GI Flashcards
1
Q
What is Barrett’s esophagitis?
A
Replacement of normal squamous epithelium with metastatic columnar epithelium, which can predispose to malignancy
2
Q
What medications can worsen symptoms of GERD?
A
Antibiotics (tetracycline), bisphosphonates, iron, NSAIDs, anticholinergics, CCBs, narcotics, benzodiazepines, and others
3
Q
When is endoscopy warranted in GERD?
A
- Patients older than 45 years of age with a new onset of symptoms
- Long-standing or frequently recurring symptoms
- Failure to respond to therapy or symptoms indicating more severe conditions such as anemia, dysphagia, or recurrent vomiting
4
Q
Appropriate lifestyle modifications for GERD
A
- Cessation of smoking
- Avoidance of eating at bedtime
- Avoidance of large meals
- Avoidance of alcohol and foods that cause irritation (tomatoes, fried foods, caffeine, etc.)
- Elevate the head of the bed
5
Q
What is the most powerful anti-GERD medication?
A
PPIs
6
Q
What treatment combination may be used in a patient with significant nighttime symptoms of GERD?
A
A combination of an H2 blocker at nighttime and a PPI in the daytime
7
Q
What some fungal causes of infectious esophagitis?
A
Candida sp. should be considered, especially if oral thrush is present
8
Q
What are some viral causes of infectious esophagitis?
A
CMV and HSV are common causes
9
Q
Besides viral and fungal causes, what are other causes of infectious esophagitis?
A
HIV, mycobacterium tuberculosis, Epstein-Barr virus, and mycobacterium avium intracellulare
10
Q
Treatment of fungal infectious esophagitis
A
Fluconazole or ketoconazole
11
Q
Treatment of HSV infectious esophagitis
A
Acyclovir
12
Q
Treatment of CMV infectious esophagitis
A
IV ganciclovir; forscarnet is indicated in cases of poor tolerability or poor response
13
Q
What are disorders of esophageal motility?
A
Neurogenic dysphagia, Zenker diverticulum, esophageal stenosis, achalasia, diffuse esophageal spasm, and scleroderma
14
Q
Dysmotility of the esophagus can be caused by what?
A
Neurologic factors, intrinsic or extrinsic blockage, or malfunction of esophageal peristalsis
15
Q
What is Zenker diverticulum?
A
Outpouching of the posterior hypo pharynx that can cause regurgitation of undigested food and liquid into the pharynx several hours after eating
16
Q
What is achalasia?
A
Global esophageal motor disorder in which peristalsis is decreased and lower esophageal sphincter tone is increased, causing slowly progressive dysphagia with episodic regurgitation and chest pain
17
Q
What are the barium swallow findings in achalasia?
A
“Parrot beak” appearance (i.e., a dilated esophagus tapering to the distal obstruction)
18
Q
Treatment of strictures in esophageal dysmotility
A
- Most benign strictures can be managed by dilation
2. Malignant strictures must be resected
19
Q
What are the most common esophageal neoplasms?
A
Squamous cell carcinomas and adenocarcinomas
20
Q
Why is is common to have esophageal neoplasms spread to the mediastinum?
A
Because the esophagus has no serosa
21
Q
What are some other causes to esophageal cancers?
A
- Cigarette smoking*
- Chronic alcohol use
- Exposure to other caustic agents (e.g., nitrosamines, fungal toxins, and other carcinogens)
- Hot foods
- Mucosal abnormalities
- Poor oral hygiene
- HPV
22
Q
What is the best initial test for esophageal CA?
A
Biphasic barium esophagram
23
Q
Treatment of esophageal CA
A
Generally surgical. Radiotherapy and adjunctive chemotherapy have been used in various combinations with or without surgery
24
Q
What is a Mallory-Weiss tear?
A
Linear mucosal tear in the esophagus, generally at the gastroesophageal junction, that occurs with forceful vomiting or retching, causing hematemesis
25
A Mallory-Weiss tear is often associated with what?
Alcohol use, but it should be considered in all cases of upper GI bleed
26
Diagnosis of Mallory-Weiss tear
Endoscopy
27
Treatment of Mallory-Weiss tear
Most resolve without treatment. A PPI may be used if the active bleed is resolved. Endoscopic injection of epinephrine or thermal coagulation may be required if bleeding does not resolve on its own
28
What are esophageal varices?
Dilations of the veins of the esophagus, generally at the distal end
29
What is the underlying causes of esophageal varices?
Portal HTN, most commonly caused by cirrhosis from either alcohol abuse or from chronic viral hepatitis. Use of NSAIDs can exacerbate bleeding
30
Budd-Chiari syndrome and esophagal varices
Budd-Chiari syndrome may cause thrombosis of the portal vein, leading to esophageal varices
31
Prevention of variceal bleeding in cirrhotic patients
Beta blockers with or without isosorbide mononitrate, along with discontinuation of hepatotoxic agents
32
What treatment may be used for esophageal varices if medical treatment is insufficient?
Endoscopic band ligation
33
Hemodynamic support in bleeding esophageal varices?
Support with high-volume fluid replacement and vasopressors and immediate control of bleeding
34
What is the preferred therapy for acute bleeds of esophageal varices?
Endoscopic band ligation. Endoscopic pharmacologic vasoconstriction (e.g., octreotide) in conjunction is highly effective as well
35
Autoimmune disorders (e.g., pernicious anemia) and other noninfectious factors cause what type of gastritis?
Type A gastritis, which involves the body of the stomach
36
H. pylori causes what type of gastritis?
Type B gastritis, which involves the antrum and body of the stomach
37
Besides gastritis, H. pylori is associated with what other conditions?
Peptic ulcer, gastric adenocarcinoma, and gastric lymphoma
38
Treatment of delayed gastric emptying
Prokinetic medications (e.g., cisapride, metoclopramide) can sometimes help to speed the movement of food through the stomach
39
What is the most common cause of PUD?
H. pylori
40
Does food help or worsen symptoms of a gastric ulcer?
It worsens, which leads to anorexia and weight loss (compared to helping with duodenal ulcers)
41
What is the most common cause of nonhemorrhagic GI bleeds?
PUD
42
Combination therapy for H. pylori regimen should be taken for 2-4 weeks. What are the treatment options?
1. PPI with clarithromycin and amoxicillin or clarithromycin and addition of metronidazole
2. Bismuth subsalicylate plus tetracycline, metronidazole, and PPI
43
Prophylactic treatment for patients with a history of ulcer who require daily NSAID use; a history of complications, such as a bleed; a need for chronic steroids or anticoagulants; or significant other cormorbidities
Misoprostol or a PPI
44
What occurs in Zollinger-Ellison syndrome (ZES)?
A gastrin-secreting tumor (gastrinoma) causes hypergastrinemia, which results in refractory PUD
45
Where are most gastrinoma found?
In the pancreas or duodenum
46
About 1/3 of gastrinoma are part of a syndrome known as what?
Multiple endocrine neoplasia type I (MEN1), an autosomal dominant condition
47
Abdominal pain in ZES may be accompanied by a secretory diarrhea that improves with what?
H2 blockers (ranitidine, cimetidine) or PPIs (omeprazole, lansoprazole)
48
Diagnostic studies in ZES
1. Fasting gastrin level
2. A secretin test
3. Endoscopy, CT, or MRI to help localize the tumor
49
Fasting gastrin level in ZES
A level greater than 150 pg/mL indicates hypergastrinemia
50
Secretin test in ZES
1. Patients are given secretin 2 U/kg IV
| 2. In most patients with ZES, the gastrin level will increase by more than 200 pg/mL
51
Treatment of ZES
1. Use of PPIs control gastrin secretion
| 2. Surgical resection of the gastrinoma should be attempted when possible
52
Signs of metastatic spread of gastric adenocarcinomas includes what?
Left supraclavicular lymphadenopathy (virchow node) and an umbilical node (Sister Mary Joseph nodule)
53
What is the most common lab finding in gastric adenocarcinoma?
Iron deficiency anemia
54
What is the most common extranodal site for non-Hodgkin lymphoma?
The stomach
55
Treatment of gastric lymphoma
Treatment is resection with or without radiation or chemotherapy
56
Norovirus source
Food, water, person to person
57
Norovirus onset of symptoms
1-3 days
58
Norovirus nausea and vomiting?
Yes
59
Norovirus diarrhea
Watery
60
Norovirus fever
Low grade
61
Norovirus duration
1-2 days
62
Norovirus therapy
Hydration (prevention: hand washing)
63
Rotavirus source
Person to person
64
Rotavirus onset of symptoms
1-3 days
65
Rotavirus nausea and vomiting?
Yes
66
Rotavirus diarrhea
Watery
67
Rotavirus fever
Low grade
68
Rotavirus duration
5-8 days
69
Rotavirus therapy
Hydration (prevention: hand washing)
70
Staphylococcus aureus (toxin) source
Food, after cooking
71
Staphylococcus aureus (toxin) onset of symptoms
1-7 hours
72
Staphylococcus aureus (toxin) nausea and vomiting?
Yes, rapid onset
73
Staphylococcus aureus (toxin) diarrhea
Cramping, some diarrhea
74
Staphylococcus aureus (toxin) fever
Uncommon
75
Staphylococcus aureus (toxin) duration
Acute (4-6 hours); total (1-2 days)
76
Staphylococcus aureus (toxin) therapy
Supportive
77
Clostridum perfringens (toxin) source
Food, before cooking
78
Clostridum perfringens (toxin) onset of symptoms
8-14 hours
79
Clostridum perfringens (toxin) nausea and vomiting?
Uncommon
80
Clostridum perfringens (toxin) diarrhea
Cramping, watery
81
Clostridum perfringens (toxin) fever
Rare
82
Clostridum perfringens (toxin) duration
24 hr.
83
Clostridum perfringens (toxin) therapy
Supportive
84
Vibrio spp. (cholera) source
Water
85
Vibrio spp. (cholera) onset of symptoms
2-3 days
86
Vibrio spp. (cholera) nausea and vomiting?
Some
87
Vibrio spp. (cholera) diarrhea
Profuse, watery
88
Vibrio spp. (cholera) fever
Rare
89
Vibrio spp. (cholera) duration
Days
90
Vibrio spp. (cholera) therapy
hydration
91
Enterotoxic escherichia coli source
Food
92
Enterotoxic escherichia coli onset of symptoms
5-15 days
93
Enterotoxic escherichia coli nausea and vomiting?
Some
94
Enterotoxic escherichia coli diarrhea
Cramping, watery
95
Enterotoxic escherichia coli fever
Low grade
96
Enterotoxic escherichia coli duration
1-5 days
97
Enterotoxic escherichia coli therapy
hydration, bismuth/loperamide
98
Giardia lamblia source
Water, person to person
99
Giardia lamblia onset of symptoms
5-25 days
100
Giardia lamblia nausea and vomiting?
Nausea
101
Giardia lamblia diarrhea
Diarrhea, bloating
102
Giardia lamblia fever
None possible
103
Giardia lamblia duration
Until treated
104
Giardia lamblia therapy
Metronidazole, 250mg twice a day for 10 days
105
Cryptosporidium source
Water, outbreaks
106
Cryptosporidium onset of symptoms
2-10 days
107
Cryptosporidium nausea and vomiting?
Yes
108
Cryptosporidium diarrhea
Watery
109
Cryptosporidium fever
Possible
110
Cryptosporidium duration
30 days (unless HIV)
111
Cryptosporidium therapy
Supportive, HIV treatment
112
Cyclospora source
Imported, uncooked foods
113
Cyclospora onset of symptoms
7 days
114
Cyclospora nausea and vomiting?
Nausea, anorexia
115
Cyclospora diarrhea
Watery
116
Cyclospora fever
low grade
117
Cyclospora duration
Weeks
118
Cyclospora therapy
Trimethoprim-sulfamethoxazole BID for 7 days
119
Salmonella (invasive) source
Poultry
120
Salmonella (invasive) onset of symptoms
6-72 hours
121
Salmonella (invasive) nausea and vomiting?
Nausea, some vomiting
122
Salmonella (invasive) diarrhea
Purulent
123
Salmonella (invasive) fever
Yes, septicemia common
124
Salmonella (invasive) duration
4-7 days
125
Salmonella (invasive) therapy
Hydration
126
Enterohemorrhagic E. coli (invasive) source
Undercooked ground beef
127
Enterohemorrhagic E. coli (invasive) onset of symptoms
12-60 hours
128
Enterohemorrhagic E. coli (invasive) nausea and vomiting?
No
129
Enterohemorrhagic E. coli (invasive) diarrhea
Purulent, bloody, cramping
130
Enterohemorrhagic E. coli (invasive) fever
Yes
131
Enterohemorrhagic E. coli (invasive) duration
5-10 days
132
Enterohemorrhagic E. coli (invasive) therapy
Supportive unless severe
133
Shigella (invasive) source
Fecal-oral
134
Shigella (invasive) onset of symptoms
1-6 days
135
Shigella (invasive) nausea and vomiting?
No
136
Shigella (invasive) diarrhea
Purulent, bloody, cramping
137
Shigella (invasive) fever
Yes
138
Shigella (invasive) duration
1-7 days
139
Shigella (invasive) therapy
Supportive
140
Campylobacter (invasive) source
Undercooked poultry
141
Campylobacter (invasive) onset of symptoms
2-5 days
142
Campylobacter (invasive) nausea and vomiting?
Some
143
Campylobacter (invasive) diarrhea
Purulent, bloody, cramping
144
Campylobacter (invasive) fever
Yes
145
Campylobacter (invasive) duration
2-5 days
146
Campylobacter (invasive) therapy
Supportive
147
Treatment of a bowel obstruction
1. NPO, nasogastric suctioning, IV fluids, monitoring
2. Partial obstruction in a hemodynamically stable patient may be managed with IV hydration and nasogastric decompression
2. Urgent surgical consultation is necessary when mechanical obstruction is suspected, especially of the large bowel
3. Pain management is necessary for patients with bowel obstruction
148
Diagnostic studies in malabsorption
1. If a 72-hour fecal fat test is normal, specific defects, such as pancreatic insufficiency and abnormal bile salt metabolism, should be considered
2. A D-xylose test will distinguish maldigestion (e.g., pancreatic insufficiency, bile salt deficiency) from malabsorption. A normal test r/o malabsorption
3. Specific tests may be used to detect vitamin B12, calcium, or albumin deficiency
149
Diagnostic studies in Celiac disease
1. IgA antiendomysial (EMA) and antitissue translutaminase (anti-tTG) antibodies are the serologic screening tests
2. Small bowel biopsy is needed to confirm the diagnosis
150
What medication may be given for refractory cases of Celiac disease?
Prednisone
151
Distribution of Crohn's disease
Mouth to anus, predominately right sided; skip areas
152
Complications of Crohn's disease
Fistulas (common), toxic megacolon, colon CA
153
Onset of Crohn's disease
Gradual
154
Depth of lesions in Crohn's disease
transmural
155
Symptoms of Crohn's disease
Diarrhea and pain
156
For acute attacks of Crohn's disease, what is the treatment?
-Oral corticosteroids (prednisone) are used with or without aminosalicylates.
157
What is added to the treatment regimen of Crohn's disease for perianal disease, fissures, or fistulae?
Metronidazole or ciprofloxacin
158
What may be added to the treatment regimen of Crohn's disease in refractory cases?
Infliximab
159
In Crohn's disease, what is the best option for maintenance therapy?
Mesalamine
160
Does smoking alleviate or aggravate the symptoms of Crohn's disease?
Aggravate
161
Ulcerative colitis onset
Sudden or gradual
162
Ulcerative colitis distribution
Distal to proximal, continuous
163
Ulcerative colitis depth of lesions
Mucosal surface
164
Ulcerative colitis symptoms
Bloody, pus-filled diarrhea; tenesmus
165
Ulcerative colitis complications
Toxic megacolon, colon CA
166
What are the mainstays of medical treatment in Ulcerative Colitis?
Topical or oral aminosalicylates and corticosteroids
167
What treatment is indicated for refractory disease of ulcerative colitis?
Immunomodulators
168
In which IBD disease is surgery curative?
UC. Segmental resection is possible, but total proctocolectomy is the most common surgical cure
169
In adults, intussusception is almost always due to what?
Neoplasm
170
Diagnostic studies of intussusception in children
Barium or air enema (it may be both diagnostic and therapeutic)
171
Diagnostic studies of intussusception in adults
CT is best means of establishing the diagnosis, but many cases are diagnosed only at surgery
-DO NOT use barium enema
172
What study should be avoided in patients with an acute episode of diverticulitis?
Barium enema (it ma lead to perforation and peritonitis)
173
Treatment of diverticulitis
1. Low-residue diet and broad-spectrum antibiotics are appropriate for patients with mild diverticulitis
2. Hospitalization for IV administration of abx, bowel rest, and analgesic often is required. An NG tube is inserted if ileus develops
174
When is surgery needed in diverticulitis?
It may be necessary in severe cases, including peritonitis, large abscesses, fistulae, or obstruction
175
Diet for patients with diverticulitis
Patients should maintain a high-fiber diet to prevent diverticulitis. Evidence has negated the need to recommend avoidance of nuts, seeds, and popcorn
176
For both acute mesenteric ischemia and chronic mesenteric ischemia, what is the typical patient population?
Older than 50 years of age and have other signs of cardiovascular or collagen vascular disease
177
Acute mesenteric ischemia causes
May be caused by arterial embolus, arterial thrombosis, or venous thrombosis
178
Intestinal infarction is more common in the small bowel or large bowel?
