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.
2
Q
Bleeding and colorectal cancer - What should be noted?
A
Some colorectal CA may bleed intermittently or not at all.
3
Q
Screening for colorectal cancer - FOBT?
A
Poor sensitivity + Poor specificity.
–> Positive predictive value 20%.
4
Q
If FOBT comes back positive, what should be done?
A
Colonoscopy, regardless.
5
Q
What percentage of colorectal tumors are palpable by DRE?
A
10%.
6
Q
Most sensitive and specific test for colorectal cancer screening?
A
Colonoscopy.
7
Q
Diagnostic test of choice for patients with a positive FOBT?
A
Colonoscopy
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.
9
Q
Barium enema as a screening method for CRCs?
A
Evaluates entire colon; complementary to flexible sigmoidoscopy.
10
Q
Disadvantage of barium enema as a screening method for CRCs?
A
Any abnormal finding needs to be evaluated by colonoscopy.
11
Q
CEA - What is its significance?
A
- NOT for screening.
- For recurrences.
- Prognostic significance - Patients with PRE-operative CEA >5ng/mL have a worse prognosis.
12
Q
Clinical staging of CRCs - How is it done?
A
CT scan of chest, abdomen, pelvis, and by physical examination (ascites, hepatomegaly, lymphadenopathy).
13
Q
Is it possible for a CRC to give metastases to the lung?
A
Yes - Via the lumbar/vertebral veins.
14
Q
What percentage of CRC patients have distant metastases at presentation?
A
20%.
15
Q
Incidence of CRC in patients with ulcerative colitis - At 20yrs and at 30yrs?
A
5-10% at 20yrs.
12-20% at 30yrs.
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.
17
Q
Gardner syndrome - Features?
A
- Polyps + osteomas
- Dental abnormalities
- Benign soft tumors
- Desmoid tumors
- Sebaceous cysts
18
Q
Gardner syndrome - Risk of CRC?
A
100% by approx. age 40.
19
Q
Turcot syndrome - Inheritance pattern?
A
AR
20
Q
Turcot syndrome - Features?
A
Polyps + cerebellar medulloblastoma or GBM.
21
Q
Peutz-Jeghers - Where do we find the hamartomas?
A
78% - Small bowel.
60% - Colon.
30% - Stomach.
22
Q
Peutz-Jeghers - Where are the pigmented spots?
A
- Lips
- Oral mucosa
- Face
- Genitalia
- Palmar surfaces
23
Q
Peutz-Jeghers - Associations with cancer?
A
- Hamartomas have very low malignant potential.
2. Slightly increased incidence in various carcinomas - stomach, ovary, breast, cervix, testicle, lung.
24
Q
Complications of Peutz-Jeghers?
A
Intussusception or GI bleeding may occur.
25
Familial juvenile polyposis coli - Features?
1. RARE - Presents in childhood, only small risk of CRC.
| 2. >10 up to HUNDREDS of juvenile colon polyps.
26
Hereditary nonpolyposis CRC - without adenomatous polyposis - Lynch syndromes?
Lynch syndrome I and II.
27
Lynch syndrome I - What happens?
1. Early onset CRC.
| 2. ABSENCE of antecedent multiple polyposis.
28
Lynch syndrome II - What happens?
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.
29
Presence of symptoms in CRC usually indicates what?
Advanced disease.
30
MC presenting symptom in CRC?
Abdominal pain.
31
MCC of large bowel obstruction in adults?
CRC
32
Right-sided CRC - Common findings?
1. Occult blood in stool.
2. Iron def. anemia.
3. Melena.
- -> Changes in bowel habits is UNCOMMON!
33
Rectal cancer - What percentage of all CRCs?
20-30%.
34
MC symptoms of rectal cancer?
Hematochezia
35
Prognosis of rectal cancer in relationship to colon cancer?
Higher recurrence rate and a lower 5-yr survival than colon cancer.
36
Only curative treatment for CRC?
Surgery
37
Radiation therapy - Indicated in colon or in rectal cancer?
In rectal cancer.
38
Follow-up after surgery of CRCs:
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.
39
Very high elevations of CEA suggest?
Liver involvement.
40
After surgery of CRCs, what percentage recurs within 3yrs?
90%.
41
Colonic polyps - Non neoplastic polyps?
Benign lesions with no malignant potential.
42
MC non neoplastic polyp?
Hyperplastic (metaplastic) polyp - 90%.
| Generally, remain small and asymptomatic.
