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Project - USMLE Step 3 > Gastroenterology > Flashcards

Gastroenterology Flashcards

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USMLE® Step 1 flashcards
1
Q

What are the complications of diverticulitis? (3)

A
  1. Free colonic perforation
  2. Abscess formation
  3. Fistula
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2
Q

What causes angiodysplasia of the colon?

A

Tortuous dilated veins in the submucosa of the colon

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3
Q

What are clinical features of angiodysplasia of the colon?

A

GI bleeding in patients over 60

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4
Q

How is agniodysplasia diagnosed and treated?

A

Diagnosed with colonoscopy and treated with colonoscopic coagulation

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5
Q

While all antibiotics are associated with C Diff, what 3 groups of antibiotics are more frequently implicated?

A

Cephalosporins, clindamycin, ampillicin

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6
Q

What are two complications of C Diff?

A

Colonic perforation and Toxic Megacolon

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7
Q

What are two clinical features of C Diff?

A

Crampy abdominal pain and profuse watery diarrhea

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8
Q

How is C Diff colitis treated?

A

Metronidazole or oral vancyomycin

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9
Q

How can C diff be diagnosed?

A

C diff toxins in stool; abdominal radiograph to rule out toxic megacolon followed by a flexible sigmiodoscopy

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10
Q

What groups of patients is metronidazole contraindicated in?

A

Babies and pregnant women

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11
Q

What are the clinical features of acute mesenteric ischemia?

A

Severe abdominal pain that is disproportionate to physical findings

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12
Q

What key lab points to intestinal infarction (and any type of general infarction)?

A

Elevated lactic acidosis

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13
Q

What is the definitive test for acute mesenteric ischemia?

A

Mesenteric angiography

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14
Q

How are all arterial causes of acute mesenteric ischemia treated?

A

Direct injection of papverine (vasodilator) into SMA

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15
Q

How are venous thrombosis treated if they cause acute mesenteric ischemia?

A

Heparin anticougulation

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16
Q

How is embolytic acute mesenteric ischemia treated?

A

Thrombolytic injection or embolectomy

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17
Q

What is the third most common cause of cancer in the United States

A

Colon Cancer

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18
Q

What type of cancers are the vast majorities of CRC?

A

Adenocarcinomas

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19
Q

What is the most specific and sensitive test for CRC?

A

Colonoscopy

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20
Q

What percent of CRC can flex sigmoidoscopy detect?

A

2/3

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21
Q

Why is CEA used in CRC?

A

As a prognostic factor, to help determine patient’s baseline before treatment. Not of any diagnostic value

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22
Q

What are two common ways CRC spreads?

A

Direct spread to other abdominoperineal organs or hematogenous spread to the lungs

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23
Q

Describe CRC screening protocol?

A

If no family history, start at age 50.

If family history, start 10 years before family member was diagnosed or age 40 (whichever is earlier)

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24
Q

What type of colonic polyps have the most malignant potential?

A

Villous adenomas (villian)

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25
Q

What type of diet shows an increased risk of CRC?

A

High fat and low fiber

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26
Q

How does IBD affect CRC risk and how does this impact screening?

A

IBD (both UC and Chron’s) increase risk of CRC, but UC increases risk more. Begin colonoscopy screening 8 years after diagnosis of IBD

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27
Q

What is the most common cause of large bowel obstruction in adults?

A

CRC

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28
Q

What is the most common non-neoplastic polyp?

A

Hyperplastic polyp

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29
Q

Are flat or pedunculated polyps more likely to be malignant?

A

Flat

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30
Q

What causes diverticulosis?

A

Increased intraluminal pressure, inner layer of colon bulges through focal areas of weakness in the colon wall, low fiber diets and positive family history

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31
Q

Where are most diverticuli located?

A

Sigmoid Colon

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32
Q

What are the clinical features of diverticulosis?

A
  1. Painless rectal bleeding
  2. LLQ discomfort (sigmoid colon)
  3. Bloating
  4. Constipation
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33
Q

How can diverticulosis be diagnosed?

A

Barium enema

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34
Q

When the large bowel is greater than ______ cm it is at risk of rupturing, peritonitis, or even death?

A

10 cm

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35
Q

How is ogilive syndrome treated?

A

IV fluids, stop narcotics and colonic decompression

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36
Q

What are the clinical features of ogilive syndrome?

A

Signs, symptoms and radiology point to a large bowel obstruction but there is no mechanical obstruction

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37
Q

Ogilive syndrome cannot be confirmed until ______ is ruled out?

A

Mechanical obstruction

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38
Q

What causes chronic mesenteric ischemia?

A

Atherosclerotic occlusive disease of main mesenteric vessels (celiac artery, SMA, IMA)

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39
Q

What are the clinical features of chronic mesenteric ischemia?

A

Dull post prandial pain

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40
Q

How is chronic mesenteric ischemia diagnosed?

A

Mesenteric angiography

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41
Q

What are some clinical features of CRC (5)?

A
  1. melena/hematochezia **
  2. abdominal pain
  3. change in bowel habits
  4. Iron Deficiency anemia *****
  5. Weight loss
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42
Q

Which sided CRC is more prone to obstruction?

A

Left (smaLLer Lumin)

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43
Q

Which sided CRC is more prone to melana? Which sided CRC is more prone to hematochezia?

A 
Melana = right
Hematochezia = left
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44
Q

What are two clinical features of rectal cancer?

