Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

ABIM > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

recent MI, combative patient, and intestinal perforation

A

relative contraindication to GI endoscopy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

procedure of choice for: evaluation of odynophagia, finding PUD, before PUD surgery, if GERD treatment fails, alarm signals, UGI bleeds, dysphagia AFTER barium swallow, foreign body removal, small bowel disease, persistent dysphagia, placement of feeding or drainage tubes

A

EGD (esophagogastroduodenoscopy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

if patient has a possible bile duct obstruction give antibiotics before

A

ERCP (endoscopic retrograde cholangiopancreatography)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

biliary obstruction, dx/tx pancreatic duct obstruction, dx of PSC (primary schlerosing cholangitis), tx of choledocholithiasis with cholangitis are indications for…

A

ERCP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

further eval of abnormal biliary or pancreatic duct imaging from CT/MRCP/EUS
other indications for…

A

ERCP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

ERCP is CONTRAINDICATED in ACUTE pancreatitis, except:

A
  1. impacted gallstones

2. ascending cholangitis (bacterial infection causing cholangitis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

bile duct obstruction, chronic pancreatitis, if acute pancreatitis doesn’t get better, and is the test of choice for PSC (primary sclerosis cholangitis)

A

MRCP (magnetic resonance cholangiopancreatography)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what visualizes the bile tract?

A

retrograde cholangiography

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what visualizes the pancreatic duct?

A

retrograde pancreatography

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

staging GIT, biliary tree, and pancreatic malignancy
diagnosing chronic pancreatitis
dx/tx pancreatitis complications
providing access to pancreatic duct or biliary tree

A

EUS (endoscopic ultrasonography)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

normal swallowing

A

deglutition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

when swallowing doesn’t proceed appropriately for any reason

A

dysphagia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

pain with swallowing

A

odynophagia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

3 main causes of dysphagia

A
  1. transfer disorders (oropharyngeal)
  2. anatomic/structural disorders
  3. motility disorders
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

you should always work up this disorder and NOT treat it empirically

A

dysphagia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

usually the 1st test performed to work up dysphagia

A

barium swallow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

definitely the 1st test performed to work up dysphagia if symptoms are SEVERE, or new-onset dysphagia with LIQUIDS

A

barium swallow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

why is barrium swallow done before endoscopy?

A
  1. avoid risk of PERFORATION if there’s DIVERTICULA or OBSTRUCTION
  2. may not need endoscopy if barium swallow is enough
  3. gives endoscopist idea of what to expect
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

if a patient has h/o reflux and presents with slight-to-moderate dysphagia for solids you can do this test first

A

EGD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

generally only done if dysphagia persists after negative barium swallow and EGD

A

esophageal manometry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

general workup of dysphagia

A
  1. barium swallow
  2. endoscopy
  3. manometry study
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

chest pain, dysphagia for SOLIDS and LIQUIDS, usually years, regurgitation

A

achalasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

finding on barium swallow in achalasia

A

bird-beak narrowing distally

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

done to diagnose and exclude a tumor at esophagogastric junction (“pseudoachalasia”)

A

EGD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

done to confirm dx of achalasia before tx

A

esophageal manometry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

absence of normal peristalsis, and non-relaxing LES

A

manometry findings in achalasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

3 distinct subtypes of achalasia seen using high resolution manometry

A
  1. traditional aperistalsis
  2. esophageal compression
  3. generalized spasm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

if you’re thinking of achalasia and see the following:
RAPID onset of symptoms, patient older than 60 years, PROGRESSIVE symptoms, and profound WEIGHT LOSS

you should worry about this…

A

cancer!

pseudoachalasia or secondary achalasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

3 treatment options for achalasia

A
  1. pneumatic dilation
  2. onabotulinum-toxin A (Botox)
  3. surgical myotomy (done via laparoscope)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

how effective is Botox for achalasia, and how often do you need to repeat therapy?

A
  • works 65% of cases
  • need to repeat every 6-12 months
  • not the greatest, but a decent alternative in patients who are high-risk for surgery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

simultaneous, nonperistaltic concentration of esophagus, worse with COLD or CARBONATED liquids

A

diffuse esophageal spasm (DES)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

causes esophageal spasms even without typical reflux symptoms

A

OCCULT REFLUX

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

barium swallow for DES shows what?

A

generally normal, but can show CORKSCREW pattern

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Type 3 achalasia, with excess, simultaneous (nonperistaltic) contractions in distal esophagus with NORMAL LES relaxation

A

high resolution manometry findings of DES

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what test is not helpful in DES workup?

A

EGD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what should be done if REFLUX is considered a possible cause of DES?

A
  • 24-hour esophageal pH recording, OR

- PPI BID for 3 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

most important part of DES tx

A

REASSURANCE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

if reassurance isn’t enough, treat DES with these:

A

1st line: DILTIAZEM or IMIPRAMINE
2nd line: isosorbide or sildenafil
3rd line: botulinum toxin injection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

SLOWLY PROGRESSIVE dysphagia- INITIALLY TO SOLIDS, then liquids

A

anatomic obstruction

  • Schatzki ring in YOUNGER patients
  • CANCER, or STRICTURE in OLDER patients
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

main problem: sxs are…: sxs precipitated by…

  1. anatomic: intermittent: solids
  2. anatomic: progressive: solids, THEN liquids
  3. anatomic: progressive: solids, THEN liquids
  4. motility/neurologic: longstanding: solids, AND liquids
  5. motility/neurologic: intermittent: solids, AND liquids (esp. COLD)
  6. various: progressive: solids AND liquids
A

disease

  1. Schatzki ring
  2. esophageal stricture
  3. cancer
  4. achalasia
  5. DES
  6. systemic sclerosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

common cause of dysphagia, YOUNGER patients

A

lower esophageal ring or Schatzki ring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

very slowly progressive, INTERMITTENT, SOLID FOOD dysphagia (meat and bread)

A

lower esophageal ring or Schatzki ring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

lower esophageal ring or Schatzki ring is ALWAYS associated with…

A

HIATAL HERNIA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

treatment for lower esophageal ring or Schatzki ring

A

1a. dilation (with bougie method),
1b. or (through-the-scope) hydrostatic balloon
2. THEN PPIs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

slowly progressive, CONSTANT (not intermittent) dysphagia for SOLID FOODS

A

esophageal stricture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

esophageal strictures are commonly d/t

A

ACID REFLUX

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

other causes of esophageal strictures

A
  1. PROLONGED NASOGASTRIC TUBE placement

2. LYE INGESTION

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

barium swallow for esophageal stricture shows what?

A

narrowing at esophagogastric junction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

how do you treat esophageal stricture?

A

dilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

what are the 3 causes of malignant esophageal obstruction?

A
  1. esophageal adenocarcinoma
  2. squamous cell carcinoma
  3. extrinsic compression from NONesophageal primary cancers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

this PROGRESSION of symptoms: SOLID food dysphagia to SOFT food, finally dysphagia with LIQUIDS
is what until proven otherwise?

A

esophageal malignancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

a rare d/o that causes dysphagia d/t UPPER esophageal web

A

Plummer-Vinson syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

what type of dysphagia is found in POSTMENOPAUSAL WOMEN, is associated with IRON-DEFICIENCY ANEMIA, and has a slightly increased risk of squamous cell esophageal cancer?

A

Plummer-Vinson syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

dysphagia to both SOLIDS AND LIQUIDS from time of onset

A

some sort of neurologic dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

examples of neurological dysfunctions causing dysphagia

A
  • STROKE
  • PARKINSONISM
  • BULBAR PALSY (lower motor neuron- ALS, MS)
  • PSEUDOBULBAR PALSY (upper motor neuron- ALS)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

if you suspect aspiration d/t neurologic dysfunction, what’s the next best step?

A

BARIUM SWALLOW to confirm dx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

more than 80% of what patients have involvement of esophagus?

A

diffuse SSc (systemic sclerosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

what is the LES pressure in patients with dysphagia d/t systemic sclerosis?

A

“wide-open” with low or NO tone/pressure

causes severe acid reflux

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

what are the 3 possible causes of dysphagia in systemic sclerosis? and what is the workup?

A
  1. esophagitis
  2. stricture
  3. impaired motility

barium swallow then EGD (to look for all 3)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

if you have esophagitis in a SSc patient what do you do?

A
  • aggressive PPI tx

- FOLLOW-UP endoscopy at 2-3 MONTHS to make sure it’s working and/or dilate strictures if any

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

what rheumatological diseases can present with dysphagia like SSc?

A

polymyositis and dermatomyositis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

immune-mediated chronic eosinophil-predominant inflammatory d/o of esophagus

A

eosinophilic (allergic) esophagitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

pathogenesis involves interleukin-5 (IL-5) and eotaxin

A

eosinophilic (allergic) esophagitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

occurs most commonly in MEN age 20-40 years

A

eosinophilic (allergic) esophagitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

strong association with ALLERGIES; environmental, food, asthma, and atopy

A

eosinophilic (allergic) esophagitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

IgE is elevated in 2/3 of patients

A

eosinophilic (allergic) esophagitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

leading symptom is recurrent attacks of dysphagia with food impaction, and usually goes undiagnosed for 4-5 years

A

eosinophilic (allergic) esophagitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

if you have PERIPHERAL eosinophilia symptoms are _____, and is found in what percentage of patients?

A

WORSE

~ 30% of patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

SCALLOPED APPEARANCE with ridges or rings (trachealization) in esophagus

A

“classic” EGD finding of EoE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

how do you confirm dx of EoE?

A

esophageal biopsies showing dense eosinophilic infiltration of esophageal epithelium (> 15 eos/HPF)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

which patients also have increased eosinophils?

A

GERD patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

EoE tx?

A
  • allergy testing
  • avoid potential allergens
  • fluticasone (BID) or viscous budesonide (usually results in a response within 1 week)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

for patients with EoE, and concomitant reflux, or PPI-responsive eosinophilic esophagitis, what medication, in addition to steroids, can be added to help with tx?

A

PPI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

odynophagia (painful swallowing) is usually d/t what?

A
  1. pill-induced esophagitis

2. opportunistic infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

common causes of pill-induced esophagitis

A
  1. doxycycline (teenager with acne)
  2. KCl
  3. ASA
  4. NSAIDs
  5. iron
  6. bisphosphonates (alendronate)
  7. quinidine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

dx and tx of pill-induced esophagitis

A
  • made solely on history

- sit in upright position and drink plenty of water

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

opportunistic infections (OIs) occur in these patients:

A
  • immunocompromised: HIV, or diabetes

- immunocompetent taking corticosteroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

common OIs are:

A
  1. Candida
  2. herpes simplex virus (HSV)
  3. cytomegalovirus (CMV)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

what to do with esophagitis with thrush in the mouth?

A
  • treat Candida empirically with FLUCONAZOLE

- if it doesn’t get better, EGD with biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

what is a genetic variable that affects PPI efficacy? and which gives the best results?

A
  • slow, moderate, and fast metabolizers

- slow metabolizers have MUCH better results than fast metabolizers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

short term adverse effect of PPI

A

COMMUNITY-ACQUIRED PNEUMONIA (CAP)

more likely within 30 days, especially within 48 hours of initialization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

long term adverse effects of PPI

A
  • FRACTURE risk is increased

- HYPOMAGNESEMIA (muscle spasms, arrhythmias, seizures)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

what happens when you stop PPIs abruptly after several months?

A

REBOUND ACID HYPERSECRETION (especially in H. pylori-NEGATIVE patients)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

should you use a PPI long-term?

when is long-term use of PPIs necessary?

A

no, it’s discouraged

Barrett esophagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

PPIs DECREASE absorption and serum levels of

A

THYROXINE and ITRACONAZOLE/KETOCONAZOLE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

PPIs INCREASE absorption and serum levels of

A

DIGOXIN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

can you give clopidogrel with omeprazole?

A

YES, benefits outweigh risk

more studies needed for slow metabolizers of clopidogrel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

gastroesophageal reflux is a result of…

A

transient relaxation of lower esophageal sphincter (LES)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

motilin, acetylcholine, and maybe gastrin INCREASE…

A

LES pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

progesterone (pregnancy increases GE reflux), chocolate, smoking, some medications (anticholinergics, especially) DECREASE…

A

LES pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

persistent, nonproductive cough, hoarse voice, clearing of throat, fullness of throat, suspect…

A

gastroesophageal reflux disease (GERD)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

most common non-cardiac chest pain (70%) cause

A

GERD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q 
nocturnal cough
frequent sore throat
hoarseness, laryngitis, clearing of throat
loss of dental enamel
exacerbation of asthma
VCD (vocal cord dysfunction)
A

extraesophageal manifestations of GERD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

what should you always ask about in the w/u of GERD patients?

A

ASTHMA SYMPTOMS; especially if they occur at night

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

w/u of suspected GERD depending on situation (6 scenarios)

A
  1. heartburn alone –> trial treatment –> improvement
  2. ALARM SYMPTOMS or persistent GERD symptoms –> endoscopy
  3. erosive esophagitis: if immunocompetent –> treat
  4. erosive esophagitis: if immunocompromised –> treat based on biopsy
  5. stricture –> treat
  6. normal= nonerosive reflux disease (NERD) (62% of patients) –> do NOTHING
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

spasm of vocal cords with associated INSPIRATORY stridor

A

vocal cord dysfunction (VCD)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

associated with increased incidence of both GERD and asthma

A

increased body mass index (BMI)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

if you’re thinking Barrett esophagus in a GERD patient…

A

do an EGD

if patient has obstructive symptoms, do a barium swallow first

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

do a 24-hour esophageal pH MONITOR for atypical cases with impedance if:

A
  1. normal EGD and still have symptoms
  2. hoarseness, coughing, or atypical chest pain, but no sxs of GERD
  3. treatment failure to PPIs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

MILD-TO-MODERATE GERD treatment

A

INITIAL:

  • RAISE HEAD OF BED
  • WEIGHT LOSS OF > 10LB if overweight

ANTISECRETORY drugs if unsuccessful

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

healing of esophagitis (not necessarily GERD) based on treatment

A

placebo= 25%
H2 blockers= 50%
PPIs= 80-95%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

tx for SEVERE GERD

A

PPIs, indefinitely

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

fundoplication indications:

A
  1. patients REFRACTORY to medical tx
  2. YOUNG patients with SEVERE disease
  3. ALTERNATIVE to PPIs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

patients with worse GERD symptoms (GERD-related cough, hoarseness) need…

A

stronger and longer treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Barrett esophagus is…

A

change from esophageal SQUAMOUS to columnar epithelium with goblet cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

SCREENING for Barrett’s is…

A

CONTROVERSIAL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

recommended guidelines for Barrett screening

A

white males > 50
long-standing GERD
elevated BMI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Barrett esophagus is associated with kind of cancer?

A

ADENOCARCINOMA ONLY

not squamous cell carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

incidence of adenocarcinoma in Barrett esophagus

A

30x normal rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

antireflux meds and surgery do what for Barrett esophagus?

A

they don’t reverse epithelial changes or eliminate cancer risk, but help with sxs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

if Barrett esophagus is found, f/u endoscopies should be done based on findings

A
  • no dysplasia: 3-5 years
  • low-grade dysplasia: 6-12 months
  • high-dysplasia without eradication therapy: 3 months
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

for HIGH-GRADE dysplasia in Barrett esophagus you should do ERADICATION therapy, which is…

A

radiofrequency ablation (RFA) or endoscopic mucosal resection (EMR)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

what other eradication therapy can be done for HIGH-GRADE dysplasia in Barrett esophagus?

A

esophagectomy, but has HIGHER MORBIDITY

should be done in centers that SPECIALIZE in them

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

2 types of esophageal cancer:

A 
1. adenocarcinoma, now more common
occurs in DISTAL 1/3
2. squamous cell
generally occurs in PROXIMAL 2/3
caused by SMOKING and ALCOHOL (especially hard liquor)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

smoking and alcohol have what effect on squamous cell carcinoma of esophagus?

A

SYNERGISTIC (multiplicative, NOT additive) carcinogenic effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

squamous cell cancer of esophagus is strongly associated with…

A

geographic location, DIET, and ENVIRONMENT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

usual presenting symptom of esophageal cancer

A

DYSPHAGIA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

treatment of esophageal cancer, if:
small and localized, then…
large or metastasized, then…

A

surgical resection

combination chemotherapy (cisplatin and 5FU) PLUS radiation PRIOR to surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

Zenker diverticulum is

A

outpouching of UPPER esophagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

common symptoms of Zenker diverticulum

A

FOUL-SMELLING BREATH

REGURGITATION of food eaten several days earlier

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

MCC of TRANSFER DYSPHAGIA (trouble initiating swallowing)

A

Zenker diverticulum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

treatment of Zenker diverticulum

A

surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

ENDOCRINAL stimulus for gastric acid release

A

gastrin (released by G cells in pylorus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

most important for postprandial gastric acid production

A

gastrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

PARACRINE stimulus for gastric acid release

A

histamine (released by ECL (enterochromaffin-like) cells in corpus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

neurocine effect, stimulation vagus nerve releases what onto G cells?

A

gastrin-releasing peptide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

what decreases production of gastrin (and therefore gastric acid)

A

somatostatin and secretin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

secretin is made by the duodenum when stomach is acidified causing:

A
  1. DECREASE in GASTRIN production

2. stimulates output of BICARBONATE from pancreas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

serum gastrin level skyrockets, when?

A

patients with achlorhydria (autoimmune gastritis), or pernicious anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

upper abdominal pain or discomfort especially after meals

A

dyspepsia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

symptoms of dyspepsia

A

epigastric fullness, belching, bloating, gnawing pain, and heartburn
(generally not severe pain)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

causes of dyspepsia

A

PUD, gastritis, GERD, biliary colic, gastroparesis, pancreatitis, and cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

classification of dyspepsia by symptoms:

A

GERD-LIKE, ULCER-LIKE (improves on anti-ulcer therapy)

DYSMOTILITY-TYPE (improves on promotility drugs, such as metoclopramide)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

recurrent upper abdominal pain with NORMAL EGD

A

NON-ULCER dyspepsia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

treatment plan for dyspepsia

A
  1. discontinue NSAIDs
  2. test and treat if H. pylori +
  3. conduct a PPI treatment trial
  4. order EGD if alarm symptoms or failure of therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

how is gastritis classified?

A

either histology or etiology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

classification of gastritis by histology:

A
  1. superficial gastritis (early, neutrophils)
  2. atrophic gastritis (mid, lymphocytes)
  3. gastric atrophy (late, gastropathy aka metaplastic atrophic gastritis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

classification of gastritis by etiology:

A

type A: Autoimmune, Atrophic, pernicious Anemia, Achlorhydria
type B: MOST COMMON form chronic gastritis (80%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

what part of the stomach does type A gastritis affect?

A

PROXIMAL stomach (fundus and corpus only)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

autoantibodies against BOTH intrinsic factor and parietal cells cause what?

A

pernicious Anemia and Achlorhydria, and secondary hypergastrinemia (> 1000 pg/mL)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

common cause of type B gastritis

A

H. pylori infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

itraconazole, ketoconazole, and thyroxine require what?

A

GASTRIC ACID for optimal absorption

fluconazole does NOT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

causes of erosive gastropathy (with subepithelial hemorrhage)

A

NSAIDS, ALCOHOL, or SEVERE PHYSIOLOGIC STRESS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

onset of erosive gastropathy in the ICU suggests

A

STRESS-RELATED MUCOSAL DAMAGE (SRMD)

a. major surgery
b. burns
c. severe CNS injuries
d. being on a ventilator
e. coagulopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

MOST EFFECTIVE treatment for SRMD

A

H2 receptor antagonist gtt or PPI gtt

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

H. pylori infection can cause:

A
  1. GASTRITIS
  2. PUD
  3. GASTRIC ADENOCARCINOMA
  4. GASTRIC B-CELL (MALT) LYMPHOMA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

who gets treated in chronic gastritis?

A

only SYMPTOMATIC patients

h/o gastric/duodenal ulcer, personal/family h/o gastric cancer, personal h/o MALT lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

test for H. pylori when:

A
  1. h/o PUD
  2. EGD showing ulcer disease, erosive gastritis, or duodenitis
  3. MALT lymphoma
  4. family h/o gastric cancer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

how is dyspepsia treated?

A
  • discontinue NSAIDs
  • test and treat if H. pylori +
  • conduct PPI trial
  • order EGD if alarm symptoms or PPI treatment failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

invasive tests for H. pylori

A
  1. EGD with biopsy= GOLD STANDARD

2. CLOtest and other rapid urease tests

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

noninvasive tests for H. pylori

A
  1. urea breath test (1st choice for treatment effectiveness)
  2. fecal antigen test (good for primary diagnosis)
  3. serologic test (not a good test)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

what interferes with urease test (CLOtest)?

A

PPIs, stop for 2 weeks before

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

which test has poor PPV for H. pylori?

A

serologic tests

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

is H. pylori treatment different for gastritis or PUD?

A

no, it’s the SAME

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

H. pylori treatment

A

triple-drug therapy

O-CLAM (omeprazole 20mg + clarithromycin 500mg + amoxicillin 1G; all BID x 10-14 days)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

should you test for H. pylori after treatment?

A

NOT recommended

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

in what situations do you test for H. pylori after treatment?

A
  1. h/o H. pylori-associated ulcer
  2. persistent dyspepsia despite test-and-treat strategy
  3. H. pylori MALT lymphoma
  4. resection of early gastric carcinoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

how soon should you test for H. pylori after treatment?

A

no sooner than 4 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

4 causes of peptic ulcer disease (PUD)

A
  1. Helicobacter pylori infection (MCC)
  2. NSAIDs
  3. high acid secreting states (Zollinger-Ellison)
  4. Crohn disease of duodenum/stomach
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

risk factors for NSAID-induced PUD

A
  1. first 3 months of use
  2. high doses
  3. elderly patient
  4. history of ulcer disease or prior UGIB
  5. cardiac disease
  6. concurrent steroid use
  7. serious illness
  8. concurrent ASA use
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

is smoking a risk factor for NSAID-induced PUD?

A
  • exacerbates ulcer in gastric/duodenal ulcer disease

- decreases healing rate and increases recurrence/perforation rate in non-H. pylori ulcers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

is ALCOHOL ulcerogenic?

A

NO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

are CORTICOSTEROIDS alone ulcerogenic?

A

NO, but they DOUBLE the risk

may be 10-FOLD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
164
Q

how do you diagnose PUD in YOUNGER/HEALTHY PATIENTS?

A
  • NO diagnosis needed; treat empirically (H2 blocker or PPI)

- or you can test and treat for H. pylori

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
165
Q

how do you diagnose PUD in ALL OTHER PATIENTS?

A

EGD

especially with melena, heme + stool, early satiety, or IDA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
166
Q

you always do EGD in PUD w/u if:

A
  1. symptoms include dysphagia or odynophagia
  2. UGIB
  3. abnormal UGI (barium swallow) or CT scan
  4. family h/o duodenal ulcer disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
167
Q

PERFORATED gastric or duodenal ulcers will show what on upright abdominal x-ray?

A

free air in peritoneal space

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
168
Q

what are CONTRAINDICATED if a perforated ulcer is suspected?

A

EGD and UGI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
169
Q

pain of ulcer vs perforated ulcer

A

gnawing vs usually severe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
170
Q

treatment of PUD

A
  1. H. pylori treatment
  2. decrease acid secretion (H2 blockers, PPIs)
  3. stop exacerbating processes (smoking, NSAIDs)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
171
Q

when is sucralfate effective, but why is it not preferred?

A
  • treatment of NON-H. pylori PUD

- has to be taken QID (PPI is once daily)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
172
Q

in which patient is sulcrafate the SHORT-TERM DOC?

A

renal patients, because it binds PO4, but shouldn’t be used long term because of aluminum accumulation and metabolic bone disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
173
Q

when should you do surgery in PUD?

A
  • UGI bleed (most common)- EGD can’t stop the bleed
  • gastric outlet obstruction- initial treatment is balloon dilation
  • perforation- laparoscopic repair
  • recurrent/refractory ulcers- rare
  • Zollinger-Ellison syndrome- remove underlying gastrinoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
174
Q

MCC of duodenal ulcers

A

H. pylori and NSAIDs

only 1-3% d/t ZES

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
175
Q

what’s better in preventing NSAID-induced ulcers?

A

PPIs and MISOPROSTOL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
176
Q

how long do you treat non-H. pylori gastric ulcers?

A

3 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
177
Q

do gastric ulcers increase gastric cancer risk?

A

NO, but NONHEALING gastric ulcers should be scoped and biopsied to rule it out

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
178
Q

leading cause of BLEEDING ulcers in the US?

A

NSAIDs

bleeding risk is DOSE-RELATED

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
179
Q

NSAID-related ulcer risk is higher in…

A

females and any patient > 70 years of age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
180
Q

what type of NSAIDs have DECREASED GI SIDE EFFECTS?

A

COX-2 inhibitors (celecoxib, meloxicam)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
181
Q

signs of SEVERE peptic ulcer bleed/high risk of rebleed

A
  • hemodynamic instability

- recurrent hematemesis or hematochezia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
182
Q

diagnostic and treatment procedure of choice for UGIB?

A

EGD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
183
Q

emergent EGD should be done in UGIB if?

A
  1. treat current bleed

2. assess risk for rebleed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
184
Q

EGD findings indicating INCREASED chance of rebleeding of ulcer?

A
  1. larger size of ulcer
  2. active bleeding during endoscopy
  3. visible vessels on non-bleeding ulcer
  4. visible clot
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
185
Q

VERY LOW chance of ulcer rebleeding?

A
  1. NO BLEEDING
  2. NO CLOT
  3. NO VISIBLE VESSELS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
186
Q

what doesn’t stop bleeding peptic ulcers?

A
  1. gastric lavage

2. IV vasoconstrictors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
187
Q
  1. Osler-Weber-Rendu (hereditary hemorrhagic telangiectasia)- telangiectasias on skin, buccal/nasal mucosa, GIT, lungs, and brain
  2. Peutz-Jeghers syndrome (PJS)- dark melanin spots on lips, buccal mucosa, and hands and feet
A

2 non-ulcer causes of UGIB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
188
Q

GASTRINOMA, continuous gastrin production, refractory ulcers, and DIARRHEA +/- STEATORRHEA

A

Zollinger-Ellison syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
189
Q

MC presentation of ZES?