43
Non neoplastic polyps in children?
Juvenile polyps (typically in children younger than 10yrs).
44
Main feature of juvenile polyps?
Highly vascular and common - should be removed.
45
Diverticulosis - What usually causes it?
Increased intraluminal pressure - Inner layer of colon bulges through focal area of weakness in colon wall --> usually an area of blood vessel penetration!
46
Risk factors for diverticulosis?
1. Low-fiber diets --> Constipation incr. intraluminal pressure.
2. Family history.
47
Clinical features of diverticulosis?
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.
48
What percentage of patients with diverticulosis is symptomatic?
Only 10-20%.
49
Test of choice in diverticulosis?
Barium enema.
50
Abdominal x-rays in diverticulosis?
Usually normal, and are NOT diagnostic.
51
Diverticulosis - Treatment?
1. High-fiber foods (such as bran) to increase stool bulk.
| 2. Psyllium (if the patient cannot tolerate pain).
52
Complications of diverticulosis?
1. Painless rectal bleeding
| 2. Diverticulitis
53
Complications of diverticulitis?
1. Bowel obstruction
2. Abscess
3. Fistulas
54
Painless rectal bleeding in diverticulosis - Percentage?
Up to 40%.
55
Painless rectal bleeding in diverticulosis - Problem?
Usually insignificant and stops spontaneously.
| Severe in 5%.
56
Diverticulitis in diverticulosis - Percentage?
15-25%
57
Free colonic perforation in diverticulitis?
UNCOMMON but catastrophic (leads to peritonitis).
58
Percentage of recurrence in patients with medically-treated diverticulitis within the first 5yrs?
About 30%.
59
Lower GI bleeding - More common in diverticulosis or diverticulitis?
Diverticulosis.
60
Diverticulosis - Test of choice?
Barium enema
61
Diverticulitis - Test of choice?
CT scan - Barium enema and colonoscopy contraindicated.
62
Why are barium enema and colonoscopy contraindicated in acute diverticulitis?
Due to risk of perforation.
63
Treatment for acute diverticulitis?
1. Mild --> IV antibiotics, bowel rest (NPO), IV fluids.
2. If symptoms persist after 3-4 days --> surgery.
3. Antibiotics for 7-10days.
64
After successful treatment of diverticulitis, what is the recurrence percentage?
About 30%.
65
Interesting relationship between aortic stenosis and bleeding AV malformations?
25% of patients with AV malformations have aortic stenosis.
66
Angiodysplasia - Percentage with massive bleeding?
15%.
67
Angiography or colonoscopy for diagnosing angiodysplasia?
Colonoscopy
68
Angiodysplasia - How often does bleeding stops spontaneously?
90%.
69
Acute or chronic Mesenteric ischemia is more common?
Acute is much more common.
70
Patients with acute mesenteric ischemia, often have what?
Preexisting heart disease - CHF, CAD.
71
Types of acute mesenteric ischemia:
1. Arterial embolism (50%)
2. Arterial thrombosis (25%)
3. Non occlusive mesenteric ischemia (20%)
4. Venous thrombosis (<10%)
72
Acute mesenteric ischemia due to arterial embolism?
Almost all emboli are of cardiac origin - A-fib, MI, Valvular disease.
73
Acute mesenteric ischemia due to arterial thrombosis:
1. Most of these patients have atherosclerotic disease at other sites.
2. Acute occlusion over preexisting atherosclerotic disease.
3. Collateral circulation has usually developed.
74
Acute mesenteric ischemia due to non occlusive mesenteric ischemia:
1. Splanchnic vasoconstriction secondary to low CO.
| 2. Typically seen in critically ill elderly patients.
75
Acute mesenteric ischemia due to venous thrombosis - Predisposing factors?
1. Infection
2. Hypercoagulable states
3. OCPs
4. Portal HTN
5. Malignancy
6. Pancreatitis
76
Presentation of acute mesenteric ischemia - Embolic?
Sudden and more painful than other causes.
77
Presentation of acute mesenteric ischemia - Arterial thrombosis?
More gradual and less severe than embolic causes.
78
Presentation of acute mesenteric ischemia - Non occlusive ischemia?
Typically in critically ill patients.
79
Presentation of acute mesenteric ischemia - Venous thrombosis?
Symptoms for several days or even weeks, with gradual worsening.
80
Overall mortality for acute mesenteric ischemia?