A

Hematochezia and mass feeling

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45
Q

What type of therapy is not indicated in CRC?

A

Radiotherapy

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46
Q

What is typical treatment for CRC?

A

Surgical recesection and adjuvant chemotherapy

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47
Q

What is followup protocol for CRC in remission?

A

Colonoscopy at 1 year and then every 3 years

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48
Q

What is genetic inheritance pattern for Peutz Jegher?

A

Autosomal dominant

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49
Q

What are the clinical features of Peutz-Jegher? (3)

A

Single or multiple HEMARTOMAS throughout the GI tract; PIGMENTED SPOTS around lips, palmar surfaces, oral mucosa; INTUSSUCEPTION or GI Bleeding

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50
Q

Where are hemartomas located in Peutz-Jegher?

A

small bowel, colon, stomach

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51
Q

What is the risk of carcinomas in Peutz-Jegher?

A

slightly increased risk of stomach, ovary, and breast cancers

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52
Q

What is malignant potential for hemartomas?

A

Low malignant potential

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53
Q

What are two hereditary nonpolyposis CRC syndromes?

A

Lynch 1 and Lynch 2

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54
Q

Describe Lynch 1

A

Early onset CRC, no antecedent multiple polyposis

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55
Q

Describe Lynch 2

A

Lynch 1 + early occurrences of other cancers

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56
Q

What generally causes colonic volvulus?

A

Twisting of a loop of intestine about its mesenteric attachment site

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57
Q

Which type of colonic volvulus is more common in kids vs adults?

A 
Kids = cecal volvulus
Adults = Sigmoid Volvulus
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58
Q

What is seen on barium enema for sigmoid volvulus?

A

Bird Beak

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59
Q

What sign on radiography helps distinguish sigmoid volvulus from cecal volvulus?

A 
sigmoid = omega sign
cecal = coffee bean sign
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60
Q

What is preferred dx and tx for colonic volvulus?

A

Sigmoidoscopy (helps untwist colon)

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61
Q

Describe genetics of familal adenomatous polyposis?

A

AD mutation in tumor supressor gene

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62
Q

What is risk of CRC in Familal adenomatous polyposis?

A

100% by 40 years old

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63
Q

How does familal adenomatous polyposis present?

A

Hundreds of adenomatous polyps in colon

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64
Q

What preventative measure is needed in patients with familal adenomatous polyposis?

A

Prophylatic colectomy

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65
Q

What are genetics and clinical presentation of Gardner syndrome?

A

Variant of familal adenomatous polyposis, autosomal dominant, patient gets polyps and osteomas and soft tissue tumors. Risk of CRC is 100% by 40 years old.

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66
Q

Turcot syndrome genetics and clinical presentation

A

Turcot syndrome can be autosomal dominant and autosomal recessive. Polyps plus CNS tumors

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67
Q

How does familal juvenile polyposis clinically present? Risk of CRC?

A

Hundreds of juvenile polyps; low risk of CRC

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68
Q

What are two problems caused by diverticulosis

A

painless GI bleeding and diverticulitis

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69
Q

What causes diverticulitis?

A

Fecal impaction in diverticulum leading to erosion and microperforation

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70
Q

How does diverticulitis present? (3)

A

Fever, leukocytosis, and LLQ pain

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71
Q

How is diverticulitis diagnosed and what is contraindicated?

A

CT scan with contrast; DO NOT give patient a colonoscopy or barium enema (risk of perforation)

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72
Q

How is diverticulitis managed?

A

NPO, antibiotics, fluids

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73
Q

When is surgery indicated for diverticulitis?

A

If symptoms persist for 3-4 days or if recurrent episodes

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74
Q

What causes acute mesenteric ischemia?

A

compromised blood supply to intestines

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75
Q

What blood vessel is affected in acute mesenteric ischemia

A

SMA

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76
Q

Patients with acute mesenteric ischemia are more likely to have underlying _______

A

Preexisting heart disease

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77
Q

How many different types of acute mesenteric ischemia are there? What are they?

A

Embolic, arterial thrombosis, nonocclusive ischemia, venous thrombosis

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78
Q

How do the symptoms vary between the four types of acute mesenteric ischemia? (Venous, embolic, nonocclusive thrombosis, arterial thrombosis)?

A

Embolic = symptoms are sudden and painful
Arterial Thrombosis = symptoms are more gradual and less severe
Nonocclusive ischemia = occurs in critically ill patients
Venous thrombosis = symptoms may be present for days or weeks with gradual worsening

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79
Q

What is definitive diagnostic test for acute mesenteric ischemia?

A

Mesenteric angiography

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80
Q

What are two of the most common causes of acute appendicitis?

A
  1. Lymphoid hyperplasia (60% of cases)

2. Fecal obstruction (35% of cases)

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81
Q

What is a risk factor for appendix perforation?

A

Delay in treatment (>24 hours of acute appendicitis)

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82
Q

What are the clinical features of acute appendicitis?

3 signs, one behavioral and one location

A
  1. Anorexia (always present). Appendicitis is unlikely if the patient is hungry
  2. Tenderness at McBurney’s point (2/3 of the way from umbilicus to right anterior superior iliac spine)
  3. Rovsing sign: deep palpation in LLQ causes referred pain in the RLQ
  4. Psoas sign: RLQ pain when right thigh is extended as patient lies on left side
  5. Obturator sign: Pain in RLQ when flexed right thigh is internally rotated when patient is supine
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83
Q

Describe how symptoms of acute appendicitis progress?

