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Step Up - Diseases Of The GIT Flashcards

1
Q

Virtually, all colorectal tumors arise from?

A

Adenomas - Majority are endoluminal adenocarcinomas arising from the mucosa.

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2
Q

Bleeding and colorectal cancer - What should be noted?

A

Some colorectal CA may bleed intermittently or not at all.

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3
Q

Screening for colorectal cancer - FOBT?

A

Poor sensitivity + Poor specificity.

–> Positive predictive value 20%.

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4
Q

If FOBT comes back positive, what should be done?

A

Colonoscopy, regardless.

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5
Q

What percentage of colorectal tumors are palpable by DRE?

A

10%.

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6
Q

Most sensitive and specific test for colorectal cancer screening?

A

Colonoscopy.

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7
Q

Diagnostic test of choice for patients with a positive FOBT?

A

Colonoscopy

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8
Q

Role of flexible sigmoidoscopy?

A

Can be used to reach the area where approx. 50-70% of polyps and cancers occur (with a 60cm scope).
–> Diagnostic in about 2/3 of all CRCs.

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9
Q

Barium enema as a screening method for CRCs?

A

Evaluates entire colon; complementary to flexible sigmoidoscopy.

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10
Q

Disadvantage of barium enema as a screening method for CRCs?

A

Any abnormal finding needs to be evaluated by colonoscopy.

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11
Q

CEA - What is its significance?

A
  1. NOT for screening.
  2. For recurrences.
  3. Prognostic significance - Patients with PRE-operative CEA >5ng/mL have a worse prognosis.
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12
Q

Clinical staging of CRCs - How is it done?

A

CT scan of chest, abdomen, pelvis, and by physical examination (ascites, hepatomegaly, lymphadenopathy).

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13
Q

Is it possible for a CRC to give metastases to the lung?

A

Yes - Via the lumbar/vertebral veins.

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14
Q

What percentage of CRC patients have distant metastases at presentation?

A

20%.

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15
Q

Incidence of CRC in patients with ulcerative colitis - At 20yrs and at 30yrs?

A

5-10% at 20yrs.

12-20% at 30yrs.

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16
Q

Which sites of the GIT are involved in FAP?

A

Colon always + the DUODENUM in 90% of cases.

Polyps may also form in the stomach, jejunum, and ileum.

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17
Q

Gardner syndrome - Features?

A
  1. Polyps + osteomas
  2. Dental abnormalities
  3. Benign soft tumors
  4. Desmoid tumors
  5. Sebaceous cysts
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18
Q

Gardner syndrome - Risk of CRC?

A

100% by approx. age 40.

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19
Q

Turcot syndrome - Inheritance pattern?

A

AR

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20
Q

Turcot syndrome - Features?

A

Polyps + cerebellar medulloblastoma or GBM.

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21
Q

Peutz-Jeghers - Where do we find the hamartomas?

A

78% - Small bowel.
60% - Colon.
30% - Stomach.

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22
Q

Peutz-Jeghers - Where are the pigmented spots?

A
  1. Lips
  2. Oral mucosa
  3. Face
  4. Genitalia
  5. Palmar surfaces
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23
Q

Peutz-Jeghers - Associations with cancer?

A
  1. Hamartomas have very low malignant potential.

2. Slightly increased incidence in various carcinomas - stomach, ovary, breast, cervix, testicle, lung.

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24
Q

Complications of Peutz-Jeghers?

A

Intussusception or GI bleeding may occur.

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25
Q

Familial juvenile polyposis coli - Features?

A
  1. RARE - Presents in childhood, only small risk of CRC.

2. >10 up to HUNDREDS of juvenile colon polyps.

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26
Q

Hereditary nonpolyposis CRC - without adenomatous polyposis - Lynch syndromes?

A

Lynch syndrome I and II.

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27
Q

Lynch syndrome I - What happens?

A
  1. Early onset CRC.

2. ABSENCE of antecedent multiple polyposis.

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28
Q

Lynch syndrome II - What happens?

A

Cancer family syndrome - All features of Lynch I + incr. number and early occurrence of other cancers - female genital tract, skin, stomach, pancreas, brain, breast, biliary tract.

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29
Q

Presence of symptoms in CRC usually indicates what?

A

Advanced disease.

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30
Q

MC presenting symptom in CRC?

A

Abdominal pain.

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31
Q

MCC of large bowel obstruction in adults?

A

CRC

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32
Q

Right-sided CRC - Common findings?

A
  1. Occult blood in stool.
  2. Iron def. anemia.
  3. Melena.
    - -> Changes in bowel habits is UNCOMMON!
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33
Q

Rectal cancer - What percentage of all CRCs?

A

20-30%.

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34
Q

MC symptoms of rectal cancer?

A

Hematochezia

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35
Q

Prognosis of rectal cancer in relationship to colon cancer?

A

Higher recurrence rate and a lower 5-yr survival than colon cancer.

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36
Q

Only curative treatment for CRC?

A

Surgery

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37
Q

Radiation therapy - Indicated in colon or in rectal cancer?

A

In rectal cancer.

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38
Q

Follow-up after surgery of CRCs:

A

Varies among physicians:

  1. Stool guaiac test
  2. Annual CT scan of abdomen/pelvis + CXR for up to 5yrs.
  3. Colonoscopy at 1yrs and then every 3yrs.
  4. CEA levels checked periodically - every 3-6months.
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39
Q

Very high elevations of CEA suggest?

A

Liver involvement.

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40
Q

After surgery of CRCs, what percentage recurs within 3yrs?

A

90%.

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41
Q

Colonic polyps - Non neoplastic polyps?

A

Benign lesions with no malignant potential.

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42
Q

MC non neoplastic polyp?

A

Hyperplastic (metaplastic) polyp - 90%.

Generally, remain small and asymptomatic.

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43
Q

Non neoplastic polyps in children?

A

Juvenile polyps (typically in children younger than 10yrs).

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44
Q

Main feature of juvenile polyps?

A

Highly vascular and common - should be removed.

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45
Q

Diverticulosis - What usually causes it?

A

Increased intraluminal pressure - Inner layer of colon bulges through focal area of weakness in colon wall –> usually an area of blood vessel penetration!

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46
Q

Risk factors for diverticulosis?

A
  1. Low-fiber diets –> Constipation incr. intraluminal pressure.
  2. Family history.
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47
Q

Clinical features of diverticulosis?

A
  1. Usually asymptomatic and discovered incidentally on barium enema or colonoscopy done for another reason.
  2. Vague LLQ discomfort, bloating, constipation/diarrhea may be present.
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48
Q

What percentage of patients with diverticulosis is symptomatic?

A

Only 10-20%.

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49
Q

Test of choice in diverticulosis?

A

Barium enema.

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50
Q

Abdominal x-rays in diverticulosis?

A

Usually normal, and are NOT diagnostic.

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51
Q

Diverticulosis - Treatment?

A
  1. High-fiber foods (such as bran) to increase stool bulk.

2. Psyllium (if the patient cannot tolerate pain).

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52
Q

Complications of diverticulosis?

A
  1. Painless rectal bleeding

2. Diverticulitis

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53
Q

Complications of diverticulitis?

A
  1. Bowel obstruction
  2. Abscess
  3. Fistulas
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54
Q

Painless rectal bleeding in diverticulosis - Percentage?

A

Up to 40%.

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55
Q

Painless rectal bleeding in diverticulosis - Problem?

A

Usually insignificant and stops spontaneously.

Severe in 5%.

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56
Q

Diverticulitis in diverticulosis - Percentage?

A

15-25%

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57
Q

Free colonic perforation in diverticulitis?

A

UNCOMMON but catastrophic (leads to peritonitis).

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58
Q

Percentage of recurrence in patients with medically-treated diverticulitis within the first 5yrs?

A

About 30%.

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59
Q

Lower GI bleeding - More common in diverticulosis or diverticulitis?

A

Diverticulosis.

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60
Q

Diverticulosis - Test of choice?

A

Barium enema

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61
Q

Diverticulitis - Test of choice?

A

CT scan - Barium enema and colonoscopy contraindicated.

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62
Q

Why are barium enema and colonoscopy contraindicated in acute diverticulitis?

A

Due to risk of perforation.

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63
Q

Treatment for acute diverticulitis?

A
  1. Mild –> IV antibiotics, bowel rest (NPO), IV fluids.
  2. If symptoms persist after 3-4 days –> surgery.
  3. Antibiotics for 7-10days.
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64
Q

After successful treatment of diverticulitis, what is the recurrence percentage?

A

About 30%.

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65
Q

Interesting relationship between aortic stenosis and bleeding AV malformations?

A

25% of patients with AV malformations have aortic stenosis.

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66
Q

Angiodysplasia - Percentage with massive bleeding?

A

15%.

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67
Q

Angiography or colonoscopy for diagnosing angiodysplasia?

A

Colonoscopy

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68
Q

Angiodysplasia - How often does bleeding stops spontaneously?

A

90%.

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69
Q

Acute or chronic Mesenteric ischemia is more common?

A

Acute is much more common.

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70
Q

Patients with acute mesenteric ischemia, often have what?

A

Preexisting heart disease - CHF, CAD.

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71
Q

Types of acute mesenteric ischemia:

A
  1. Arterial embolism (50%)
  2. Arterial thrombosis (25%)
  3. Non occlusive mesenteric ischemia (20%)
  4. Venous thrombosis (<10%)
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72
Q

Acute mesenteric ischemia due to arterial embolism?

A

Almost all emboli are of cardiac origin - A-fib, MI, Valvular disease.

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73
Q

Acute mesenteric ischemia due to arterial thrombosis:

A
  1. Most of these patients have atherosclerotic disease at other sites.
  2. Acute occlusion over preexisting atherosclerotic disease.
  3. Collateral circulation has usually developed.
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74
Q

Acute mesenteric ischemia due to non occlusive mesenteric ischemia:

A
  1. Splanchnic vasoconstriction secondary to low CO.

2. Typically seen in critically ill elderly patients.

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75
Q

Acute mesenteric ischemia due to venous thrombosis - Predisposing factors?

A
  1. Infection
  2. Hypercoagulable states
  3. OCPs
  4. Portal HTN
  5. Malignancy
  6. Pancreatitis
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76
Q

Presentation of acute mesenteric ischemia - Embolic?

A

Sudden and more painful than other causes.

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77
Q

Presentation of acute mesenteric ischemia - Arterial thrombosis?

A

More gradual and less severe than embolic causes.

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78
Q

Presentation of acute mesenteric ischemia - Non occlusive ischemia?

A

Typically in critically ill patients.

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79
Q

Presentation of acute mesenteric ischemia - Venous thrombosis?

A

Symptoms for several days or even weeks, with gradual worsening.

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80
Q

Overall mortality for acute mesenteric ischemia?

A

60-70% - If bowel infarction has occurred, mortality can exceed 90%.

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81
Q

Classic presentation of acute mesenteric ischemia?

A

Acute onset of severe abdominal pain DISPROPORTIONATE to physical findings.
Examination may appear benign even when there is severe ischemia - This can lead to delay in diagnosis.

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82
Q

Signs of intestinal infarction in acute mesenteric ischemia?

A
  1. Hypotension
  2. Tachypnea
  3. Lactic acidosis
  4. Fever
  5. Altered mental status
    Eventually leading to shock.
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83
Q

Which biochemical component needs to be checked if acute mesenteric ischemia is suspected?

A

Lactate level

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84
Q

Acute mesenteric ischemia - Definitive diagnostic test?

A

Mesenteric angiography

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85
Q

Is a plain abdomen film necessary in acute mesenteric ischemia?

A

To exclude other causes of abdominal pain.

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86
Q

Acute mesenteric ischemia - What do we see on barium enema?

A

“Thumbprinting” due to thickened Edematous mucosal folds.

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87
Q

Supportive measures for acute mesenteric ischemia?

A

IV fluids and broad-spectrum antibiotics.

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88
Q

Therapy of choice for all arterial causes of acute mesenteric ischemia?

A

Direct intra-arterial infusion of papaverine (vasodilator) into the superior mesenteric system during arteriography.

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89
Q

Do we give Thrombolytics in patients with acute mesenteric ischemia?

A

May be indicated in some patients with embolic acute mesenteric ischemia.

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90
Q

Treatment of choice for acute mesenteric ischemia due to venous thrombosis?

A

Heparin

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91
Q

Surgery for acute mesenteric ischemia - When?

A

May be needed in ALL types of acute mesenteric ischemia if signs of peritonitis develop.

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92
Q

Chronic mesenteric ischemia - Presentation?

A
  1. Causes by atherosclerotic occlusive disease of main mesenteric vessels.
  2. Abdominal angina.
  3. Significant weight loss.
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93
Q

Chronic mesenteric ischemia - What confirms the diagnosis?

A

Mesenteric angiography

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94
Q

Chronic mesenteric ischemia - Definitive treatment?

A

Surgical Revascularization and leads to pain relief in 90% of cases.

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95
Q

Ogilvie’s syndrome - What happens?

A

Unusual problem in which signs, symptoms, and radiographic findings of large bowel obstruction are present, but there is NO MECHANICAL OBSTRUCTION.

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96
Q

Ogilvie’s syndrome - Commom causes:

A
  1. Recent surgery or trauma.
  2. Serious medical illnesses (sepsis, malignancy)
  3. Medications (narcotics, psychotropic drugs, malignancy)
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97
Q

Ogilvie’s syndrome - Treatment?

A
  1. Stopping any offending agent (narcotics) and supportive measures (IV fluids, electrolyte repletion).
  2. Decompression with gentle enemas or nasogastric suction may be helpful if above fail.
  3. Surgical decompression with cecostomy or colostomy is a last resort.
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98
Q

3 antibiotics frequently associated with Pseudomembranous colitis?

A
  1. Clindamycin
  2. Ampicillin
  3. Cephalosporins
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99
Q

What is the max colonic Distention in which the risk of impending rupture is very high?

A

> 10cm diameter.

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100
Q

Complications of severe pseudomembranous colitis:

A
  1. Toxic megacolon
  2. Colonic perfusion
  3. Anasarca, electrolyte disturbances
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101
Q

Diagnosis of pseudomembranous colitis:

A

Demonstration of C.difficile toxins is diagnostic - results take at least 24h. 95% sensitivity.

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102
Q

What is the importance of abdominal radiograph in pseudomembranous colitis?

A

To rule out toxic Megacolon and perforation.

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103
Q

Drug of choice in pseudomembranous colitis?

A

Metronidazole

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104
Q

Where is metronidazole contraindicated?

A

Infants or pregnant patients.

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105
Q

When do we use oral vanco instead of metronidazole?

A

If the patient is resistant to metro or cannot tolerate it.

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106
Q

Recurrence of pseudomembranous colitis?

A

15-35% within 2-8wks after successful treatment.

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107
Q

Role of abdominal radiograph in pseudomembranous colitis?

A

To rule out toxic megacolon and perforation.

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108
Q

Role of cholestyramine in pseudomembranous colitis treatment?

A

May be used as an adjuvant treatment to improve diarrhea.

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109
Q

Colonic volvulus - Definition?

A

Defined as twisting of a loop of intestine about its mesenteric attachment site.

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110
Q

Colonic volvulus - Complication?

A

May result in obstruction or vascular compromise - potential for necrosis and/or perforation if untreated.

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111
Q

MC site of colonic volvulus?

A

The sigmoid colon - 75% of all cases.

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112
Q

Is cecal volvulus common?

A

25% of cases.

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113
Q

Risk factors for colonic volvulus:

A
  1. Chronic illness
  2. Age
  3. Institutionalization
  4. CNS disease
  5. Chronic constipation - laxative abuse - antimotility drugs
  6. Prior abdominal surgery
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114
Q

Risk for cecal volvulus?

A

Due to congenital lack of fixation of the right colon and tends to occur in younger patients.

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115
Q

Colonic volvulus - Presentation:

A
  1. Acute onset of colicky abdominal pain.
  2. Obstipation, abdominal distention.
  3. Anorexia
  4. Nausea
  5. Vomiting
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116
Q

Diagnosis - Sigmoid volvulus - Plain abdominal film:

A

Omega loop sign (or bent inner-tube shape) indicates a dilated sigmoid colon.

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117
Q

Cecal volvulus - Diagnosis - Plain abdominal film:

A

Coffee bean sign indicates a large air-fluid level in RLQ.

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118
Q

Role of sigmoidoscopy in diagnosing colonic volvulus?

A

Preferred diagnostic and therapeutic test for sigmoid volvulus –> Leads to successful treatment (untwisting and decompression) in many cases.

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119
Q

Barium enema - colonic volvulus?

A

Reveals the narrowing of the colon at the point where it is twisted (“bird’s beak”).

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120
Q

Treatment of sigmoid volvulus:

A

> 70% decompression via sigmoidoscopy.

–> Recurrence is HIGH –> Elective sigmoid colon resection is recommended.

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121
Q

Treatment of cecal volvulus?

A

Emergent surgery is indicated.

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122
Q

Gold standard for diagnosing cirrhosis:

A

Liver biopsy.

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123
Q

Cirrhosis - Distortion of liver anatomy causes 2 major events:

A

A. Decreased blood flow through the liver.

B. Impairment of biochemical functions.

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124
Q

How do we assess hepatic functional reserve?

A

Child’s classification –> Measure disease severity and is a predictor of morbidity and mortality.

125
Q

MCC of cirrhosis:

A

Alcoholic liver disease –> Range of conditions from fatty liver (reversible, due to acute ingestion) to cirrhosis (reversible).

126
Q

Percentage of heavy drinkers that develop alcoholic cirrhosis:

127
Q

2nd MCC of cirrhosis:

A

Chronic hep C/B.

128
Q

Cause of cirrhosis after bone marrow transplantation:

A

Hepatic veno-occlusive disease.

129
Q

Components of Child’s classification:

A
  1. Ascites
  2. Bilirubin
  3. Encephalopathy
  4. Nutritional status
  5. Albumin
130
Q

Child A:

A

Ascites: None
Bilirubin: 3.5

131
Q

Child B:

A 
Ascites: Controlled
Bilirubin: 2.0-2.5
Encephalopathy: Minimal
Nutritional status: Good
Albumin: 3.0-3.5
132
Q

Child C:

A 
Ascites: Uncontrolled
Bilirubin: >3.0
Encephalopathy: Severe
Nutritional status: Poor
Albumin: <3.0
133
Q

What may be used to lower portal HTN?