A

diarrhea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
190
Q

initial w/u of ZES?

A

serum gastrin level (while off PPI therapy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
191
Q

treatment of newly diagnosed ZES?

A

exploratory surgery with RESECTION OF PRIMARY TUMOR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
192
Q

DRUG OF CHOICE for ZES?

A

PPI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
193
Q

persistently high gastrin levels can cause?

A

gastric CARCINOIDS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
194
Q

gastric carcinoids are caused by?

A

CHRONIC HYPERGASTRINEMIC STATES

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
195
Q

types of gastric carcinoids

A
  • type 1 (70-80%)= AUTOIMMUNE GASTRITIS/PERNICIOUS ANEMIA
  • type 2 ( 5%)= ZES as MEN1
  • type 3 (30%)= SPONTANEOUS (most aggressive)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
196
Q

sometimes gastric carcinoids occur in?

A

patients with VITILIGO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
197
Q

do gastric carcinoids cause carcinoid syndrome?

A

yes, but ALMOST NEVER (they are very slow growing)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
198
Q

4 malignancies of stomach

A
  1. adenocarcinoma (MOST COMMON- 95%)
  2. carcinoids
  3. lymphoma
  4. GIST (gastrointestinal stromal tumors; e.g. leiomyosarcoma)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
199
Q

2 types of gastric adenocarcinoma

A
  1. PROXIMAL DIFFUSE

2. DISTAL INTESTINAL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
200
Q

DISTAL gastric cancer has strong association with?

A

ENVIRONMENTAL factors, especially:

  • little fruits and vegetables, a lot of dried, smoked, and salted foods
  • nitrates and nitrites
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
201
Q

what is most often associated with GASTRIC CANCER?

A

ACANTHOSIS NIGRICANS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
202
Q

what don’t cause gastric cancer?

A

ALCOHOL nor GASTRIC ULCERS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
203
Q

diagnostic procedure of choice for nonhealing ulcer

A

endoscopy with multiple biopsies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
204
Q

should you use tumor markers, such as CEA and AFP, for gastric cancer?

A

NO, they are NOT USEFUL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
205
Q

treatment of gastric cancer

A
  • remove cancer and adjacent LNs

- adjuvant combination chemoradiation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
206
Q

what are symptoms of dumping syndrome postprandial vasomotor?

A

PALPITATIONS, SWEATING, and LIGHTHEADNEDESS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
207
Q

2 types of dumping syndrome

A
  1. EARLY- occurs 30 minutes after eating (hyperosmolality of food and fluid shifts in small bowel)
  2. LATE- occurs 90 minutes after eating (probably d/t hypoglycemia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
208
Q

treatment of dumping syndrome

A
  • restrict sweets
  • separate liquids and solids
  • eat frequent small meals
  • high protein
  • complex carbohydrates
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
209
Q

what is blind loop syndrome?

A
  • BACTERIAL OVERGROWTH leading to FAT and B12 MALABSORPTION

- LOW D-XYLOSE ABSORPTION TEST

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
210
Q

what is afferent loop syndrome?

A
  • ABDOMINAL BLOATING and PAIN 20-60 minutes after eating

- vomiting relieves symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
211
Q

gastroparesis

A
  • delayed gastric emptying (early satiety)

- N/V/abdominal pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
212
Q

gastroparesis in diabetics

A

highly VARIABLE gastric emptying

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
213
Q

w/u for delayed gastric emptying

A
  • RULE OUT obstruction first

- CONFIRM with radiolabeled solid meal (gastric emptying study)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
214
Q

metoclopramide FDA WARNING for LONG-TERM USE

A

extrapyradmidal side effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
215
Q

can erythromycin be used for gastroparesis?

A

NOT VERY USEFUL (can be used acutely)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
216
Q

family members at increased risk of IBD and patient has increased risk of GI cancer in?

A

BOTH, Crohn disease (CD) and ulcerative colitis (UC),

but much higher in UC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
217
Q

complication in both CD and UC, and barium enema is CI in acute exacerbation

A

TOXIC MEGACOLON

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
218
Q

more likely to get CD

A

SMOKERS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
219
Q

split by bacteria in COLON into MESALAMINE (active component) and SULFAPYRADINE

A

sulfasalazine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
220
Q

INEFFECTIVE for CD of SMALL BOWEL

A

sulfasalazine (because it won’t be split into active metabolite)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
221
Q

is the cause of adverse effects of sulfasalazine

A

SULFAPYRIDINE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
222
Q

treats perianal abscesses and fistulas in CD

A

metronidazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
223
Q

enteric-coated corticosteroid with FEWER SYSTEMIC SIDE EFFECTS than prednisone, used for small bowel CD and colon (mild-to-moderate) UC

A

budesonide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
224
Q

PREDNISONE-SPARING, used in both CD and UC, take 3-4 MONTHS to show effect

A

6-mercaptopurine (6-MP) and azathioprine (metabolizes to 6-MP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
225
Q

CD and UC treatment with bone marrow suppressive effects

A

6-mercaptopurine (6-MP) and azathioprine (metabolizes to 6-MP)
MONITOR CBC MONTHLY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
226
Q
  • monoclonal antibodies to TNF-a

- given for MODERATE-TO-SEVERE CD, FISTULOUS CD, and REFRACTORY UC

A

infliximab
certolizumab pegol
adalimumab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
227
Q

infliximab, certolizumab pegol, adalimumab concerns:

A

TB REACTIVATION, but MOST COMMON side effect is URI

check for TB and hepatitis B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
228
Q

drugs proven to decrease relapse rate in CD

A

6-mercaptothioprine, azathioprine, methotrexate, and infliximab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
229
Q
  • lesions: focal, SKIP, deep
  • course: indolent
  • less responsive to prednisone in acute flares
  • granulomas are pathognomonic
  • rectal sparing in 50%
  • abscesses, fistulas
  • small bowel involvement in > 50%
A

Crohn disease (CD)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
230
Q
  • lesions: shallow, CONTINUOUS
  • course: more acute
  • very responsive to prednisone in acute flares
  • NO granulomas
  • rectum ALWAYS involved
  • NO perianal disease
  • backwash ileitis in
A

ulcerative colitis (UC)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
231
Q

drugs that decrease relapse in UC

A

ALL standard drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
232
Q

CD age of presentation

A

20’s or 30’s

but can be any age (70’s-80’s smaller peak)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
233
Q

long-term (> 8 years) CD should be screened how often for cancer?

A

every other year

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
234
Q

common in patients with Crohn disease

A

osteoporosis (abnormal bone density, vitamin D deficiency d/t malabsorption, and/or steroids)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
235
Q

STRING SIGN

A

“string” of contrast going through lumen of terminal ileum in CD

if seen elsewhere in colon, it’s called APPLE-CORE lesion, suggests CANCER

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
236
Q

serologic marker for UC

A

p-ANCA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
237
Q

serologic marker for CD

A

ASCA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
238
Q

extraintestinal manifestations of IBD usually seen in patients with?

A

COLITIS

  • so usually associated with UC, but can be seen in CD that involves the colon
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
239
Q

terminal ileum problems in CD usually NOT found in UC

A
  1. calcium oxalate kidney stones
  2. steatorrhea
  3. gallstones
  4. B12 deficiency
  5. hypocalcemia (from vitamin D malabsorption)
  6. bile acid-induced diarrhea
  7. nutrient malabsorption
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
240
Q

CD gallstone type?

A

PIGMENT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
241
Q

when does B12 MALABSORPTION occur?

A

> 60cm terminal ileum resection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
242
Q

when does bile acid-induced diarrhea occur?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
243
Q

treatment for bile acid-induced diarrhea

A

BILE ACID SEQUESTRANTS (cholestyramine, colestipol)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
244
Q

when does steatorrhea occur?

d/t DECREASED proximal gut concentration of bile salts

A

> 100cm of distal ileum resection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
245
Q

treatment for steatorrhea in CD patients

A

LOW-FAT DIET

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
246
Q

treatment for MILD CD with COLON disease only

A

5-ASA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
247
Q

treatment for FLARES of CD

A

prednisone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
248
Q

1st line drug for mild-to-moderate CD of ileum or ileocecal disease

A

budesonide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
249
Q

helpful with fistulas and getting off steroids

A

infliximab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
250
Q

can develop POSITIVE ANA, SEVERE FUNGAL INFECTION, LYMPHOMA, and MS from this CD medication

A

infliximab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
251
Q

incidence of RECURRENCE AFTER SURGERY in CD depends on what?

A
  1. site- ileocolic is highest

2. nature of complication- obstruction, perforation, and abscesses have higher rate of recurrence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
252
Q

treatment scenarios for CD:

COLON ONLY

A

sulfasalazine or mesalamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
253
Q

treatment scenarios for CD:

ANY ILEUM or SMALL BOWEL

A

slow-release mesalamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
254
Q

treatment scenarios for CD:

ONLY ILEUM or SMALL BOWEL

A

slow-release mesalamine or budesonide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
255
Q

treatment scenarios for CD:

FISTULA or PERIANAL

A
  • infliximab (or other immunomodulators), metronidazole, or ciprofloxacin
  • 6-MP also used
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
256
Q

treatment scenarios for CD:

incomplete acute small bowel obstruction

A

corticosteroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
257
Q

screen CD patients for?

A

OSTEOPOROSIS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
258
Q

inflammation ALWAYS starts in RECTUM, extends proximally, ALWAYS confined to COLON

A

ulcerative colitis (UC)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
259
Q

INFECTIOUS causes of colitis

A
  • E. coli O157:H7 (EHEC)
  • Shigella
  • Salmonella
  • Yersinia
  • Campylobacter
  • C. difficile
  • E. histolytica (amebiasis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
260
Q

how is UC diagnosed?

A

colonoscopy or sigmoidoscopy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
261
Q

UC patient that develops jaundice, itching and cholestatic LFTs

A

PRIMARY SCLEROSING CHOLANGITIS (PSC)

“JSEM” mnemonic

  • Joints
  • Skin
  • Eyes
  • Mouth

(this mnemonic leaves out primary sclerosing cholangitis; PSC)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
262
Q

PANcolitis for 8 YEARS or LEFT-SIDED colitis for 15 YEARS should have…

A

a colonoscopy every 1-2 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
263
Q

treatment for UC?

A

CURED with SURGERY (but difficult to do)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
264
Q

for MILD DISEASE of UC, treatment

A
  • sulfasalazine PO
  • mesalamine PO
  • rectal mesalamine
  • hydrocortisone enema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
265
Q

for MODERATE-to-SEVERE DISEASE of UC, treatment

A

prednisone PO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
266
Q

treatment of fulminant UC

A
  • hospitalize

- IV corticosteroids, infliximab, or cyclosporine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
267
Q

treatment of fulminant UC if symptoms persist for > 48 hours

A

colectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
268
Q

IBD buzzwords

tenesmus

A

UC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
269
Q

IBD buzzwords

rectal bleeding

A

UC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
270
Q

IBD buzzwords

fecal soiling

A

think fistula= CD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
271
Q

IBD buzzwords

hydronephrosis without stones

A

obstruction from inflammatory mass= CD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
272
Q

IBD buzzwords

pneumaturia

A

think fistula to the bladder= CD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
273
Q

definition of diarrhea

A

> 200-250 g/day of stool

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
274
Q

normal average daily stool output

A

150-180 grams/day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
275
Q

diarrhea duration

A
  • acute = 1 month
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
276
Q

etiology of acute diarrhea

A

commonly INFECTIOUS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
277
Q

diagnosis of acute diarrhea

A

check diet and travel history

guaiac test and fecal WBCs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
278
Q

distinction between infectious diarrhea and IBD

A

BOTH can have crypt abscesses, but crypt distortions ONLY in IBD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
279
Q

treatment for INVASIVE diarrhea

A
  • quinolones (especially ciprofloxacin)

- macrolides for Campylobacter (high quinolone resistance)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
280
Q

should you treat Salmonella with antibiotics?

A

NO, PROLONG infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
281
Q

should you use antibiotics for E. coli O157:H7 (EHEC) infection?

A

NO! CONTRAINDICATED!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
282
Q

3 mechanisms of chronic diarrhea

A

OSMOTIC
SECRETORY
INCREASED MOTILITY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
283
Q

stool osmalality calculated=

A

2 x (stool [Na+] + stool [K+])

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
284
Q

stool osmolar gap=

A

290 - stool osmolality calculated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
285
Q

SOG > 50

A

osmotic diarrhea

added osmoles are present causing diarrhea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
286
Q

SOG

A

normal stool, OR secretory diarrhea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
287
Q

in secretory diarrhea, patient is at risk of?

A

ELECTROLYTE DEFICIENCY (> 1L stool/day, meaning increased secretion of electrolytes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
288
Q

does a 24-48-hour fast decrease secretory diarrhea?

A

NO, except in fatty acid- and bile acid-related diarrheas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
289
Q

does a 24-hour fast help with osmotic diarrhea?

A

YES

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
290
Q

MOST COMMON cause of osmotic diarrhea

A

lactase deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
291
Q

causes of dysmotility diarrhea

A
  • antibiotics
  • hyperthyroidism
  • carcinoid
  • irritable bowel syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
292
Q

disease with both osmotic and secretory diarrhea

A

CELIAC disease

(malabsorption of carbohydrates= osmotic
malabsorption of fat= secretory)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
293
Q

disease with osmotic, secretory, and dysmotility

A

EXUDATIVE diarrhea

(inflammation= causes altered motility
malabsorption= causes osmotic and secretory diarrhea)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
294
Q

diarrhea and weight loss in AIDS patient WITHOUT FEVER BUT HAS LOW CD4 COUNT, suspect

A 
noninvasive organisms:
Cryptosporidia (usual cause)
E. histolytica
Giardia
Isospora
Strongyloides
AIDS enteropathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
295
Q

diarrhea and weight loss in AIDS patient WITH FEVER, think

A 
Mycobacterium
Campylobacter
Salmonella
Cryptococcus
Histoplasma
CMV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
296
Q

VOLUME: > 1L diarrhea/day in AIDS patient

A

AIDS-associated diarrhea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
297
Q

chronic bloody stools, think

A

UC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
298
Q

chronic loose stools, chronic RLQ abdominal cramping, think

A

CD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
299
Q

with GI tumors, when does carcinoid syndrome occur?

A

ONLY when it metastasizes to the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
300
Q

PAROXYSMAL FLUSHING; crampy, explosive DIARRHEA; and HYPOTENSIVE TACHYCARDIA

A

carcinoid syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
301
Q

can cause NIACIN DEFICIENCY (pellagra)

A

carcinoid syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
302
Q

diagnosis of carcinoid

A

check 24-hour urine for 5-HIAA (5-hydroxyindoleacetic acid); > 25mg/d

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
303
Q

microscopic colitis (both COLLAGENOUS and LYMPHOCYTIC colitis)

A

chronic secretory, watery diarrhea

normal colonoscopy, only seen on microscopic biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
304
Q

diagnosis of chronic diarrhea

A

stage 1: labs
stage 2: more diagnostic tests
stage 3: EGD and colonoscopy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
305
Q

“BIG 6” blood tests for malabsorption

A
  1. albumin
  2. Ca++
  3. cholesterol
  4. carotene
  5. serum iron (all LOW)
  6. PT (PROLONGED)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
306
Q

2 subdivisions of malabsorption

A
  1. MUCOSAL TRANSPORT (something wrong with intestinal uptake)
  2. DIGESTION (not enough digestive enzymes)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
307
Q

what is celiac disease?

A

autoimmune gluten-sensitive enteropathy (small bowel villous atrophy and crypt hypertrophy causing malabsorption)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
308
Q

celiac disease can cause what in children?

A

GROWTH RETARDATION

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
309
Q

deficiencies caused by celiac disease

A 
iron
folic acid
calcium
vitamin D
vitamin B12 (rarely)
vitamin K
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
310
Q

dermatologic manifestation of celiac disease

A

dermatitis herpetiformis (vesicopapular rash)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
311
Q

4 diagnostic criteria of celiac disease

A
  1. evidence of malabsorption
  2. positive tissue transglutaminase Ab test OR antiendomysial Ab test
  3. positive response to gluten-free diet
  4. abnormal small bowel biopsy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
312
Q

treatment of celiac disease

A

LIFETIME GLUTEN-FREE DIET

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
313
Q

what test to order in the following patient?

a 16-year-old presents with a diagnosis of bipolar disorder

A

tissue transglutaminase Ab or IgA antiendomysial Ab for celiac disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
314
Q

what test to order in the following patient?

a 33-year-old presents with bone pain in his spine and legs

A

tissue transglutaminase Ab or IgA antiendomysial Ab for celiac disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
315
Q

what test to order in the following patient?

a 28-year-old presents with a pruritic papulovesicular eruption on her extensor elbows and knees

A

tissue transglutaminase Ab or IgA antiendomysial Ab for celiac disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
316
Q

what test to order in the following patient?

a 30-year-old presents with heme-negative stool and low Hb, MCV, and FERRITIN

A

tissue transglutaminase Ab or IgA antiendomysial Ab for celiac disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
317
Q

what is tropical sprue?

A

malabsorption with partial villous atrophy

maybe caused by infectious organism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
318
Q

treatment of tropical sprue

A

tetracycline or doxycycline for 3-6 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
319
Q

cause of whipple disease?

A

Tropheryma whipplei

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
320
Q

cardinal tetrad of symptoms of whipple disease

A
  1. arthralgias (MOST COMMON symptom preceding diagnosis)
  2. abdominal pain
  3. weight loss
  4. diarrhea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
321
Q

diagnostic procedure of choice for whipple disease

A

EGD with small bowel biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
322
Q

small bowel biopsy finding in whipple disease

A

FOAMY MACROPHAGES that are POSITIVE for PAS staining

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
323
Q

treatment of whipple disease

A
  • CEFTRIAXONE or IV PCN for 14 days

- THEN TMP/SMX FOR 1 YEAR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
324
Q

RELAPSE of whipple disease manifests with

A

CNS SYMPTOMS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
325
Q

short bowel syndrome happens when?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
326
Q

complications of short bowel syndrome

A
  • CALCIUM OXALATE kidney stones (2/2 steatorrhea)

- gastric acid hypersecretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
327
Q

treatment of short bowel syndrome

A

low-fat diet
small frequent meals
vitamin supplements
TPN if needed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
328
Q

eosinophilic gastroenteritis can mimic

A

INTESTINAL LYMPHOMA and REGIONAL ENTERITIS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
329
Q

2 main causes of malabsorption d/t decreased digestion

A
  1. pancreatic insufficiency

2. bile acid deficiency

330
Q

causes of pancreatic insufficiency

A
  • chronic pancreatitis
  • pancreatic cancer
  • cystic fibrosis
331
Q

determine pancreatic insufficiency with

A

qualitative stool exam

332
Q

what must be ruled out if there is evidence of pancreatic insufficiency in patients > 55 years of age?

A 
PANCREATIC CANCER
(do a CT scan)
333
Q

causes of bile acid deficiency

A
  • ileal resection (> 100cm) (reuptake of bile acids)
  • severe liver disease (liver produces bile acids)
  • Zollinger-Ellison syndrome (increased acidity causes precipitation of bile acids
  • bacterial overgrowth (causes breakdown of bile acids)
334
Q

best indicator of malabsorption

A

STEATORRHEA

335
Q

“gold standard” for determining steatorrhea

A

3-day, quantitative fecal fat measurement

steatorrhea if > 14g/d of fecal fat

336
Q

best SCREENING test for steatorrhea

A

Sudan stain test

337
Q

steatorrhea from what causes the MOST fecal fat? (can be > 50g/d)

A

PANCREATIC INSUFFICIENCY

338
Q

first step in diagnosing malabsorption

A

determine if small bowel MUCOSAL problem or DIGESTIVE problem

test for celiac disease or chronic pancreatitis

339
Q

requires normal transmucosal transport, and doesn’t need pancreatitic enzymes to be digested

A

D-xylose

340
Q

NORMAL D-xylose test indicates

A

NORMAL mucosal transport

and PANCREATIC INSUFFICIENCY is MORE LIKELY

341
Q

LOW D-xylose test indicates

A

NOT SPECIFIC, but if patient has STEATORRHEA, then small bowel disease

342
Q

if LOW D-xylose test, next step?

A

SMALL BOWEL BIOPSY

343
Q

moderate STEATORRHEA, but presenting c/o ABDOMINAL DISTENTION

A

bacterial overgrowth

344
Q

macrocytosis with HIGH folate and LOW B12 levels

A

bacterial overgrowth (they make more folate, but decrease B12 absorption)

345
Q

conditions causing bacterial overgrowth

A
  • structural abnormalities (AFTER ILEOCECAL RESECTION)
  • motility disorders (DIABETES, and SCLERODERMA)
  • achlorhydria
  • immune disorders
346
Q

bacterial overgrowth is associated with

A

ROSACEA

347
Q

diagnosis of bacterial overgrowth?

A

LACTULOSE HYDROGEN BREATH TEST

and sometimes a C14-glycocholate test

348
Q

TREAT bacterial overgrowth EMPIRICALLY with

A

RIFAXIMIN (nonabsorbable antibiotic) for 2 weeks, then off for 1 week, and repeat indefinitely

349
Q

> 60cm of terminal ileum resected

A

B12 deficiency

350
Q
A

bile acid uptake is DECREASED

bile acid makes it to colon, causing bile acid-induced diarrhea

351
Q

> 100cm of terminal ileum resected

A

bile acid uptake is LOST

synthesis can’t keep up with LOSS –> bile acid deficiency –> fat malabsorption

352
Q

majority of causes of constipation

A

IDIOPATHIC

353
Q

RECENT ONSET of constipation
NO CHANGES TO DIET
NO NEW MEDICATIONS

A

suggests OBSTRUCTING lesion

354
Q

ACQUIRED MEGACOLON

A
  • traumatic sacral nerve damage
  • MS
  • Chagas disease
  • aganglionic megacolon (Hirschsprung’s)
355
Q

what causes CHAGAS DISEASE and where is it found?

A

Trypanosoma cruzi

Central and South America

356
Q

Trypanosoma cruzi infection causes

A
  • ACHALASIA
  • cardiomyopathy
  • acquired megacolon
357
Q

common drugs that cause constipation

A

many, but ANTIcholinergics, and ESPECIALLY most NARCOTICS

358
Q

one of the most common causes of constipation

A

dehydration

359
Q

endocrine disorders that can cause constipation

A

DIABETES MELLITUS

HYPOTHYROIDISM

360
Q

who gets worked up for constipation?

A

patients that also have:

WEIGHT LOSS, RECTAL BLEEDING, or ANEMIA

361
Q

w/u for constipation with other symptoms

A
  • colonoscopy (to r/o cancer, or strictures)

- serum Ca++ and TSH (to exclude hyper/hypocalcemia and hypothyroidism; DM comes from the history)

362
Q

test for intractable constipation

A

colonic transit function with 24 radiopaque markers (“Sitz markers”)

363
Q

abnormal colonic transit function test

A

more than or equal to 5 markers

if markers spread THROUGHOUT colon = GENERALIZED COLONIC INERTIA

CLUSTERING of markers in RECTOSIGMOID colon = pelvic floor dysfunction

364
Q

treatment of constipation

A

dietary fiber > 20g/day and fluid intake

365
Q

what kind of constipation does increased fiber and water help with?

A

colonic inertia, but NOT pelvic floor dysfunction

366
Q

presentation of fecal impaction

A

sudden onset watery stools/incontinence in a person with chronic constipation

367
Q

treatment of fecal impaction

A

REMOVE impaction

368
Q

in patients > 50 years of age with new-onset IBS-like symptoms, you should?

A

check for other causes

369
Q

characteristic IBS symptoms

A
  • abdominal relieved by defecation
  • change in stool frequency/consistency
  • NO NOCTURNAL SYMPTOMS
370
Q

treatment of IBS

A

REASSURANCE

371
Q

colon cancer risk factors

A 
age > 50
adenomatous polyps
UC and CD
BRCA1 mutation
acromegaly
obesity
smoking
diets high in calories and animal fat
372
Q

hereditary risk factors for colon cancer

A

1st degree relatives with colon cancer OR adenomatous polyps
FAP
HNPCC

373
Q

endocarditis caused by either Streptococcus bovis or Clostridium septicum is associated with

A

COLON CANCER

374
Q

most GI cancers arise from

A

ADENOMAS

375
Q

adenomas with “ADVANCED” features

“ADVANCED” means likely to develop cancer

A

high-grade dysplasia
villous histology
size > 10mm

376
Q

do HYPERPLASTIC polyps have malignant potential?

A

NO

contain NO features of dysplasia

377
Q

1 OR 2 small tubular ADENOMAS with low-grade dysplasia

A

repeat colonoscopy 5-10 years after initial polypectomy

378
Q

3-10 ADENOMAS

A

repeat colonoscopy in 3 years

379
Q

1 adenoma > 1cm

A

repeat colonoscopy in 3 years

380
Q

any adenoma with VILLOUS features or HIGH-GRADE dysplasia

A

repeat colonoscopy in 3 years

381
Q

> 10 ADENOMAS

A

repeat colonoscopy

382
Q

SESSILE adenomas that are removed piecemeal

A

repeat colonoscopy in 2-6 MONTHS

383
Q

genetics of FAP

A

AUTOSOMAL DOMINANT (AD)

384
Q

4 types of familial polyposis syndromes in DECREASING cancer potential

A
  1. FAP (familial adenomatous polyposis)
  2. Gardner syndrome
  3. Peutz-Jeghers syndrome
  4. juvenile polyposis
385
Q

HUNDREDS OF ADENOMAS in the COLON

100% RISK OF CANCER

A

FAP

386
Q

REQUIRE PROPHYLACTIC PROCTOCOLECTOMY by AGE 20!