A

Classically starts in the epigastrium, moves towards umbilicus, and then to RLQ.

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84
Q

How is acute appendicitis diagnosed?

A

Clinical diagnosis, however, CT scan is useful in cases where diagnosis is unclear

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85
Q

How is acute appendicitis treated?

A

Laparoscopic appendectomy

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86
Q

What are carcinoid tumors and where are they usually located?

A

Located usually in the appendix but can be found anywhere. Composed of neuroendocrine cells and secrete serotonin

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87
Q

What percent of patients with carcinoid tumors go on to develop carcinoid syndrome? What are the risk factors for metastasis of carcinoid tumors? How are carcinoid tumors treated?

A
  1. 10%
  2. Risk factors for metastasis is location and size of tumor (increase in size = higher chance of metastasis), appendix carcinoid tumors are less likely to metastasize but illeal have the greatest likelihood of spreading
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88
Q

What are some symptoms of carcinoid syndrome?

A

Cutaneous flushing, diarrhea, sweating, wheezing, abdominal pain, and heart valve dysfunction

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89
Q

Describe pathogenesis of acute pancreatitis?

A

Inflammation of the pancreas resulting from prematurely activated pancreatic digestive enzymes that invoke pancreatic tissue autodigestion

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90
Q

What are the two forms of acute pancreatitis and how do they differ in mortality and morbidity?

A
  1. Mild form is most common and responds well to supportive treatment.
  2. Severe form has significant morbidity and mortality
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91
Q

What are the two biggest causes of acute pancreatitis?

A
  1. Alcohol abuse (40%) and

2. Gallstones (40%)

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92
Q

What are the clinical features of acute pancreatitis?

A

Abdominal pain in the epigastric region
50% of cases will radiate to the back
Pain characterized as dull steady, worse with meals

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93
Q

What three signs indicate hemorrhagic pancreatitis?

A
  1. Grey Turn sign: flank ecchymosis
  2. Cullen sign: periumbilical ecchymosis
  3. Fox sign: ecchymosis of the inguinal ligament
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94
Q

What diagnostic test is confirmatory for acute pancreatitis?

A

CT scan

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95
Q

What are some lab tests to check for in acute pancreatitis? (5)

A
  1. Serum amylase (nonspecific) however five times the upper limit is highly specific
  2. Serum lipase: more specific than amylase
  3. LFTs: to identify gallstones as a cause
  4. WBC
  5. LDH
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96
Q

What are the acronyms for acute pancreatitis prognosis?

A
  1. GA-LAW for admissions criteria

2. C HOBBS for initial 48 hours criteria

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97
Q

What are two types of pancreatic necrosis? and how can someone distinguish between them?

A
  1. Sterile pancreatic necrosis - infection may develop, but half of these cases resolve spontaneously
  2. Infected pancreatic necrosis - high mortality rate: surgical debridement and antibiotics are indicated

Distinguish between them using CT-guided percutaneous aspiration and Gram stain/culture

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98
Q

What is a pancreatic pseudocyst and when does it appear in relation to an episode of acute pancreatitis?

A

Encapsulated fluid collection that appears 2-3 weeks after an acute attack

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99
Q

How are pancreatic pseudocysts diagnosed?

A

CT-scan

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100
Q

What are some complications of pancreatic pseudocysts?

A

Rupture, infection, fistula, hemorrhage into cyst

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101
Q

What is the treatment for pancreatic pseudocysts?

A

Cysts < 5 cm: observation

Cysts > 5 cm: drain either percutaneously or surgically

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102
Q

When does a pancreatic abscess develop?

A

4-6 weeks after acute pancreatitis

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103
Q

What is a respiratory complication of acute pancreatitis?

A

Adult respiratory distress syndrome

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104
Q

What is treatment for mild acute pancreatitis?

A
  1. NPO
  2. IV fluids
  3. Pain control (fentanyl and meperidine over morphine)
  4. Nasogastric tube
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105
Q

How is severe acute pancreatitis treated?

A
  1. Admit to ICU

2. Early enteral nutrition in the first 72 hours via nasojejunal tube

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106
Q

What is diagnostic for chronic pancreatitis? (2)

A
  1. Chronic epigastric pain

2. Calcifications seen on CT Scan

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107
Q

What is the most common cause of chronic pancreatitis?

A
  1. Alcohol abuse (80%)
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108
Q

Describe what happens in chronic pancreatitis?

A

Persistent and chronic inflammation of the pancreas leads to fibrotic tissue replacing pancreatic parenchyma and alteration of the pancreatic ducts. Endocrine and exocrine functions of the pancreas are impaired.

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109
Q

What are some clinical features of chronic pancreatitis?

A
  1. Severe pain in the epigastrium
  2. Radiates to the back (50%)
  3. Chronic in nature
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110
Q

What is the initial test of choice for chronic pancreatitis?

A

CT scan

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2
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111
Q

What are serum amylase and lipase levels in chronic pancreatitis?

A

Not elevated, (possibly normal)

112
Q

What are some complications of chronic pancreatitis (4)

A
  1. Pancreatic cancer (recurrent chronic pancreatitis increases risk of cancer)
  2. Diabetes mellitus (loss of islets of langerhans)
  3. Pseudocyst formation
  4. Malabsorption and steatorrhea (loss of exocrine pancreatic function)
113
Q

How is chronic pancreatitis managed?

A
  1. Nonoperatively: Narcotics for pain, bowel rest, pancreatic enzymes and H2 blockers, insulin, and short low-fat meals
  2. Surgery: Pancreatic duct drainage to decompress the dilated pancreatic duct; Pancreatic resection (Whipple procedure)
114
Q

What are some risk factors for pancreatic cancer?

A
  1. Age (> 60 years old)
  2. African American
  3. Diabetes Mellitus
  4. Chronic pancreatitis
  5. Alcohol use
  6. SMOKING (MOST IMPORTANT)
115
Q

What is the most common location of pancreatic cancer?

A

75% are in the pancreatic head

116
Q

What are the clinical features of pancreatic cancer?

A
  1. Abdominal pain (vague, dull)
  2. Jaundice
  3. Weight loss
  4. Migratory thrombophlebitis (10% of cases)
117
Q

What is one sign on physical exam that indicates pancreatic cancer

A

Courvoisier sign: palpable gallbladder

118
Q

What are two tumor markers for pancreatic cancer and what is the test of choice?

A

Test of choice is CT scan and tumor markers are CEA and CA19-9

119
Q

What is treatment for pancreatic cancer?

A

Whipple - low survival rates

120
Q

What are causes of Peptic ulcer disease (3)

A
  1. H pylori infection
  2. NSAID use (inhibits prostaglandin production which leads to impaired mucosal defenses)
  3. Acid hypersecretory states (Zollinger-Ellison Syndrome)
121
Q

What are some unproven causes of peptic ulcer disease that the public thinks about?

A 
Emotional stress (malcolm in the middle)
Type A personality disorder
Caffeine and coffee intake
122
Q

What are the clinical features of peptic ulcer disease?

A
  1. Epigastric pain (aching or gnawing in nature)

2. Nausea/vomiting, early satiety, weight loss)

123
Q

What is the most accurate test in diagnosing ulcers?

A

Endoscopy (biopsy is necessary to rule out malignancy)

124
Q

What type of ulcers require biopsy? (Gastric or duodenal)?

A

Gastric ulcers require biopsy, duodenal ulcers do not

125
Q

How is H pylori infection detected?

A

Urease detection via urea breath test

126
Q

How is zollinger-ellison syndrome diagnosed?

A

Serum gastric measurement

127
Q

Describe the pathogenesis of duodenal and gastric ulcers?

A

Duodenal ulcers are caused by an increase in offensive factors (higher rates of basal and gastric acid secretion).

Gastric ulcers are caused by a decrease in defensive factors

128
Q

Is H pylori infection more likely to cause ulcers in duodenal ulcers or gastric ulcers?

A

More likely to be the cause of duodenal ulcers

129
Q

Which types of ulcers (gastric or duodenal) are more likely to be malignant?

A

Gastric ulcers are more likely to be malignant

130
Q

Where are most gastric ulcers located?

A

On the lesser curvature of the stomach

131
Q

How does pain defer in gastric and duodenal ulcers in relation to eating?

A

In duodenal ulcers, eating relives pain.

In gastric ulcers, eating does not relieve pain

132
Q

How is peptic ulcer disease treated? (3)

A
  1. avoid NSAIDS
  2. Eradicate H pylori infection
  3. Appropriate use of antisecretory drugs
133
Q

How is H pylori infection eradicated?

A

For initial treatment, use triple therapy (PPI, amoxicillin, and clarithromycin).

For retreatment, use quadruple therapy (PPI, bismuth, metronidazole, and tetracycline)

134
Q

What are two categories of acid suppression drugs and what is their MOA?

A
  1. H2 blockers (-tidine drugs). Block histidine based parietal cell acid secretion.
  2. PPIs (-prazole): Block H+/K+ ATPase pump directly in the parietal cell membrane
135
Q

What are some causes of acute gastritis? (3) What does acute gastritis mean?

A

NSAIDs/asprin use, smoking, H pylori infection

It means inflammation of the gastric mucosa

136
Q

How is acute gastritis managed?

A

If patient has low or moderate levels of pain, empiric treatment with acid suppression is appropriate. If this fails, investigate using endoscopy or ultrasound.

137
Q

What can be seen on imaging for gastric ulcer perforation?

A

On CXR, patient will have free air under the diaphragm,

138
Q

How is gastric ulcer perforation managed?

A

Surgery to close it up

139
Q

What are the symptoms of gastric ulcer perforation?

A

Acute, severe abdominal pain, signs of peritonitis, hemodynamic instability.

140
Q

What is the most common cause of UPPER GI bleeding?

A

Peptic ulcer disease

141
Q

What is the best diagnostic study in diagnosing patients with epigastric pain?

A

Upper GI endoscopy because it can diagnose esophagitis, PUD, gastritis, rule out cancers of esophagus and stomach

142
Q

What is the most common cause of chronic gastritis and how is it managed?

A

Most common cause is H pylori infection and managed with eradication of H pylori infection

143
Q

What type of cancers are most gastric cancers?

A

Adenocarcinomas

144
Q

Where are gastric cancers more common?

A

Japan

145
Q

What are some risk factors for gastric cancer?

A

High intake of preserved foods like smoked fish

H pylori infections

146
Q

What are the clinical features of gastric cancer?

A

Abdominal pain and weight loss

147
Q

What is the most accurate test for gastric cancer?

A

Endoscopy

148
Q

How is gastric cancer treated?

A

Surgery

149
Q

What are the following:

Krukenberg tumor?
Blumer's shelf?
Sister Mary Joseph Node?
Virchow node?
Irish node?
A

Krukenberg - gastric cancer that metastasized to the ovaries

Blumer’s shelf - gastric cancer that metastasized to the rectum (palpate on rectal exam)

Sister Mary Joseph - gastric cancer that metastasized to the periumbilical lymph node

Virchow - gastric cancer that metastasized to the supraclavicular lymph nodes

Irish node - gastric cancer that spread to the left axillary

150
Q

What is gastric lymphoma?

A

A type of non-hodgkin lymphoma that arises in the stomach

151
Q

What is the clinical difference between partial and complete small bowel obstruction?

A

In partial obstruction, patients can still pass gas and have bowel movements. In complete obstruction, patients are usually unable to pass gas or have bowel movements unless the gas or feces are in the colon/distal to obstruction

152
Q

What are the clinical features of proximal obstruction and distal small bowel obstruction?

A

In partial obstruction, patients have frequent vomiting, severe pain, minimal abdominal distention

In distal obstruction, patients have less frequent vomiting, and significant abdominal distention

153
Q

What are some systemic symptoms of small intestine obstruction?

A

Dehydration from vomiting leads to systemic signs like tachycardia, hypochloremia, hypokalemia, and metabolic alkalosis, and hypotension

154
Q

What is a dangerous complication of small bowel obstruction?

A

Excessive extraluminal pressure can lead to a compromise of the blood supply causing strangulation of the intestine and subsequent gangrene, peritonitis, or perforation of the bowel.

155
Q

What is the most common cause of small bowel obstruction in adults?

A

Adhesions from previous abdominal surgery

156
Q

How can you distinguish small bowel obstruction from strangulation of the intestines?

A

In strangulation, patient may have peritonitis, fever, hematemesis, increased lactic acidosis, and abdominal pain is severe and continuous.

In your garden variety small bowel obstruction, pain is cramping.

157
Q

What the clinical features of small bowel obstruction?

A

Cramping abdominal pain, nausea, vomiting (may be feculent), obstipation (absence of gas or stool), abdominal distention.

158
Q

How is small bowel obstruction diagnosed?

A

abdominal plain films show obstruction or dilated loops of small bowel, and air-fluid levels proximal to point of obstruction.

159
Q

How is small bowel obstruction treated?

A

If it is partial and no signs of strangulation, give fluids, withhold food, give nasogastric tube.

If it is complete or if signs of strangulation, perform exploratory laparotomy

160
Q

What distinguishes paralytic ileus from small bowel obstruction or colonic obstruction on imaging?

A

In paralytic obstruction, there is a uniform distribution of gas in the small bowel, colon and rectum

161
Q

What is celiac sprue?

A

Hypersensitivity to gluten

162
Q

What are the symptoms of celiac sprue?

A

Diarrhea, weight loss, abdominal distention, bloating, weakness, and fatigue

163
Q

What skin disorder is associated with celiac sprue and what percentage of patients with celiac sprue have this skin disorder?

A

Dermatitis herpetiformis (papulovesicular lesion on extensor surfaces) is found in 10-20% of patients with celiac disease

164
Q

What does biopsy in celiac sprue show?

A

flattening of the villi in the proximal small bowel which causes malabsorption (fat soluble vitamin malabsorption)

165
Q

What is Whipple Disease?

A

Rare infection caused the infection by bacterium Tropheryma Whipplei

166
Q

How is Whipple Disease diagnosed?

A

PAS-postive macrophages are seen in the lamina propria containing non-acid fast gram-positive bacteria

167
Q

What is tropical sprue?

A

Environmental enteropathy that occurs in people who livin in or visit tropical areas

168
Q

What can be seen on endoscopy in patients with tropical sprue?

A

Flattening of villi

169
Q

How is tropical sprue managed?

A

Treated with antibiotics and folic acid

170
Q

What are the symptoms of tropical sprue?

A

Similar as the symptoms of celiac sprue: weight loss, diarrhea, cramps, fatigue, and malabsorption.

171
Q

What is the cause of tropical sprue?

A

Unknown, expected to be caused by bacterial overgrowth

172
Q

What are two effects that are caused by a distortion of liver anatomy in hepatic cirrhosis?

A
  1. Decreased blood flow through the liver with subsequent hypertension in portal circulation has widespread manifestations such as ascites, peripheral edema, splenomegaly, and varicosity of veins.
  2. Liver failure leads to decreased albumin synthesis and decreased clotting factor synthesis
173
Q

What are some causes of liver cirrhosis

A 
Alcohol abuse 
Chronic Hepatitis B
Chronic Hepatitis C
Alpha 1 antitrypsin deficiency 
Autoimmune hepatitis 
Primary biliary cirrhosis
NASH
174
Q

What are some classic signs of chronic liver disease?

A

Ascites, varices, gynecomastia, testicular atrophy, palmar erythema, spider angiomas, hemorrhoids, caput medusa

175
Q

What procedure can decrease portal hypertension in the setting of liver cirrhosis?

A

TIPS (transjugular intrahepatic portal systemic shunt)

176
Q

What can be used to prevent esophageal varices from bleeding? (prophylactic measures)

A

Use non-selective beta blockers

177
Q

How can emergent esophageal variceal bleeding be treated?

A

Treatment of bleeding esophageal varices involves pharmacological treatment with IV octreotide in addition to endoscopic treatment (variceal ligation or sclerotherapy)

178
Q

What are some causes of ascites?

A 
Portal Hypertension
CHF
chronic renal disease
malignancy
hypoalbuminemia
179
Q

What is caput medusa?

A

Distension of abdominal wall veins

180
Q

How can ascites be managed (in most cases)

A

Using salt restriction and diuretics

181
Q

What are complications of liver failure (AC, 9H)

A 
Ascites
Coagulopathy
Hypoalbuminemia
Portal Hypertension
Hyperammonemia
Hepatic encephalopathy 
Hepatorenal syndrome
Hypoglycemia
Hyperbilirubinemia
Hypertension
HCC
182
Q

What is measured and what is the cutoff for causes of ascites when performing a diagnostic paracentesis?

A

Measure serum ascites albumin gradient.

If SAAC is > 1.1 portal hypertension is cause for ascites

If SAAC is <=1.1, portal hypertension is unlikely

183
Q

When should a patient with ascites undergo therapeutic paracentesis?

A

If patient has tense ascites that is causing shortness of breath or early satiety

184
Q

What is a cause of hepatic encephalopathy?

A

Toxic metabolite ammonia builds up in the body because the liver cannot remove it

185
Q

What are clinical features of hepatic encephalopathy?

A

Stupor, confusion, poor concentration, decreased mental functions, asterixis (flapping tremor)

186
Q

What is used to prevent hepatic encephalopathy and how does it work?

A

Lactulose prevents absorption of ammonia.

187
Q

What is used to treat hepatic encephalopathy?

A

Rifaximin because it kills bowel flora that produce ammonia

188
Q

What are the clinical features of spontaneous bacterial peritonitis?

A

Look for fever and/or changes in mental status in a patient with known ascites

rebound tenderness, fever, vomiting

189
Q

What are some etiological causes of SBP?

A

E coli (most common)
Klebsiella
Strep pneumo

190
Q

How is SBP diagnosed?

A

Paracentesis that shows presence of WBC in ascitic fluid (WBC > 500 PMN > 250)

191
Q

How is SBP treated?

A

Broad spectrum antibiotics followed by specific antibiotics once cause has been identified

Repeat paracentesis in 2-3 days to document a decrease in ascitic fluid PMN (<250)

192
Q

What is hepatorenal syndrome and what does it indicate?

A

Progressive renal failure secondary to renal hypoperfusion. Indicates end-stage liver disease

193
Q

Kidneys are _____ in terms of morphology and they ____ respond to volume expansion in hepatorenal syndrome

A

Kidneys are normal in terms of morphology and they do not respond to volume expansion in hepatorenal syndrome

194
Q

What are the clinical features of hepatorenal syndrome?

A

Azotemia, oliguria, hyponatremia, hypotension, low urine sodium (<10 mEq/L)

195
Q

Why are estrogens elevated in liver cirrhosis and how does this clinical manifest (4)

A

Estrogens are elevated because the liver can no longer catabolize estrogens.

Clinical features of hyperestrinism:

  1. Spider angiomas
  2. Palmar erythema
  3. Gynecomastia
  4. Testicular atrophy
196
Q

What are the genetics of Wilson’s disease?

A

Autosomal Recessive

197
Q

What is the pathology of Wilson’s disease?

A

Mutations in ATP7B gene lead to impairment in copper excretion and incorporation of copper into ceruloplasmin, a cooper binding protein that is necessary for copper excretion

198
Q

What are some of the organs affected by Wilson’s disease? (4)

A
  1. Liver (can cause cirrhosis)
  2. Cornea (Kayser-Fleischer rings)
  3. CNS findings (Extrapyramidal signs such as parkinsonian symptoms (resting tremor, rigidity, bradykinesia) and Psychiatric disturbances)
  4. Renal involvement
199
Q

What lab value should be tested for in patients suspected of having Wilson’s disease?

A

Decreased serum ceruloplasmin levels

200
Q

What is the treatment for Wilson’s disease? (2)

A
  1. Chelating agents like d-penicillamine

2. Zinc to prevent uptake of dietary cooper

201
Q

What are the genetics of hemochromatosis?

A

Autosomal recessive

202
Q

What is the pathogenesis of hemochromatosis?

A

Excessive iron absorption in the intestines buildups in various organs. Iron causes free radicals to buildup in the body.

203
Q

What organs are affected by hemochromatosis? (5)

A
  1. Skin
  2. Liver
  3. Pancreas
  4. Heart
  5. Joints
204
Q

What are the complications of hemochromatosis? (6)

A
  1. Heart: cardiomyopathies
  2. Liver: Cirrhosis
  3. Pancreas: Diabetes Mellitus
  4. Joints: Arthritis
  5. Skin: Bronzelike skin
  6. Hypogonadism: amenorrhea, impotence, loss of libido.
205
Q

What happens to iron, ferratin, transferrin saturation, TIBC, and what test is required for diagnosis of hemochromatosis?

A
  1. Elevated serum iron
  2. Elevated serum ferritin
  3. Elevated transferrin saturation
  4. Decreased TIBC
  5. Liver biopsy confirms diagnosis
206
Q

How is hemochromatosis treated?

A

Repeated phlebotomies

207
Q

What are three kinds of benign liver tumors?

A
  1. Focal nodular hyperplasia
  2. Cavernous hemangiomas (most common type of liver tumor)
  3. Hepatocellular adenoma
208
Q

When should a benign liver tumor be investigated for possible resection?

A

When greater than 5 cm

209
Q

What type of benign liver tumor is not associated with oral contraceptives as a risk factor?

