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First Aid > Gastroenterology 4 > Flashcards

Gastroenterology 4 Flashcards

1
Q

What is Acalculous cholecystitis and what is it caused by?

A

Acute cholecystitis not due to gallstones.

Caused by gall bladder ischemia and stasis (commonly in critically ill patients).

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2
Q

AIDS Cholangiopathy is a result of what?

A

Chronic infection involving biliary tree, usually involving Cryptosporidium (most common) and CMV.

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3
Q

What is Ascending Cholangitis?

A

Stone blocks flow of bile (cholestasis) → GI bacteria ‘ascend’ in biliary tree and cause infections.

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4
Q

What is the clinical triad and pentad seen in Ascending Cholangitis?

A

Charcot’s triad: Fever, abdominal pain, jaundice.

Reynolds pentad: Fever, abdominal pain, jaundice, confusion, hypotension. Indicates sepsis and shock from infection.

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5
Q

What 3 diagnostic labs are seen in Ascending Cholangitis?

A

↑ WBC, ↑ Alk Phos&raquo_space; ↑ AST/ALT, ↑ conjugated bilirubin (and total).

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6
Q

What are 3 common bacteria that cause Ascending Cholangitis?

A

Gram negatives: E. coli, Klebsiella, Enterobacter.

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7
Q

What is a rare cause of Ascending Cholangitis? What is a hallmark of this infection?

A

Clonorchis sinensis (Chinese liver fluke found in infected fish).

Will see peripheral eosinophilia due to helminth infection.

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8
Q

What are 2 treatment therapies for Ascending Cholangitis?

A

Antibiotics with Gram negative and anaerobic coverage.

Examples include Ampicillin-sulbactam and Ciprofloxacin-Metronidazole.

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9
Q

What is Endoscopic retrograde cholangiopancreatography (ERCP)?

A

Combination of endoscopy and fluoroscopy, can inject dye into bile duct to visualize obstruction or use tools on endoscope to pull out stone.

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10
Q

What is Gallstone ileus?

A

Massive gallstone erodes through gallbladder wall → Creates fistula with small intestine → large stone can cause bowel obstruction at ileocecal valve.

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11
Q

What is a key radiologic imaging finding seen in Gallstone ileus?

A

Air in the biliary tree.

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12
Q

What can obstruction of common bile duct by stone lead to?

A

Cholangitis or acute pancreatitis.

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13
Q

What is gallbladder carcinoma?

A

Rare adenocarcinoma from chronic inflammation.

Risk factors include chronic cholecystitis (untreated gallstone disease) and chronic salmonella infection: S. typhi can remain in carrier state in gall bladder.

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14
Q

What is Biliary Atresia? What are 3 symptoms seen?

A

Idiopathic biliary obstruction in neonates.

Symptoms include jaundice, pale stools, dark urine.

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15
Q

What may ultrasound of a patient with Biliary atresia reveal?

A

Gallbladder absent or abnormal, absence of common bile duct.

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16
Q

What is the treatment for Biliary atresia?

A

Kasai procedure: Create conduit for bile drainage using small intestine.

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17
Q

What is Biliary Cirrhosis?

A

Old term used for liver damage due to biliary obstruction i.e. gallstone, pancreatic cancer.

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18
Q

What is Primary Biliary Cirrhosis?

A

Autoimmune disorder, T-cells attack interlobular bile ducts → Granulomatous inflammation.

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19
Q

Primary Biliary Cirrhosis is more common among which gender?

A

Women.

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20
Q

What are the 2 most common initial symptoms in Primary Biliary Cirrhosis?

A

Fatigue and pruritus (often precedes jaundice, may be worse at night).

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21
Q

What is a key symptom of Primary Biliary Cirrhosis?

A

ITCHING!!!

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22
Q

What 2 antibodies are commonly present in Primary Biliary Cirrhosis?

A

Anti-mitochondrial antibodies (hallmark), Anti-nuclear antibodies.

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23
Q

What are 3 abnormal LFTs seen in Primary Biliary Cirrhosis?

A

Markedly elevated alkaline phosphatase, may see mild elevations AST/ALT, ↑ bilirubin occurs late.

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24
Q

What is a key non-liver lab finding in Primary Biliary Cirrhosis?