60-70% - If bowel infarction has occurred, mortality can exceed 90%.
81
Classic presentation of acute mesenteric ischemia?
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.
82
Signs of intestinal infarction in acute mesenteric ischemia?
1. Hypotension
2. Tachypnea
3. Lactic acidosis
4. Fever
5. Altered mental status
Eventually leading to shock.
83
Which biochemical component needs to be checked if acute mesenteric ischemia is suspected?
Lactate level
84
Acute mesenteric ischemia - Definitive diagnostic test?
Mesenteric angiography
85
Is a plain abdomen film necessary in acute mesenteric ischemia?
To exclude other causes of abdominal pain.
86
Acute mesenteric ischemia - What do we see on barium enema?
"Thumbprinting" due to thickened Edematous mucosal folds.
87
Supportive measures for acute mesenteric ischemia?
IV fluids and broad-spectrum antibiotics.
88
Therapy of choice for all arterial causes of acute mesenteric ischemia?
Direct intra-arterial infusion of papaverine (vasodilator) into the superior mesenteric system during arteriography.
89
Do we give Thrombolytics in patients with acute mesenteric ischemia?
May be indicated in some patients with embolic acute mesenteric ischemia.
90
Treatment of choice for acute mesenteric ischemia due to venous thrombosis?
Heparin
91
Surgery for acute mesenteric ischemia - When?
May be needed in ALL types of acute mesenteric ischemia if signs of peritonitis develop.
92
Chronic mesenteric ischemia - Presentation?
1. Causes by atherosclerotic occlusive disease of main mesenteric vessels.
2. Abdominal angina.
3. Significant weight loss.
93
Chronic mesenteric ischemia - What confirms the diagnosis?
Mesenteric angiography
94
Chronic mesenteric ischemia - Definitive treatment?
Surgical Revascularization and leads to pain relief in 90% of cases.
95
Ogilvie's syndrome - What happens?
Unusual problem in which signs, symptoms, and radiographic findings of large bowel obstruction are present, but there is NO MECHANICAL OBSTRUCTION.
96
Ogilvie's syndrome - Commom causes:
1. Recent surgery or trauma.
2. Serious medical illnesses (sepsis, malignancy)
3. Medications (narcotics, psychotropic drugs, malignancy)
97
Ogilvie's syndrome - Treatment?
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.
98
3 antibiotics frequently associated with Pseudomembranous colitis?
1. Clindamycin
2. Ampicillin
3. Cephalosporins
99
What is the max colonic Distention in which the risk of impending rupture is very high?
>10cm diameter.
100
Complications of severe pseudomembranous colitis:
1. Toxic megacolon
2. Colonic perfusion
3. Anasarca, electrolyte disturbances
101
Diagnosis of pseudomembranous colitis:
Demonstration of C.difficile toxins is diagnostic - results take at least 24h. 95% sensitivity.
102
What is the importance of abdominal radiograph in pseudomembranous colitis?
To rule out toxic Megacolon and perforation.
103
Drug of choice in pseudomembranous colitis?
Metronidazole
104
Where is metronidazole contraindicated?
Infants or pregnant patients.
105
When do we use oral vanco instead of metronidazole?
If the patient is resistant to metro or cannot tolerate it.
106
Recurrence of pseudomembranous colitis?
15-35% within 2-8wks after successful treatment.
107
Role of abdominal radiograph in pseudomembranous colitis?
To rule out toxic megacolon and perforation.
108
Role of cholestyramine in pseudomembranous colitis treatment?
May be used as an adjuvant treatment to improve diarrhea.
109
Colonic volvulus - Definition?
Defined as twisting of a loop of intestine about its mesenteric attachment site.
110
Colonic volvulus - Complication?
May result in obstruction or vascular compromise - potential for necrosis and/or perforation if untreated.
111
MC site of colonic volvulus?
The sigmoid colon - 75% of all cases.
112
Is cecal volvulus common?
25% of cases.
113
Risk factors for colonic volvulus:
1. Chronic illness
2. Age
3. Institutionalization
4. CNS disease
5. Chronic constipation - laxative abuse - antimotility drugs
6. Prior abdominal surgery
114
Risk for cecal volvulus?
Due to congenital lack of fixation of the right colon and tends to occur in younger patients.
115
Colonic volvulus - Presentation:
1. Acute onset of colicky abdominal pain.
2. Obstipation, abdominal distention.
3. Anorexia
4. Nausea
5. Vomiting
116
Diagnosis - Sigmoid volvulus - Plain abdominal film:
Omega loop sign (or bent inner-tube shape) indicates a dilated sigmoid colon.