A

Focal nodular hyperplasia

210
Q

What are the two types of hepatocellular carcinoma and what is the difference between the two?

A

Nonfibrolamellar and fibrolamellar

Nonfibrolamellar is associated with Hep B, Hep C, and cirrhosis and is usually not resectable.

Fibrolamellar is not associated with Hep B, Hep C, and cirrhosis and is usually resectable

211
Q

What are some risk factors for hepatocellular carcinomas?

A

Hep B, Hep C, alcohol abuse, AAT deficiency, hemochromatosis, Wilson’s disease, smoking

212
Q

What are the clinical features of hepatocellular carcinomas?

A

Abdominal Pain, weight loss, anorexia, signs and symptoms of chronic liver disease

213
Q

What percentage of non-alcoholic steatohepatitis patients develop liver cirrhosis?

A

10-15%

214
Q

How is non-alcoholic steatohepatitis usually discovered?

A

Mild elevation in AST and ALT

215
Q

What causes Hydatid liver cysts, what is the risk with having this infection and how are they treated?

A

Caused by infection from Echinococcus granulosus tapeworm.

If cysts rupture, they may cause fatal anaphylactic shock.

They are treated with surgery and after surgical resection, the patient gets mebendazole

216
Q

What is the cause of pyogenic liver abscesses?

A

Obstruction of bile causes a breeding ground to form for bacteria.

217
Q

Describe the pathogenesis for Budd-Chiari Syndrome?

A

Liver disease caused by occlusion of hepatic venous outflow which leads to hepatic congestion and subsequent microvascular ischemia

218
Q

What are the clinical features of Budd-Chiari Syndrome?

A

Hepatomegaly, ascites, abdominal pain, jaundice, and variceal bleeding

219
Q

What is the treatment for Budd-Chiari syndrome?

A

Medical therapy is usually not enough, surgery is usually needed

220
Q

What are the three main causes of jaundice?

A

Hemolysis, Liver disease, and biliary obstruction

221
Q

Describe how hemoglobin is broken down (3)

A

Hemoglobin is broken down in the spleen into unconjugated bilirubin.

Unconjugated bilirubin is not water soluble and travels with albumin to the liver.

The liver conjugates bilirubin and excretes into the urine

222
Q

Dark urine is seen with conjugated or unconjugated bilirubin?

A

Only seen with conjugated bilirubin

223
Q

What is so dangerous about a buildup of unconjugated bilirubin?

A

Unconjugated bilirubin can cross the blood brain barrier causing neurological deficits

224
Q

What are two major causes of conjugated hyperbilirubinemia?

A
  1. Decreased intrahepatic excretion of bilirubin (conjugated bilirubin is stuck in the liver)
  2. Extrahepatic biliary obstruction (ie gallstones)
225
Q

What are two major causes of unconjugated hyperbilirubinemia?

A
  1. Excessive production of bilirubin (hemolytic anemia)
  2. Impaired bilirubin conjugation due to decrease function of UDP glucoronosyltransferase (two subtypes = Gilbert syndrome and Crigler-Najjar syndrome)
226
Q

What precipitates Gilbert syndrome and what are the genetics of Gilbert Syndrome?

A

Fasting, fever, alcohol, infection

Autosomal dominant

227
Q

What is the function of UDP glucuronosyltransferase?

A

Conjugates unconjugated bilirubin into conjugated bilirubin

228
Q

ALT or AST is more specific for liver damage?

A

ALT is more specific

AST is less Specific

229
Q

What are the upper cutoff levels for AST and ALT in alcoholic hepatitis?

A

AST is never > 500

ALT is never > 300

230
Q

If ALT and AST are moderately elevated (high hundreds to thousands) think of? (1)

A

acute viral hepatitis

231
Q

If AST and ALT are mildly elevated (low hundreds) think of? (2)

A

chronic viral hepatitis or acute alcoholic hepatitis

232
Q

What levels of AST and ALT are seen in acetaminophen toxicity?

A

> 10,0000

233
Q

What value is affected by decreased hepatic function? PT or PTT?

A

PT. Liver synthesizes factors 1, 2, 5, 7, 9, 10, 12, 13

234
Q

Normal levels of what makes cholestasis unlikely?

A

Normal levels of Alkaline phosphatase makes cholestasis unlikely

235
Q

Why does one check GGT along with Alkaline phosphatase and what does this show?

A

Alkaline phosphatase is also found in bone, gut, placenta.

GGT helps confirm that elevated alkaline phosphatase is due to hepatic issues.

If GGT is normal, but alkaline phosphatase is elevated consider bone disease or pregnancy

If GGT and alkaline phosphatase are elevated consider hepatic origin (hepatic bile obstruction)

236
Q

How is hepatic functional reserve measured in patients with liver cirrhosis?

A

Child-Pugh Score

237
Q

What does cholelithiasis refer to?

A

Stones in the gallbladder

238
Q

What are the four types of gallstones and what diseases are each associated with?

A
  1. Green/Yellow gallstones = cholesterol gallstones, associated with obesity, diabetes, hyperlipidemia
  2. Black gallstones = pigment gallstones, associated with hemolysis
  3. Brown gallstones = biliary tract infection
  4. Mixed gallstones = combination of above
239
Q

What causes the pain in biliary colic?

A

Biliary colic refers to temporary obstruction of the cystic duct due to gallstones. The pain occurs as the gallbladder contracts against an obstructed cystic duct.

240
Q

What forms the common hepatic duct?

A

The right and left hepatic ducts join to form the common hepatic duct

241
Q

What duct is the outflow from the gallbladder?

A

The cystic duct

242
Q

What makes up the common bile duct?

A

The cystic duct joins with the common hepatic duct (which is made up of the right and left hepatic ducts)

243
Q

Describe the pain associated with biliary colic? (location, what makes it worse, how long does it last, any referred pain?)

A

Typically presents in the RUQ and epigastrium. Pain is worse after meals. Pain lasts only a few hours. Boas sign is referred right subscapular pain of biliary colic.

244
Q

What are some complications of biliary colic? (2)

A

Cholecystitis, choledocholithiasis

245
Q

How is biliary colic diagnosed?

A

RUQ ultrasound

246
Q

How is biliary colic treated?

A

No treatment if the patient is asymptomatic. Elective cholecystectomy if the patient has recurrent bouts of biliary colic

247
Q

What causes the pain in acute cholecystitis and how long does this pain last?

A

Pain in acute cholecystitis is from gallbladder wall inflammation. This pain lasts several days

248
Q

Define acute cholecystitis?

A

Obstruction of the cystic duct (not infection) induces acute inflammation of the gallbladder wall.

249
Q

What are the symptoms (3) and signs (1) of acute cholecystitis?

A

Symptoms:

  1. Symptoms are pain in RUQ or epigastrium. May radiate to the right shoulder/scapula.
  2. Nausea/vomiting
  3. Anorexia

Signs:
Murphy’s sign = inspiratory arrest during deep palpation of the RUQ.

250
Q

What are the findings of acute cholecystitis on RUQ ultrasound?

A

Thickened gallbladder wall, pericholecystic fluid, distended gallbladder, presence of stones

251
Q

When could acute cholecystitis be ruled out? (test). What is seen in a positive HIDA scan?

A

If Hida scan is normal, acute cholecystitis is ruled out. If gallbladder is not visualized, acute cholecystitis is confirmed.

252
Q

What is the treatment for acute cholecystitis?

A

Cholecystectomy

253
Q

What is gallstone ileus and what does it cause?

A

Gallstone enters the bowel lumen and gets stuck causing bowel obstruction (1-2% of cases of bowel obstruction are from gallstone ileus.

254
Q

What is acalculous cholecystitis?

A

Acute cholecystitis without a stone obstructing the cystic duct

255
Q

What causes acalculous cholecystitis and what are the signs and symptoms?

A

Severe illness is the cause. Signs and symptoms are the same as acute cholecystitis

256
Q

How is acalculous cholecystitis treated?

A

Treated with emergent cholecystectomy.

257
Q

What are some life-threatening complications of acute cholecystitis?

A

Gangrene and Gallbladder Perforation

258
Q

What does choledolithiasis refer to?

A

Gallstones in the common bile duct

259
Q

What are the clinical features of choledocholithiasis?

A

Patients may be asymptomatic for years. Symptoms, when present, include RUQ or epigastric pain and jaundice.

260
Q

How sensitive is RUQ US for choledocholithiasis?

A

50% sensitive. Normal RUQ scan does not rule out choledocholithiasis.

261
Q

What are the labs can you expect for choledocholithiasis

A

Total and direct bilirubin is elevated. ALK-P is elevated

262
Q

What is the gold standard for diagnosis and treatment for choledocholithiasis?

A

ERCP

263
Q

How are the presenting symptoms different for choledocholithiasis and acute cholecystitis?

A

Patients with CBD stones may be asymptomatic for years. However, unlike patients with cholelithiasis, in which biliary colic may lead to acute cholecystitis, the onset of choledocholithiasis can signal the development of life-threatening complications like cholangitis and pancreatitis.

264
Q

Do patients with acute cholecystitis have jaundice?

A

No

265
Q

What two disorders affect the cystic duct?

A
  1. Biliary colic

2. Acute cholecystitis

266
Q

What disorders affect the common bile duct?

A
  1. Cholangitis

2. Choledocholithiasis

267
Q

What is cholangitis?

A

Infection of the biliary tract secondary to obstruction which leads to biliary stasis and bacterial overgrowth

268
Q

What is Charcot triad and what disease process does it indicate?

A

RUQ pain
Jaundice
Fever

Indicates cholangitis

269
Q

What is Reynolds Pentad and what disease process does it indicate?

A 
RUQ pain
Jaundice
Fever
Septic Shock
Altered Mental Status
270
Q

What are the lab findings in cholangitis?

A

Leukocytosis
Hyperbilirubinemia
Increased LFTs (mild)

271
Q

How is cholangitis treated?

A

IV antibiotics and IV fluids

Closely monitor hemodynamics, BP and urine output.

Once patient has been afebrile for 48 hours, consider ERCP, PTC (catheter drainage), or laparotomy (T-tube insertion)

272
Q

What is the most deadly complication of cholangitis?

A

Hepatic abscess

273
Q

What is gallbladder cancer associated with?

A

Elderly patients with a history of gallstones or porcelain gallbladder.

274
Q

What is the pathology underlying primary sclerosing cholangitis?

A

Intra and extra hepatic bile ducts thicken and have luminal narrowing.

275
Q

What is the pathology for primary biliary cirrhosis?

A

Intrahepatic bile duct destruction

276
Q

Which is associated with UC, primary biliary cirrhosis or primary sclerosing cholangitis?

A

PSC is associated with UC

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