A

Serum lipids may be markedly elevated.

Xanthomas may be present.

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25
Q

What will imaging show in Primary Biliary Cirrhosis?

A

Absence of biliary obstruction.

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26
Q

What is a typical case presentation of Primary Biliary Cirrhosis?

A

Woman with itching, fatigue, markedly elevated Alk Phos, positive anti-mitochondrial antibodies.

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27
Q

What are 2 treatments for Primary Biliary Cirrhosis?

A

Ursodeoxycholic acid: Only effective therapy, replaces endogenous bile acids and prevents disease progression.

Liver transplant.

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28
Q

Primary Biliary Cirrhosis is associated with what other condition?

A

Other autoimmune disorders, most common is Sjogren’s.

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29
Q

What is Primary Sclerosing Cholangitis?

A

Autoimmune disorder that leads to inflammation, fibrosis, strictures in biliary tree.

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30
Q

Primary Sclerosing Cholangitis is strongly associated with what other condition?

A

Ulcerative colitis.

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31
Q

What are 3 clinical features of Primary Sclerosing Cholangitis?

A

Strictures obstruct bile flow → Symptoms of biliary obstruction: RUQ pain, fatigue, jaundice.

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32
Q

What 3 abnormal LFTs are seen in Primary Sclerosing Cholangitis?

A

Elevated alkaline phosphatase, elevated conjugated bilirubin, usually mildly elevated AST/ALT.

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33
Q

What 2 antibodies are commonly seen/elevated in Primary Sclerosing Cholangitis?

A

Elevated IgM levels, positive p-ANCA.

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34
Q

What is a histopathology finding in Primary Sclerosing Cholangitis?

A

Periductal fibrosis (‘Onion skin’ fibrosis of bile ducts).

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35
Q

What is used to confirm diagnosis of Primary Sclerosing Cholangitis? What is the finding?

A

Cholangiogram: ERCP, MRCP (MRI cholangiography).

Biliary strictures and dilations (‘beading’) is seen.

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36
Q

What are 2 treatments for Primary Sclerosing Cholangitis?

A

Endoscopic therapy: Dilation or stenting of strictures in bile ducts.

Liver transplant.

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37
Q

Patients with Primary Sclerosing Cholangitis have an increased risk for what?

A

Cholangiocarcinoma.

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38
Q

What is Cholangiocarcinoma? Symptoms?

A

Cancer of bile duct epithelial cells.

Symptoms arise from bile duct obstruction.

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39
Q

What are 2 risk factors for Cholangiocarcinoma?

A

Primary sclerosing cholangitis (ulcerative colitis), Clonorchis sinensis (Chinese liver fluke).

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40
Q

What is the difference between Gastritis, Erosion, and Ulcer?

A

Gastritis: inflammation of mucosa.

Erosion: loss of epithelial layer, may extend into muscularis mucosa but will not break through. Ulcer: loss of mucosal layer.

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41
Q

In what 2 regions are ulcers mostly found in the GI tract?

A

Stomach, duodenum.

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42
Q

What type of infiltrate is seen on biopsy in Acute and Chronic gastritis?

A

Acute: Neutrophil.

Chronic: Lymphocytes, plasma cells, macrophages.

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43
Q

What are the 2 common causes of Chronic gastritis?

A

Autoimmune (type A), H. pylori (type B).

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44
Q

What are symptoms of dyspepsia?

A

Dyspepsia = indigestion.

Symptoms include nausea, vomiting, loss of appetite, abdominal pain.

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45
Q

What are symptoms of acute gastritis? They are often worsened by…

A

Dyspepsia, food.

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46
Q

What are the 2 underlying mechanisms that lead to acute gastritis?

A

Excess acid, loss of protection (mucous, bicarbonate).

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47
Q

ACh and histamine [stimulate/inhibit] acid production.

A

Stimulate.

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48
Q

Prostaglandins [stimulate/inhibit] acid production.

A

Inhibit.

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49
Q

Where are parietal cells found in the stomach?

A

Fundus and body.

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50
Q

What are 4 common causes of acute gastritis?

A

NSAIDS: block prostaglandin production, increases acid production.

Alcohol: directly damages mucosa, Chemotherapy: inhibits epithelial cell replication, H. Pylori.

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51
Q

What is Curling’s ulcer?

A

Occurs in burn patients.

Loss of skin → loss of fluids, decrease plasma volume → hypotension → decreased mucosal perfusion → mucosal damage.

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52
Q

Any patient with extensive burns are usually put on what drug to prevent Curling’s ulcer?

A

PPI.

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53
Q

What are Cushing’s ulcers caused by?

A

Increased intracranial pressure i.e. tumor, hemorrhage → increased vagal stimulation → ↑ Ach to stomach → Excess acid production, gastritis/ulcer.

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54
Q

What are Stress ulcers caused by?

A

Shock, sepsis, trauma → ↓ mucosal perfusion → loss of protective barrier of mucous/bicarb.

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55
Q

What is used as prophylactic therapy for Stress ulcers?

A

Proton pump inhibitors (offered to all ICU patients).

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56
Q

Patients with Chronic gastritis are often _______ until complications develop.

A

Asymptomatic.

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57
Q

Autoimmune gastritis is also known as?

A

Pernicious anemia.

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58
Q

Pernicious anemia affects what part of the stomach?

A

Body/fundus (where parietal cells are located).

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59
Q

Autoimmune gastritis is more common in [M/W].

A

Women.

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60
Q

Pernicious anemia is associated with what other disease?

A

Gastric adenocarcinoma.

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61
Q

What is the most common cause of Chronic gastritis?

A

H. pylori.

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62
Q

What type of bacteria is H. pylori?

A

Gram negative rod.

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63
Q

H. pylori causes ulcers in what region of the GI tract?

A

Antrum of stomach.

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64
Q

An important virulence factor of H. pylori is ______. What is the function and what does it cause?

A

Urease.

Hydrolyzes urea → produces ammonium (alkaline) → protects bacteria from stomach acid and forms ammonium chloride which damages stomach.

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65
Q

H. pylori is associated with what 2 malignancies?

A

Gastric Adenocarcinoma, MALT lymphoma (highly associated): B cell cancer.

66
Q

What are 3 ways to diagnose H. pylori?

A

Biopsy, Urea breath test, Stool antigen.

67
Q

How is the urea breath test performed?

A

Patients swallow urea with isotopes (carbon-14 or carbon-13).

Detection of isotope-labelled carbon dioxide in exhaled breath indicates presence of urease.

68
Q

What does the ‘triple therapy’ for H. pylori consist of?

A

Proton pump inhibitor, Clarithromycin, Amoxicillin/Metronidazole.

69
Q

What is Metaplastic Atrophic Gastritis? What is a key pathology finding?

A

Chronic gastritis → intestinal metaplasia.

Key path finding: Goblet cells appear in stomach.

70
Q

Solitary ulcers in peptic ulcer disease are found in what 2 locations? Which is more common?

A

Antrum of stomach (~10%), Proximal duodenum (~90%).

71
Q

What are 3 risk factors for peptic ulcer disease?

A

NSAIDs, H. pylori infection, Smoking.

72
Q

Duodenal ulcers are almost always related to _____. Why?

A

H. pylori.

Can increase gastric acid production.

73
Q

What is a rare cause of Duodenal Ulcers? How does it present?

A

Zollinger-Ellison Syndrome.

Often multiple ulcers in distal duodenum or jejunum.

74
Q

Epigastric pain from Duodenal Ulcer [improves/worsens] with food. Why?

A

Improves, meal stimulates secretion of bicarb.

75
Q

Duodenal Ulcers are [commonly/almost never] cancerous.

A

Almost never.

76
Q

Brunner’s Gland Hypertrophy is seen in what condition?

A

Peptic ulcer disease.

77
Q

What are 3 complications of duodenal ulcers?

A

Upper GI Bleeding: More common when located posteriorly, Pancreatitis, Perforation.

78
Q

When duodenal ulcers cause bleeding, what is the usual source?

A

Gastroduodenal artery.

79
Q

Upper GI bleeding is bleeding above what landmark?

A

Ligament of Treitz.

80
Q

What are 2 symptoms of Upper GI bleed?

A

Melena (lower GI bleed results in Hematochezia), Hematemesis.

81
Q

Gastric or duodenal Ulcer perforation leads to what finding on CXR?

A

Air under diaphragm (pneumoperitoneum).

82
Q

What is the usual source of bleeding in duodenal ulcers?

A

Gastroduodenal artery

83
Q

Upper GI bleeding is bleeding above what landmark?

A

Ligament of Treitz

84
Q

What are 2 symptoms of Upper GI bleed?

A
  • Melena (lower GI bleed results in Hematochezia)
  • Hematemesis
85
Q

Gastric or duodenal ulcer perforation leads to what finding on CXR?

A

Air under diaphragm (pneumoperitoneum)

86
Q

Where are gastric ulcers commonly located in the stomach?

A

Lesser curvature

87
Q

Gastric ulcer rupture causes bleeding from what artery?

A

Left gastric artery

88
Q

Does abdominal pain from gastric ulcer improve or worsen after meals?

A

Worsens, food stimulates acid release

89
Q

What are 2 causes of gastric ulcer?

A
  • H. Pylori
  • Adenocarcinoma (often biopsied)
90
Q

What are 2 complications of gastric ulcers?

A
  • Perforation
  • Upper GI bleeding
91
Q

What is the treatment for gastric/duodenal ulcers?

A
  • Proton pump inhibitors are therapy of choice
  • Treat H. pylori if indicated
92
Q

Proton pump inhibitors are often used empirically for dyspepsia symptoms in what conditions?

A

GERD, gastritis, ulcers

93
Q

What percentage of gastric carcinomas are adenocarcinomas?

A

95%

94
Q

What is the clinical presentation early in gastric carcinoma?

A
  • Usually asymptomatic until advanced
  • Non-specific symptoms i.e. weight loss, abdominal pain, early satiety
95
Q

What are the 2 types of gastric carcinoma?

A

Intestinal, Diffuse

96
Q

Intestinal gastric carcinoma grossly appears as what? Where is it commonly found?

A
  • Large ulcer with irregular margins
  • Lesser curvature of stomach
97
Q

Intestinal gastric carcinoma results from what?

A

Intestinal metaplasia due to H. pylori, autoimmune gastritis

98
Q

Intestinal gastric carcinoma is more common among what demographic?

A

Older men

99
Q

What are 4 risk factors for intestinal gastric carcinoma besides chronic gastritis?

A
  • Smoking
  • Alcohol consumption
  • Nitrosamines: found in smoked meats, linked to cancer by case control studies
  • Type A blood: mechanism unclear
100
Q

What is a morphologic finding in diffuse type gastric carcinoma? What is a common symptom?

A
  • Stomach diffusely thickened (linitis plastica), made up of gastric mucosa cells
  • Early satiety
101
Q

What special type of cells are found in diffuse gastric carcinoma?

A

Signet ring cells, mucin forms and nucleus is pushed to periphery

102
Q

What is the most common site of metastasis of gastric carcinoma?

A

Liver

103
Q

Gastric adenocarcinoma is associated with what 2 skin findings?

A
  • Acanthosis Nigricans
  • Leser-Trelat sign: ‘Explosive onset’ of multiple itchy seborrheic keratoses
104
Q

Leser-Trelat sign is associated with many malignancies, which is the most common?

A

Gastric adenocarcinoma

105
Q

What are 2 nodular findings in gastric carcinoma?

A
  • Virchow’s node: Left supraclavicular node (drains stomach)
  • Sister Mary Joseph nodule: Metastasis to periumbilical region, palpable on exam
106
Q

What is a Krukenberg tumor? What cells are often seen on pathology?

A
  • Bilateral ovarian tumor secondary to metastasis from another site, most common from gastric adenocarcinoma
  • Signet cells often seen on pathology
107
Q

What percentage of patients with dyspepsia have an organic cause?

A

25%

108
Q

What are the organic causes of dyspepsia?

A

Gastritis, ulcers, cancer, H. Pylori

109
Q

What is the next step in diagnostics for patient with dyspepsia +/- Age>55, alarm symptoms (weight loss, early satiety)?

A

Endoscopy

110
Q

What is hypertrophic gastropathy?

A

Rare disorder characterized by enlarged rugal folds, caused by hyperplasia

111
Q

What is Menetrier’s disease? What does this lead to?

A

Hyperplasia of mucous cells due to unknown cause, leading to excessive gastric mucous secretions, loss of acid, and protein loss (hypoalbuminemia → edema, facial swelling)

112
Q

Menetrier’s disease is more common in which gender?

A

Men (3:1 ratio)

113
Q

Menetrier’s disease can lead to what other disease?

A

Gastric adenocarcinoma

114
Q

What are some clinical manifestations of fat malabsorption?

A
  • Steatorrhea
  • Pale if bile is absent (no bilirubin)
  • Voluminous stools
  • Greasy, foul smelling stools that float
  • Loss of fat soluble vitamins
115
Q

What is a clinical manifestation of carbohydrate malabsorption?

A

Watery diarrhea

116
Q

What is a clinical manifestation of protein malabsorption?

A

Edema (loss of albumin)

117
Q

What are the different types of diarrhea?

A

Steatorrhea, Inflammatory, Watery: Secretory, osmotic

118
Q

How do you calculate stool osmotic gap? How do you interpret this?

A

290 - (2[Na]+2[K])stool

Osmotic gap >50 = osmotic diarrhea; Osmotic gap <50 = secretory causes

119
Q

What is celiac disease? What is the mechanism of disease?

A

Autoimmune disease triggered by gluten exposure, leads to destruction of small intestinal villi

120
Q

Gluten is a combination of what 2 compounds?

A

Gliadin and Glutenin

121
Q

What is the pathogenic component of gluten? Why?

A

Gliadin is deamidated via tissue transglutaminase (tTG) → Deamidated gliadin is immunogenic

122
Q

What genes are associated with celiac disease?

A

HLA-DQ2 and HLA-DQ8

123
Q

What are 3 histological features seen in celiac disease?

A
  • Blunting of villi
  • Crypt hyperplasia
  • Lymphocytes in lamina propria
124
Q

Celiac disease is common in what demographic?

A

Whites of northern European descent

125
Q

What are 3 antibodies seen in celiac disease? Which is most accurate?

A
  • Anti-gliadin (rarely tested – poor accuracy)
  • Anti-tissue transglutaminase
  • Anti-endomysial
  • IgA endomysial and tTG have highest accuracy, IgG testing can also be done if patient is IgA deficient
126
Q

What are 3 key diagnostic tests for celiac disease?

A
  • Biopsy
  • IgA levels
  • Anti-tTG
127
Q

What area of the GI tract is most commonly affected by celiac disease?

A

Duodenum

128
Q

What are 4 symptoms of celiac disease?

A
  • Flatulence, bloating, Steatorrhea
  • Iron deficiency anemia
129
Q

What are 3 complications associated with celiac disease?

A
  • Small ↑ risk small bowel malignancy (rare condition)
  • Adenocarcinoma
  • Enteropathy-associated T-cell lymphoma (EATL)
130
Q

Celiac patient adherent to gluten-free diet with worsening symptoms is suggestive of what?

A

Cancer

131
Q

What is dermatitis herpetiformis? What is it caused by?

A
  • Herpes-like lesions on skin associated with celiac disease
  • Caused by IgA deposition in dermal papillae
132
Q

What is tropical sprue? Where does it occur?

A
  • Malabsorption due to unknown infectious agent, leads to blunting of villi
  • Occurs in the tropics (Caribbean)
133
Q

What is a key difference between tropical sprue and celiac disease?

A

Different location
- Celiac: Duodenum most common
- Tropical: Entire small bowel affected

134
Q

Celiac disease and tropical sprue may be associated with what deficiency?

A
  • Celiac disease: iron deficiency anemia
  • Tropical sprue: Folate/B12 deficiency
135
Q

How does a typical case of tropical sprue present?

A

Patient is a traveler to tropics with chronic diarrhea and malabsorption

136
Q

Tropical sprue should be treated with what?

A
  • Antibiotics (usually tetracycline)
  • Folate supplementation
137
Q

What is Whipple disease?

A
  • Caused by Tropheryma whipplei
  • Systemic infection that involves small intestines, joints, brain, heart
138
Q

What type of bacteria is Tropheryma whipplei?

A

Gram-positive rod

139
Q

Whipple’s disease is most common in what demographic?

A

White, European men

140
Q

What are the 4 cardinal features of Whipple’s disease? What are 4 other features seen?

A
  • Diarrhea
  • Abdominal pain
  • Weight loss
  • Joint pains (migratory arthralgias large joints)
  • Mesenteric lymphadenopathy
  • Hyperpigmentation
  • Confusion with CNS involvement
  • Culture negative Endocarditis
141
Q

How is Whipple’s disease diagnosed? What is the classic finding?

A

Biopsy of small intestine: PAS positive foamy macrophage seen in lamina propria

142
Q

What is the treatment for Whipple’s disease?

A

Ceftriaxone (different treatments for extra-intestinal disease)

143
Q

Lactose is composed of what molecules?

A

Galactose and glucose

144
Q

Lactose is digested by what?

A

Brush border enzyme lactase

145
Q

Failure to digest lactose leads to what?

A

High volume, watery diarrhea

146
Q

What are the 3 causes of lactose intolerance? Which is most common?

A
  • Lactase non-persistence (most common): Enzyme levels fall with aging
  • Congenital lactase deficiency (rare)
  • Secondary deficiency due to mucosal injury i.e. viral infection, Celiac’s
147
Q

What brush border enzyme is first lost following GI illness? Why?

A

Lactase, due to distal location on villi

148
Q

How is lactose intolerance often diagnosed? What 2 diagnostic tests can be done?

A
  • Often clear from history
  • Lactose breath hydrogen test
  • Lactose tolerance test (rarely done)
149
Q

How to perform lactose breath hydrogen test? What do the test results mean?

A
  • Patient ingests lactose then measure exhaled hydrogen level
  • If lactose intolerant, bacteria will ferment lactose → ↑ Hydrogen
150
Q

How to perform the lactose tolerance test? What do the test results mean?

A
  • Monitor blood glucose level after lactose consumption
  • Should rise if lactose → galactose and glucose
151
Q

There is usually a small or large amount of organisms in the small intestines?

A

Small (should be nearly sterile)

152
Q

Bacterial overgrowth in the small intestine can cause what?

A

Malabsorption (bloating, flatulence, abdominal discomfort, chronic diarrhea, vitamin deficiencies)

153
Q

What are 2 causes of bacterial overgrowth in small intestines?

A
  • Altered motility: diabetes mellitus (enteric nerve damage), scleroderma
  • Partial/intermittent obstruction: adhesions, Crohn’s disease
154
Q

What are 2 diagnostic tests used for bacterial overgrowth in small intestines?

A
  • Jejunal aspirate (gold standard): not commonly done
  • Lactulose test: laxative, bacteria will metabolize some into H+ (high H+ = bacterial overgrowth)
155
Q

What is the treatment for bacterial overgrowth in small intestines?

A

Antibiotics

156
Q

What are the 3 underlying mechanisms of increased fat malabsorption?

A
  • Loss of bile (liver, biliary disease)
  • Loss of pancreatic enzymes
  • Loss of small bowel (resection)
157
Q

What is the fecal fat test?

A
  • Stool collected over 1-3 days
  • Amount of fat measured, Normal <7 grams per day
158
Q

What is the D-xylose test? How is it performed?

A
  • Tests carbohydrate absorption small intestine
  • After fasting, pt ingests D-xylose (monosaccharide absorbed in intestine, no enzyme required) → D-xylose then measured in serum/urine
  • Intact mucosa = rise in D-xylose seen
159
Q

What 2 tests can be used to diagnose sugar malabsorption?

A
  • Stool pH: most sugars cause acidic pH
  • Clinitest: detects undigested sugars, works best in children
160
Q

What is the clinical presentation of acute pancreatitis?

A
  • Epigastric pain, classically radiating to back
  • Nausea/Vomiting
161
Q

What are the 2 most common triggers for acute pancreatitis?

A

Gallstones, alcohol (triggers release of pancreatic enzymes, exact mechanism unclear)

162
Q

What are 2 classic physical exam findings seen in acute pancreatitis? These findings are also found in what condition?

A

Cullen’s sign: periumbilical hemorrhage
Grey Turner’s sign: flank hemorrhage

Due to spread of necrosis from enzyme-induced damage; Ruptured ectopic pregnancy

First Aid (18 decks)

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