117
Cecal volvulus - Diagnosis - Plain abdominal film:
Coffee bean sign indicates a large air-fluid level in RLQ.
118
Role of sigmoidoscopy in diagnosing colonic volvulus?
Preferred diagnostic and therapeutic test for sigmoid volvulus --> Leads to successful treatment (untwisting and decompression) in many cases.
119
Barium enema - colonic volvulus?
Reveals the narrowing of the colon at the point where it is twisted ("bird's beak").
120
Treatment of sigmoid volvulus:
>70% decompression via sigmoidoscopy.
| --> Recurrence is HIGH --> Elective sigmoid colon resection is recommended.
121
Treatment of cecal volvulus?
Emergent surgery is indicated.
122
Gold standard for diagnosing cirrhosis:
Liver biopsy.
123
Cirrhosis - Distortion of liver anatomy causes 2 major events:
A. Decreased blood flow through the liver.
| B. Impairment of biochemical functions.
124
How do we assess hepatic functional reserve?
Child's classification --> Measure disease severity and is a predictor of morbidity and mortality.
125
MCC of cirrhosis:
Alcoholic liver disease --> Range of conditions from fatty liver (reversible, due to acute ingestion) to cirrhosis (reversible).
126
Percentage of heavy drinkers that develop alcoholic cirrhosis:
15-20%.
127
2nd MCC of cirrhosis:
Chronic hep C/B.
128
Cause of cirrhosis after bone marrow transplantation:
Hepatic veno-occlusive disease.
129
Components of Child's classification:
1. Ascites
2. Bilirubin
3. Encephalopathy
4. Nutritional status
5. Albumin
130
Child A:
Ascites: None
Bilirubin: 3.5
131
Child B:
```
Ascites: Controlled
Bilirubin: 2.0-2.5
Encephalopathy: Minimal
Nutritional status: Good
Albumin: 3.0-3.5
```
132
Child C:
```
Ascites: Uncontrolled
Bilirubin: >3.0
Encephalopathy: Severe
Nutritional status: Poor
Albumin: <3.0
```
133
What may be used to lower portal HTN?
TIPS - Transjugular intrahepatic portal-systemic shunt.
134
What happens when a patient develops complications of cirrhosis?
They have "decompensated" disease, with high morbidity and high mortality.
135
Treatment of bleeding esophageal varices - Options:
1. Variceal ligation/banding
2. Endoscopic sclerotherapy
3. IV vasopressin
4. IV octreotide infusion
5. Other options
136
Treatment of varices - Variceal ligation/banding:
1. Initial endoscopic TREATMENT OF CHOICE.
2. Effective control of active bleeding.
3. Lower rate of rebleeding than sclerotherapy.
137
Treatment of varices - Sclerotherapy:
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
MC complication of cirrhosis:
Ascites
139
Abdominal US can detect as little as how much of ascitic fluid?
30mL.
140
Indications for paracentesis in ascites:
1. New-onset ascites
2. Worsening ascites
3. Suspected spontaneous bacterial peritonitis
141
In most cases, how can we manage ascites?
By salt restriction and diuretics in most cases.
142
Treatment of ascites:
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
DDx of ascites:
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
Monitoring patients with cirrhosis:
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
Precipitants of hepatic encephalopathy:
1. Alkalosis
2. Hypokalemia (due to diuretics)
3. Sedating drugs (narcotics, sleeping medications)
4. GI bleeding
5. Systemic infections
6. Hypovolemia
146
Treatment of hepatic encephalopathy:
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
What may precipitate hepatorenal syndrome often?
Infections and diuretics.
148
Clinical features of hepatorenal syndrome:
1. Azotemia
2. Oliguria
3. Hyponatremia
4. Hypotension
5. Low urine sodium (<10mEq/L)
149
Treatment of hepatorenal syndrome:
Liver transplantation is the only cure. In general, the prognosis is very poor, and the condition is usually fatal without liver transplantation.
150
Complications of liver failure - AC, 9H:
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
SBP - Up to what percentage of patients hospitalized for ascites?
Up to 20%.
152
SBP - Mortality?
20-30%.
153
SBP - What to look for?
Look for fever and/or change in mental status in a patient with known ascites.
154
SBP - Does it recur?
Up to 70% in first year.
155
SBP - Etiologic agents:
1. E.coli (MC)
2. Klebsiella
3. S.pneumoniae
156
Diagnosis of SBP:
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
SBP - Treatment:
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
Signs of ACUTE liver failure:
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
Treatment of coagulopathy in acute liver failure:
Fresh frozen plasma
160
HCC - Percentage in patients with cirrhosis:
10-25%.
161
How long does the patient have to withdraw alcohol in order to be eligible for a liver transplantation?
More than 6 months.
162
Wilson inheritance pattern?
AR
163
Wilson - Age of presentation?
5-35.
164
Wilson - Renal involvement?
1. Aminoaciduria
| 2. Nephrocalcinosis
165
Wilson - Diagnosis?
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
Wilson - What if diagnosed regarding the family?
Must also be screened as well.
167
Wilson - Treament:
1. D-penicillamine
2. Zinc --> Prevents uptake of dietary Cu.
3. Liver transplantation (if unresponsive to therapy or fulminant liver failure).
168
Hemochromatosis - Inheritance pattern:
AR
169
Hemochromatosis - Diagnosis:
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
Hemochromatosis - Treatment:
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
Hepatocellular adenoma - Which patients?
Often seen in young women 15-40yrs.
172
Hepatocellular adenoma - Risk factors:
1. OCPs
2. Female sex
3. Anabolic steroid use
173
Hepatocellular adenoma - Complications:
1. Hemoperitoneum
174
Hepatocellular adenoma - Diagnosis:
1. CT scan
2. US
3. Hepatic arteriography (most accurate but invasive).
175
Hepatocellular adenoma - Treatment:
1. Discontinue OCPs.
| 2. Surgically resect tumors >5cm that do not regress after stopping OCPs - otherwise there is a risk of rupture.
176
MC benign tumor of the liver?
Cavernous hemangioma
177
Cavernous hemangioma - Complications:
1. Rupture with hemorrhage
2. Obstructive jaundice
3. Coagulopathy
4. CHF secondary to a large AV shunt
5. Gastric outlet obstruction.
178
Cavernous hemangiomas - Diagnosis:
1. US
2. CT scan
3. IV contrast
4. Biopsy is CONTRAINDICATED because of risk of rupture and hemorrhage.
179
Cavernous hemangiomas - Treatment:
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
Focal nodular hyperplasia - Occurs in?
Women of reproductive age.
181
Focal nodular hyperplasia - Association with OCPs?
NO ASSOCIATION.
182
Focal nodular hyperplasia - Symptoms?
Usually asymptomatic - Hepatomegaly may be present - Treatment NOT NECESSARY IN MOST CASES.
183
HCC - Pathologic subtypes:
1. Non fibrolamellar (most common).
| 2. Fibrolamellar
184
Non fibrolamellar HCC - Features:
1. Hep B and C
2. Cirrhosis
3. Usually unresectable with very short survival time (months)
185
Fibrolamellar HCC - Features:
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
Prognosis of HCC:
If unresectable: less than 1yr.
| If resectable: 25% of patients are alive at 5yrs.
187
Diagnosis of HCC - Liver biopsy:
REQUIRED for definitive diagnosis.
188
Diagnosis of HCC - Lab tests:
1. Hep B and C serology.
2. LFTs
3. Coagulation tests
189
Diagnosis of HCC - Imaging studies:
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
Diagnosis of HCC - AFP:
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
HCC - Treatment:
1. Liver resection - in the 10% of patients who have resectable tumors.
2. Liver transplantation if diagnosis is made early.
192
NASH - What happens:
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
NASH - Associated with:
1. Obesity
2. Hyperlipidemia
3. DM
- -> Some patients have none of these.
194
NASH - Course:
Usually asymptomatic - Benign course --> Cirrhosis develops in 10%-15%.
195
NASH - How is it found?
Typically discovered on routine lab tests - mild elevation of AST ALT.
196
NASH - Treatment:
Not clearly established.
197
Gilbert's syndrome - Inheritance pattern:
AD
198
Hemobilia - What happens?
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
Hemobilia - Etiology:
1. MCC trauma
2. Papillary thyroid carcinoma
3. Surgery (eg cholecystectomy, CBD exploration).
4. Tumors
5. Infections
200
Hemobilia - Clinical features:
1. GI bleeding - melena/hematemesis.
2. Jaundice
3. RUQ pain
201
Hemobilia - Diagnosis:
Arteriogram is diagnostic.
| Upper GI endoscopy shows blood coming out of ampulla of Vater.
202
Hemobilia - Treatment:
Resuscitation (may require transfusion). If bleeding is severe, surgery is necessary:
--> Options include ligation of hepatic arteries or arteriogram with embolization of vessel.
203
Hydatid liver cysts - Caused by:
1. Echinococcus granulosus
2. Echinococcus multilocularis
Cysts more commonly occur in the right lobe of the liver.
204
Hydatid liver cysts - Complications:
1. Small cysts are asymptomatic.
| 2. Larger cysts may cause RUQ pain and rupture into the peritoneal cavity --> fatal anaphylactic shock.
205
Hydatid liver cysts - Treatment:
1. Surgical resection --> caution to avoid spilling contents of the cyst into the peritoneal cavity.
2. Mebendazole is given after surgery.
206
MC location for a liver (BOTH pyogenic and amebic) abscess:
Right lobe.
207
2 types of liver abscess:
1. Pyogenic
| 2. Amebic
208
Pyogenic liver abscess - MCC?
Biliary tract obstruction.
209
Pyogenic liver abscess - Causative organisms:
1. E.coli
2. Klebsiella
3. Proteus
4. Enterococcus
5. Anaerobes
210
Pyogenic liver abscess - Clinical features:
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
Pyogenic liver abscess - Diagnosis:
1. US
2. CT scan
3. Elevates LFTs
212
Pyogenic liver abscess - Prognosis:
Fatal if untreated.
Treatment - IV antibiotics and percutaneous drainage of abscess.
--> Reduces mortality to about 5-20%.
Surgical drainage is sometimes necessary.
213
Amebic liver abscess - Common in men or women?
Men - 9:1 - Particularly homosexual men. Transmitted through fecal-oral contact.
214
Amebic liver abscess - Diagnosis:
Serologic testing (IgG enzyme immunoassay) establishes diagnosis.
215
Amebic liver abscess - Treatment:
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
Budd-Chiari syndrome - Etiology:
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
Budd-Chiari - Diagnosis:
Hepatic venography - Serum ascites albumin gradient >1.1g/dL.
218
Budd-Chiari - Treatment:
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
3 Major causes of jaundice:
1. Hemolysis
2. Liver disease
3. Biliary obstruction
220
Jaundice with dark urine?
Only seen with high CONJUGATED bilirubin.
221
Dark urine and pale stools sign a diagnosis of conjugated or unconjugated hyperbilirubinemia?
CONJUGATED
222
Bilirubin metabolism - From where does bilirubin come?
80% from Hb (RBC breakdown). The rest comes from myoglobin breakdown and liver enzymes.
223
Clinical features of cholestasis:
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
If there is no hemolysis, isolated hyperbilirubinemia (unconjugated) may indicate?
Gilbert syndrome
225
What do severely elevated (>10.000) ALT, AST indicate?
Extensive hepatic necrosis has occured.
1. Ischemia, shock liver - prolonged hypotension or circulatory collapse.
2. Acetaminophen toxicity.
3. Severe viral hepatitis.
226
Elevated AST, ALT in asymptomatic patients?
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
ALP - Besides liver, also found in?
1. Bone
2. Gut
3. Placenta
228
ALP is very high (10-fold) - What should we think?
Think of extrahepatic biliary tract obstruction OR intrahepatic cholestasis (eg PBC or drug-induced cirrhosis).
229
What should be done if ALP is elevated?
Measure GGT to make sure the elevation is HEPATIC IN ORIGIN (rather than bone or intestinal).
230
ALP is elevated, but GGT is normal?
Consider bone disease or pregnancy.
231
Decr. albumin - what do we think?
1. Chronic liver disease
2. Nephrotic syndrome
3. Malnutrition
4. Inflammatory states
232
PT is prolonged - What does it tell us about liver?
ADVANCED liver disease.
233
Cholesterol stones (yellow to green) - associated with?
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
Pigment stones - Associations?
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
Majority of gallstones are of which type?
Mixed ones.
236
Biliary colic - timing?
Pain after eating and at night.
237
What is the Boa's sign?
Referred right subscapular pain of biliary colic.
238
Percentage of patients with biliary colic that develop acute cholecystitis within 2 years?
30%
239
Diagnosis of cholelithiasis?
RUQ US - sensitivity + specificity >95% for stones >2mm.
| CT/MRI are alternatives
240
Signs of biliary tract obstruction:
1. Elevated ALP, GGT.
2. Elevated conjugated bilirubin.
3. Jaundice
4. Pruritus
5. Clay-colored stools
6. Dark urine
241
Acute cholecystitis is due to what?
Obstruction of the cystic duct - Not infection.
242
Percentage of patients with gallstones that develop acute cholecystitis?
10%.
243
Signs of acute cholecystitis:
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
Acute cholecystitis diagnosis - Test of choice?
RUQ US.
245
CT role in acute cholecystitis:
It is as accurate as US but is more sensitive in identifying complications of acute cholecystitis (eg perforation, abscess, pancreatitis).
246
Diagnosis of acute cholecystitis - Radionuclide scan role:
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
Positive HIDA means?
The gallbladder is NOT visualized - If so for 4hr after injection, diagnosis of acute cholecystitis is confirmed.
248
Complications of acute cholecystitis:
1. Gangrenous cholecystitis.
2. Perforation of gallbladder.
3. Emphysematous cholecystitis.
4. Cholecystoenteric fistula with gallstone ileus.
5. Empyema of gallbladder.
249
Gallstone ileus:
Gallstone enters bowel lumen via cholecystoenteric fistula - gets "stuck" in terminal ileum and causes obstruction.
- Accounts for 1-2% of bowel obstruction.
250
Treatment of acute cholecystitis - What to do first?
1. Admit the patient.
2. Hydration with IV fluids
3. Bowel rest (NPO)
4. IV antibiotics
5. Analgesics
6. Correction of electrolyte abnormalities
251
Acute cholecystitis surgery?
Early surgery is preferred (24-48h). Recurrence rate with non surgical treatment is as high as 70%.
252
Acalculous cholecystitis - Percentage of patients with acute cholecystitis?
10% usually idiopathic and seen in patients with severe underlying disease.
253
Signs and symptoms of acalculous cholecystitis:
Same as for acute calculous cholecystitis.
254
Choledocholithiasis - Primary vs secondary stones:
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
Choledocholithiasis - clinical features:
1. Asymptomatic for years.
| 2. Symptoms when present, include RUQ or epigastric pain and jaundice.
256
Complications of CBD stones:
1. Cholangitis
2. Obstructive jaundice
3. Acute pancreatitis
4. Biliary colic
5. Biliary cirrhosis
257
Choledocholithiasis - Diagnosis - Lab tests
Total and direct bilirubin levels are elevated, as well as ALP.
258
Choledocholithiasis - Initial study for diagnosis:
RUQ US, but is not a sensitive study for choledocholithiasis.
Detects only in 50%, so it cannot be used to rule out diagnosis.
259
Choledocholithiasis - Diagnosis - Gold standard:
ECPR (perhaps MRCP). Sensitivity + specificity of 95% and should followe US.
Diagnostic + Therapeutic.
260
Choledocholithiasis - May be asymptomatic for years but the onset of symptoms may indicate what?
Development of life-threatening complications such as cholangitis and acute pancreatitis.
261
Cholangitis - etiology:
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
Do the following in patients with cholangitis:
1. Blood cultures.
2. IV fluids.
3. IV antibiotics AFTER blood cultures obtained.
4. Decompress CBD when patient stable.
263
Cholangitis - Clinical features - Charcot triad:
1. RUQ pain.
2. Jaundice.
3. Fever.
Present in only 50-70%.
264
Cholangitis - Reynolds pentad:
Charcot triad + septic shock + altered mental status.
| Rapidly fatal.
265
Cholangitis - Initial study:
RUQ US
266
Cholangitis - Lab:
1. Hyperbilirubinemia
2. Leukocytosis
3. Mild elevation in serum transaminases
267
Cholangitis - Treatment:
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
What is the most serious and dreaded complication of acute cholangitis?
Hepatic abscess - High mortality rate.
269
Risk factors for carcinoma of the gallbladder:
1. Gallstones
2. Cholecystoenteric fistula
3. Porcelain gallbladder
270
Carcinoma of the gallbladder - Clinical features:
1. Non specific - suggest extrahepatic bile duct obstruction.
2. Palpable gallbladder is a sign of advanced disease.
271
Why to do a prophylactic cholecystectomy in a patient with porcelain gallbladder?
Approx. 50% of patients with porcelain gallbladder will develop carcinoma of the gallbladder.
272
UC is present in what percentage of patients with PSC?
50-70%. Course of PSC is unaffected by a colectomy done for UC.
273
PSC - Diagnosis:
ERCP and PTC are diagnostic studies of choice.
| Lab tests show cholestatic LFTs.
274
PSC - Complications:
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
PSC - Treatment:
1. Only liver transplantation is curative.
2. ERCP for stent placement - may relieve symptoms.
3. Cholestyramine for pruritus.
276
Secondary biliary cirrhosis - Etiology:
1. Long-standing mechanical obstruction.
2. Sclerosing cholangitis
3. CF
4. Biliary atresia
277
PBC - Lab findings:
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
PBC - Treatment:
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
Cholangiocarcinoma - Locations:
1. Proximal 3rd of CBD - most common, called Klatskin's tumor.
2. Distal extrahepatic - best chance for resectability.
3. Intrahepatic - least common.
280
Klatskin' tumors:
1. Involve junction of the right + left hepatic ducts.
| 2. Very poor prognosis because they are unresectable.
281
Cholangiocarcinoma - Risk factors:
1. PSC is the major risk factor in the US.
| 2. Other include --> UC, choledochal cysts, Clonorchis sinensis infection (Hong Kong).
282
Choledochal cysts - More common in women or men?
Women 4:1.
283
Choledochal cysts - Clinical features:
1. Epigastric pain
2. Jaundice
3. Fever
4. RUQ mass
284
Choledochal cysts - Complications:
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
Choledochal cysts - Best non invasive test?
US
286
Choledochal cysts - Definitive test for diagnosis:
ERCP.
287
Choledochal cysts - Treatment:
Surgery - Complete resection of the cyst with a biliary-enteric anastomosis to restore continuity of biliary system with bowels.
288
Bile duct stricture - Etiology:
1. MCC is iatrogenic injury (prior biliary surgery such as cholecystectomy, liver transplantation).
2. Recurring choledocholithiasis
3. Chronic pancreatitis
4. PSC
289
Bile duct stricture - Clinical features:
Those of obstructive jaundice.
290
Bile duct strictures - Complications:
1. Secondary biliary cirrhosis.
2. Liver abscess
3. Ascending cholangitis
291
Biliary dyskinesia - What happens?
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
Biliary dyskinesia - How do we make the diagnosis?
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
Biliary dyskinesia - Treatment options:
1. Laparoscopic cholecystectomy
| 2. Endoscopic sphincterotomy
294
Acute appendicitis - Pathogenesis:
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
Perforation of the appendix - Features:
1. 20% of cases.
| 2. Risk factors --> Delay in treatment (>24h) and extremes of ages.
296
Signs of appendiceal rupture:
1. High fever
2. Tachycardia
3. Marked leukocytosis
4. Peritoneal signs
5. Toxic appearance
297
Psoas sign in acute appendicitis:
RLQ pain when right thigh is extended as patient lies on left side.
298
Obturator sign in acute appendicitis:
Pain in RLQ when flexed right thigh is internally rotated when patient is supine.
299
Acute appendicitis - Diagnosis:
Clinical. Lab is supportive.
CT sensitive 98-100%.
US sensitive 90%.
300
Percentage of patients with carcinoid tumor that develop carcinoid syndrome?
10%.
301
Features of carcinoid syndrome:
1. Cutaneous flushing
2. Diarrhea
3. Sweating
4. Wheezing
5. Abdominal pain
6. Heart valve dysfunction
302
Forms of acute pancreatitis:
1. Mild - responds to treatment.
| 2. Severe - Necrotizing with significant morbidity and mortality.
303
Post-ERCP pancreatitis - How often?
10% of ECRP.
304
Drugs causing acute pancreatitis:
1. Sulfonamides
2. Thiazide diuretics
3. Furosemide
4. Estrogens
5. HIV medication
+ others.
305
Recurrences are common in which type of acute pancreatitis?
Alcoholic pancreatitis.
306
Hemorrhagic pancreatitis - 3 signs:
1. Grey-Turner's sign (flank ecchymoses).
2. Cullen's sign (periumbilical ecchymoses).
3. Fox's sign (ecchymosis of INGUINAL ligament).
307
Acute pancreatitis - Diagnosis:
1. Clinical
2. Lab is supportive
3. CT is confirmatory
308
Serum amylase use in acute pancreatitis diagnosis:
If levels are more than 5x the UPPER LIMIT of normal, there is a high specificity for acute pancreatitis.
309
3rd MC cancer in the US?
Colorectal
