Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Upper GI > Clinical > Flashcards

Clinical Flashcards

1
Q

Most potent acid inhibitor for GERD?

A

PPIs

-heals erosive esophagitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

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

A

No

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the main reason for GERD?

A

LES dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Typical GERD symptoms?

A
  • heartburn
  • regurgitation
  • difficulty swallowing
  • water brash: hyper salivation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Atypical GERD?

A
  • chronic cough
  • cavities
  • chest pain
  • hoarse
  • asthma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Complications of GERD?

A
  • bleeding
  • stricture
  • ulcers
  • Barrett’s
  • Cancer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Barrett’s esophagus?

A

metaplastic columnar epithelium replaces stratified squamous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Factors that Increase risk of GERD?

A
  • nocturnal acid
  • age
  • white
  • male
  • obesity
  • tobacco
  • family history
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Factors that decrease risk of GERD?

A

CagA+ H. pylori

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Most common esophageal cancer?

A

Adenocarcinoma of lower 1/3

  • arise from BE
  • nocturnal heartburn is risk factor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Clinical EoE in adults?

A
  1. Dysphagia
  2. Food impaction
  3. Heartburn
  4. Regurgitation
  5. Chest pain
  6. Odynophagia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Clinical EoE in children?

A
  1. abdominal pain
  2. Heartburn
  3. Regurgitation
  4. N/V
  5. Dysphagia
  6. Failure to thrive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Linear furrows, exudates, and concentric rings in esophagus?

A

Eosinophilic Esophagitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Eoe complications?

A
  • longitudinal rent

- perforation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Histo diagnosis of EoE?

A

> 15 eosinophils per HPF on biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Treatment of EoE?

A
  1. elimination diet
  2. PPI
  3. Swallow steroids for adults (Fluticasone)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

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

A

achalasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How to diagnose achalasia?

A
  • barium swallow shows dilated esophagus and beak like narrowing
  • manometry shows elevated LES resting pressures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Treatment for achalasia?

A
  • nitrates
  • ca blockers
  • botulinum
  • pneumatic balloon
  • myotomy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Boerhaave syndrome?

A
  • sudden increase in esophageal pressure with negative intrathoracic pressure causes perforation
  • severe retching
  • severe retrosternal chest pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How to diagnose esophageal perforation?

A
  • CXR shows free air
  • CT
  • gastrograffin swallow
  • EGD if surgery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Prophylaxis of esophageal varices?

A
  • nonselective beta blockers

- EVL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Nutcracker esophagus?

A

> 220 mmHg distal esophageal peristaltic pressures

-hypercholinergic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Complicated symptoms of GERD?

A
  • dysphagia
  • odynophagia
  • bleeding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

How should GERD be diagnosed?

A

clinically, no tests

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Management of GERD?

A
  1. weight loss
  2. elevate bed
  3. eliminate food triggers
  4. PPI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

ADR of Nissen?

A
  • flatulence

- adbominal distention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

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

A
  1. Rule out mechanical obstruction first

2. Gastric Scintigraphy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Gastroparesis pathophys?

A

MMC and phasic antral motility are impaired

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Most common cause of gastroparesis?

A

idiopathic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Noninvasive tests for H. pylori?

A
  • Urea breath test
  • Stool antigen
  • serology
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

When to test for H. pylori?

A
  • active ulcer
  • history of ulcers
  • MALT
  • if going to be treated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Highest risk of PUD?

A

NSAIDS users with H. pylori

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

ZE?

A
  • gastrinoma secreting hyper gastrin in duodenum (70%) or pancreas
  • PUD develops in duodenum (90%)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Causes of gastritis?

A
  • infections
  • drugs
  • autoimmune hypersensitivity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Causes of gastropathy?

A
  • drugs
  • bile reflux
  • stress
  • hypovolemia
  • chronic vascular congestion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Enlarged gastric folds Ddx?

A
  • Chronic gastritis (lymphoid hyperplasia/h. pylori)
  • tumors
  • ZE
  • Menetrier’s
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Menetrier’s?

A
  • enlarged rugal folds (foveolar hyperplasia)
  • decreased acid (parietal atrophy)
  • protein losing gastropathy
  • hypoalbumin
  • associated with CMV and H. pylori
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Most common benign tumor of stomach?

A

leiomyoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Highest incidence of gastric cancer?

A

Japan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Volvulus?

A
  • stomach rotates
  • organoaxial: greater curve swings up
  • mesenteroaxial: antrum rotates to the left
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Cholesterol stones?

A
  • monohydrate crystals
  • mucin
  • unconjugated Br
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Black pigment stones?

A
  • cirrhosis, hemolysis, TPN
  • unconjugated Br
  • calcium
  • mucin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Brown pigment stones?

A
  • stasis, infection (radiolucent)
  • unconjugated
  • anaerobes
  • mcuin
  • ca salts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Gallstone pathophys?

A
  1. Increased cholesterol and decreased bile salts causes supersaturation
  2. central calcium nidus
  3. GB stasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Is a CT a good test for gallstones?

A

no unless calcified

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

MRCP for gallstones?

A

highly sensitive if stones > 1cm

-doesnt detect small stones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Best test for imaging gallstones?

A
  1. EUS

2. ERCP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Ultrasound results for chronic cholecystitis?

A

hyper echoic foci with shadowing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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?

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?

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?

114
Q

Adolescent with anorexia, ascites, and peripheral edema.

Diagnosis?

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?

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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions