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ITE '23 > Ch. 11 Abd & GI Emergencies > Flashcards

Ch. 11 Abd & GI Emergencies Flashcards

1
Q

What is the treatment for pill esophagitis?

A

Instruct patients to drink 8 oz of water with each pill and then remain upright for at least 30 minutes. Full symptom relief may take
up to 6 weeks.

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2
Q

What is the treatment for esophagitis caused by C albicans?

A

mild disease & not immunocompromised: Clotrimazole troches or nystatin swish and swallow for 1-2 weeks

Advanced disease and/or immunocompromised:
Oral fluconazole or itraconazole for 3-4 weeks.

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3
Q

What is the treatment for esophagitis caused by CMV?

A

IV ganciclovir or foscarnet

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4
Q

What is the treatment for esophagitis caused by HSV?

A

Oral acyclovir or valacyclovir

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5
Q

How is GERD treated?

A

an empiric trial of proton pump inhibitor (PPI) for 4-6 weeks

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6
Q

What are alarm symptoms for GERD that may necessitate need for upper endoscopy with biopsy?

A

dyphagia
odynophagia
weight loss
anemia
long-standing symptoms
blood in stool
age > 50

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7
Q

What are the only two behavior modifications proven to improve sx of GERD?

A

elevate head of bed
weight loss

but should be advised in combination with PPI

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8
Q

What are 4 conditions found to be associated with use of PPIs?

A
  1. pneumonia
  2. atrophic gastritis (hypergastrinemia)
  3. enteric infections (c diff)
  4. hip fractures
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9
Q

When should PPIs be avoided?

A

Patients with acute coronary syndrome on clopidogrel
- associated with increased reinfarction

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10
Q

Caustic ingestions with acids cause _______ necrosis.

A

Coagulation

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11
Q

Caustic ingestions with alkalis cause ______ necrosis.

A

Liquefactive

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12
Q

Ingestion of household bleach is unlikely to cause serious problems unless > ______ (volume) has been ingested.

A

> 100 mL

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13
Q

What is the workup for a caustic ingestion?

A

if perforation suspected –> CXR or CT; +/- upper endoscopy

IV fluids, IV pain medications, and IV PPI; +/- abx

do not give anything by mouth; do not give activated charcoal

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14
Q

What is Hamman sign?

A

Mediastinal crunch heard during systole with auscultation of the heart (not respiration)
Indicates Esophageal perforation

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15
Q

What tests should be considered if concerned for perforation?

A

Plain CXR and/or lateral neck film
if normal –> does not exclude

Obtain esophagram using WATER-SOLUBLE contrast +/- EGD

Do NOT use BARIUM as it can worsen mediastinitis

can consider CT

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16
Q

How can pleural fluid from thoracentesis be used to increase suspicion for esophageal perforation?

A

elevated amylase levels

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17
Q

If you diagnose esophageal perforation, what is the next step?

A

keep NPO
administer broad spectrum abx
surgical consultation

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18
Q

How is achalasia diagnosed?

A

Bird’s beak on barium swallow

–> refer to GI for endoscopy and confirmatory manometry

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19
Q

What is the treatment for achalasia?

A

Typically outpatient GI referral for:
surgical myotomy vs dilation vs botulinum
toxin injections.

Medical options include nifedipine or nitrates before meals to decreases LES pressure.

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20
Q

What triad makes up Plummer-Vinson Syndrome?

A

Triad of dysphagia, glossitis, and iron-deficiency anemia – commonly see esophageal webs

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21
Q

In foreign body ingestions, where does obstruction typically occur in children?

A

In children < 4 years, this is the level of the cricopharyngeus muscle (C6)

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22
Q

When is emergent endoscopy indicated for foreign body ingestions?

A

sharp objects or disc batteries in the esophagus,
or for objects causing obstruction with inability to handle secretions

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23
Q

When is urgent endoscopy (<24 hours) indicated for foreign body ingestions?

A

for smooth objects or food impaction
in the esophagus, sharp or large (> 6 cm) objects in the stomach/duodenum, or magnets

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24
Q

How long can esophageal coins be observed?

A

12-24 hours

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25
Q

How long can disc/standard batteries be observed in the stomach?

A

up to 48 hours

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26
Q

How long can blunt objects be observed in the stomach?

A

up to 3 weeks

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27
Q

What anatomical landmark differentiates upper from lower GI bleeding?

A

Ligament of Treitz

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28
Q

What medications should be given in upper GI bleeds?

A

PPIs - bolus then drip
Octreotide (if variceal bleeding)
IV antibiotics (third gen cephalosporin or fluoroquinolone) (if cirrhosis)
Consult GI early

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29
Q

What is the treatment for GI bleeding with elevated INR?

A

Vitamin K + FFP +PCC

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30
Q

What are risk factors for aortoenteric fistula?

A

prosthetic aortic grafts = most common
aortic aneurysms, aortitis, postradiation, tumors, or trauma

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31
Q

Where do aortoenteric fistulas most commonly occur?

A

third or fourth portion of the duodenum is most commonly involved,
followed by the jejunum and ileum

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32
Q

How is aortoenteric fistulas diagnosed?

A

CT or angiography

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33
Q

What is the treatment for aortoenteric fistulas?

A

emergent laparotomy

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34
Q

What is the most common cause of gastritis?

A

Helicobacter pylori bacterial infection

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35
Q

How is H pylori diagnosed?

A

Urea breath test, endoscopic
biopsy, and stool antigen may be used
for diagnosis and to confirm adequate
treatment.

(serologic tests are useful but cannot be used for test of cure)

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36
Q

Where are gastrinomas typically found?

A

Duodenum, pancreas or lymph nodes

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37
Q

How are gastrinomas diagnosed?

A

Elevated fasting serum gastrin level (off H2-blocker or PPI) with gastric pH < 2
■ Multiple ulcers in abnormal locations on endoscopy
■ Imaging to identify tumor ± mets (somatostatin receptor scintigraphy with SPECT [single-photon emission computed tomography])

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38
Q

What two nodes are classic findings described in gastric cancer?

A

Virchow now - supraclavicular
Sister Mary Joseph nodule - umbilicus

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39
Q

What is a Krukenberg tumor?

A

mucinous signet cells that metastasize to the ovaries – may lead to palpable ovarian masses

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40
Q

What do you call a palpable nodule on rectal exam due to metastatic gastric cancer?

A

Blumer shelf

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41
Q

How is giardia lamblia diagnosed?

A

trophozoites or cysts in stool

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42
Q

What is the treatment for giardia lamblia?

A

metronidazole

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43
Q

What foods are notorious for noninvasive gastroenteritis caused by staph aureus?

A

previously cooked foods that sit out for several hours: ham, egg salad, potato salad
onset within 1-6 hours of ingestion

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44
Q

what is the typical onset of sx in viral gastroenteritis?

A

11-72 hours

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45
Q

What is the treatment for viral gastroenteritis?

A

Self-limited; supportive care
with PO or IV hydration and
antiemetics

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46
Q

What is the treatment for gastroenteritis caused by staph aureus?

A

Supportive care with IV fluids
and symptomatic treatment;
antibiotics ineffective

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47
Q

What types of food is implicated in gastroenteritis caused by clostridium perfringens? Onset of sx?

A

previously cooked or reheated meats and poultry
8-24h

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48
Q

What is the onset of symptoms of gastroenteritis caused by vibrio cholera?

A

2-6d

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49
Q

What foods are commonly implicated in gastroenteritis caused by vibrio cholera?

A

raw or undercooked seafood,
fecal–oral, contaminated
water, often raw oysters, large
inoculum required

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50
Q

What is the treatment for gastroenteritis caused by vibrio cholera?

A

Fluid resuscitation is critical;
significant electrolyte imbalance
can occur. doxy or macrolide
may shorten course

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51
Q

What is the most common cause of chronic diarrhea in AIDS patients?

A

Cryptosporidum

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52
Q

What is the treatment of gastroenteritis caused by cryptosporidium?

A

Immunocompetent: Supportive
care, ± nitazoxanide

Immunodeficient: Restore
immune status, HARRT.
Nitazoxanide, paromomycin,
and azithromycin are no longer
recommended

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53
Q

What is the onset of action of symptoms with scombroid fish poisoning?

A

20-60 minutes after ingestion

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54
Q

What are the signs and symptoms of scombroid fish poisoning?

A

histamine intoxication:
facial flushing, throbbing headache, nausea,
vomiting, diarrhea, abdominal cramps,
bronchospasm (severe).

Heat-stabile toxin with histamine like property, not due to allergic reaction

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55
Q

What is the treatment for scombroid fish poisoning?

A

H1/H2 blockers; albuterol for
wheezing. Rarely may require Tx
as anaphylaxis

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56
Q

What is the onset of symptoms in Ciguatera fish poisoning?

A

2-6 h after ingestion of ciguatoxin
found in carnivorous fish (eg,
grouper, snapper, barracuda,
king fish, jack)

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57
Q

What types of fish may give you ciguatoxin fish poisoning?

A

carnivorous fish (eg, grouper, snapper, barracuda,
king fish, jack)

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58
Q

What is a classic finding in ciguatoxin fish poisoning?

A

reversal of hot and cold sensation
(pathognomonic, worsen with alcohol
consumption)

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59
Q

What is the treatment for ciguatoxin fish poisoning?

A

Supportive care.
Amitriptyline effective for neuropathic pain.
+/- Single dose mannitol in stable, fluid resuscitated pts with neuro sx
Atropine for bradycardia.

Abstinence from alcohol, nuts, seafood for
6 mo

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60
Q

What are the symptoms of Typhoid fever?

A

intractable fever, bradycardia, “rose spots”
caused by salmonella typhi

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61
Q

What is the treatment for salmonella gastroenteritis?

A

ciprofloxacin if severe illness or immunocompromised

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62
Q

What is the treatment for shigella gastroenteritis?

A

same as salmonella – ciprofloxacin if severe illness or immunocompromised

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63
Q

What pathogens may cause gastroenteritis that mimics appendicitis?

A

campylobacter jejuni
Yersinia enterocolitica

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64
Q

What is the treatment for campylobacter jejuni?

A

Azithromycin if severely ill or immunocompromised

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65
Q

How is Vibrio parahaemolyticus spread?

A

ingestion of raw or undercooked fish or shellfish

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66
Q

How is vibrio parahaemolyticus treated?

A

If severe: Doxycycline;
Alt: ciprofloxacin, azithromycin.
For proven bacteremia, add ceftriaxone

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67
Q

Which antibiotics are most commonly implicated as contributing to c. diff infections?

A

Clindamycin, cephalosporins, quinolones

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68
Q

How is c diff diagnosed?

A

Stool C diff toxin

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69
Q

What is the treatment for c diff?

A

stop offending antibiotic
treat with PO metronidazole for mild to moderate cases
PO vanc for severe cases

(IV vanc is ineffective)

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70
Q

How is entamoeba histolytica treated?

A

Metronidazole acutely,
then iodoquinol or paromomycin to
clear intestinal cysts;
antibiotics will usually sufficiently treat
abscess as well

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71
Q

What is the treatment for EHEC 0157:H7?

A

Supportive care; antibiotics not recommended as they may increase incidence of HUS, especially in children

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72
Q

What toxin is produced by EHEC 0157:H7?

A

Shiga toxin – cytotoxic to intestinal vascular endothelium.

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73
Q

The presence of gross or occult blood and fecal leukocytes suggests _____ cause of gastroenteritis.

A

bacterial

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74
Q

What position for XR is most sensitive for detecting pneumoperitoneum?

A

left lateral decubitus

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75
Q

Which form of IBD has skip lesions?

A

Crohn disease

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76
Q

In which form of IBD is perianal involvement common?

A

Crohn’s disease
(UC always involves rectum, but not necessarily perianal region)

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77
Q

Which form of IBD has LINEAR ulcerations, noncaseating granulomas on pathology?

A

Crohns

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78
Q

Which form of IBD has crypt abscesses, epithelial necrosis, and mucosal ulceration?

A

Ulcerative Colitis

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79
Q

In which form of IBD are fistulas and strictures common?

A

Crohns

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80
Q

Which form of IBD has transmural inflammation?

A

Crohns

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81
Q

What is first line therapy for Crohns disease?

A

5-aminosalicylic acid (5-ASA) (sulfasalazine, or the newer, less toxic mesalamine)
+ steroids for symptom flares

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82
Q

What is the treatment for severe or refractory Crohns?

A

immunomodulating agents (azathioprine, 6-MP, methotrexate) and anti-TNF (tumor necrosis factor) therapies.

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83
Q

How can toxic megacolon by diagnosed in UC?

A

plain films

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84
Q

What is the treatment for mild to moderate Ulcerative Colitis?

A

5-ASA derivatives (sulfasalazine, mesalamine)
are the mainstay of therapy with corticosteroids (PO ± rectal) indicated
for persistent symptoms or flare while on 5-ASA.

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85
Q

What is the treatment for severe ulcerative colitis?

A

corticosteroids (PO/IV ± rectal) and immunosuppressants (eg, anti-TNF, cyclosporine).

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86
Q

What types of medications should be avoided in ulcerative colitis?

A

NSAIDs, which may worsen IBD

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87
Q

How is toxic megacolon defined?

A

colon dilated > 6 cm on radiographs with signs of systemic toxicity

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88
Q

What is the most common cause of SBO in early childhood?

A

intussusception

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89
Q

What is the gold standard for diagnosing SBO?

A

CT Abd/Pelvis with IV and PO contrast (though IV contrast alone is often sufficient)

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90
Q

What is the rule of 2s for Meckel Diverticulum?

A

2% prevalence, 2% symptomatic, 2:1 maleto-
female ratio, 2 ft proximal to ileocecal
valve, and half of those symptomatic are
< 2 years of age.

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91
Q

Meckel diverticulum is caused by incomplete obliteration of the fetal __________ duct.

A

omphalomesenteric

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92
Q

What is the most common congenital abnormality of the GI tract?

A

Meckel diverticulum

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93
Q

What percentage of Meckel diverticulum contain heterotopic tissue?

A

60% – usually gastric

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94
Q

How is Meckel diverticulum diagnosed?

A

A technetium scan (definitive dx is made surgically)

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95
Q

How is the diagnosis of steathorrhea made?

A

Quantitative stool fat

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96
Q

______ are thought to result from low-fiber diets and resultant increased colonic pressure.

A

Diverticula

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97
Q

What is the difference between uncomplicated and complicated diverticulitis?

A

Complicated diverticulitis involves inflammation extending beyond pericolonic fat with abscess formation and/or microperforation

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98
Q

What is the treatment for uncomplicated diverticulitis?

A

oral antibiotics with gramnegative
and anaerobic coverage (quinolone + metronidazole, OR amoxclavulanate),
NSAIDs, and narcotics for pain relief. Liquid diet provides some relief of symptoms but is not required.

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99
Q

What is the treatment for complicated diverticulitis?

A

IV antibiotics. Keep NPO, and obtain
surgical consultation for all patients with peritonitis or perforation

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100
Q

What is the obturator sign?

A

pain induced by passively flexing and internally rotating the right hip – +appendicitis

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101
Q

What is the psoas sign?

A

It is elicited in the left lateral decubitus position by extension of the right hip – +appendicitis

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102
Q

What is Rovsing sign?

A

It is positive when palpation to the left lower quadrant (LLQ) causes RLQ pain; it’s indicative of right-sided peritoneal irritation

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103
Q

What is the test of choice for diagnosing appendicitis in pregnant patients and children?

A

Graded compression ultrasound

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104
Q

What ultrasound findings are consistent with appendicitis?

A

noncompressible appendix or > 6 mm in diameter

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105
Q

What is the most specific finding of appendicitis on CT scan?

A

The presence of periappendiceal
fat stranding is the most specific finding

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106
Q

Besides surgical consultation, how is appendicitis managed?

A

Keep NPO
give fluids
antibiotics – Pip/Tazo or Ertapenem
Pain medications

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107
Q

What causes acute radiation proctocolitis?

A

Oxygen-free radicals cause cellular DNA damage and slowed replacement of normally sloughed intestinal epithelium, leading
to ulcerations. Submucosal inflammation causes increased secretions and bleeding.

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108
Q

What causes chronic radiation proctocolitis?

A

Progressive endarteritis causes decreased perfusion. Worsening bowel ischemia causes ulceration, scarring, narrowing and possibly
perforation.

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109
Q

How is radiation proctocolitis diagnosed?

A

Chronic disease is a diagnosis of exclusion; neither endoscopy nor biopsy is diagnostic, but they may show suggestive changes and/or exclude alternative diagnoses

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110
Q

What is the test of choice for suspected fistula due to radiation proctocolitis?

A

MRI

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111
Q

What is the treatment for radiation proctocolitis?

A

Steroids or sucralfate enemas, decreased radiation doses, and stool softeners may
help. Limited evidence supports topical steroids + metronidazole in chronic disease.

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112
Q

How is IBS defined?

A

Rome III Criteria
recurrent abdominal pain/discomfort for >/= 3 days/month in the last 3 months AND at least two of the following:
- improvement with defecation
- change in stool frequency
- and/or change in stool form

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113
Q

What are alarm systems that would argue against IBS?

A

onset after age 50
weight loss
anorexia
bloody stools
nocturnal diarrhea

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114
Q

Cecal diameter > ___ cm is associated with higher risk of perforation

A

12 cm

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115
Q

What is the most common cause of large bowel obstruction?

A

Colorectal cancer

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116
Q

What is the treatment for sigmoid volvulus?

A

Attempt decompression with scope or rectal tube;
resection and fixation are indicated for unsuccessful attempts and strangulation.

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117
Q

How are sigmoid and cecal volvulus diagnosed?

A

abdominal XR; may need contrast enema

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118
Q

What is the most common abdominal emergency in children <2?

A

Intussusception

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119
Q

How is intussusception diagnosed?

A

Ultrasound usually diagnostic; shows “target sign.”
Contrast enema is diagnostic and therapeutic. Can also be seen on CT.

120
Q

What do you call Dilatation usually
of the cecum and right colon in the absence of a mechanical obstruction?

A

Acute Colonic Pseudo-obstruction (Ogilvie syndrome)

121
Q

How is Colonic pseudo-obstruction diagnosed?

A

CT or water-soluble enema is diagnostic.

122
Q

How is colonic pseudo-obstruction treated?

A

Conservative management initially (bowel rest, rectal tube, hydration, correct electrolytes avoid medications that slow colonic motility).

123
Q

What is the most common cause of perirectal abscess?

A

obstruction of anal gland –> local polymicrobial abscess formation

124
Q

Where do perianal abscesses typically form?

A

posterior midline

125
Q

How should perianal abscesses be drained?

A

Use a cruciate or elliptical incision as close to the anus as possible to minimize fistula formation. Simple linear incisions may be used
but require packing and 24-hour follow-up.

Sitz baths
Abx not necessary unless febrile, leukocytosis, or immunocompromised

126
Q

How are anal fistulas diagnosed?

A

Transrectal ultrasound/endosonography or MRI preferred. CT and fistulography have limited capacity to define small abscesses and tracts.

127
Q

Are antibiotics indicated for pilonidal abscess?

A

No, just I&D and surgical follow-up

128
Q

What is proctitis?

A

inflammation of the rectal mucosa

129
Q

What is the most common cause of proctitis?

A

STIs, but can also be due to enteric pathogens, radiation treatments, or ulcerative colitis

130
Q

What is pruritus ani?

A

Painless, uncontrollable itching/scratching of perianal area

131
Q

What is the treatment for HPV (condyloma acuminata) proctitis?

A

topicals (podophyllin, trichloroacetic
acid, 5-FU); refer for cryotherapy,
laser ablation, or excision

132
Q

What is the most frequent cause of rectal bleeding in infants and children?

A

anal fissures

133
Q

Where do anal fissures typically occur?

A

posterior midline

134
Q

What is the treatment for anal fissures?

A

Begins with meticulous anal hygiene and the WASH regimen: Warm water, Analgesics, Stool softeners, High-fiber diet. Hot sitz baths relieve
sphincter spasm.

135
Q

All patients should undergo _______ after removal of rectal foreign bodies to look for mucosal injury and/or perforation.

A

sigmoidoscopy

136
Q

Internal hemorrhoids are located proximal to the _______ line.

A

dentate

137
Q

What defines uncomplicated hemorrhoids?

A

nonthrombosed external and nonprolapsed internal

138
Q

What is the treatment for uncomplicated hemorrhoids?

A

warm sitz baths
bulk laxatives/high fiber diet
over the counter topicals
(avoid prolonged topical corticosteroid use)

139
Q

What is the treatment for prolapsed internal hemorrhoids?

A

Surgical referral for: band ligation, sclerotherapy, or hemorrhoidectomy
Emergent hemorrhoidectomy is indicated for non-reducible, thrombosed, or gangrenous internal hemorrhoids.

140
Q

What is the treatment for thrombosed external hemorrhoids <48 hours old?

A

may be excised in the ED to relieve pain
Lidocaine with epinephrine (to minimize bleeding) should be injected at the dome of the hemorrhoid, followed by an elliptical
incision and clot removal. The wound should be packed and the patient should begin sitz baths at home

141
Q

What 3 things may be associated with incomplete rectal prolapse, besides constipation and diarrheal illness?

A

Cystic fibrosis, malnutrition, parasitic infections

142
Q

What is the cause for complete rectal prolapse (all layers)?

A

laxity of attachment structures, usually elderly women with chronic constipation

143
Q

What is the treatment for complete rectal prolapse (all layers)?

A

Attempt manual reduction with gentle, continuous pressure, ± sedation;
surgery is necessary if reduction fails.

Treat constipation.

Refer all adults for endoscopy to rule out underlying lesion/lead point (eg, IBD, tumor, polyps, rectal ulcer).

144
Q

Rectal cancers proximal to the dentate line are typically what types of cancer?

A

Adenocarcinoma, melanoma,
transitional cell carcinoma, Kaposi
sarcoma, villous adenoma

145
Q

Rectal cancers distal to the dentate line are typically what types of cancer?

A

Squamous cell carcinoma, Bowen
(SCC in situ) basal cell carcinoma,
Paget disease (AdenoCa

146
Q

How does relation to dentate line correlate with outcome/prognosis?

A

proximal to dentate line = high grade malignant potential (mets early, poor prognosis)

distal to dentate line = lower grade malignant potential (slow to metastasize)

147
Q

What is a large risk factor for anal cancer?

A

HIV

148
Q

What do you call anorectal pain in the absence of an identifiable organic disorder?

A

proctalgia

149
Q

What is levator ani syndrome?

A

dull pressure brought on by defecation
and prolonged sitting

150
Q

What is proctalgia fugax?

A

intense, painful anorectal spasms lasting < 30 minutes

151
Q

Jaundice usually results from bilirubin levels > ___ mg/dL and deposition in body tissues.

A

> 3mg/dL

152
Q

Where does jaundice typically occur first?

A

under the tongue
then in conjunctiva
then spreads caudally

153
Q

What type of hyperbilirubinemia is caused by Crigler-Najjar syndrome?

A

Unconjugated (Indirect)

due to defective UDP-glucuronyl transferase

154
Q

What type of hyperbilirubinemia is caused by Dubin-Johnson Syndrome?

A

Conjugated (Direct) Hyperbilirubinemia

due to abnormal transport of conjugated bilirubin into biliary system

155
Q

What type of hyperbilirubinemia is caused by Gilbert Disease?

A

Unconjugated (Indirect)

due to reduced activity of UDP-glucuronyl transferase

156
Q

What type of hyperbilirubinemia is caused by Rotor syndrome?

A

Conjugated (Direct) hyperbilirubinemia

due to impaired canalicular export of conjugated bilirubin

157
Q

What type of hyperbilirubinemia is caused by ineffective erythropoiesis (ie thalassemia, folate or B12 deficiency)?

A

Unconjugated (indirect)

158
Q

What type of hyperbilirubinemia is caused by hepatitis (viral, alcoholic, autoimmune) or shock liver?

A

conjugated (direct)

159
Q

Which type of hyperbilirubinemia would you see LFT and alk phos elevation?

A

conjugated (direct) hyperbilirubinemia

160
Q

Which type of hyperbilirubinemia would you have normal stool and urine color?

A

unconjugated (indirect)

161
Q

Which type of hyperbilirubinemia would you have dark urine and light-colored stool?

A

Conjugated (Direct) Hyperbilirubinemia

162
Q

What is the imaging modality of choice in a jaundiced patient?

A

ultrasound

163
Q

What is the most common reason for liver transplantation in the US?

A

Hepatitis C

164
Q

What is the most common cause of hepatitis in the US?

A

viral hepatitis

165
Q

What virus causes hepatitis A?

A

RNA picornavirus

166
Q

How is Hepatitis A transmitted?

A

fecal-oral via contaminated food and water and sexual practices

167
Q

What are the signs and symptoms of Hepatitis A?

A

flulike illness, RUQ pain, followed by onset of jaundice and pruritus
PEx: hepatosplenomegaly and jaundice

168
Q

What two foods are most commonly implicated in Hepatitis A infection?

A

Shellfish and green onions

169
Q

What lab finding is diagnostic of hepatitis A infection?

A

Elevated Anti-HAV IgM is diagnostic in the symptomatic patient

170
Q

What is the treatment for Hepatitis A infection?

A

Supportive
If unvaccinated & exposed –> prophylaxis with HAV vaccine (preferred) or immune globulin (IG)

If immunosuppressed –> administer both vaccine and IG

171
Q

What should be avoided in active Hep A infections?

A

alcohol and hepatotoxic meds (eg acetaminophen)

172
Q

When should food handlers return to work if infected with Hep A?

A

when jaundice clears
(IgM will remain elevated for 3-6 months, IgG remains elevated for life)

173
Q

What type of virus is Hepatitis B?

A

double stranded DNA virus

174
Q

What percent of those infected with Hep B with develop chronic infection?

A

10%

175
Q

How does age at infection relate to risk of chronic infection?

A

inversely related; older = lower risk, younger = higher risk of chronic infection

176
Q

What percentage of patients with chronic Hep B develop cirrhosis?

A

15-20%

177
Q

What percentage of patients with chronic Hep B develop hepatocellular carcinoma?

A

10-15%

178
Q

What is the most common cause of Hep B infection worldwide?

A

maternal –> fetal

179
Q

What are the symptoms of Hep B?

A

similar to Hep A

flulike illness, RUQ pain, followed by onset of jaundice and pruritus
PEx: hepatosplenomegaly and jaundice

180
Q

How is active Hep B infection diagnosed?

A

HBsAg: Hepatitis B surface antigen (acute or chronic active infection)

181
Q

What lab findings are consistent with immunity from Hep B due to vaccination?

A

+Hepatitis B surface antibody only (no core antibody)

182
Q

What lab findings are consistent with immunity from Hep B due to recovery from prior infection?

A

+Hep B surface antibody AND +Anti-HBc IgG (Hep B core Antibody IgG)

183
Q

Which lab findings is related to Hepatitis B infectivity?

A

HBeAg: Hepatitis Be antigen; proportional to the quantity of intact virus and, therefore, infectivity.

184
Q

What is the treatment for acute hepatitis due to Hepatitis B?

A

Treatment of acute hepatitis is primarily supportive with avoidance of hepatotoxic
agents; transfer to transplant-capable center should occur in fulminate hepatitis.

185
Q

What is the treatment for chronic hepatitis B?

A

Treatment strategies for chronic HBV typically include PegIFN or nucleos(t)ide analogs
(eg, entecavir and tenofovir)

186
Q

What is post-exposure prophylaxis for completely vaccinated person exposed to HBsAg positive source?

A

Completely vaccinated persons should
receive booster.

187
Q

What is post-exposure prophylaxis for partially vaccinated person exposed to HBsAg positive source?

A

Partially vaccinated persons should receive hepatitis B immune globulin (HBIG) within 24 hours and complete their vaccination series.

188
Q

What is post-exposure prophylaxis for unvaccinated person exposed to HBsAg positive source?

A

Unvaccinated persons should receive HBIG and hepatitis B vaccine.

189
Q

What is post-exposure prophylaxis for and person exposed to HBsAg unknown person?

A

Initiate or complete the vaccination
series.

190
Q

What is the most common cause of blood-borne infection?

A

Hepatitis C

191
Q

What is the most common caused of chronic liver disease in the US?

A

Hepatitis C

192
Q

What percentage of Hep C infections will develop chronic infection?

A

75-85%

193
Q

What is the most common cause of Hep C infection?

A

Injection drug use or blood product transfusion prior to 1992 are the predominant causes in the United States and Europe. (Needle stick, dialysis,
and other parenteral exposures are also implicated.)

194
Q

What are the symptoms of acute Hepatitis C virus infection?

A

Most patients are asymptomatic; may have mild flulike symptoms and jaundice.

195
Q

What are the symptoms of chronic Hepatitis C infection?

A

Chronic HCV: Usually asymptomatic until cirrhosis develops. Also may present with cryoglobulinemia associated with a vasculitic skin rash (leukocytoclastic vasculitis), arthralgias, sicca syndrome, and membranoproliferative glomerulonephritis

196
Q

How is Acute hepatitis C diagnosed?

A

RNA polymerase chain reaction (PCR) and HCV Ab

197
Q

How is Hep C screening performed?

A

HCV antibody (positive 4-6 weeks after infection) and qualitative PCR (positive 1-2 weeks after infection); screen patients with risk factors or
persistently elevated transaminases

198
Q

How is Hep C confirmatory testing performed?

A

Qualitative PCR or recombinant immunoblot assay (RIBA)

199
Q

How is Chronic Hep C treated?

A

sofosbuvir, peginterferon, and/or ribavirin
can be curative in selected patients.

200
Q

What type of virus is Hepatitis D?

A

a defective RNA virus

201
Q

Hepatitis D is a defective RNA virus that requires simultaneous presence of host hepatitis __ virus to replicate.

A

B

202
Q

How is Hepatitis D diagnosed?

A

positive anti-HDV.

203
Q

How is hepatitis D treated?

A

interferons.

204
Q

How is Hepatitis E transmitted?

A

fecal-oral transmission

205
Q

In what population is mortality from Hepatitis E high?

A

pregnant patients (10-20%)

206
Q

How is hepatitis E diagnosed?

A

positive anti-HEV IgM (acute infection) and anti-HEV (prior exposure)

207
Q

What is treatment for Hep E?

A

supportive

208
Q

What are risk-factors for drug-induced hepatitis?

A

advanced age
female gender
increasing # of prescription meds
underlying liver disease
renal insufficiency
poor nutrition

209
Q

What is treatment for autoimmune hepatitis?

A

varies by case, but typically with steroids and/or azathioprine

210
Q

How is liver cirrhosis defined?

A

hepatocellular injury leading to fibrosis and nodular regeneration

211
Q

What are the sigmata/physical exam findings in liver cirrhosis?

A

Palmar erythema, spider telangiectasia,
Dupuytren contractures, gynecomastia, testicular atrophy, Terry nails (white
opacification of proximal two-third of the nail)

212
Q

What are signs & symptoms of portal HTN?

A

Caput medusae, splenomegaly, ascites, varices

213
Q

What is the gold standard fo dx of liver cirrhosis?

A

Liver biopsy

214
Q

What is the medical management of ascites?

A

restrict dietary sodium and consider diuretic therapy (spironolactone ± loop diuretic)

215
Q

What typically causes SBP?

A

translocation of bacteria from the intestines to the ascitic fluid

216
Q

What is the most common organism implicated in SBP?

A

The most common organism implicated is Escherichia coli.
Other organisms include Streptococcus and Enterococcus spp

217
Q

How is SBP diagnosed?

A

paracentesis with
PMNs >250 cells/mm^3.

218
Q

What is the treatment for SBP?

A

Third-generation cephalosporin (eg, cefotaxime)

219
Q

When should SBP prophylaxis be initiated?

A

indicated for cirrhotic patients
1. hospitalized with GI bleed (3 days);
2. ascites with total protein < 1.5 g/dL (while hospitalized); or
3. ascites in a pt w/ a hx of SBP

220
Q

What medication(s) are used for SBP prophylaxis?

A

Fluoroquinolones or TMP-SMX once daily

221
Q

What causes hepatic encephalopathy in liver failure patients?

A

accumulation of nitrogenous waste products

222
Q

What is asterixis?

A

wrist flaps rhythmically when held in extension);

223
Q

What is fetor hepaticus?

A

musty breath in liver cirrhosis patient with hepatic encephalopathy

224
Q

How is hepatic encephalopathy diagnosed?

A

Diagnosis is clinical. Blood ammonia levels are typically elevated but do not correlate with degree of encephalopathy

225
Q

What is the treatment for hepatic encephalopathy?

A

Lactulose, given PO, PR, or by NGT (adverse effects include dehydration and hypokalemia from diarrhea). Oral neomycin, rifaximin, or
metronidazole.

226
Q

What is hepatorenal syndrome?

A

a type of subacute or acute kidney injury in patients with severe cirrhosis.

227
Q

What is the prognosis in someone with hepatorenal syndrome?

A

The prognosis is poor;
median survival is 10-14 days
2-month mortality is 90%

228
Q

What is the most common cause of hepatic abscess in the US?

A

due to biliary obstruction or cholangitis

229
Q

What bacteria are implicated in hepatic abscess?

A

polymicrobial

230
Q

Primary amebic liver abscesses are due to which organism?

A

Entamoeba histolytica

231
Q

How is liver abscess diagnosed?

A

CT or RUQ US
Abscess aspiration and culture are definitive

232
Q

What is the treatment for liver abscesses?

A

Start empiric therapy covering both pyogenic and amoebic abscess (metronidazole,
and either ceftriaxone or piperacillin-tazobactam).

233
Q

What is the most common malignant tumor of the liver?

A

Hepatocellular carcinoma

234
Q

What is the major risk factor for HCC?

A

cirrhosis;
other associated risk factors: aflatoxin exposure, a1-antitrypsin deficiency, hemochromatosis

235
Q

What is the treatment for HCC?

A
  1. Local regional therapy (radiofrequency ablation, chemoembolization) is not curative but often is performed as a bridge to liver transplantation.
  2. Liver transplant or surgical resection can be curative for limited stages without extrahepatic metastasis.
  3. Systemic chemotherapy is used for palliation only.
236
Q

What is the most common benign neoplasm of the liver?

A

hemangioma

237
Q

What causes increase of hepatic hemangiomas?

A

use of exogenous hormones

238
Q

What do you call hypervascular mass of hepatocytes?

A

focal nodular hyperplasia

239
Q

What are risk factors for hepatic adenomas?

A

common in women in 30s and 40s
strongly linked to oral contraceptive use
increased size with hormone use

240
Q

What is the treatment for hepatic adenomas?

A

resection – advised to prevent necrosis and rupture

241
Q

What is cholelithiasis most commonly composed of?

A

cholesterol stones

242
Q

What are risk factors for cholesterol GB stones?

A

increased age, female gender, obesity, rapid weight loss, CF, parity, certain drugs, and
family history.

243
Q

What element is in GB pigment stones?

A

calcium

244
Q

What are risk factors for pigment stones (GB)?

A

chronic intravascular hemolysis (eg, sickle cell disease, spherocytosis) and biliary infection

245
Q

What is the treatment for choledocholithiasis?

A

Endoscopic retrograde cholangiopancreatography (ERCP) with sphincterotomy for removal of stone, followed by semielective cholecystectomy

246
Q

What are risk factors for acalculous cholecystitis?

A

TPN
trauma
burn victims

247
Q

In suspected cholecystitis, what is the next step when ultrasound is equivocal?

A

HIDA scan

248
Q

What is gas in the gallbladder wall indicative of?

A

emphasymatous cholecystitis

249
Q

What is a risk factor for emphasymatous cholecystitis?

A

diabetes and gas-producing organisms

250
Q

What is the treatment for cholecystitis, besides surgical consultation?

A

antibiotics: pip/tazo or ertapenem

251
Q

In unstable patients, what is an alternative to cholecystectomy?

A

percutaneous drain placement

252
Q

What do you call an infection of the biliary tree resulting from biliary obstruction and stasis?

A

acute bacterial cholangitis

253
Q

What pathogens are commonly implicated in acute cholangitis?

A

E coli, Enterobacter,
Pseudomonas

254
Q

What are risk factors for acute cholangitis?

A

gallstones (85% of cases),
bile duct stricture, ampullary carcinoma, and pancreatic pseudocyst

255
Q

What do you call the autoimmune process characterized by progressive inflammation of the biliary tree, often associated with UC?

A

Primary Sclerosing Cholangitis (PSC)

256
Q

What is Charcot’s triad and what is it indicative of?

A

RUQ pain, jaundice, and fever
acute cholangitis

257
Q

What is reynolds pentad?

A

RUQ pain, jaundice, and fever
+hypotension, +AMS

=severe cholangitis (often termed acute suppurative cholangitis)

258
Q

How is acute cholangitis diagnosed and treated?

A

Ultrasound or CT; ERCP is both diagnostic and therapeutic.

259
Q

How is acute cholangitis treated?

A

Pip/tazo

OR
Cefazolin/Cefuroxime/Ceftriaxone/Cefotaxime/Ciprofloxacin
PLUS metronidazole,

260
Q

How is acute suppurative cholangitis treated?

A

Abx PLUS
emergent bile duct decompression via ERCP sphincterotomy, percutaneous transhepatic drainage, or open decompression

261
Q

What is AIDS Cholangiopathy and at what CD4 count is it typically seen?

A

several pathological processes associated with biliary obstruction and resultant inflammation/cholangitis seen in AIDS patients,
typically with CD4 counts < 200/mm3.

262
Q

Which AIDS-associated infections are commonly implicated in AIDS Cholangiopathy?

A

CMV, mycobacterium avium complex [MAC], cryptosporidium

263
Q

What are the two most common causes of pancreatitis in US adults?

A

EtOH and gallstones (accounts for 80% of pancreatitis)

264
Q

What are the two most common causes of pancreatitis in US adults?

A

EtOH and gallstones (accounts for 80% of pancreatitis)

265
Q

What is the most common cause of pancreatitis in children in US?

A

trauma

266
Q

What medications are known to cause pancreatitis?

A

Azathioprine, pentamidine, sulfonamides, thiazide diuretics, 6MP,
valproic acid, dideoxyinosine

267
Q

What two viruses are implicated in pancreatitis?

A

mumps, coxsackie B

268
Q

What parasite can occasionally cause pancreatitis?

A

Ascaris lumbricoides

269
Q

What do you call umbilical ecchymosis associated with retroperitoneal hemorrhage due to pancreatitis?

A

Cullen Sign

270
Q

What do you call flank ecchymosis associated with retroperitoneal hemorrhage due to pancreatitis?

A

Grey Turner Sign

271
Q

What lab value is diagnostic of pancreatitis?

A

Lipase >3x normal

272
Q

What AST/ALT ratio suggests EtOH abuse?

A

AST/ALT ratio >2

273
Q

What other metabolic/electrolyte disturbances are commonly seen in pancreatitis?

A

hyperglycemia, hypocalcemia

274
Q

What is used to estimate mortality of patients with pancreatitis, based on initial and 48-hour lab values?

A

Ranson criteria

275
Q

What is the only effective treatment for pancreatitis in the first 24-48 hours?

A

IV fluid hydration

276
Q

How is adequate fluid hydration assessed in treatment of pancreatitis?

A

Adequate fluid replacement can be assessed by
1. improvement in vital signs (goal heart rate <120 beats/minute, mean arterial pressure between 65 to 85 mmHg),
2. urine output (>0.5 to 1 cc/kg/hour) and
3. reduction in hematocrit (goal 35 to 44 percent) and BUN over 24 hours,

277
Q

Should antibiotics be given in acute pancreatitis?

A

NOT indicated unless necrotizing infection, septic, or unstable

278
Q

What is the treatment for gallstone pancreatitis?

A

ERCP for stone removal and cholecystectomy following recovery but prior to discharge

279
Q

When should you suspect necrotizing pancreatitis?

A

Suspect in setting of a persistently elevated
WBC count (7-10 days), high fever, and shock (organ failure)

280
Q

What is a pancreatic pseudocyst?

A

A collection of pancreatic fluid walled off by
granulation tissue

281
Q

When is drainage indicated for pancreatic pseudocysts?

A

resolves spontaneously in about 50%.
Drainage not required unless the pseudocyst
is present for > 6-8 weeks and is enlarging and symptomatic

282
Q

What type of cancer is 90% of pancreatic cancers?

A

pancreatic ductal adenocarcinomas, mostly in the pancreatic head

283
Q

What are risk factors for pancreatic cancer?

A

smoking, chronic pancreatitis, a first-degree
relative with pancreatic cancer, obesity, and DM

284
Q

What is Courvoisier sign?

A

a palpable, nontender gallbladder associated with pancreatic cancer

285
Q

What is Trousseau sign?

A

migratory thrombophlebitis associated with pancreatic cancer

286
Q

How can pancreatic cancer be identified?

A

CT scan

If a mass is not visualized, use ERCP or endoscopic ultrasound for better
visualization and consider fine-needle aspiration.

287
Q

What is the most common etiology of mesenteric ischemia?

A

most commonly (> 50%) due to occlusive embolism involving the SMA

288
Q

What is the classic physical exam finding of mesenteric ischemia?

A

abdominal pain out of proportion to clinical
examination

289
Q

What is the most common risk factor for mesenteric ischemia?

A

atrial fibrillation

290
Q

How is mesenteric ischemia diagnosed?

A

CT angiography or conventional angiography

291
Q

What is the treatment for mesenteric ischemia?

A

IV fluids
Antibiotics
Heparin
General or Vascular surgery consult

292
Q

Asplenic patients are at risk of infection due to encapsulated organisms and gram negatives which include?

A

Neisseria meningitidis, Haemophilus influenzae, and Streptococcus pneumoniae

E coli, Pseudomonas aeruginosa

293
Q

What findings are common on peripheral blood smear in asplenic patients?

A

Howell Jolly bodies
Pocked erythrocytes
(both normally removed by the spleen)

294
Q

What antibiotics should be given to all asplenic patients presenting with fever?

A

antibiotics targeting S pneumoniae (eg, ceftriaxone ± vancomycin)

295
Q

What is the difference between splenomegaly and hypersplenia?

A

Slenomegaly = enlargement of the spleen
hypersplenism = increased destruction of blood cells by the enlarged spleen

296
Q

What length on US constitutes splenomegaly?

A

> 13 cm

297
Q

Why is thrombocytopenia often seen in hypersplenism due to portal HTN, hematologic malignancies, and hemolytic anemias?

A

due to splenic sequestration

ITE '23 (20 decks)

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