A

TIPS - Transjugular intrahepatic portal-systemic shunt.

134
Q

What happens when a patient develops complications of cirrhosis?

A

They have “decompensated” disease, with high morbidity and high mortality.

135
Q

Treatment of bleeding esophageal varices - Options:

A
  1. Variceal ligation/banding
  2. Endoscopic sclerotherapy
  3. IV vasopressin
  4. IV octreotide infusion
  5. Other options
136
Q

Treatment of varices - Variceal ligation/banding:

A
  1. Initial endoscopic TREATMENT OF CHOICE.
  2. Effective control of active bleeding.
  3. Lower rate of rebleeding than sclerotherapy.
137
Q

Treatment of varices - Sclerotherapy:

A
  1. Sclerosing substance is injected into varices during endoscopy.
  2. This controls acute bleeding in 80-90% of cases.
  3. UP TO 50% of patients may have re-bleeding.
138
Q

MC complication of cirrhosis:

139
Q

Abdominal US can detect as little as how much of ascitic fluid?

140
Q

Indications for paracentesis in ascites:

A
  1. New-onset ascites
  2. Worsening ascites
  3. Suspected spontaneous bacterial peritonitis
141
Q

In most cases, how can we manage ascites?

A

By salt restriction and diuretics in most cases.

142
Q

Treatment of ascites:

A
  1. Bed rest, a low-sodium diet, and diuretics (furosemide + spironolactone).
  2. Perform therapeutic paracentesis if tense ascites, SOB, or early satiety is present.
  3. Peritoneovenous shunt or TIPS to reduce portal HTN.
143
Q

DDx of ascites:

A
  1. Cirrhosis, portal HTN.
  2. CHF.
  3. Chronic renal disease
  4. Massive fluid overload.
  5. Tuberculous peritonitis.
  6. Malignancy
  7. Hypoalbuminemia
  8. Peripheral vasodilation secondary to endotoxin-induced release of NO, which leads to increased renin secretion (and thus secondary hyperaldosteronism).
  9. Impaired liver inactivation of aldosterone.
144
Q

Monitoring patients with cirrhosis:

A
  1. Order periodic lab values every 3-4months - CBC, renal function tests, electrolytes, LFTs, and coagulation tests.
  2. Perform an endoscopy to determine the presence of esophageal varices.
  3. If HCC is suspected, perform a CT-guided biopsy for diagnosis.
145
Q

Precipitants of hepatic encephalopathy:

A
  1. Alkalosis
  2. Hypokalemia (due to diuretics)
  3. Sedating drugs (narcotics, sleeping medications)
  4. GI bleeding
  5. Systemic infections
  6. Hypovolemia
146
Q

Treatment of hepatic encephalopathy:

A
  1. Lactulose prevents absorption of ammonia.
  2. Neomycin - kills bowel flora, so decreases ammonia production by intestinal bacteria.
  3. Diet: Limit protein to 30-40 g/day.
147
Q

What may precipitate hepatorenal syndrome often?

A

Infections and diuretics.

148
Q

Clinical features of hepatorenal syndrome:

A
  1. Azotemia
  2. Oliguria
  3. Hyponatremia
  4. Hypotension
  5. Low urine sodium (<10mEq/L)
149
Q

Treatment of hepatorenal syndrome:

A

Liver transplantation is the only cure. In general, the prognosis is very poor, and the condition is usually fatal without liver transplantation.

150
Q

Complications of liver failure - AC, 9H:

A
  1. Ascites
  2. Coagulopathy
  3. Hypoalbuminemia
  4. portal Hypertension
  5. Hyperammonemia
  6. Hepatic encephalopathy
  7. Hepatorenal syndrome
  8. Hypoglycemia
  9. Hyperbilirubinemia/jaundice
  10. Hyperestrinism
  11. HCC
151
Q

SBP - Up to what percentage of patients hospitalized for ascites?

A

Up to 20%.

152
Q

SBP - Mortality?

153
Q

SBP - What to look for?

A

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

154
Q

SBP - Does it recur?

A

Up to 70% in first year.

155
Q

SBP - Etiologic agents:

A
  1. E.coli (MC)
  2. Klebsiella
  3. S.pneumoniae
156
Q

Diagnosis of SBP:

A

Established by paracentesis and examination of ascitic fluid for WBCs (especially PMNs). Gram stain with culture, and sensitivities.

  • -> WBC>500, PMN>250.
  • -> Positive ascites culture; culture-negative SBP is common as well.
157
Q

SBP - Treatment:

A
  1. Broad-spectrum antibiotic therapy.
  2. Give specific antibiotic once organism is identified.
  3. Clinical improvement should be seen in 24-48hrs.
  4. Repeat paracentesis in 2-3 days to document a decrease in ascitic fluid PMN (<250).
158
Q

Signs of ACUTE liver failure:

A

ANY of the following may be present:

  1. Coagulopathy
  2. Jaundice
  3. Hypoglycemia (liver stores glycogen)
  4. Hepatic encephalopathy
  5. Infection
  6. Elevated LFT values
  7. Any complication associated with cirrhosis
159
Q

Treatment of coagulopathy in acute liver failure:

A

Fresh frozen plasma

160
Q

HCC - Percentage in patients with cirrhosis:

161
Q

How long does the patient have to withdraw alcohol in order to be eligible for a liver transplantation?

A

More than 6 months.

162
Q

Wilson inheritance pattern?

163
Q

Wilson - Age of presentation?

164
Q

Wilson - Renal involvement?

A
  1. Aminoaciduria

2. Nephrocalcinosis

165
Q

Wilson - Diagnosis?

A

By determining the following:

  1. Hepatic disease.
  2. Decr. ceruloplasmin levels –> Range within normal DO NOT exclude diagnosis.
  3. Liver biopsy - significantly elevated Cu concentration.
166
Q

Wilson - What if diagnosed regarding the family?

A

Must also be screened as well.

167
Q

Wilson - Treament:

A
  1. D-penicillamine
  2. Zinc –> Prevents uptake of dietary Cu.
  3. Liver transplantation (if unresponsive to therapy or fulminant liver failure).
168
Q

Hemochromatosis - Inheritance pattern:

169
Q

Hemochromatosis - Diagnosis:

A
  1. Markedly elevated serum iron and serum ferritin.
  2. Elevated iron sat (transferrin saturation).
  3. Decr. TIBC.
  4. Liver biopsy - determines hepatic iron concentration - REQUIRED for diagnosis.
  5. Genetic testing for chromosomal abnormalities.
170
Q

Hemochromatosis - Treatment:

A
  1. Perform repeated phlebotomies –> Treatment of choice –> Improves survival dramatically if initiated early in the course of the disease.
  2. Treat any complications - CHF, DM, hypothyroidism, arthritis.
  3. Consider liver transplantation in advanced cases.
171
Q

Hepatocellular adenoma - Which patients?

A

Often seen in young women 15-40yrs.

172
Q

Hepatocellular adenoma - Risk factors:

A
  1. OCPs
  2. Female sex
  3. Anabolic steroid use
173
Q

Hepatocellular adenoma - Complications:

A
  1. Hemoperitoneum
174
Q

Hepatocellular adenoma - Diagnosis:

A
  1. CT scan
  2. US
  3. Hepatic arteriography (most accurate but invasive).
175
Q

Hepatocellular adenoma - Treatment:

A
  1. Discontinue OCPs.

2. Surgically resect tumors >5cm that do not regress after stopping OCPs - otherwise there is a risk of rupture.

176
Q

MC benign tumor of the liver?

A

Cavernous hemangioma

177
Q

Cavernous hemangioma - Complications:

A
  1. Rupture with hemorrhage
  2. Obstructive jaundice
  3. Coagulopathy
  4. CHF secondary to a large AV shunt
  5. Gastric outlet obstruction.
178
Q

Cavernous hemangiomas - Diagnosis:

A
  1. US
  2. CT scan
  3. IV contrast
  4. Biopsy is CONTRAINDICATED because of risk of rupture and hemorrhage.
179
Q

Cavernous hemangiomas - Treatment:

A
  1. Most cases do not require treatment.

2. Consider resection if the patient is symptomatic or if there is a high risk of rupture (as with large tumors).

180
Q

Focal nodular hyperplasia - Occurs in?

A

Women of reproductive age.

181
Q

Focal nodular hyperplasia - Association with OCPs?

A

NO ASSOCIATION.

182
Q

Focal nodular hyperplasia - Symptoms?

A

Usually asymptomatic - Hepatomegaly may be present - Treatment NOT NECESSARY IN MOST CASES.

183
Q

HCC - Pathologic subtypes:

A
  1. Non fibrolamellar (most common).

2. Fibrolamellar

184
Q

Non fibrolamellar HCC - Features:

A
  1. Hep B and C
  2. Cirrhosis
  3. Usually unresectable with very short survival time (months)
185
Q

Fibrolamellar HCC - Features:

A
  1. Usually NOT associated with hep B and C or cirrhosis.
  2. More often resectable; relatively longer survival time.
  3. Seen most commonly in adolescents and young adults.
186
Q

Prognosis of HCC:

A

If unresectable: less than 1yr.

If resectable: 25% of patients are alive at 5yrs.

187
Q

Diagnosis of HCC - Liver biopsy:

A

REQUIRED for definitive diagnosis.

188
Q

Diagnosis of HCC - Lab tests:

A
  1. Hep B and C serology.
  2. LFTs
  3. Coagulation tests
189
Q

Diagnosis of HCC - Imaging studies:

A
  1. US
  2. CT scan (chest, abdomen, pelvis)
  3. MRI or MRA if surgery is an option –> provide more detail about the anatomy of the tumor.
190
Q

Diagnosis of HCC - AFP:

A

Tumor marker elevation (AFP) is useful as a screening tool.
Elevated in 40-70% of patients with HCC.
ALSO helpful in monitoring response to therapy.

191
Q

HCC - Treatment:

A
  1. Liver resection - in the 10% of patients who have resectable tumors.
  2. Liver transplantation if diagnosis is made early.
192
Q

NASH - What happens:

A

Histology of the liver is identical to that in patients with alcoholic liver disease, BUT these patients do not have a history of alcohol use!

193
Q

NASH - Associated with:

A
  1. Obesity
  2. Hyperlipidemia
  3. DM
    - -> Some patients have none of these.
194
Q

NASH - Course:

A

Usually asymptomatic - Benign course –> Cirrhosis develops in 10%-15%.

195
Q

NASH - How is it found?

A

Typically discovered on routine lab tests - mild elevation of AST ALT.

196
Q

NASH - Treatment:

A

Not clearly established.

197
Q

Gilbert’s syndrome - Inheritance pattern:

198
Q

Hemobilia - What happens?

A

Refers to blood draining into the duodenum via the common bile duct - Source of bleeding can be anywhere along the biliary tract, the liver, or the ampullary region.

199
Q

Hemobilia - Etiology:

A
  1. MCC trauma
  2. Papillary thyroid carcinoma
  3. Surgery (eg cholecystectomy, CBD exploration).
  4. Tumors
  5. Infections
200
Q

Hemobilia - Clinical features:

A
  1. GI bleeding - melena/hematemesis.
  2. Jaundice
  3. RUQ pain
201
Q

Hemobilia - Diagnosis:

A

Arteriogram is diagnostic.

Upper GI endoscopy shows blood coming out of ampulla of Vater.

202
Q

Hemobilia - Treatment:

A

Resuscitation (may require transfusion). If bleeding is severe, surgery is necessary:
–> Options include ligation of hepatic arteries or arteriogram with embolization of vessel.

203
Q

Hydatid liver cysts - Caused by:

A
  1. Echinococcus granulosus
  2. Echinococcus multilocularis
    Cysts more commonly occur in the right lobe of the liver.
204
Q

Hydatid liver cysts - Complications:

A
  1. Small cysts are asymptomatic.

2. Larger cysts may cause RUQ pain and rupture into the peritoneal cavity –> fatal anaphylactic shock.

205
Q

Hydatid liver cysts - Treatment:

A
  1. Surgical resection –> caution to avoid spilling contents of the cyst into the peritoneal cavity.
  2. Mebendazole is given after surgery.
206
Q

MC location for a liver (BOTH pyogenic and amebic) abscess:

A

Right lobe.

