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Upper GI > Clinical > Flashcards

Clinical Flashcards

1
Q

Most potent acid inhibitor for GERD?

A

PPIs

-heals erosive esophagitis

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2
Q

Does the grade of esophagitis correlate with the degree of symptoms?

A

No

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3
Q

What is the main reason for GERD?

A

LES dysfunction

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4
Q

Causes of GERD?

A
  1. Defective esophageal clearance (dysmotility)
  2. Hiatal Hernia
  3. LES dysfxn (decreased pressure)
  4. Delayed gastric emptying
  5. Increased intrabdominal pressure (GPEG)
  6. Increased transient relaxation of LES
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5
Q

Typical GERD symptoms?

A
  • heartburn
  • regurgitation
  • difficulty swallowing
  • water brash: hyper salivation
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6
Q

Atypical GERD?

A
  • chronic cough
  • cavities
  • chest pain
  • hoarse
  • asthma
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7
Q

Complications of GERD?

A
  • bleeding
  • stricture
  • ulcers
  • Barrett’s
  • Cancer
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8
Q

Barrett’s esophagus?

A

metaplastic columnar epithelium replaces stratified squamous

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9
Q

Factors that Increase risk of GERD?

A
  • nocturnal acid
  • age
  • white
  • male
  • obesity
  • tobacco
  • family history
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10
Q

Factors that decrease risk of GERD?

A

CagA+ H. pylori

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11
Q

Middle aged white obese male with reflux for 20 years.

  1. Diagnosis?
  2. Treatment?
A
  1. GERD

2. PPI for 3 weeks then endoscopy

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12
Q

Factors that increase risk of esophageal squamous cell ca?

A
  • smoking
  • alcohol
  • low veggie intake
  • hot liquids
  • achalasia
  • lye ingestion
  • Tylosis (hyperkeratosis of palms and feet)
  • Bisphosphonates
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13
Q

Treatment of esophageal squamous cell ca?

A
  1. Endoscopy with biopsy
  2. CT/MRI for metastases
  3. Endoscopic ultrasound if negative
  4. chemo/radiation
  5. Palliation
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14
Q

Most common esophageal cancer?

A

Adenocarcinoma of lower 1/3

  • arise from BE
  • nocturnal heartburn is risk factor
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15
Q

Clinical EoE in adults?

A
  1. Dysphagia
  2. Food impaction
  3. Heartburn
  4. Regurgitation
  5. Chest pain
  6. Odynophagia
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16
Q

Clinical EoE in children?

A
  1. abdominal pain
  2. Heartburn
  3. Regurgitation
  4. N/V
  5. Dysphagia
  6. Failure to thrive
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17
Q

Linear furrows, exudates, and concentric rings in esophagus?

A

Eosinophilic Esophagitis

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18
Q

Eoe complications?

A
  • longitudinal rent

- perforation

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19
Q

Histo diagnosis of EoE?

A

> 15 eosinophils per HPF on biopsy

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20
Q

Treatment of EoE?

A
  1. elimination diet
  2. PPI
  3. Swallow steroids for adults (Fluticasone)
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21
Q

Pathophys of achalasia?

A
  • degeneration of neurons in esophageal wall leads to lack of inhibition of LES so LES cannot relax and loss of peristalsis in distal esophagus
  • caused by Chagas (trypanosome cruz)
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22
Q

Dysphagia to solids and liquids with regurgitation onto pillow at night?

A

achalasia

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23
Q

How to diagnose achalasia?

A
  • barium swallow shows dilated esophagus and beak like narrowing
  • manometry shows elevated LES resting pressures
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24
Q

Treatment for achalasia?

A
  • nitrates
  • ca blockers
  • botulinum
  • pneumatic balloon
  • myotomy
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25
Q

Boerhaave syndrome?

A
  • sudden increase in esophageal pressure with negative intrathoracic pressure causes perforation
  • severe retching
  • severe retrosternal chest pain
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26
Q

How to diagnose esophageal perforation?

A
  • CXR shows free air
  • CT
  • gastrograffin swallow
  • EGD if surgery
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27
Q

HIV+ patient with odynophagia, who inhales corticosteroids. EGD shows white mucosal plaques down esophagus.