A

FAP

387
Q

giant stomach tumors in FAP patients are

A

BENIGN

388
Q

variant of FAP with multiple OSTEOMAS

A

Gardner syndrome

389
Q

patient has multiple osteomas found incidentally on an x-ray

what do you do?

A

colonoscopy!

390
Q

variant of FAP with multiple hamartomatous polyps in small bowel, and freckles on lips and buccal mucosa

A

Peutz-Jeghers syndrome

391
Q

variant of FAP with > 10 juvenile polyps

A

juvenile polyposis

392
Q

hereditary nonpolyposis colon cancer a.k.a.

A

Lynch syndrome

393
Q

colorectal, endometrial, small bowel, ureter, or renal pelvis cancer in:
3 FIRST DEGREE relatives, over at least 2 generations, with at least 1 person diagnosed

A

hereditary nonpolyposis colon cancer (HNPCC)

394
Q

women in families with HNPCC have an increased incidence of

A

OVARIAN and ENDOMETRIAL cnacer

395
Q

screening of patient with HNPCC risks starts at

A

age 25

396
Q

colorectal cancer screening

ASYMPTOMATIC
MORE THAN OR EQUAL TO 50 YEARS of age
NEGATIVE FAMILY HISTORY

A

colonoscopy every 10 years

397
Q

USPSTF recommends AGAINST screening for colorectal cancer in which patients

A

> 85 years of age

398
Q

colorectal cancer screening

increased-risk patients

A

start at age 40 or 10 YEARS before age of index cancer was diagnosed, WHICHEVER IS FIRST

399
Q

screening procedure of choice in patient with ANY 1st degree relative with colon cancer or an adenomatous polyp

A

COLONOSCOPY

400
Q

test that can be done if you can’t do a colonoscopy

A

CT colonography

401
Q

screen for what in OLDER patients after episode of DIVERTICULITIS

A

SIGMOID COLON CANCER

402
Q

where does colon cancer almost always metastasize to?

A

LIVER (via portal circulation)

403
Q

where does colon cancer metastasize to if it only involves the RECTUM?

A

lung, bone, and brain WITHOUT liver mets (bypasses portal circulation)

404
Q

1st treatment option for colon cancer and potentially curative

A

SURGICAL RESECTION

405
Q

what is the adjuvant chemotherapy protocol for colon cancer?

A

FOLFOX

  • FOlinic acid (leucovorin)
  • 5-FU
  • OXaliplatin
406
Q

adjuvant chemo effective in colon cancer only when?

A

stage 3 or locally advanced stage 2

407
Q

radiation therapy prior to surgery only helpful in colon cancer for?

A

RECTAL lesions

408
Q

4 types of diverticular disease

A
  1. asymptomatic diverticulosis (most common)
  2. painful diverticulosis
  3. diverticular bleeding
  4. diverticulitis
409
Q

luminal narrowing of colon
pencil-thin stools
bouts of colicky pain relieved by BM

A

symptomatic diverticulosis

410
Q

treatment of symptomatic diverticulosis

A

BULKING AGENTS (psyllium or methylcellulose)

411
Q

MOST COMMON cause of colonic bleeding

A

diverticular bleeding

412
Q

2nd most common cause of colonic bleeding (more severe bleeds)

A

ANGIODYSPLASIA

413
Q

PAINLESS, MAROON STOOL

A

diverticular bleeding

414
Q

treatment for diverticular bleeding

A

IVF, PRBCs if needed, r/o UGI, colonoscopy if bleeding doesn’t stop

415
Q

UGI bleed is suggested by

A

BUN/Cr ratio > 30:1

416
Q

cause of diverticulitis

A

MICROPERFORATIONS

417
Q 
LLQ pain
fever
high WBC
LLQ tenderness
NO BLEEDING
A

diverticulitis

418
Q

look for what on physical exam in diverticulitis

A

SIGMOID MASS (palpable, tender sigmoid)

419
Q

most useful test in assessing diverticulitis

A

CT scan

420
Q

AVOID what in diverticulitis

A

COLONOSCOPY (d/t risk of perforation)

421
Q

treatment of diverticulitis should cover which organisms?

A

AEROBIC and ANAEROBIC GRAM-NEGATIVE organmisms

422
Q

treatment of MILD diverticulitis

A

METRONIDAZOLE (gram-negative ANaerobic coverage)
plus
CIPROFLOXACIN OR TMP/SMX (gram-negative aerobic coverage)
as outpatient

423
Q

treatment of MODERATE-to-SEVERE diverticulitis

A

DUAL-drug therapy (BEST!)

  • aminoglycoside or ciprofloxacin (gram-negative aerobic)
    PLUS
  • clindamycin or metronidazole (gram-negative anaerobic)

or single-drug therapy that has both gram-negative aerobic and anaerobic coverage

424
Q

can present similarly to diverticulitis

and patients > 50 years of age need flex-sig/colonoscopy in 4-8 weeks

A

PERFORATION from sigmoid COLON CANCER

425
Q

angiodysplasia = vascular ectasia = AVM

A

2nd most common cause of lower GI bleeding in elderdly

426
Q

hereditary condition with multiple AVMs

A

hereditary hemorrhagic telangiectasias (Osler-Weber-Rendu)

427
Q

recurrent melanotic stools, with NEGATIVE EGDs and colonoscopies, you should

A

video capsule endoscopy (VCE)

428
Q

most common cause of SMALL INTESTINE obstruction

A

postoperative ADHESIONS

429
Q

most common causes of COLONIC obstruction (in decreasing frequency)

A

CARCINOMA –> DIVERTICULITIS –> VOLVULUS

430
Q

persistent vomiting, obstipation, and constipation

A

suggest obstruction

431
Q

confirm diagnosis of obstruction with

A

flat and upright abdominal film

432
Q

fluid levels SAME HEIGHT on either side of loop

A

PARALYTIC ILEUS

433
Q

4 types of intestinal ischemia

A
  1. ischemic colitis (MOST COMMON)
  2. chronic mesenteric ischemia
  3. acute mesenteric ischemia (70% mortality)
  4. mesenteric venous thrombosis
434
Q

ABDOMINAL PAIN and MAROON stools

A

ischemic colitis

435
Q

areas affected by nonocclusive ischemia

A

splenic flexure
descending colon
sigmoid colon

(inferior mesenteric circulation)

436
Q

ischemic colitis cause

A

most often, NO SPECIFIC CAUSE found

437
Q

possible ischemic colitis causes

A
  • LOW-FLOW CONDITIONS (CHF)
  • medications/cocaine
  • HYPERCOAGULABLE states
438
Q

sudden LLQ pain with urge to defecate, followed by passage of RED-TO-MAROON stool w/i 1 day

A

ischemic colitis

439
Q

what do you see on abdominal x-ray (KUB) in ischemic colitis?

A

submucosal hemorrhage and edema (mildest injury)

440
Q

what do you see with barium enema in ischemic colitis?

A

“THUMBPRINTING”

441
Q

1st diagnostic test done for ischemic colitis

A

CT scan

442
Q

do this with peritoneal signs in setting of suspected ischemic colitis

A

COLONOSCOPY withOUT bowel prep

443
Q

is angiography done for ischemic colitis?

A

usually NOT

444
Q

another name for chronic mesenteric ischemia

A

INTESTINAL ANGINA

445
Q

classic triad of chronic mesenteric ischemia

A
  1. abdominal pain after meals
  2. abdominal bruit
  3. weight loss (from tolerating only smaller meals)
446
Q

pain in chronic mesenteric ischemia (intestinal angina) is d/t episodes of what?

A

INADEQUATE blood FLOW brought on by DIGESTION

447
Q

suspect what if ABDOMINAL PAIN is OUT OF PROPORTION to physical findings

A

mesenteric vascular ischemia

448
Q

1-3 HOURS OF DULL, GNAWING abdominal pain about 30 minutes after eating

A

chronic mesenteric ischemia

449
Q

diagnosis of chronic mesenteric ischemia

A

based on SYMPTOMS

450
Q

tests that can be done to help in the diagnosis of chronic mesenteric ischemia

A

MRA or CT ANGIOGRAM

451
Q

most severe and life-threatening form of intestinal ischemia (MORTALITY RATE OF 70%- even with treatment!)

A

ACUTE MESENTERIC ISCHEMIA

452
Q

etiology of acute mesenteric ischemia

A

thromboembolus in a mesenteric artery –> loss of blood flow to corresponding SMALL INTESTINE and/or ASCENDING COLON

453
Q

symptoms of acute mesenteric ischemia

A

ACUTELY ILL with vomiting, diarrhea, and rectal blood

454
Q

bowel infarction leads to

A

LACTIC ACIDOSIS

455
Q

diagnostic test for acute mesenteric ischemia

A

CT ANGIOGRAPHY unless there is evidence of PERFORATION

456
Q

treatment of acute mesenteric ischemia

A

possible embolectomy, or surgery for dead-bowel resection

457
Q

mesenteric VENOUS thrombosis (MVT) is associated with

A

hypercoagulable states

458
Q

mesenteric VENOUS thrombosis (MVT) may be

A

ACUTE, SUBACUTE, or CHRONIC

459
Q

diagnostic procedure of choice for mesenteric VENOUS thrombosis (MVT)

A

CT

460
Q

treatment of ACUTE MVT

A

THROMBOLYTICS and LONG-TERM ANTICOAGULANTS

461
Q

treatment of CHRONIC MVT

A

sclerotherapy or portosystemic shunts

462
Q

most common causes of acute pancreatitis

A

ALCOHOL ABUSE and GALLSTONES

463
Q

diagnostic test that can cause acute pancreatitis in 2-5% of patients

A

endoscopic retrograde cholangiopancreatography (ERCP)

464
Q 
acidosis (eg, DKA)
hyertriglyceridemia
hypercalcemia
trauma
obstruction of ampulla of Vater (eg, pancreatic cancer)
A

other causes of acute pancreatitis

465
Q

biliary microlithiasis
cystic fibrosis
hereditary pancreatitis
hypertriglyceridemia

A

possibly overlooked causes of acute pancreatitis labeled as “idiopathic”

466
Q

elevated enzymes in acute pancreatitis

A

amylase and lipase (> 3x normal)

467
Q

may cause spuriously NORMAL amylase level!

A

acute pancreatitis with high triglyceride levels

468
Q

triglyceride levels > 1,000 mg/dL can cause

A

pancreatitis

469
Q

classification for acute pancreatitis (2 out of 3 must be present to make the diagnosis)

A
  1. upper abdominal pain radiating through to the back
  2. serum amylase or lipase 3x upper limit of normal
  3. cross sectional imaging consistent with acute pancreatitis
470
Q

severity of acute pancreatitis directly related to

A

degree of pancreatic NECROSIS (10-25% have necrosis) and if necrotic tissue is INFECTED

471
Q

mortality of acute pancreatitis if necrotic tissue is NOT infected

A

10%

472
Q

mortality of acute pancreatitis if necrotic tissue IS infected

A

30%

473
Q

overall mortality rate for acute pancreatitis

A

5-10%

474
Q

severe pancreatitis causes

A

shock and MULTIORGAN FAILURE

475
Q

hemoconcentration
SBP 130 bpm
PO2

A

indicators of severe pancreatitis

476
Q

most COMMON skin finding in severe pancreatitis

A

ERYTHEMA of flanks

extravasated pancreatic exudates

477
Q

faint blue discoloration around umbilicus (includes HEMOPERITONEUM)

A

Cullen sign

478
Q

bluish-reddish-purple or greenish-brown discoloration of flanks

A

Turner sign

479
Q

characteristic, but NOT pathognomonic for acute pancreatitis

A

Cullen and Turner signs

480
Q

severity scoring systems for acute pancreatitis

A

APACHE II and BISAP

481
Q

BISAP scoring for MORTALITY

A 
BUN > 25
impaired mental status
SIRS
age > 60 years
pleural effusion
482
Q

SIRS criteria

A

temperature 100.4
HR > 90
RR > 20 OR pCO2 12 OR 10% bands

483
Q

current AGA recommendations for acute pancreatitis

A

if APACHE II score greater than or equal to 8 OR organ failure at 72 hours; get a CT to check for necrosis

484
Q

associated with 2x increase in mortality in acute pancreatitis

A

morbid obesity (BMI > 30)

485
Q

pancreatic necrosis best confirmed by

A

CT SCAN or MRI

486
Q

pancreatic necrosis is severe if?

A

GREATER THAN OR EQUAL TO 30%

487
Q

do this daily for acute pancreatitis

A

SIRS evaluation

488
Q

occurs within 48 HOURS of PAIN onset in acute pancreatitis

A

ACUTE FLUID COLLECTION

489
Q

occurs in first 1-2 weeks of acute pancreatitis (may resemble pseudocyst)

A

NECROTIC TISSUE

490
Q

diagnosis and treatment of infected pancreatic necrosis

A

endoscopic or CT-guided aspiration

491
Q

may occur after A MINIMUM OF 4 WEEKS after acute pancreatitis

A

pseudocyst

492
Q

what size pseudocyst probably won’t resolve on its own?

A

> 5cm

493
Q

if pancreatic pseudocyst persists > 3-6 months and causes symptoms, then what?