Small bowel
179
Chronic mesenteric ischemia clinical features
Presents as abdominal angina, with pain occurring 10-30 minutes after eating, which is relieved somewhat by squatting or lying down. Physical exam is normal
180
Acute mesenteric ischemia clinical features
Presents with sudden onset of severe abdominal pain out of proportion to examination findings. Later in the process, involuntary guarding, rebound, and heme-positive stool may develop
181
All patients with ischemic bowel disease should have what study done?
Duplex u/s of the mesenteric arteries, which may be confirmed by angiography
182
Treatment for acute mesenteric ischemia or chronic mesenteric ischemia
Surgical revascularization. Hydration is also a critical factor
183
What is toxic megacolon?
It is extreme dilation and immobility of the colon and represents a true emergency.
184
Toxic megacolon can be caused by Hirschsprung disease. What is this disease?
It is a congenital aganglionosis of the colon, leading to functional obstruction in the newborn
185
In adults, toxic megacolon occurs as a complication of what?
UC, Crohn colitis, pseudomembranous colitis, and specific infectious causes (particularly amebiasis, Shigella sp., Campylobacter sp., and Clostridium difficile)
186
Toxic megacolon treatment
1. Decompression of the colon is required. In some cases, colostomy or even complete colonic resection may be required
2. Careful attention must be paid to fluid and electrolyte balance
187
Which type of colonic polyps carry the lowest risk of dysplasia?
Hyperplastic polyps
188
Which type of colonic polyps carry the highest risk of malignancy?
Villous polyps
189
Family members of those with familial polyposis syndrome should be evaluated how often?
Every 1-2 years beginning at 10-12 years of age. Elective colectomy may be an option for high-risk individuals
190
Having a single distal hyperplastic poly requires follow-ups how often?
Every 10 years
191
Having multiple hyperplastic polyps, hyperplastic polyps at sites rather than distal, or tubular polyps requires follow-ups how often?
Every 5 years
192
Villous polyps requires follow-ups how often?
Every 3 years
193
Clinical features of right-sided colon CA lesions
They typically cause chronic blood loss and iron deficiency anemia. Obstruction is uncommon
194
Clinical features of left-sided colon CA lesions
Circumferential, causing change in bowel habits and obstructive symptoms
195
Treatment of colon CA
1. Treatment is by surgical resection, which is accompanied by chemotherapy in patients with stage III (Dukes C or higher) or higher (and sometimes in stage II [Dukes B]) lesions
2. Radiation may be used for rectal tumors
196
An anorectal abscess is a result of what?
Infection
197
A fistula is a result of what?
Chronic complication of abscess
198
What is a anorectal fistula?
An open tract between two epithelium-lined areas and most commonly is associated with deeper anorectal abscesses
199
Treatment of an anorectal abscess
Requires surgical drainage, followed by warm-water cleansing, analgesics, stool softeners, and high-fiber diet (WASH regimen)
200
Treatment of anorectal fistuale
Treated surgically
201
What are anal fissures?
Linear lesions in the rectal wall most commonly found on the posterior midline
202
Treatment of anal fissure
Treatment includes bulking agents and increased fluids to avoid straining. Sitz baths will relieve acute pain.
203
What medications may help with healing of an anal fissure?
Topical nitroglycerin ointment or topical styptic, such as silver nitrate (1-2%) or gentian violet solution (1%)
204
Stage I internal hemorrhoids
Confined to the anal canal and may bleed with defecation
205
Stage II internal hemorrhoids
Protrude from the anal opening but reduce spontaneously. Bleeding and mucoid discharge may occur
206
Stage III internal hemorrhoids
Require manual reduction after bowel movements. Patients may develop pain and discomfort
207
Stage IV internal hemorrhoids
Chronically protruding and risk strangulation
208
Stages I and II internal hemorrhoids can be managed how?
With a high-fiber diet and increased fluids. Bulk laxatives may be helpful
209
Higher stage hemorrhoidal disease may benefit from what treatment?
From suppositories with anesthetic and astringent properties
210
Surgical treatment of hemorrhoids is indicated for whom?
Those unresponsive to conservative treatment and all stage IV hemorrhoids
211
What are the surgical options for hemorrhoids?
Injection, rubber band ligation, or sclerotherapy
212
Treatment of pilonidal disease
1. Treatment is surgical drainage, which may be supplemented with antibiotics
2. Follicle removal may be required, with unroofing of sinus tracts
213
What are complications of fecal impaction?
Urinary tract obstruction and infection, spontaneous perforation of the colon, and stercoral ulcer where the mass has pressed on the colon
214
Fecaliths may cause and develop what?
Appendicitis
215
More proximal fecal impaction generally indicates what?
neoplasm
216
Anal cancer is caused by what?
HPV and is a common finding among women with HPV and people with HIV infection, particularly men who have sex with men (MSM)
217
Treatment of anal cancer
Surgical
218
What is the most common cause of appendicitis?
Fecalith
219
What are the most common causes of pancreatitis?
Cholelithiasis or alcohol abuse
220
What are some indications of a grave prognosis?
Severe hypovolemia, adult respiratory distress syndrome, and tachycardia of greater than 130 bpm
221
Hemorrhagic pancreatitis may cause bleeding where?
Into the flanks (Grey Turner sign) or umbilical area (Cullen sign)
222
Which is the most sensitive and specific test for acute pancreatitis?
Serum lipase (but only with elevations of threefold or greater)
223
Ranson criteria for poor prognosis for pancreatitis: leukocyte count
>16,000/µL
224
Ranson criteria for poor prognosis for pancreatitis: blood glucose level
>200 mg/dL
225
Ranson criteria for poor prognosis for pancreatitis: lactate dehydrogenase
>350 IU/dL (normal <20-50 IU/dL)
226
Ranson criteria for poor prognosis for pancreatitis: AST
>250 IU/dL (normal <120 IU/dL)
227
Ranson criteria for poor prognosis for pancreatitis: Arterial PO2
<60 mm Hg
228
Ranson criteria for poor prognosis for pancreatitis: Base deficit
>4 mEq/L
229
Ranson criteria for poor prognosis for pancreatitis: Calcium
Falling
230
Ranson criteria for poor prognosis for pancreatitis: BUN
Rising
231
Treatment for acute pancreatitis
1. Oral intake must be stopped to prevent continued secretion of pancreatic juices
2. Fluid volume must be restored and maintained. Parenteral hyperalimentation should be started early to prevent nutritional depletion
3. Pain is managed with an opioid. Antibiotics should be considered
4. The patient must be monitored closely for complications
232
Complications of acute pancreatitis
Pancreatic pseudocyst, renal failure, pleural effusion, hypocalcemia, and pancreatic abscess
233
What is the classic triad of chronic pancreatitis?
Pancreatic calcification, steatorrhea, and DM
234
Treatment of chronic pancreatitis
1. Treatment is as for acute pancreatitis. A low-fat diet should be recommended at discharge
2. Surgical removal of part of the pancreas can control pain
3. The only definitive treatment for chronic pancreatitis is to address the underlying cause, which most commonly is alcohol
235
What is Courvoisier sign?
It is a palpable gallbladder that may be seen in pancreatic CA
236
Treatment of pancreatic CA
1. Treatment is surgical resection (modified Whipple procedure) in those w/o metastases
2. Subsequent radiation and chemotherapy are controversial
237
What are complications of choledocholithiasis?
Cholecystitis, pancreatitis, and acute cholangitis
238
What is the Charcot triad?
RUQ tenderness, jaundice, and fever that is found in acute cholangitis
239
What is Reynolds pentad?
RUQ tenderness, jaundice, fever, altered mental status, and hypotension
240
What is the optimal procedure both for diagnosis and treatment of acute cholangitis?
ERCP (however it should not be done until the patient is stable)
241
What is the initial treatment of acute cholangitis?
Antibiotics (generally a fluoroquinolone, a cephalosporin, ampicillin, or gentamicin with metronidazole), fluid and electrolyte replacement, and analgesia are the initial treatment
242
What is primary sclerosing cholangitis (PSC)?
Chronic thickening of the bile duct walls of unknown etiology, although 80% are associated with inflammatory bowel disease, generally UC
243
PSC is strongly associated with what?
Cholangiocarcinoma as well as with an increased risk of pancreatic and colorectal carcinoma
244
What is the most common presenting features of PSC?
Jaundice and pruritus
245
Treatment of PSC
1. Localized strictures may be relieved with balloon dilation and stent placement. Long-term stenting increases the risk of cholangitis
2. Liver transplant is the only treatment with a known survival benefit
246
What is the most common cause of acute hepatitis?
Viral; toxins (e.g., alcohol) are the second most common cause
247
How is hepatitis A and E transmitted?
Fecal-oral contamination and can be prevented by maintaining a sanitary water supply and hand washing
248
How is hepatitis B, C, and D transmitted?
Parenterally or by mucous membrane contact
249
Hepatitis D is seen only in conjunction with what?
hepatitis B
250
Immunoglobulin M antibody to hepatitis A virus (anti-HAV) can be detect with what?
the onset of clinical disease but it disappears after several months.
251
What does HAV IgG indicate?
Resolved hepatitis A
252
What does hepatitis B surface antigen (HBsAg) indicate?
Ongoing infection of any duration
253
What does antibody against hepatitis B surface antigen (anti-HBs) indicate?
immunity by past infection or vaccination
254
When is hepatitis B core antibody (anti-HBc) present and what does it indicate?
It is present between the disappearance of HBsAg and the appearance of anti-HBs, indicating acute hepatitis
255
What does hepatitis B envelope antigen (HBeAg) indicate?
Active infection that is highly contagious
256
What does hepatitis B envelope antigen antibody (anti-HBe) indicate?
A lower viral titer
257
What medication regimen will cover hepatitis B and the additional antiretroviral medication that will cover the HIV infection?
Tenofovir with either emtricitabine or lamivudine
258
What is the goal of therapy with hepatitis C?
Reduction of viral RNA to undetctable at 6 months posttherapy
259
What is the maximum daily dose of acetaminophen in adults?
4 g
260
What can be given for acetaminophen toxicity?
Acetylcysteine
261
What does spontaneous bacterial peritonitis present with?
Fevers, chills, worsening ascites, and abdominal pain
262
What diuretic may be given in cirrhosis?
Spironolactone, 100 mg daily
263
How is spontaneous bacterial peritonitis treated?
With antibiotics (cefotaxime 2 g IV q 8 hours)
264
Liver abscess is generally caused by what organisms?
Entamoeba histolytica or the coliform bacteria
265
Treatment of liver abscess
Antibiotics (ampicillin-sulbactam) and percutaneous drainage or surgical excision
266
Benign liver neoplasms include what?
Cavernous hemangioma, hepatocellular adenoma, and infantile hemangioendothelioma
267
The liver is a common site of metastasis for other primary cancers, especially which ones?
lung and breast cancers.
268
Primary hepatocellular carcinoma is associated with what?
hepatitis B, hepatitis C, aflatoxin B1 exposure, and cirrhosis
269
Alpha-fetoprotein may be elevated in what conditions?
hepatic carcinoma, chronic hepatitis C, and cirrhosis
270
Should needle biopsy be performed in liver neoplasm?
It should not be perfomred if the tumor is resectable for fear of seeding
271
Indirect hernias
Most common; passage of intestine through the internal inguinal ring down the inguinal canal, may pass into the scrotum
272
Direct hernias
Passage of intestine through external inguinal ring at Hesselbach triangle, rarely enters the scrotum
273
Femoral hernia
Least common; passage through femoral ring
274
Ventral hernia occurs when?
When there is a weakening in the anterior abdominal wall and may be either incisional or umbilical
275
Esophageal atresia presents in newborns as what?
As excessive saliva and choking or cough with attempts to feed
276
What will establish the diagnosis of esophageal atresia?
Inability to pass a nasogastric tube
277
Treatment of esophageal atresia
Surgical; pulmonary aspiration should be prevented in the interim by suction and withholding of oral feedings
278
Why does a diaphragmatic hernia cause immediate respiratory distress in the newborn?
Because the affected lung is compressed by pressure from abdominal contents
279
A diagnosis of a diaphragmatic hernia can be made how?
If bowel sounds are heard in the chest
280
Radiography of a diaphragmatic hernia shows what?
Loops of bowel in the involved hemithorax, with displacement of the heart and mediastinal structures
281
Treatment of a diaphragmatic hernia
Surgical
282
Lab findings in pyloric stenosis
U/S will generally demonstrate the lesion (olive-shaped mass) while barium swallow will show delayed emptying and a "string sign"
283
Hirschsprung disease (congenital megacolon) is caused by what?
Congenital absence of Meissner and Auerbach autonomic plexuses enervating the bowel wall
284
Symptoms of Hirschsprung disease
Constipation or obstipation, vomiting, and failure to thrive
285
Treatment of Hirschsprung disease
Surgical resection of the affected bowel
286
Vitamin A sources
Liver, fish oils, fortified milk, eggs
287
Vitamin A function(s)
Vision, epithelial cell maturity, resistance to infection, antioxidant
288
Vitamin A at-risk groups
Elderly, alcoholics, liver disease
289
Vitamin A deficiency
Night blindness, dry skin
290
Vitamin A toxicity
Skin disorders, hair loss, teratogenicity
291
Vitamin D sources
Fortified mild
292
Vitamin D function
Calcium regulation, cell differentiation
293
Vitamin D at-risk groups
Elderly, shut-ins with low sun exposure
294
Vitamin D deficiency
Rickets, osteomalacia
295
Vitamin D toxicity
Hypercalcemia, kidney stones, soft-tissue deposits
296
Vitamin E sources
Plant oils, wheat germ, asparagus, peanuts, margarine
297
Vitamin E function(s)
Retard cell aging, vascular and red cell wall integrity, antioxidant
298
Vitamin E at-risk groups
Rare
299
Vitamin E deficiency
Hemolytic anemia, degenerative nerve changes
300
Vitamin E toxicity
Inhibition of vitamin K, myalgia, HA, weakness
301
Vitamin K sources
Liver, green leafy vegetables, broccoli, peas, green beans
302
Vitamin K function(s)
clotting
303
Vitamin K at-risk groups
Rare
304
Vitamin K deficiency
Bleeding
305
Vitamin K toxicity
Anemia, jaundice
306
Thiamin sources
Pork, grains, dried beans, peas, brewer's yeast
307
Thiamin function(s)
Carbohydrate metabolism, nerve function
308
Thiamin at-risk groups
Alcoholism, poverty
309
Thiamin deficiency
Beriberi (nervous tingling, poor coordination, edema, weakness, cardiac dysfunction)
310
Thiamin toxicity
N/A
311
Riboflavin sources
Milk, spinach, liver, grains
312
Riboflavin function(s)
Energy
313
Riboflavin at-risk groups
N/A
314
Riboflavin deficiency
Oral inflammation, eye disorders
315
Riboflavin toxicity
N/A
316
Niacin sources
Bran, tuna, salmon, chicken, beef, liver, peanuts, grains
317
Niacin function(s)
Energy, fat metabolism
318
Niacin at-risk groups
Poverty, alcoholism
319
Niacin deficiency
Flushing
320
Niacin toxicity
N/A
321
Pantothenic acid sources
Liver, broccoli, eggs
322
Pantothenic acid function(s)
Energy, fat metabolism
323
Pantothenic acid at-risk groups
Alcoholism
324
Pantothenic acid deficiency
Tingling, fatigue, HA
325
Biotin sources
Cheese, eggs, cauliflower, peanut butter, liver
326
Biotin function(s)
Glucose production, fat synthesis
327
Biotin at-risk groups
Alcoholism
328
Biotin deficiency
Dermatitis, tongue pain, anemia, depression
329
Biotin toxicity
N/A
330
Vitamin B6 (pyridoxine) sources
Animal protein, spinach, broccoli, bananas, salmon
331
Vitamin B6 (pyridoxine) function(s)
Protein metabolism, neurotransmitter synthesis, hemoglobin
332
Vitamin B6 (pyridoxine) at-risk groups
Adolescents, alcoholism
333
Vitamin B6 (pyridoxine) deficiency
HA, anemia, seizures, flaky skin, sore tongue
334
Vitamin B6 (pyridoxine) toxicity
Nerve destruction
335
Folate sources
Green leafy vegetables, orange juice, grains, organ meats
336
Folate function(s)
DNA synthesis
337
Folate at-risk groups
Alcoholism, pregnancy
338
Folate deficiency
Megaloblastic anemia, sore tongue, diarrhea, mental disorders
339
Folate toxicity
N/A
340
Vitamin B12 (cobalamin) sources
Animal foods
341
Vitamin B12 (cobalamin) function(s)
Folate metabolism, nerve function
342
Vitamin B12 (cobalamin) at-risk groups
Elderly, vegans
343
Vitamin B12 (cobalamin) deficiency
Megaloblastic anemia, poor nerve function
344
Vitamin B12 (cobalamin) toxicity
N/A
345
Vitamin C sources
Citrus fruits, strawberries, broccoli, greens
346
Vitamin C function(s)
Collagen synthesis, hormone function, neurotransmitter synthesis
347
Vitamin C at-risk groups
Alcoholism, elderly men
348
Vitamin C deficiency
Scurvy (poor wound healing, petechiae, bleeding gums)
349
Vitamin C toxicity
Diarrhea
