q

What are type III peptic ulcers?

A

Prepyloric with acid hypersecretion

54
Q

What are type IV peptic ulcers?

A

Gastric cardia without acid hypersecretion (disruption in mucosal defense)

55
Q

What are type V peptic ulcers?

A

Any location in stomach: associated with NSAID use so no acid hypersecretion (disruption in mucosal defense)

56
Q

How id diagnosis of perforated PUD established?

A

Clinical exam: guarding with palpation and muscle rigidity

Confirmed by radiology findings

57
Q

What labs do we send in suspected perforated PUD?

A 
CBC
Blood chemistry
- Look for elevated WBC, CRP, decreased albumin, elevated BUN/Cr
- Amylase/Lipase to r/o pancreatitis
- LFTs: cholecystitis or cholelithiasis
58
Q

What imaging do we order for suspected perforated PUD?

A

Acute abdominal series or upright CXR

59
Q

What is the classic finding on abdominal or chest XR in perforated PUD?

A

Pneumoperitoneum: hyperlucent area under one or both hemidiaphragms
- Also look retroperitoneal for posterior gastric!

60
Q

What studies are contraindicated in suspected perforated PUD?

A
  • Barium UGI series (causes barium peritonitis)

- Upper endoscopy (can exacerbate with air)

61
Q

What is the role of CT scan in workup of perforated peritonitis?

A

CT scan with gastrografin: Diagnose pneumoperitoneum and confirm diagnosis
- Also can tell if spontaneously sealed itself

62
Q

What is morbidity and mortality of perforated peptic ulcer?

A

> 25%

63
Q

What is definitive management of perforated peptic ulcer?

A
  • ICU admission
  • Volume resuscitation
  • NGT placement
  • Antibiotics for sepsis
  • Triple therapy if H pylori positive
64
Q

How do we treat duodenal ulcer perforation?

A

Primary closure with omental patch

65
Q

How do we treat gastric ulcer perforation?

A

Primary closure, biopsy omental patch vs. wedge resection

66
Q

What is important to rule out in patient with any gastric ulcer?

A

Malignancy

67
Q

What are two possible causes of ulcers?

A

Acid hypersecretion

Mucosal defense hyposecretion

68
Q

What are the key findings in perforated ulcer? PE, labs, imaging

A

PE: acute abdomen with diffuse peritonitis
Labs: Elevated WBC
Imaging: free air under diaphragm (XR) and CT

69
Q

What are key features of Boerhaave’s syndrome?

A
  • CP after forceful vomiting
  • Crepitus with palpation around the sternum
  • L sided pleural effusion
  • SIRS
70
Q

What are the risk factors for Boerhaave’s syndrome?

A
  • Alcoholics

- Overeating –> aggressive vomiting

71
Q

Why is Boerhaave’s syndrome so often unrecognized?

A

CP has such a large differential

72
Q

What is Mackler’s triad? what’s it for?

A

Vomiting
Thoracic pain
SubQ emphysema
- Suggests Boerhaave’s

73
Q

What are clinical signs most often observed in Boerhaave’s?

A

Vomiting > thoracic pain > dyspnea ? epigastric pain ? dysphagia

74
Q

What is most specific sign of an esophageal rupture?

A

SubQ emphysema = pathognomonic

75
Q

How does Boerhaave’s present differently than Mallory Weiss?

A

Boerhaave’s: thoracic pain radiating to back, L pleural effusion, sepsis
M-w: Upper GI bleed

76
Q

What are most common causes of esophageal perforation?

A
  • Iatrogenic injury during upper endoscopy: most common
  • Blunt or penetrating trauma
  • Foreign body ingestion
  • Perforating malignancy
  • Only 10-20% Boerhaave’s
77
Q

How does Boerhaave’s most commonly present?

A

Thoracic pain radiating to the lower back and aggravated by swallowing

78
Q

What is the pathophysiology of Boerhaave’s?

A

Transmural esophageal perforation 2/2 increased intragastric pressure induced by vomiting

79
Q

Why do patients with Boerhaave’s become so septic?

A
  • Gross contamination of mediastinum
  • Often leads to rupture of pleura as well: 2/2 gastric and bilious contents eroding through the lining
  • Once pleura disrupted, gross contamination of pleural cavity also occurs
  • Mediastinitis / pleuritis eventually lead to sepsis
80
Q

What is first step in workup of suspected Boerhaave’s?

A

CXR: should see L pleural effusion and atelectasis, but can be normal if it has not been > 1 hour

81
Q

If CXR is questionable in suspected Boerhaave’s, what is the next diagnostic step?

A

CT with oral contrast:

  • Identify extent of perforation
  • Assists in decision on surgical approach
  • If not Boerhaave’s, helps id another differential
82
Q

Is there a role for endoscopy in Boerhaave’s?

A

No: more air into esophagus can enlarge the opening/hole

83
Q

What are the initial steps in management of a Boerhaave’s patient?

A
  • IVF resuscitation
  • NPO
  • Antibiotics to over oral bacteria + fungal
  • PPI to reduce secretions
  • Place arterial line if hemodynamically unstable
84
Q

What is the key timeframe for detection and treatment in Boerhaave’s?

A

Within 24 hours!

85
Q

Who gets conservative management with Boerhaave’s? What is conservative?

A

Contained leak w/in mediastinum:

  • NPO
  • NGT
  • IV antibiotics / fluids
  • Parenteral nutrition
86
Q

What is the goal for surgery for Boerhaave’s?

A

Within 24 hours

87
Q

What is standard treatment(surgery) for Boerhaave’s?

A
  • Debride necrotic tissue around perforation
  • Primary suture closure
  • Cover with pedicle flap
88
Q

What causes death in Boerhaave’s?

A

Contamination of mediastinum and pleura: leads to sepsis, shock and multi organ failure

89
Q

In which patients is conservative management considered for Boerhaave’s?

A

Minimal comorbidites
No signs of sepsis / shock
Perforation < 24 h
Leak that is small/contained or has self-sealed

90
Q

What is the mortality of Boerhaave’s?

A

50%

91
Q

What is the differential for vague abdominal pain, weight loss, difficulty eating and melena?

A 
PUD
GERD
Panreatitis
Cholelithiasis
Hiatal hernia
Gastric outlet obstruction
SBO
Gastric cancer
92
Q

What to think: weight loss and positive FOBT?

A

Malignancy until proven otherwise

93
Q

What is triple therapy for H. pylori?

A

Amoxicillin
Clarithromycin
Omeprazole

94
Q

Why don’t we screen for gastric cancer?

A

Not cost effective due to low rate in US

95
Q

Why is mortality rate so high for gastric cancer?

A
  • No screening
  • By the time sx appear, already stage III to IV
  • Sx of gastric cancer are vague
96
Q

What are most common symptoms for a patient with gastric cancer?

A

1 Weight loss
2 Abdominal pain
Perhaps dyphagia, nausea, early satiety, rarely a palpable mass

97
Q

Are there specific findings on physical exam for gastric cancer?

A

Usually non specific, often absent
If present:
- Palpable L supraclavicular nodes (Virchow’s nodes)
- Periumbilical lymphadenopathy (SMJ nodes)
- Left axillary node (Irish’s node)

98
Q

What are the 2 types of gastric adenocarcinoma?

A

1 Intestinal type

2 Diffuse type

99
Q

What are hallmark features of intestinal type gastric adenocarcinoma?

A
  • Arises from gastric mucosa usually in distal stomach
  • Sporadic: high exposure to tobacco, alcohol, poor diet
  • Largely decreased due to H. pylori eradication
100
Q

What are hallmark features of diffuse type gastric adenocarcinoma?

A
  • Arises from lamina propria and grows in infiltrative, submucosal pattern
  • Leads to gastric thickening without discrete mass often in proximal stomach
101
Q

What is linitis plastica?

A

Diffuse type gastric cancer: if it infiltrates the entire gastric wall / esophagus / duodenum = linitis plastica.
- High mortality rate!

102
Q

What is the vascular supply to the stomach and where do those arteries branch from?

A 
L/R gastrics: lesser curve
L/R gastroepiploics: greater curve
L gastric: celiac
R gastric: common hepatic
L gastroepiploic: splenic
R gastroepiploic: R gastric / common hepatic
103
Q

Why do patients with gastric cancer get iron deficiency anemia?

A

slow intermittent bleeding of the tumor

104
Q

What is the best way to diagnose a patient with suspected gastric cancer?

A

Upper endoscopy: visualize and biopsy lesion

105
Q

Once diagnosis of gastric cancer is established, what further workup is recommended?

A

1 Endoscopic ultrasound: assess tumor size, depth and lymph node involvement for TNM staging
2 CT abdomen to see if surgical candidate, r/o liver mets
3 PET scan: look for mets and nodes

106
Q

Why is staging of gastric tumor important?

A

To determine intervention: surgery vs. chemo vs. radiation

107
Q

When do we use chemotherapy in locally advanced gastric cancer?

A

Before surgery!

108
Q

What stages of gastric cancer get preoperative chemotherapy?

A

Stage 1B or higher

109
Q

What is the benefit of postoperative chemo and radiation in gastric cancer?

A

Improved overall survival

110
Q

What is the surgical approach for gastric cancer in the distal stomach?

A

Subtotal gastrectomy

111
Q

What is the surgical approach for gastric cancer in the proximal stomach?

A

Proximal or total gastrectomy

112
Q

What are the margins of gastric cancer stage R0 resection?

A

5cm

113
Q

How many lymph nodes should be taken in gastric cancer surgery? Why?

A

> 15 to properly stage

114
Q

How do we treat MALT lymphoma in the stomach?

A
  1. Low grade: H. pylori eradication

2. High grade: chemo

115
Q

Why does the 5 year mortality remain high for gastric cancer?

A

Advanced disease present at diagnosis

116
Q

What gene mutation has been shown to often be present in gastric cancers?

A

HER2 - do genetic testing before induction chemotherapy

117
Q

What other types of gastric cancers are there, besides adeno?

A

GIST: mesenchymal tumors
Gastric carcinoids
Gastric lymphoma

118
Q

Why do patients get dumping syndrome after gastric resection?

A

Absence of regulatory effect of the pyloric sphincter: hyperosmolar state in the small intestine leads to increased water secretion into the lumen, leading to diarrhea and hypotension

119
Q

What are common complications after a gastric resection?

A 
Diarrhea
Darly satiety
Dumping syndrome
Anastomotic leak
SBO
Internal hernia
120
Q

How are anastomotic leaks identified?

A
  • Presentation: peritonitis, fevers, tachycardia, leukocytosis, sepsis
  • Confirm with upper GI with gastrografin: will see contrast extravasation
121
Q

How do we treat anastomotic leak?

A
  1. Source control: reoperate to repair suture line and abdominal washout/drainage
  2. Post op: NPO with TPN, NGT to reduce gastric contents
122
Q

What do we NOT do as first treatment for anastomotic leak?

A

Resection and revision of anastomosis: control it to try and salvage initial operation!

123
Q

What are GIST tumors?

A

Smooth, submucosal tumors that express C-KIT and CD117

Surgery Clerkship (16 decks)

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