207
Q

2 types of liver abscess:

A
  1. Pyogenic

2. Amebic

208
Q

Pyogenic liver abscess - MCC?

A

Biliary tract obstruction.

209
Q

Pyogenic liver abscess - Causative organisms:

A
  1. E.coli
  2. Klebsiella
  3. Proteus
  4. Enterococcus
  5. Anaerobes
210
Q

Pyogenic liver abscess - Clinical features:

A
  1. Fever
  2. Malaise
  3. Anorexia
  4. Weight loss
  5. Nausea
  6. Vomiting
  7. RUQ pain
  8. Jaundice
  9. Patients may appear quite ill
211
Q

Pyogenic liver abscess - Diagnosis:

A
  1. US
  2. CT scan
  3. Elevates LFTs
212
Q

Pyogenic liver abscess - Prognosis:

A

Fatal if untreated.
Treatment - IV antibiotics and percutaneous drainage of abscess.
–> Reduces mortality to about 5-20%.
Surgical drainage is sometimes necessary.

213
Q

Amebic liver abscess - Common in men or women?

A

Men - 9:1 - Particularly homosexual men. Transmitted through fecal-oral contact.

214
Q

Amebic liver abscess - Diagnosis:

A

Serologic testing (IgG enzyme immunoassay) establishes diagnosis.

215
Q

Amebic liver abscess - Treatment:

A

IV metronidazole is effective treatment in most cases.
Therapeutic aspiration of the abscess (image-guided percutaneous aspiration) may be necessary if the abscess is large (high risk of rupture), or if there is no response to medical therapy.

216
Q

Budd-Chiari syndrome - Etiology:

A
  1. Hypercoagulable states
  2. Myeloproliferative disorders (polycythemia vera)
  3. Pregnancy
  4. Chronic inflammatory diseases
  5. Infection
  6. Various cancers
  7. Trauma
  8. IDIOPATHIC 40% OF CASES.
217
Q

Budd-Chiari - Diagnosis:

A

Hepatic venography - Serum ascites albumin gradient >1.1g/dL.

218
Q

Budd-Chiari - Treatment:

A
  1. Medical therapy is unsatisfactory - anticoagulation, thrombolytics, diuretics.
  2. Surgery is eventually necessary in most cases - Balloon angioplasty with stent placement in IVC, portocaval shunts.
  3. Liver transplantation if cirrhosis is present.
219
Q

3 Major causes of jaundice:

A
  1. Hemolysis
  2. Liver disease
  3. Biliary obstruction
220
Q

Jaundice with dark urine?

A

Only seen with high CONJUGATED bilirubin.

221
Q

Dark urine and pale stools sign a diagnosis of conjugated or unconjugated hyperbilirubinemia?

A

CONJUGATED

222
Q

Bilirubin metabolism - From where does bilirubin come?

A

80% from Hb (RBC breakdown). The rest comes from myoglobin breakdown and liver enzymes.

223
Q

Clinical features of cholestasis:

A
  1. Jaundice, gray stools, dark urine.
  2. Pruritus
  3. Elevated ALP
  4. Elevated serum CHOLESTEROL (impaired excretion)
  5. Skin xanthomas (local accumulation of cholesterol)
  6. MALABSORPTION OF FATS AND FAT-SOLUBLE VITAMINS
224
Q

If there is no hemolysis, isolated hyperbilirubinemia (unconjugated) may indicate?

A

Gilbert syndrome

225
Q

What do severely elevated (>10.000) ALT, AST indicate?

A

Extensive hepatic necrosis has occured.

  1. Ischemia, shock liver - prolonged hypotension or circulatory collapse.
  2. Acetaminophen toxicity.
  3. Severe viral hepatitis.
226
Q

Elevated AST, ALT in asymptomatic patients?

A
  1. Autoimmune hep
  2. Hep B
  3. Hep C
  4. Drugs or toxins
  5. Ethanol
  6. Fatty liver (hypertriglyceridemia)
  7. Growth (tumors)
  8. Hemodynamic disorders (CHF).
  9. Iron (hemochromatosis), copper (Wilson), or AAT def.
227
Q

ALP - Besides liver, also found in?

A
  1. Bone
  2. Gut
  3. Placenta
228
Q

ALP is very high (10-fold) - What should we think?

A

Think of extrahepatic biliary tract obstruction OR intrahepatic cholestasis (eg PBC or drug-induced cirrhosis).

229
Q

What should be done if ALP is elevated?

A

Measure GGT to make sure the elevation is HEPATIC IN ORIGIN (rather than bone or intestinal).

230
Q

ALP is elevated, but GGT is normal?

A

Consider bone disease or pregnancy.

231
Q

Decr. albumin - what do we think?

A
  1. Chronic liver disease
  2. Nephrotic syndrome
  3. Malnutrition
  4. Inflammatory states
232
Q

PT is prolonged - What does it tell us about liver?

A

ADVANCED liver disease.

233
Q

Cholesterol stones (yellow to green) - associated with?

A
  1. Obesity
  2. Diabetes
  3. Hyperlipidemia
  4. Multiple pregnancies
  5. OCPs
  6. Crohn’s, ileac resection
  7. Advanced age
  8. Native American ancestry
  9. Cirrhosis
  10. CF
234
Q

Pigment stones - Associations?

A
  1. Black stones usually found in the gallbladder and are associated with either hemolysis (eg sickle cell disease, thalassemia, hereditary spherocytosis, artificial cardiac valves).
  2. Alcoholic cirrhosis.
235
Q

Majority of gallstones are of which type?

A

Mixed ones.

236
Q

Biliary colic - timing?

A

Pain after eating and at night.

237
Q

What is the Boa’s sign?

A

Referred right subscapular pain of biliary colic.

238
Q

Percentage of patients with biliary colic that develop acute cholecystitis within 2 years?

239
Q

Diagnosis of cholelithiasis?

A

RUQ US - sensitivity + specificity >95% for stones >2mm.

CT/MRI are alternatives

240
Q

Signs of biliary tract obstruction:

A
  1. Elevated ALP, GGT.
  2. Elevated conjugated bilirubin.
  3. Jaundice
  4. Pruritus
  5. Clay-colored stools
  6. Dark urine
241
Q

Acute cholecystitis is due to what?

A

Obstruction of the cystic duct - Not infection.

242
Q

Percentage of patients with gallstones that develop acute cholecystitis?

243
Q

Signs of acute cholecystitis:

A
  1. RUQ tenderness, rebound tenderness in RUQ.
  2. Murphy sign is PATHOGNOMONIC - Not present in many cases.
  3. Hypoactive bowel sounds
  4. Low-grade fever.
  5. Leukocytosis.
244
Q

Acute cholecystitis diagnosis - Test of choice?

245
Q

CT role in acute cholecystitis:

A

It is as accurate as US but is more sensitive in identifying complications of acute cholecystitis (eg perforation, abscess, pancreatitis).

246
Q

Diagnosis of acute cholecystitis - Radionuclide scan role:

A

Hepatoiminodiacetic acid (HIDA).
Used when US is inconclusive. Its sensitivity and specificity parallel that of US.
If HIDA is normal, acute cholecystitis can be ruled out.

247
Q

Positive HIDA means?

A

The gallbladder is NOT visualized - If so for 4hr after injection, diagnosis of acute cholecystitis is confirmed.

248
Q

Complications of acute cholecystitis:

A
  1. Gangrenous cholecystitis.
  2. Perforation of gallbladder.
  3. Emphysematous cholecystitis.
  4. Cholecystoenteric fistula with gallstone ileus.
  5. Empyema of gallbladder.
249
Q

Gallstone ileus:

A

Gallstone enters bowel lumen via cholecystoenteric fistula - gets “stuck” in terminal ileum and causes obstruction.
- Accounts for 1-2% of bowel obstruction.

250
Q

Treatment of acute cholecystitis - What to do first?

A
  1. Admit the patient.
  2. Hydration with IV fluids
  3. Bowel rest (NPO)
  4. IV antibiotics
  5. Analgesics
  6. Correction of electrolyte abnormalities
251
Q

Acute cholecystitis surgery?

A

Early surgery is preferred (24-48h). Recurrence rate with non surgical treatment is as high as 70%.

252
Q

Acalculous cholecystitis - Percentage of patients with acute cholecystitis?

A

10% usually idiopathic and seen in patients with severe underlying disease.

253
Q

Signs and symptoms of acalculous cholecystitis:

A

Same as for acute calculous cholecystitis.

254
Q

Choledocholithiasis - Primary vs secondary stones:

A
  1. Primary originate in the CBD - usually pigmented stones.
  2. Secondary originate in the gallbladder and then pass into the CBD (usually cholesterol or mixed stones). These account for 95% of all cases.
255
Q

Choledocholithiasis - clinical features:

A
  1. Asymptomatic for years.

2. Symptoms when present, include RUQ or epigastric pain and jaundice.

256
Q

Complications of CBD stones:

A
  1. Cholangitis
  2. Obstructive jaundice
  3. Acute pancreatitis
  4. Biliary colic
  5. Biliary cirrhosis
257
Q

Choledocholithiasis - Diagnosis - Lab tests

A

Total and direct bilirubin levels are elevated, as well as ALP.

258
Q

Choledocholithiasis - Initial study for diagnosis:

A

RUQ US, but is not a sensitive study for choledocholithiasis.
Detects only in 50%, so it cannot be used to rule out diagnosis.

259
Q

Choledocholithiasis - Diagnosis - Gold standard:

A

ECPR (perhaps MRCP). Sensitivity + specificity of 95% and should followe US.
Diagnostic + Therapeutic.

260
Q

Choledocholithiasis - May be asymptomatic for years but the onset of symptoms may indicate what?

A

Development of life-threatening complications such as cholangitis and acute pancreatitis.

261
Q

Cholangitis - etiology:

A
  1. 60% of cases is due to choledocholithiasis.
  2. Pancreatic and biliary neoplasms.
  3. Post-op strictures
  4. Invasive procedures such as ERCP or PTC
  5. Choledochal cysts.
262
Q

Do the following in patients with cholangitis:

A
  1. Blood cultures.
  2. IV fluids.
  3. IV antibiotics AFTER blood cultures obtained.
  4. Decompress CBD when patient stable.
263
Q

Cholangitis - Clinical features - Charcot triad:

A
  1. RUQ pain.
  2. Jaundice.
  3. Fever.
    Present in only 50-70%.
264
Q

Cholangitis - Reynolds pentad:

A

Charcot triad + septic shock + altered mental status.

Rapidly fatal.

265
Q

Cholangitis - Initial study:

266
Q

Cholangitis - Lab:

A
  1. Hyperbilirubinemia
  2. Leukocytosis
  3. Mild elevation in serum transaminases
267
Q

Cholangitis - Treatment:

A
  1. IV antibiotics + fluids –> Most patients respond rapidly.
  2. Decompress CBD via PTC (catheter drainage)
  3. ERCP sphincterectomy
  4. Laparotomy (T-tube section) once the patient is stabilized, or emergently if the condition does not respond to antibiotics.
268
Q

What is the most serious and dreaded complication of acute cholangitis?

A

Hepatic abscess - High mortality rate.

269
Q

Risk factors for carcinoma of the gallbladder:

A
  1. Gallstones
  2. Cholecystoenteric fistula
  3. Porcelain gallbladder
270
Q

Carcinoma of the gallbladder - Clinical features:

A
  1. Non specific - suggest extrahepatic bile duct obstruction.
  2. Palpable gallbladder is a sign of advanced disease.
271
Q

Why to do a prophylactic cholecystectomy in a patient with porcelain gallbladder?

A

Approx. 50% of patients with porcelain gallbladder will develop carcinoma of the gallbladder.

272
Q

UC is present in what percentage of patients with PSC?

A

50-70%. Course of PSC is unaffected by a colectomy done for UC.

273
Q

PSC - Diagnosis:

A

ERCP and PTC are diagnostic studies of choice.

Lab tests show cholestatic LFTs.

274
Q

PSC - Complications:

A
  1. Cholangiocarcinoma (in up to 20-30% of patients).
  2. Recurrent bouts of cholangitis (15%).
  3. Can progress to secondary biliary cirrhosis, portal HTN, and liver failure.
275
Q

PSC - Treatment:

A
  1. Only liver transplantation is curative.
  2. ERCP for stent placement - may relieve symptoms.
  3. Cholestyramine for pruritus.
276
Q

Secondary biliary cirrhosis - Etiology:

A
  1. Long-standing mechanical obstruction.
  2. Sclerosing cholangitis
  3. CF
  4. Biliary atresia
277
Q

PBC - Lab findings:

A
  1. Hallmark is anti-mt abs (98% specificity).
  2. Perform a liver biopsy to confirm diagnosis.
  3. Cholestatic LFTs.
  4. Elevated cholesterol, HDL
  5. Elevated IgM
278
Q

PBC - Treatment:

A
  1. Symptomatic for pruritus (cholestyramine) and osteoporosis (calcium, biphosphonates, vitD).
  2. Ursodeoxycholic acid (hydrophilic bile acid) has been shown to slow progression of the disease.
  3. Liver transplantation is the only curative treatment available.
279
Q

Cholangiocarcinoma - Locations:

A
  1. Proximal 3rd of CBD - most common, called Klatskin’s tumor.
  2. Distal extrahepatic - best chance for resectability.
  3. Intrahepatic - least common.
280
Q

Klatskin’ tumors:

A
  1. Involve junction of the right + left hepatic ducts.

2. Very poor prognosis because they are unresectable.

281
Q

Cholangiocarcinoma - Risk factors:

A
  1. PSC is the major risk factor in the US.

2. Other include –> UC, choledochal cysts, Clonorchis sinensis infection (Hong Kong).

282
Q

Choledochal cysts - More common in women or men?

A

Women 4:1.

283
Q

Choledochal cysts - Clinical features:

A
  1. Epigastric pain
  2. Jaundice
  3. Fever
  4. RUQ mass
284
Q

Choledochal cysts - Complications:

A
  1. Cholangiocarcinoma - most feared - risk is about 20% over 20yrs.
  2. Hepatic abscess
  3. Recurrent cholangitis/pancreatitis.
  4. Rupture
  5. Biliary obstruction
  6. Cirrhosis
  7. Portal HTN
285
Q

Choledochal cysts - Best non invasive test?

286
Q

Choledochal cysts - Definitive test for diagnosis:

287
Q

Choledochal cysts - Treatment:

A

Surgery - Complete resection of the cyst with a biliary-enteric anastomosis to restore continuity of biliary system with bowels.

288
Q

Bile duct stricture - Etiology:

A
  1. MCC is iatrogenic injury (prior biliary surgery such as cholecystectomy, liver transplantation).
  2. Recurring choledocholithiasis
  3. Chronic pancreatitis
  4. PSC
289
Q

Bile duct stricture - Clinical features:

A

Those of obstructive jaundice.

290
Q

Bile duct strictures - Complications:

A
  1. Secondary biliary cirrhosis.
  2. Liver abscess
  3. Ascending cholangitis
291
Q

Biliary dyskinesia - What happens?

A

Motor dysfunction of the sphincter of Oddi, which leads to recurrent episodes of biliary colic without any evidence of gallstones on diagnostic studies such as US, CT scan, and ERCP.

292
Q

Biliary dyskinesia - How do we make the diagnosis?

A

By HIDA scan.
Once the gallbladder is filled with labeled radionuclide, give CCK IV, then determine the ejection fraction of the gallbladder.
If low –> Dyskinesia is likely.

293
Q

Biliary dyskinesia - Treatment options:

A
  1. Laparoscopic cholecystectomy

2. Endoscopic sphincterotomy

294
Q

Acute appendicitis - Pathogenesis:

A

60% –> Lumen of the appendix is obstructed by HYPERPLASIA of lymphoid tissue.
35% –> A fecalith.
Other –> Foreign body, or other rare causes (parasite or carcinoid tumor 5% of cases).

295
Q

Perforation of the appendix - Features:

A
  1. 20% of cases.

2. Risk factors –> Delay in treatment (>24h) and extremes of ages.

296
Q

Signs of appendiceal rupture:

A
  1. High fever
  2. Tachycardia
  3. Marked leukocytosis
  4. Peritoneal signs
  5. Toxic appearance
297
Q

Psoas sign in acute appendicitis:

A

RLQ pain when right thigh is extended as patient lies on left side.

298
Q

Obturator sign in acute appendicitis:

A

Pain in RLQ when flexed right thigh is internally rotated when patient is supine.

299
Q

Acute appendicitis - Diagnosis:

A

Clinical. Lab is supportive.
CT sensitive 98-100%.
US sensitive 90%.

300
Q

Percentage of patients with carcinoid tumor that develop carcinoid syndrome?

301
Q

Features of carcinoid syndrome:

A
  1. Cutaneous flushing
  2. Diarrhea
  3. Sweating
  4. Wheezing
  5. Abdominal pain
  6. Heart valve dysfunction
302
Q

Forms of acute pancreatitis:

A
  1. Mild - responds to treatment.

2. Severe - Necrotizing with significant morbidity and mortality.

303
Q

Post-ERCP pancreatitis - How often?

A

10% of ECRP.

304
Q

Drugs causing acute pancreatitis:

A
  1. Sulfonamides
  2. Thiazide diuretics
  3. Furosemide
  4. Estrogens
  5. HIV medication
    + others.
305
Q

Recurrences are common in which type of acute pancreatitis?

A

Alcoholic pancreatitis.

306
Q

Hemorrhagic pancreatitis - 3 signs:

A
  1. Grey-Turner’s sign (flank ecchymoses).
  2. Cullen’s sign (periumbilical ecchymoses).
  3. Fox’s sign (ecchymosis of INGUINAL ligament).
307
Q

Acute pancreatitis - Diagnosis:

A
  1. Clinical
  2. Lab is supportive
  3. CT is confirmatory
308
Q

Serum amylase use in acute pancreatitis diagnosis:

A

If levels are more than 5x the UPPER LIMIT of normal, there is a high specificity for acute pancreatitis.

309
Q

3rd MC cancer in the US?

A

Colorectal

Internal Medicine (106 decks)

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