  1. Diagnosis?
  2. Treatment?
A
  1. Candidiasis

2. Fluconazole

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28
Q

Prophylaxis of esophageal varices?

A
  • nonselective beta blockers

- EVL

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29
Q

Treatment of esophageal varices hemorrhage?

A
  • EVL
  • blood with clotting factors
  • Octreotide (somatostatin) to decrease portal pressures
  • Quinolones or Ceftriaxone
  • balloon
  • surgery
  • TIPS
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30
Q

Nutcracker esophagus?

A

> 220 mmHg distal esophageal peristaltic pressures

-hypercholinergic

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31
Q

Complicated symptoms of GERD?

A
  • dysphagia
  • odynophagia
  • bleeding
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32
Q

How should GERD be diagnosed?

A

clinically, no tests

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33
Q

Management of GERD?

A
  1. weight loss
  2. elevate bed
  3. eliminate food triggers
  4. PPI
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34
Q

Factors that predict poor response to medical therapy of GERD?

A
  1. nocturnal reflux
  2. LES dysfxn
  3. mixed gastric and duodenal reflux
  4. mucosal injury
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35
Q

Hiatal hernia causes?

A
  1. Phrenesophageal ligament degeneration
    - aging
    - smoking
  2. Increased intra-abdominal pressure
    - obesity (BMI > 30 increases risk 4.2)
    - straining
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36
Q

Types of hiatal hernias?

A
  1. GE junction above diaphragm = most common
  2. Fundus herniates above diaphragm
  3. GE and Fundus herniate
  4. GE, Fundus, and other organs herniate
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37
Q

Gold standard treatment of Hiatal hernias?

A
  1. Nissen fundoplication
    - 360 degree wrap
  2. Toupet
    - 270 degree
  3. Dor
    - wrap anterior to esophagus
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38
Q

ADR of Nissen?

A
  • flatulence

- adbominal distention

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39
Q

Old female with chronic DM presents with early satiety, epigastric pain, and vomiting of undigested food.

Diagnosis?

A
  1. Diabetic gastroparesis
  2. pyloric stenosis
  3. achalasia
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40
Q

If you suspect gastroparesis, what’s your next step?

A
  1. Rule out mechanical obstruction first

2. Gastric Scintigraphy

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41
Q

Gastroparesis pathophys?

A

MMC and phasic antral motility are impaired

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42
Q

Most common cause of gastroparesis?

A

idiopathic

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43
Q

Protective factors of the stomach? causes of disruption?

A
  1. mucous (acid)
  2. hydrophobicity (h. pylori)
  3. bicarbonate (NSAIDS)
  4. blood flow (ischemia)
  5. prostaglandins (NSAIDS)
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44
Q

Noninvasive tests for H. pylori?

A
  • Urea breath test
  • Stool antigen
  • serology
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45
Q

When to test for H. pylori?

A
  • active ulcer
  • history of ulcers
  • MALT
  • if going to be treated
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46
Q

Highest risk of PUD?

A

NSAIDS users with H. pylori

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47
Q

ZE?

A
  • gastrinoma secreting hyper gastrin in duodenum (70%) or pancreas
  • PUD develops in duodenum (90%)
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48
Q

How to diagnose ZE?

A
  • Fasting serum Gastrin levels (>1000 pg/mL)
  • gastric pH < 2
  • Secretin test
  • screen for MEN1 (PTH, Ca, prolactin)
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49
Q

Causes of gastritis?

A
  • infections
  • drugs
  • autoimmune hypersensitivity
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50
Q

Causes of gastropathy?

A
  • drugs
  • bile reflux
  • stress
  • hypovolemia
  • chronic vascular congestion
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51
Q

Enlarged gastric folds Ddx?

A
  • Chronic gastritis (lymphoid hyperplasia/h. pylori)
  • tumors
  • ZE
  • Menetrier’s
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52
Q

Menetrier’s?

A
  • enlarged rugal folds (foveolar hyperplasia)
  • decreased acid (parietal atrophy)
  • protein losing gastropathy
  • hypoalbumin
  • associated with CMV and H. pylori
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53
Q

Most common benign tumor of stomach?

A

leiomyoma

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54
Q

Highest incidence of gastric cancer?

A

Japan

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55
Q

Volvulus?

A
  • stomach rotates
  • organoaxial: greater curve swings up
  • mesenteroaxial: antrum rotates to the left
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56
Q

Cholesterol stones?

A
  • monohydrate crystals
  • mucin
  • unconjugated Br
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57
Q

Black pigment stones?

A
  • cirrhosis, hemolysis, TPN
  • unconjugated Br
  • calcium
  • mucin
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58
Q

Brown pigment stones?

A
  • stasis, infection (radiolucent)
  • unconjugated
  • anaerobes
  • mcuin
  • ca salts
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59
Q

Gallstone pathophys?

A
  1. Increased cholesterol and decreased bile salts causes supersaturation
  2. central calcium nidus
  3. GB stasis
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60
Q

Is a CT a good test for gallstones?

A

no unless calcified

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61
Q

MRCP for gallstones?

A

highly sensitive if stones > 1cm

-doesnt detect small stones

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62
Q

Best test for imaging gallstones?

A
  1. EUS

2. ERCP

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63
Q

Biliary colic from chronic cholecystitis?

A
  • stone is in neck of cystic duct, intermittent obstruction
  • fibrosis and inflammation
  • shrunken GB and RA sinuses if recurrent
  • epigastric pain radiating to right shoulder
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64
Q

Ultrasound results for chronic cholecystitis?

A

hyper echoic foci with shadowing

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65
Q

Most common complication of gallstone disease?

A

Acute cholecystitis

  • 90% from chronically obstructed stone
  • young females
66
Q

Pathophys of acute cholecystitis?

A

cystic duct is obstructed by gallstone which damages GB mucosa stimulating prostaglandin synthetase
-secretions and inflammation with bacteria (50%)

67
Q

40 year old female with RUQ pain, elevated Br (<4), and inspiratory arrest (murphys).

  1. Diagnosis?
  2. if Br >4?
A
  1. Acute cholecystitis

2. Choledocholithiasis

68
Q

Ddx of acute cholecystitis?

A
  • Appendicitis

- Pancreatitis

69
Q

Choledocholithiasis?

A

stone in CBD

70
Q

Patient with RUQ pain, fever, jaundice, hypotension, and confusion. ALT > 150. Elevated direct bilirubin.

Diagnosis?

A

Choledocholithiasis with ascending cholangitis

71
Q

Acalculous cholecystitis?

A
  • GB inflammation without stones
  • elderly, HIV, vasculitis, infection, BMT
  • treat with antibiotics and cholecystectomy
72
Q

Causes of acalculous cholecystitis?

A
  • prolonged fasting
  • immobility (no CCK)
  • hemodynamic instability (ischemia)
73
Q

Cholesterolosis?

A

accumulation of lipid in GB mucosa

74
Q

Patient with epigastric pain that radiates to the back, N/V, and diarrhea. Labs show elevated lipase.

Diagnosis?

A

Acute pancreatitis

75
Q

Key histories for acute pancreatitis?

A
  • Biliary disease
  • Chronic alcohol abuse
  • Binge drinking
  • HyperTG
  • Post-op
  • Cystic fibrosis
76
Q

Xray of acute pancreatitis?

A
  1. Colon cut off sign
    - edema of pancreas compressing on splenic flexure with distention and sympathetic ileus
  2. Sentinel loop
    - due to ileus
77
Q

Purtscher retinopathy?

A

thrombi in eye indicating acute pancreatitis

78
Q

What enzyme is always elevated in acute pancreatitis?

A

Lipase

-amylase but not as specific

79
Q

Why use abdominal ultrasound?

A

suspected biliary disease

-not used for pancreatitis

80
Q

Why use MRCP?

A

noninvasive image of biliary and pancreatic ducts

-use if choledocholithiasis is suspected

81
Q

Test done if acute pancreatitis is severe?

A

Abdominal CT

82
Q

What is severe acute pancreatitis?

A
  • severe inflammatory infiltrate
  • necrosis
  • gland dysfunction
  • multi organ failure
  • admitted to ICU
83
Q

Ranson criteria for pancreatitis on admission?

A
  • age 55
  • WBC > 16,000
  • Glucose > 200
  • LDH > 350
  • AST > 250
84
Q

Ranson criteria within 48 hours?

A
  • Hct drops >10%
  • BUN increases by 5
  • Calcium < 8
  • pO2 < 60
  • Base deficit > 4
  • Fluid sequestration > 6 L
85
Q

Patient with epigastric pain, weight loss, steatorrhea, and DM. Low trypsinogen and high glucose.

Diagnosis?

A

Chronic pancreatitis

86
Q

Pathognomic test for chronic pancreatitis?

A

KUB and CT shows calcium deposits on pancreas and pseudocysts
-ERCP is gold standard to diagnose but less invasive option is done first

87
Q

Patient is having worsening symptoms after 4 weeks from bout of acute pancreatitis

A

Necrotizing pancreatitis

88
Q

CT/MRI results of necrotizing pancreatitis?

A

Dead tissue will not take up IV contrast and appear black

-air indicates infection

89
Q

Signs of necrotizing pancreatitis, hemorrhagic?

A

Cullen sign
-bluish discoloration around umbilicus secondary to hemoperitoneum

Grey Turner sign
-red brown purple flank secondary to retroperitoneal blood

90
Q

Treatment of acute pancreatitis?

A
  1. NPO
  2. IVF (D5W)
  3. Analgesics
  4. Imipenem Abx
  5. TPN if Ranson >3
91
Q

AST normal value? Where synthesized?

A

8-45

Liver, heart, muscles
-found in mitochondria

92
Q

ALT normal value? Where synthesized?

A

7-55

  • 20-25 females
  • 30-35 males

Liver cells
-more specific to liver disease than AST

93
Q

AST:ALT in a 2:1 ratio?

A

Alcoholic hepatitis

94
Q

Patient with ALT/AST 10x higher than normal, asterixis, confusion, and prolonged PT.

A

Acute liver failure with encephalopathy

95
Q

ALP normal value? Where made?

A

45-115

Made in liver and bones

96
Q

ALP >4x normal and high GGT. Mild elevation of AST/ALT. Diagnosis?

A

cholestasis

97
Q

High ALP and normal GGT. Diagnosis?

A

Bone disease

98
Q

GGT normal value? Where made?

A

9-48

made in liver cells and biliary epithelial cells

99
Q

LDH use?

A

122-222

useful for MI or hemolysis

100
Q

Why does PT and INR increase in liver disease?

A
  • decreased synthesis of clotting factors

- Vit k deficiency

101
Q

Low albumin in hepatic test means?

A

chronic liver disease

102
Q

Normal bilirubin levels?

A

0.2-1.2

103
Q

Elevated bilirubin with normal ALP. Diagnosis?

A

genetic disorder or hemolysis

104
Q

Elevated conjugated Br?

A
  • biliary obstruction
  • intrahepatic cholestasis
  • liver injury
105
Q

What conjugates Br?

A

UDP-glucuronosyltransferase

106
Q

College student with fatigue and jaundice. High unconjugated Br.

  1. Diagnosis?
  2. Pathophys?
  3. Treatment?
A
  1. Gilbert Syndrome
  2. Mild reduction in UDP-G
  3. Phenobarbital
107
Q

Infant 2 weeks after birth with extensive jaundice and increased unconjugated Br. Dies shortly after.

Diagnosis?

A

Crigler Najjar Type 1

  • lack of conjugating enzyme
  • Type 2 less severe
108
Q

Patient with elevated conjugated Br, jaundice, and a black liver.

Diagnosis?

A

Dubin johnson

-inability to transport Br to bile canaliculi

109
Q

Patient with elevated conjugated Br and no black liver.

Diagnosis?

A

Rotor

110
Q

Patient with cirrhosis, DM, and hyperpigmentation of skin. Elevated Ferritin >500.

Diagnosis?
Pathophys?
Treatment?

A

Hemochromatosis

  • HFE gene 282Y
  • increased intestinal iron absorption which is normally regulated by Hepcidin
  • treat with phlebotomy
  • women delayed symptoms due to menstruation
111
Q

A1-AT function?

A
  • produced in hepatocytes

- inhibits elastase

112
Q

Most common deficient allele in A1-AT?

A

z allele results in emphysema and eventual cirrhosis

113
Q

Child with jaundice, ascites, and poor nutrition.

Diagnosis?

A

A1-AT

114
Q

Adolescent with anorexia, ascites, and peripheral edema.

Diagnosis?

A

A1-AT

115
Q

Diagnosis of A1-AT? Treatment?

A
  • serum A1-AT
  • PCR to detect Z
  • treat symptoms
116
Q

40 year old female with pruritus, fatigue, hepatosplenomegaly, xanthomas, elevated ALP and IgM, and antimitochondrial antibodies.

Diagnosis?
Treatment?

A

Primary Biliary Cholangitis

  • T cell autoimmune interlobular duct damage
  • treat with Ursodiol
  • watch bone health
117
Q

Man with ulcerative colitis, pruritis, and elevated ALP.

Diagnosis?

A

Primary sclerosing cholangitis

  • fibrosis of intra and extra hepatic ducts
  • diagnose with cholangiography
118
Q

Man who doesn’t drink, has mildly elevated LFTs and hepatic steatosis.

Diagnosis?

A

Nonalcoholic fatty liver disease

  • insulin resistance from obesity, DM, dyslipidemia, metabolic
  • no inflammation
  • inflammation seen in NASH
119
Q

Young man with cirrhosis, Kayser fleisher rings around corneas, jaundice, and behavioral changes. Labs show decreased Ceruloplasmin and increased urine copper.

Diagnosis?
pathophys?
Treatment?

A

Wilson disease

  • abnormal copper transport protein
  • autosomal recessive
  • treat with D-penicillamine, Trientine, or zinc to bind copper
120
Q

First test if liver suggest cholestasis?

A

ultrasound

  • 95% sensitive for gallstones
  • noninvasive and cheap
  • may miss small lesions
121
Q

Uses for CT?

A
  • hepatomegaly
  • intrahepatic tumors
  • portal HTN
  • biliary tree dilation

-it is noninvasive but is expensive, uses contrast, and radiation

122
Q

Use of MRI?

A

most accurate for liver lesions but is expensive and contrast can cause kidney problems

123
Q

Use of PET?

A

smaller lesions and metastatic disease

124
Q

Use of Cholescintigraphy (HIDA)?

A

cholecystitis or gallstone

125
Q

Use of MRCP?

A

intrahepatic and extra hepatic bile ducts for gallstones, strictures, or dilatation and is noninvasive

126
Q

Use of ERCP?

A

invasive but more reliable than MRCP and can extract stones or insert stents
-risk of pancreatitis

127
Q

Use of PTC?

A

invasive evaluation of biliary tree

-risks fever, bacteria, peritonitis, hemorrhage

128
Q

Treatment for fulminant hepatitis?

A

urgent transplant

129
Q

Presentation of HAV?

A

Children asymptomatic

Adults symptomatic

130
Q

HBsAg+ for 6 months?

A

Chronic HBV

131
Q

HBsAg-, HBcAb+, HBsAb+?

A

past HBV resolved, no vaccine

132
Q

HBsAg-, HBcAb-, HBsAb+?

A

immune, no vaccine

133
Q

HBsAg-, HBcAb+, HBsAb-?

A

past HBV resolved, need vaccine

134
Q

Extrahepatic manifestations of HBV?

A
  • PAN
  • MGN
  • HCC
135
Q

Treatment of HBV?

A

Entacavir or Tenofovir if:

  • cirrhotic
  • INR >1.5 and Br >3 (acute)
  • chronic with extrahepatics
136
Q

Superinfection with HDV?

A

chronic HBV is then infected with HDV on top

137
Q

Coinfection of HBV and HDV?

A

most will clear HBV and then HDV will resolve

138
Q

Acute HCV?

A

flu like symptoms with mildly elevated ALT

139
Q

Chronic HCV?

A
  • persistent 6 months

- low albumin, elevated INR, hyperBr, thrombocytopenia means advanced cirrhosis or HCC

140
Q

Pregnant woman from another country presents with liver issues and dies.

Diagnosis?

A

HEV

141
Q

Micronodular cirrhosis?

A

alcoholic hepatitis

142
Q

AST:ALT elevated 2:1, elevated GGT, and elevated MCV.

Diagnosis?

A

Acute alcoholic hepatitis

-treat by abstaining from alcohol

143
Q

Inflammation, fibrosis, and steatosis with no history of alcohol.

Diagnosis?

A

NASH

-treat with aerobic exercise and bariatric surgery

144
Q

Patient with elevated liver enzymes, what should you always ask?

A

new medications, OTC, herbal supplements

145
Q

Most common cause of acute liver failure in US? Treatment?

A

acetaminophen

  • safe 1-4mg/day
  • treat with N-acetylcysteine
146
Q

Type 1 autoimmune hepatitis antibodies? Treatment?

A

ANA
ASMA
anti-F actin

  • must biopsy
  • treat with immunosuppression
147
Q

95% of portal HTN caused by?

A

intrahepatic (cirrhosis)

148
Q

Causes of ascites?

A
  • cirrhosis (75%)
  • Neoplasms (10%)
  • CHF (5%)
  • hypoalbumin
149
Q

Tests performed on ascites?

A

paracentesis

  • high albumin gradient > 1.1mg (cirrhosis)
  • low gradient (nephrotic)
  • ANC >250 (bacterial peritonitis)
150
Q

Treatment of cirrhotic ascites?

A
  • abstain from alcohol and salt
  • moderate ascites- use diuretic
  • refractory- remove fluid and consider TIPS or liver transplant
151
Q

Spontaneous bacterial peritonitis? Pathophys? Organism? Treatment?

A

complication of ascites

  • infection of ascitic fluid without intraabdominal source
  • bacteria traverse into LN
  • E. Coli most common
  • ANC >250
  • Treat with 3rd gen Cephalosporin
152
Q

Treatment of varices?

A
  1. IVF and blood with clotting factors
  2. Octreotide
    - somatostatin splanchnic vasoconstrictor
  3. Control bleeding with Endoscopy
  4. Liver transplant
153
Q

Patient with low BP, bounding pulses, jaundice, clubbing, palmar erythema, spider nevi, edema, and ascites.

Diagnosis?

A

Hepatorenal syndrome

154
Q

How to diagnose hepatorenal syndrome?

A
  • low GFR (need diuretic withdrawal)
  • urine Na <10mmol
  • Urine osmolality > plasma
155
Q

Type 1 hepatorenal?

A
  • double creatinine
  • > 221umol/L
  • GFR <20cc/min
  • hypotension
  • death in 8-10 weeks
  • treat with vasoconstrictors, dialysis, and fluids
156
Q

TIPS treatment?

A
  • reduces portal pressure
  • connects portal vein to hepatic veins
  • suppresses RAAS
157
Q

Definitive treatment for hepatorenal?

A
  • liver transplant

- limited benefit in type 1 because they die before operation

158
Q

Patient with cirrhosis, asterixis, and mental status change.

Diagnosis?
Pathophys?
Treatment?

A

Hepatic encephalopathy

  • necessary to diagnose fulminant hepatitis
  • increased ammonia and gut toxins get to brain due to lack of liver breakdown
  • usually a precipitating cause like electrolyte imbalance, GI bleed, Drugs, infection, diet
  • treat by lactulose which increases gut H+ that binds NH3
  • Neomycin, Metronidazole, Rifaximin
159
Q

Why osteoporosis in cirrhosis?

A
  • malabsorption of Vit D
  • decreased calcium ingestion
  • bone resorption > formation

-screen with DEXA

160
Q

What is the first indication of Portal HTN?

A

Splenomegaly

-TTP, Leukopenia, recurrent infections

161
Q

Why does coagulopathy occur in cirrhosis?

A

decreased synthesis of clotting factors

  • Vit K dependent (2, 7, 9, 10)
  • treat with IV Vit K

Impaired clearance of anticoagulants

TTP from splenomegaly

Upper GI (5 decks)

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