A

drain it

494
Q

may occur 4-6 WEEKS after acute severe pancreatitis with severe pancreatic necrosis

A

ABSCESS

495
Q

pancreatic abscess on upright abdominal x-ray

A

“SOAP BUBBLE sign”

496
Q

diagnosis of pancreatic abscess

A

CT-GUIDED PERCUTANEOUS ASPIRATE (90% accurate)

497
Q

diagnosis of acute pancreatitis

A

gallbladder US to r/o gallstones

498
Q

treatment of acute pancreatitis

A

supportive care: NPO, LR, NGT feeds (in protracted acute pancreatitis patients)

499
Q

when do you give systemic antibiotics in acute pancreatitis?

A

ONLY if there is ESTABLISHED infection

500
Q

IVF protocol for acute pancreaitis

A

LR is crystalloid of choice (decreased incidence of SIRS)

  • 20mL/kg bolus
  • then continuous infusion at 3mL/kg/hr for 6-8 hours
  • if fluid responsive: 1.5mL/kg/hr
  • if fluid refractory: give another 20mL/kg bolus and continuous infusion at 3mL/kg/hr
  • recheck at 16 hours
501
Q

if amylase is still elevated after 10 days, think of

A

leaking pseudocyst

502
Q

recurrent acute pancreatitis with NO evidence of gallstones or alcohol abuse may be d/t

A

MICROLITHIASIS

do elective cholecystectomy

503
Q

gastric varices WITHOUT esophageal varices

A

ONLY happens with splenic vein thrombosis

504
Q

complication of both severe ACUTE pancreatitis and CHRONIC pancreatitis

A

splenic vein thrombosis

505
Q

criteria for resumption of oral feeds in acute pancreatitis

A
  1. bowel sounds present and passing flatus/stools
  2. doesn’t need narcotics
  3. patient is hungry and wants to eat
506
Q 
acute pancreatitis
acute cholecystitis
intestinal infarction
diabetic ketoacidosis
perforated ulcer
salpingitis
ectopic pregnancy
A

can cause elevated AMYLASE

507
Q

common cause of chronic pancreatitis

A

chronic alcohol ingestion, > 10 years

508
Q

fecal fat/day in chronic pancreatitis

A

> 40g/day

late stage may be > 100g/day

509
Q

late chronic pancreatitis patients develop

A

STEATORRHEA and DIABETES MELLITUS

510
Q

diagnostic triad for CHRONIC pancreatitis

A
  1. pancreatic calcification
  2. diabetes
  3. steatorrhea
511
Q

PROCEDURE OF CHOICE for diagnosis of chronic pancreatitis

A

CT scan of abdomen

512
Q

diagnosis of chronic pancreatitis on CT of abdomen is made IF

A
  • calcified pancreas, OR
  • dilated pancreatic duct, OR
  • atrophic pancreas
513
Q

best test to diagnose chronic pancreatitis, BUT requires a skilled gastroenterologist

A

endoscopic ultrasound

514
Q

if initial tests are negative, but you still suspect chronic pancreatitis do this

A

MRCP (NO risk of causing pancreatitis)

515
Q

only advantage of ERCP over MRCP in chronic pancreatitis

A

endoscopic removal of CALCIFIC STONES

516
Q

pancreatic duct has stenoses and dilations seen on MRCP and ERCP visualized as

A

“CHAIN OF LAKES”

517
Q

most sensitive test for pancreatic exocrine function

A

SECRETIN TEST

518
Q

how diabetes in chronic pancreatitis different?

A

decrease in insulin AND glucagon

519
Q

low glucagon in chronic pancreatitis can lead to?

A

HYPOglycemia

520
Q

do patients with diabetes from chronic pancreatitis develop retinopathy and nephropathy?

A

NO, usually NOT

521
Q

treatment of chronic pancreatitis

A

alcohol and tobacco cessation
pancreatic enzymes supplementation
decreasing dietary fat
antioxidants

522
Q

SERUM IGG4 level greater than or equal to 2x normal

A

autoimmune pancreatitis

523
Q

JAUNDICE, (unexplained upper) ABDOMINAL PAIN, and/or WEIGHT LOSS

A

pancreatic cancer

524
Q

pancreatic cancer: HEAD of pancreas

A

painLESS jaundice, present early

525
Q

pancreatic cancer: BODY and TAIL of pancreas

A

PAIN and WEIGHT LOSS, more advanced

526
Q

helical CT, CTA, EUS-guided FNA biopsy, and laparoscopy to diagnose

A

pancreatic cancer

527
Q

treatment of pancreatic cancer

A

RESECTION

528
Q

most common reasons for tumor unresectability of pancreatic cancer

A
  • distant metastases

- local invasion of major vessel

529
Q

surgical candidate + mass in HEAD of pancreas + appears resectable

A

do a pancreaticoduodenectomy (Whipple resection)

530
Q

serum marker for pancreatic cancer

A

CA 19-9

531
Q

if pancreatic cancer has already metastasized

A

AVOID surgery

place STENT with ERCP to palliate biliary obstruction

532
Q

ONLY time you use ERCP for pancreatic cancer

A

to place a STENT to help with biliary obstruction

533
Q

glucagon-secreting, alpha-cell tumor of pancreas

A

glucagonoma

534
Q 
scaly NECROLYTIC ERYTHEMA
weight loss
anemia
diarrhea
persistent HYPERglycemia
plasma glucagon > 1,000pg/dL
A

GLUCAGONOMA

535
Q

insulin-secreting, beta-cell tumor of pancreas

A

insulinoma

536
Q

serum gastrin > 500 in patient who is able to secrete gastric acid (not on PPI, no prior peptic ulcer)

A

gastrinoma

537
Q

tumor that secretes vasoactive intestinal peptide (VIP)

A

VIPoma

538
Q

VIPomas cause

A

PROFUSE SECRETORY DIARRHEA (“pancreatic cholera”)

539
Q

is cholelithiasis associated with hypercholesterolEMIA?

A

NO

540
Q

pathophysiology of cholelithiasis

A
  1. abnormal bile secretion
  2. accelerated nucleation of microcrystals to MACROcrystals
  3. defective GB emptying
541
Q

cholelithiasis associated with

A

obesity
OCPs
clofibrate treatment
ileal disease/resection

542
Q

75% of gallstones are composed of

A

radioLUCENT CHOLESTEROL (pure or mixed)

the rest are bile pigment gallstones

543
Q

cholelithiasis symptoms

A

RUQ pain (20-60 minutes, especially after fatty meal)

544
Q

diagnose cholelithiasis

A

ULTRASOUND (90% sensitive)

545
Q

best test for confirming acute CYSTIC duct obstruction (ie, ACUTE CHOLECYSTITIS)

A

HIDA SCAN (cholescintigraphy)

546
Q

treatment of cholelithiasis, if patient has gallstones and SYMPTOMATIC

A

elective cholecystectomy

547
Q

ACALCULOUS cholecystitis

A

occurs only in SERIOUSLY ILL patients; eg, major trauma, burns, after major surgeries

548
Q

alkaline phosphatase and bilirubin in typical gallbladder cases

A

NOT elevated

549
Q

INCREASING LEVELS of ALP and bilirubin (> 4mg/dL) suggest

A

COMMON DUCT STONE

choledocholithiasis

550
Q

post-cholecystectomy patient with PERSISTENT PAIN

A

COMMON DUCT STONE

choledocholithiasis

551
Q

treatment for common duct stones

A

ERCP

552
Q

OBSTRUCTIVE (common duct stones) or HEPATOCELLULAR

A

cholestasis

553
Q

Charcot’s triad:

  1. biliary colic (abdominal pain)
  2. fever
  3. jaundice
A

acute cholangitis

554
Q

Reynold’s pentad:

  1. biliary colic (abdominal pain)
  2. fever
  3. jaundice
  4. SEPTIC SHOCK
  5. AMS
A

suppurative cholangitis (ascending cholangitis)

555
Q

treatment acute cholangitis

A

PARENTERAL ANTIBIOTICS
IV HYDRATION
BILIARY DRAINAGE

556
Q

best procedure for diagnosis and treatment of suppurative cholangitis (ascending cholangitis)

A

ERCP WITH ENDOSCOPIC SPHINCTEROTOMY

557
Q

treatment for EMPHYSEMATOUS cholecystitis

A

emergent laparotomy with cholecystectomy AND antibiotics

558
Q

antibiotics for suppurative cholangitis and emphysematous cholecystitis must cover

A

GRAM-NEGATIVE and ANAEROBIC organisms

559
Q

do NOT use this antibiotic for suppurative cholangitis and emphysematous cholecystitis

A

CEFTRIAXONE (can cause biliary sludge; NO anaerobic coverage)

560
Q

X-ray showing GB with CALCIFIED OUTLINE

A

“porcelain gallbladder”

suggests CANCER

561
Q

treatment for porcelain gallbladder

A

OPEN cholecystectomy

562
Q

nonsuppurative, progressive, destructive cholangiolitis

SLOW onset, 95% ARE WOMEN- MIDDLE-AGED

A

primary biliary cholangitis (PBC)

563
Q

florid duct lesion on liver biopsy

A

pathognomonic for primary biliary cholangitis (PBC)

564
Q

90% of primary biliary cholangitis (PBC) have positive

A

ANTIMITOCHONDRIAL ANTIBODY test (> 1:40)

degree of elevation does NOT correlate with severity of disease

565
Q

PBC patient who present with symptoms have

A

ADVANCE disease

566
Q

FATIGUE
HIGH ALKALINE PHOSPHATASE
ITCHING (first on palms and soles, then throughout body)

A

primary biliary cholangitis (PBC)

567
Q

PBC course

A

indolent, but RELENTLESSLY PROGRESSIVE

568
Q

ALKALINE PHOSPHATASE 2-5x above normal

A

PBC

569
Q

hallmark test for PBC

A

ANTIMITOCHONDRIAL ANTIBODY test

570
Q

NOT a good indicator of severity of PBC

A

antimitochondrial antibody test

571
Q

antimitochondrial antibody test can be positive in PBC, and?

A

autoimmune hepatitis, and drug-induced chronic hepatitis

572
Q

diagnosis of PBC is confirmed ONLY with

A

LIVER BIOPSY

573
Q

PBC patients also have a high hepatic level of?

A

COPPER

as do patients with primary sclerosing cholangitis and Wilson disease

574
Q

treatment of biliary cirrhosis

A

URSODIOL (ursodeoxycholate- a synthetic bile acid)

575
Q

what SLOWS progression of primary biliary cirrhosis?

A

URSODIOL

576
Q

BIOCHEMICAL RESPONSE to ursodiol leads to

A

DRAMATIC SLOWING of progression of PBC

577
Q

treatment has what effect on LATE disease of PBC?

A

NO EFFECT

578
Q

what is recommended for late disease of PBC?

A

liver transplantation

579
Q

AAAABCs of PBC

A

Antimitochondrial Antibody Attack INCREASES Alk phos and CAUSES obstructive Biliary lesions and liver Cirrhosis

580
Q

indolent, 70% males, average age of 45

A

primary sclerosing cholangitis (PSC)

581
Q

PSC is strongly associated with

A

COLITIS (MAINLY UC [up to 75% of PSC patients have UC])

582
Q

ALL PSC patients should have a

A

COLONOSCOPY

583
Q

any UC patient with persistent, greater than or equal to 2x increase in ALKALINE PHOSPHATASE should be screened for

A

PSC

584
Q

cause of PSC?

A

unknown

585
Q

pathophysiology of PSC

A

intra- and extrahepatic biliary tract sclerosis leading to OBSTRUCTIVE JAUNDICE and CIRRHOSIS

586
Q

elevated BILIRUBIN and ALKALINE PHOSPHATASE
elevated hepatic COPPER
but NEGATIVE antimitochondrial antibody test

A

primary sclerosing cholangitis (PSC)

587
Q

8-15% of PSC patients develop

A

CHOLANGIOCARCINOMA

suspect if PSC patients abruptly worsen

588
Q

diagnose PSC

A

MRCP

589
Q

MRCP, ERCP, or transhepatic cholangiography shows what for PSC?

A

“BEADED” appearance

590
Q

liver biopsy shows what for PSC?

A

“onion skin” fibrosis in portal triads

establishes the diagnosis

591
Q

treatment of sclerosing cholangitis

A

LIVER TRANSPLANTATION

592
Q

should you use ursodeoxycholic acid (UDCA) in PSC?

A

no, recommend AGAINST UDCA, and if on it in the past, recommend DISCONTINUING it

593
Q

jaundice, increased alk phos, h/o chronic diarrhea or IBD, ESPECIALLY UC, must rule out?

A

PSC with MRCP or ERCP

594
Q

sclerosing CHOLangitis, COLitis, high CHOLestatic bili, and alk phos; negative antimitochondrial Ab, cirrhosis, and liver failure

abnormal MRCP or ERCP

A

PSC

595
Q

female, no IBD, cancer is rare, UDCA is effective

A

PBC (primary biliary cholangitis

596
Q

male, IBD, (UC) 8-15% risk of cholangiocarcinoma, UDCA is NOT effective

A

PSC (primary sclerosing cholangitis)

597
Q

enzyme more liver-specific than AST

A

ALT (Liver)

598
Q

alcoholic hepatitis AST:ALT ratio

A

AST:ALT ratio is about 3:1

alcohol damages MITOCHONDRIA

599
Q

viral hepatitis AST:ALT ratio

A

ALT > AST

ALT is more liver-specific

600
Q

nonalcoholic fatty liver disease (NAFLD)2 hepatitis ALT:AST ratio

A

ALT:AST ratio is > 2:1

NAFLD is also more liver-specific

601
Q

alkaline phosphatase comes from

A

LIVER and BONES

602
Q

check this when elevated alkaline phosphatase, but normal bilirubin and tranaminases

A

GGT (gamma glutamyl transpeptidase)

603
Q

if transaminases are elevated order this:

and if still elevated:

A
  • reorder labs to confirm
  • order hepatitis panel (A, B, C)
  • iron and ferritin (r/o hemochromatosis)
604
Q

if alk phos and GGT are elevated, next test

A

abdominal ultrasound (look for dilated biliary ducts or metastatic liver lesions)

605
Q

what type of virus is hepatitis A?

A

RNA

606
Q

hepatitis A is easily transmitted by?

A

fecal-oral route (food or water)
or sexually transmitted

NO transplacental transmission!

607
Q

NO carrier or persistent states, but can cause PROLONGED CHOLESTASIS (increased bili and alk phos) up to 4 months

A

hepatitis A

608
Q

diagnosis of acute hepatitis A infection

A

high titers of anti-HAV IgM in serum

IgG indicates previous infection

609
Q
  • high-risk sexual behavior
  • IV drug use
  • recommended for all > 1 year of age
  • chronic liver disease
A

indications for HAV vaccine

610
Q

patients with hepatitis B and C need

A

HAV vaccine (can be fulminant)

611
Q

onset of jaundice with hepatitis A

A

3 WEEKS

612
Q

onset of jaundice with hepatitis B

A

3 MONTHS

613
Q

means you’re producing hepatitis B virus

A

HBsAg

614
Q

indicates past exposure to EITHER:
hepatitis B VIRION, or
vaccine

A

HBsAb

usually indicates IMMUNITY

615
Q

what HB antigen DOES NOT CIRCULATE in the serum?

A

HBcAg

616
Q

best marker for PREVIOUS exposure to HBV

A

HBcAb IgG

617
Q

HB antigen IS secreted from hepatocytes and circulates in serum

A

HBeAg

618
Q

correlates with the QUANTITY OF INTACT VIRUS and, therefore, INFECTIVITY and liver INFLAMMATION

A

HBeAg

619
Q

indicates active virions and high infectivity

A

HBsAg AND HBeAg

620
Q

only hepatitis virus composed of DNA

A

hepatitis B

621
Q

hepatitis is strongly associated with

A

POLYARTERITIS NODOSA (PAN)

622
Q

HBsAg +
anti-HBc -
anti-HBs -

A

acute infection

623
Q

HBsAg +
anti-HBc +
anti-HBs -

A

3 possibilities:

1) acute infection (IgM anti-HBc)
2) chronic Hep B (high ALT, IgG anti-HBC)
3) inactive carrier (normal enzymes, IgG anti-HBc)

624
Q

HBsAg -
anti-HBc -
anti-HBs +

A

2 possibilities:

1) remote infection
2) immunized

625
Q

HBsAg -
anti-HBc +
anti-HBs +

A

remote infection

626
Q

HBsAg -
anti-HBc +
anti-HBs -

A

3 possibilities:

1) window disease
2) remote infection
3) false positive

627
Q

HBsAg +
anti-HBc +
anti-HBs +

A

more than 1 infection;

eg, IVDA or renal dialysis patient with both ACUTE and CHRONIC hepatitis B (infected with different strains)

628
Q

SERUM SICKNESS-LIKE symptoms of hepatitis B

A

fever, arthritis, urticaria, and angioedema

629
Q

hepatitis B prodromal symptoms constitutional get better when?

A

onset of jaundice

630
Q

what do you give a newborn of a mother with hepatitis B?

A

BOTH hep B immune globulin (HBIG)
and
hepatitis B vaccination

631
Q

asymptomatic patient has HBsAg

EITHER patient is a carrier OR has early hepatitis B

A

initially, follow closely

632
Q

what do you give sexual contacts and infants cared for by a patient with acute HBV infection?

A

HBIG
AND
HBV vaccinations

633
Q

what do you give pregnant patient with acute HBV infection?

A

HBIG
AND
HBV vaccinations

634
Q

how is likelihood of developing CHRONIC HBV related to AGE?

A

INVERSELY

90% chance in infants; 25-50% chance in children 1-5 years; 5% chance in older children and adults

635
Q

what are 2 types of hepatitis B carrier states?

A
  1. inactive carrier state (asymptomatic with NORMAL liver enzymes)
  2. chronic active hepatitis B
636
Q

how do you confirm chronic hepatitis B diagnosis?

A

LIVER BIOPSY

637
Q

what happens to patients with INACTIVE carrier states if they become IMMUNOCOMPROMISED?

A

CAN develop severe exacerbations

638
Q

chronic hepatitis B progresses to

A

CIRRHOSIS

639
Q

chronic hepatitis B strongly associated with

A

HEPATOCELLULAR CARCINOMA (HCC)

640
Q

in chronic hepatitis B, screen for HCC every?

A

6 months with abdominal ULTRASOUND

641
Q

should you use alpha-fetoprotein (AFP) to screen for HCC?

A

NO, not sensitive or specific enough

642
Q

when do you treat chronic active hepatitis B?

A

HBV DNA > 20,000 and ALT > 2x ULN

643
Q

when do you treat chronic active hepatitis B with CIRRHOSIS?

A

treat compensated cirrhosis when HBV DNA > 2,000

treat DEcompensated cirrhosis when HBV DNA > 200

644
Q

only treatment for end-stage liver disease

A

liver transplantation

645
Q

what type of virus is hepatitis C?

A

single-strand RNA virus

646
Q

most common liver disease in the US

A

NAFLD (nonalcoholic fatty liver disease)

647
Q

2nd most common liver disease in the US

A

hepatitis C

648
Q

most common HCV GENOTYPE in the US

A

GENOTYPE 1 (> 70%)

LESS responsive to treatment

649
Q

risk factors for hepatitis C

A

drugs, sex, blood, needles

650
Q

porphyria cutanea tarda (PCT) is associated ONLY with

A

hepatitis C

not B

651
Q

what should you do within 2-4 months after exposure to hepatitis C?

A

RECHECK for loss of HCV RNA (PCR) to make sure it’s not chronic

652
Q

how do you check for immunity to hepatitis C?

A

HCV RNA

HCV Ab does NOT confer immunity (just means prior infection)

653
Q

what percentage of HCV infections become CHRONIC?

A

70-80%

654
Q

what percentage of chronic HCV develop end-stage cirrhosis?

A

25% of the 70-80% that develpp chronic HCV after 20-25 years

655
Q

in chronic hepatitis C, screen for HCC every?

A

6 months with abdominal ULTRASOUND

656
Q

1 reason for liver transportation in the US

A

chronic HCV infection

657
Q

MIXED cryoglobulinemia is STRONGLY associated with?

A

chronic hepatitis C

658
Q

treat CHRONIC hepatitis C and elevated liver enzymes

A

COMBINATION of:
pegylated INF-a
ribavirin (RNA polymerase inbibitor)
telaprevir or boceprevir (protease inhibitors)

659
Q

adverse effect of ribavirin

A

HEMOLYTIC ANEMIA

660
Q

what can worsen when a patient is on INF-a?

A

depression

661
Q

what type of virus is hepatitis D?

A

RNA

662
Q

hepatitis D needs what?

A

COEXISTENT hepatitis B virus infection

663
Q

suspect what if sudden decompensation in patient with chronic hepatitis B?

A

hepatitis D

664
Q

what type of virus is hepatitis E?

A

single-strand RNA

665
Q

how is hepatitis E transmitted?

A

fecal-oral route (food or water)

commonly after monsoon flooding

666
Q

carries very high risk for fulminant hepatitis in 3rd trimester of pregnancy

(20% fatality rate)

A

hepatitis E

667
Q

TRAVELER with acute hepatitis and NEGATIVE STANDARD SEROLOGY (hep A, B), think of?

A

hepatitis E

668
Q

does HGV cause chronic liver disease?

A

no evidence that it does

669
Q

differential diagnoses of chronic hepatitis

A, B, C, D, F

A 
A= autoimmune
B= hepatitis B
C= hepatitis C
D1= hepatitis D (only with hep B)
D2= drugs
D3= diseases
F= NAFLD
670
Q

MOST SENSITIVE and LEAST SPECIFIC for autoimmune hepatitis

A

ANA

671
Q

about 80% sensitive and MORE SPECIFIC than ANA for autoimmune hepatitis

A

anti-SMA antibody (smooth muscle antibody)

672
Q

more SPECIFIC and SENSITIVE for autoimmune hepatitis

A

anti-actin antibody (AAA)

673
Q

MOST SPECIFIC, but NOT SENSITIVE

A

anti-SLA (soluble liver antigen)

674
Q

confirm diagnosis of autoimmune hepatitis

A

LIVER BIOPSY

675
Q

treatment of autoimmune hepatitis

A

PREDNISONE or BUDESONIDE

+/- AZATHIOPRINE

676
Q

CONTRAINDICATED and EXACERBATES autoimmune hepatitis

A

IFN-a

677
Q

is there a cure for autoimmune hepatitis?

A

NO CURE

678
Q

toxic, intermediate compound NAPQI, and glutathione depletion

A

acetaminophen toxicity

679
Q

2-FOLD effect

  • increased P-450 system
  • an already decreased glutathione supply
A

alcohol-acetaminophen syndrome

680
Q

long-term users of moderate-to-heavy alcohol should be cautious of?
and, are at risk for?

A

taking NORMAL or higher levels of acetaminophen

at risk for SEVERE HEPATIC TOXICITY or LIVER FAILURE

681
Q

can develop liver toxicity by not eating for 3-4 days and taking

A

THERAPEUTIC doses of acetaminophen

682
Q

most common cause of FULMINANT hepatitis in the US

A

acetaminophen toxicity

683
Q

alcoholic liver disease results in?

A

MACROvesicular fat accumulation

684
Q

this enzyme is DISPROPORTIONATELY HIGH in alcoholic liver disease

A

GGT

685
Q

AST is virtually always

A

alcoholic liver injury

686
Q

can cause indolent, asymptomatic liver disease that progresses to cirrhosis

A

methotrexate (MTX)

687
Q

young woman on OCPs who has a mass in her liver

A

ADENOMA

688
Q

EXCLUSIVELY occurs in children

A

Reye syndrome

689
Q

viral illness, CONCURRENT ASA use, progressive encephalopathy

A

Reye syndrome

MIRCROvesicular fat accumulation
(50% mortality)

690
Q

looks just like alcoholic liver disease, but NO h/o alcohol abuse

A

NASH aka NAFLD

691
Q

75-80% of “CRYPTOGENIC” cirrhosis is d/t

A

NAFLD

692
Q

DROP is a metabolic syndrome with:

A

Dyslipidemia
insulin Resistence
Obesity
increased blood Pressure

693
Q

treatment of NAFLD

A

weight loss, DM and hyperlipidemia control

694
Q

treatment for biopsy-proven NASH

A

vitamin E

695
Q

associated with CHRONIC LIVER DISEASE of ANY type and AFLATOXIN exposure

A

hepatocellular carcinoma (HCC, “hepatoma”)

696
Q

MOST COMMON cause of HCC in the US

A

ALCOHOLIC liver disease, with CONCURRENT HEPATITIS C (75%)

697
Q 
tender hepatomegaly
BRUIT in RUQ
bloody ascites
high alk phos
very high AFP
A

HCC

698
Q

hypercalcemia (PTHrP)
hypoglycemia (high demand)
watery diarrhea
FUO

A

HCC-associated PARANEOPLASTIC syndrome

699
Q
  • esophageal variceal hemorrhage
  • hepatic encephalopathy
  • hepatorenal syndrome
  • prolonged PT
A

complications of cirrhosis

700
Q

SIZE of varices correlates with

A

risk of bleeding

701
Q

should be prescribed to ALL patient with medium to large varices- whether or not they have had bleeding

A

nonselective beta-blockers

propranolol or nadolol

702
Q

should you perform sclerotherapy to prevent a 1st hemorrhage in medium to large varices?

A

NO, appear to make things worse

703
Q

what do you do for a patient with cirrhosis and small esophageal varices?

A

NOTHING- only BIG varices bleed!

704
Q

primary therapy of actively bleeding varices

A

ENDOSCOPIC BANDING or SCLEOTHERAPY

preferably with somatostatin

705
Q

give all cirrhotic patients with bleeding or ascites prophylactic PO or IV what?
to prevent what?

A

antibiotics (3rd generation cephalosporin or quinolones)

SBP (spontaneous bacterial peritonitis)
AKI
decrease mortality

706
Q

should be prescribed to ALL patients who have had bleeding varices to decrease the chance of rebleeds

A

B-blocker

propranolol or nadolol

707
Q

only used for varices that REbleed

A

TIPS (transjugular intrahepatic portosystemic shunt)

708
Q 
GI bleed
hypovolemia
hypoxia
hypokalemia
sedatives
tranquilizers
portal venous obstruction
infections
alkalosis (which, increases ammonia/ammonium ratio)
A

things that can cause hepatic encephalopathy or make it worse

709
Q

signs of hepatic encephalopathy

A

fetor hepaticus
hyperreflexia
asterixis
altered mental status

710
Q

treatment of hepatic encephalopathy

A

lactulose (goal of about 3 BM/day)

rifaximin, metronidazole, rifampin, or vancomycin

acarbose

probiotics

711
Q

diagnosis of hepatorenal syndrome

A

diagnosis of exclusion

712
Q

urine sodium in hepatorenal syndrome is

A

very low (commonly

713
Q

treatment of hepatorenal syndrome

A

albumin
midodrine (a1 agonist)
octreotide (stimulates fluid absorption from GI tract)

714
Q

if prothrombin time (PT) in alcoholic is prolonged

A

EASILY CORRECTED with IM vitamin K

715
Q

accumulation of fluid in peritoneal cavity

A

ASCITES

716
Q

lymphatic blockage (trauma, tumors- especially primary lymphona, TB, and filariasis), NOT cirrhosis or CHF

A

CHYLOUS ascites

717
Q

bloody ascitic fluid suggests

A

tumor

718
Q

cloudy ascitic fluid suggests

A

infection

719
Q

milky ascitic fluid suggests

A

lymphatic obstruction

720
Q

what do you do if ascitic cell count is > 250 PMNs?

A

C&S and start antibiotics

721
Q

a serum-to-ascites albumin gradient (SAAG) > 1.1 g/dL indicates

A

portal hypertension

722
Q

definition of SAAG

A

albumin (serum) - albumin (ascites)

723
Q

high albumin in ascites and NO portal HTN

A

SAAG

724
Q

used to treat refractory ascites caused by cirrhosis

A

TIPS (transjugular intrahepatic portosystemic shunt)

725
Q

common complication of TIPS

A

ENCEPHALOPATHY

726
Q

peritoneal fluid with > 250 PMN/mL in patient with ascites

A

SBP (spontaneous bacterial peritonitis)

727
Q
  • ascites protein
A

risk factors of SBP

728
Q

patient with SBP risk factors should receive either

A

INTERMITTENT (preferred) or continuous PROPHYLACTIC PO antibiotics
(usually PO quinolone)

729
Q

2 other possibilities that must be ruled out before assuming diagnosis of SBP

A
  1. neutrocytic ascites

2. primary bacterial peritonitis (PBP)

730
Q

PMNs > 250/mL with NO evidence of SBP and negative cultures

A

neutrocytic ascites

731
Q

d/t perforated viscus

protein > 1 g/dL, frequently > 3 g/dL
glucose 5,000
ascites fluid LDH > serum LDH

A

(PBP) primary bacterial peritonitis

732
Q

treatment for active SBP

A

cefotaxime or other 3rd generation cephalosporin
AND
IV ALBUMIN

733
Q

do NOT diurese more than this amount in treatment of ascites

A

> 1 L/d

734
Q

okay to do what daily during INITIAL TREATMENT of recent-onset ascites or severe REFRACTORY ascites

A

daily paracenteses

735
Q

okay to do daily paracenteses IF patient’s renal function is normal AND there is:

A
  • NO GI bleeding
  • NO sepsis
  • NO portosystemic encephalopathy (PSE)
736
Q

with large-volume paracentesis (5 L or more)

A

replace 6-8 grams albumin for each liter of fluid removed

737
Q

main finding in hereditary liver diseases

A

hyperbilirubinemia

738
Q

only this type of bilirubin passes the glomeruli and is excreted in the urine

A

CONJUGATED

739
Q

bilirubinRUIA results only come from

A

CONJUGATED hyperbilirubinemia

740
Q

bilirubinRUIA is an indication of

A

cholestasis (because bilirubin is conjugated in liver)

741
Q

very common, benign, chronic disorder resulting in mild, UNconjugated hyperbilirubinemia

A

Gilbert syndrome

742
Q

UNCONJUGATED bilirubin

A

INDIRECT = WITHOUT BILIRUBINURIA

743
Q

jaundice may come and go, typically brough on by

A

physical stress (surgery, exertion, and infection), alcohol, and alcohol

744
Q

Gilbert syndrome genetics

A

AUTOSOMAL DOMINANT with variable penetrance

745
Q

diagnosis of Gibert syndrome

A

increased UNconjugated bilirubin after prolonged fasting

746
Q

treatment of Gilbert syndrome

A

NO treatment needed

747
Q

increased CONJUGATED bilirubin after major surgery

A

BENIGN POSTOPERATIVE CHOLESTASIS

748
Q

a1-antitrypsin deficiency treatment

A

liver transplant (or both, liver and lung transplant)

749
Q

2 types of hemochromatosis

A
  1. genetic

2. acquired

750
Q

GENETIC form of hemochromatosis

A

HFE gene

autosomal recessive (AR)

751
Q

ACQUIRED form of hemochromatosis

A

2/2 blood transfusions

752
Q

abnormally increased intestinal iron absorption leading to tissue deposition

A

BOTH genetic and acquired hemochromatosis

753
Q

suspect this in a thin 50-year-old with new onset DM

A

secondary diabetes, “bronze diabetes” 2/2 hemochromatosis

754
Q

25-30% risk of HCC in patients with cirrhosis caused by

higher than any other cause

A

hemochromatosis

755
Q

diagnosis of hemochromatosis is SUGGESTED by

A

high serum IRON, FERRITIN, and TRANSFERRIN

756
Q

CONFIRMS diagnosis stages fibrosis of hemochromatosis

A

liver biopsy

757
Q

confirm diagnosis for hereditary type of hemochromatosis

A

assay for HFE gene

758
Q

initial treatment of hemochromatosis

A

weekly phlebotomy

759
Q

treatment of hemochromatosis

A

phlebotomy 4x/year with goal ferritin between 50-100ng/mL

760
Q

liver disease OR neurologic/psychiatric dysfunction in ADOLESCENTS

A

Wilson disease

761
Q

impaired excretion of copper into bile –> excess copper in body tissues (especially liver)

A

Wilson disease

762
Q

LOW serum ceruloplasmin and URINARY copper level is HIGH

A

Wilson disease

763
Q

pathognomonic for Wilson disease

A

Kayser-Fleischer rings with slit-lamp exam

764
Q

what CONFIRMS Wilson disease diagnosis?

A

liver biopsy

765
Q

what also has a high liver copper level, besides Wilson disease?

A

PBC and PSC

766
Q

screen for Wilson disease in?

A

adults (especially

767
Q

3 screening test for Wilson disease

A
  1. serum ceruloplasmin
  2. slit-lamp exam
  3. urine copper
768
Q

treatment of Wilson disease

A

2-PHASE process

  1. chelation with PENICILLAMINE
  2. maintenance chelation and low-copper diet
769
Q

CURE for Wilson disease

A

liver transplant

770
Q

only treatment of fulminant Wilson disease (severe hemolytic anemia and high serum copper)

A

liver transplant

771
Q

liver disease during pregnancy

1st trimester

A

mild increase in AST and ALT

772
Q

liver disease during pregnancy

2nd trimester

A

best time for surgery for symptomatic gallstone patients

773
Q

liver disease during pregnancy

3rd trimester

A

fulminant hepatitis d/t HEPATITIS E

774
Q

MICROvesicular fat deposition

modest elevation of AST/ALT/bili

associated with encephalopathy, hypoglycemia, preeclampsia, pancreatitis, DIC, and renal failure

A

fatty liver of pregnancy

775
Q

HELLP syndrome

SEVERE VARIANT OF PREECLAMPSIA

A

Hemolysis
Elevated Liver enzymes
Low Platelets

776
Q

ITCHING and increased AP/bili/AST/ALT

A

intrahepatic cholestasis of pregnancy

777
Q

Model for End-stage Liver Disease (MELD) scale predicts

A

MORTALITY risk

778
Q

MELD > 20

A

candidate for transplant

779
Q

NOT a contraindication to liver transplant

A

TIPS procedure

780
Q

jaundice in those

A

acute viral hepatitis (MCC; 85-90%)

781
Q

jaundice in those 40-60 years old

A

chronic cirrhosis (50-70%)

782
Q

obstructive jaundice in those 60-80 years old

A

common duct stone or pancreatic cancer (80%)

783
Q

outside of USA
jaundice
eosinophilia

A

ascariasis

784
Q

US results determine next test to be done:

DILATED common bile duct AND STONES

A

ERCP

785
Q

US results determine next test to be done:

DILATED common bile duct and NO stones

A

CT (think pancreatic cancer) or EUS

786
Q

US results determine next test to be done:

dilated intrahepatic ducts

A

CT

787
Q

US results determine next test to be done:

dilated ducts and testing to exclude PSC

A

MRCP

788
Q

US results determine next test to be done:

if NO dilated ducts

A

liver BIOPSY

789
Q

vitamin deficiencies
time until onset of symptoms

weeks

A

WATER-SOLUBLE VITAMINS
MAGNESIUM
ESSENTIAL FATTY ACIDS

790
Q

vitamin deficiencies
time until onset of symptoms

months

A

COPPER

VITAMIN K

791
Q

vitamin deficiencies
time until onset of symptoms

year

A

VITAMINS A and D
SELENIUM
CHROMIUM

792
Q

vitamin deficiencies
time until onset of symptoms

several years

A

IRON

COBALT

793
Q

vitamin deficiencies
time until onset of symptoms

many years

A

B12

794
Q

major cause of blindness in developing countries

earliest symptom is night blindness

A

vitamin A deficiency

795
Q

BERBERI

A

vitamin B1 (THIAMINE) deficiency

796
Q

2 major manifestations of thiamine deficiency

A

wet and dry beriberi

797
Q

heart failure, ascites, and peripheral edema

A

wet beriberi

798
Q

(confined to the nervous system)

peripheral neuropathy, Wernicke encephalopathy, and Korsakoff syndrome

A

dry beriberi

799
Q

closet drinker who develops ophthalmoplegia or nystagmus post-surgery

A

Wernicke encephalopathy

800
Q

always give this to an alcoholic before IV dextrose infusion

A

thiamine (B1)

801
Q

PHENOTHIAZINES and TRICYCLIC ANTIDEPRESSANTS increase tendency to develop

A

riboflavin (B2) deficiency

802
Q

isoniazid, cycloserine, and pencillamine cause

A

pyridoxine (B6) deficiency

803
Q

MACROcytic anemia, smooth tongue, and peripheral neuropathy

A

cobalamin (B12) deficiency

804
Q

PELLAGRA (3 D’s: dermatitis, diarrhea, and dementia)

seen in CARCINOID syndrome, and INH usage

A

niacin (B3) deficiency

805
Q

vitamin C deficiency causes

A

SCURVY

806
Q

PETECHIAL hemorrhages and ECCHYMOSES

perifollicular hemorrhage

A

scurvy

807
Q

rickets in children

osteomalacia in adults

A

vitamin D deficiency

808
Q

older patient with musculoskeletal pain/weakness, especially if h/o fat MALABSORPTION or VEGETARIANISM

A

consider vitamin D deficiency

809
Q

areflexia and decreased vibration and position sense

A

vitamin E deficiency

810
Q

causes of hypervitaminosis A

A

eating polar bear liver

vitamin supplements

811
Q

symptoms of hypervitaminosis A

A

headache and flaky skin

812
Q

symptoms of hypervitaminosis B6 (pyridoxine)

A

peripheral neuropathy with NORMAL motor and sensory function, but ABSENT positional and vibratory sensation

813
Q

can cause marked POTENTIATION OF ORAL ANTICOAGULANTS

A

vitamin E hypervitaminosis

814
Q

vitamin C hypervitaminosis

A

increase incidence of OXALATE renal stones

815
Q

can cause acanthosis nigricans and cholestatic jaundice

A

niacin (B3) hypervitaminosis

816
Q

helps MAINTAIN THE INTEGRITY OF THE SMALL INTESTINAL WALL (the loss of which is associated with the onset of multisystem failure)

A

ENTERIC feeding

817
Q

chronically malnourished patients (especially those with resting bradycardia, hypotension, or body weight

A

REFEEDING SYNDROME d/t rapid refeeding

818
Q

monitor what in refeeding syndrome

A

phosphate and potassium

819
Q

what are GERD ALARM SYMPTOMS?

A
  • nausea/emesis
  • chronic GI bleeding
  • family h/o PUD
  • weight loss
  • anorexia
  • IDA
  • abnormal physical exam
  • long duration of frequent symptoms
  • tx failure with full dose PPI
  • dysphagia/odynophagia
820
Q

w/u of suspected esophageal cancer

A
  • barium swallow may be done
  • EGD is ALWAYS done to confirm via BIOPSY
  • CT scan and endoscopic US are used for staging
821
Q
  • RF-negative peripheral polyarthritis
  • ankylosing spondylitis
  • erythema nodosum
  • pyoderma gangrenosum
  • iritis/episcleritis/uveitis
  • venous thrombosis
  • pericholangitis
  • primary sclerosing cholangitis
  • aphthous ulcers
A

extraintestinal manifestations of IBD

ABIM (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions