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GI Flashcards

1
Q

causes of oropharyngeal dysphagia

A

muscular or neurologic disorders, most commonly stroke, Parkinson disease, ALS, MG, and muscular dystrophy

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2
Q

what test to rule out oropharyngeal disease

A

videofluroscopy

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3
Q

signs of zenker diverticulum

A

present with regurgitation of undigested food, gurgling sound in the chest, and severe halitosis.

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4
Q

how to differentiate mechanical vs motility abnormality in esophageal dysphagia

A

Solid-food dysphagia is most often caused by a structural esophageal abnormality.

Dysphagia for solids and liquids or for liquids alone suggests an esophageal motility abnormality such as achalasia

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5
Q

how would you describe a esophageal web or schazki ring (distal esophageal ring)

A

Solid-food dysphagia that occurs episodically for months to years

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6
Q

how does achalasia occur

A 
degeneration of the myenteric plexus with failure of the lower
esophageal sphincter (LES) to relax in response to swallowing and absent peristalsis
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7
Q

does achalasia affect solid, liquids or both and common presenting symptom

A

both

presents with nonacidic regurgitation of undigested food

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8
Q

diagnostics for achalasia

A

Diagnostic evaluation should be performed in the following order:
• barium swallow: the preferred screening test when diagnosis is suspected clinically;
shows “bird’s beak” narrowing of the GE junction
• esophageal manometry: documents the absence of peristalsis and incomplete relaxation of the LES with swallows
• upper endoscopy: to rule out adenocarcinoma (pseudoachalasia) at the GE
junction

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9
Q

what infectious disease is associated with achalasia

A

• If the patient has a history of travel to South America, suspect Chagas disease as
the cause of achalasia

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10
Q

tx for achalasia

A

Laparoscopic surgical myotomy of the LES and endoscopic pneumatic dilation of the
esophagus are first-line therapies for achalasia.

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11
Q

a patient without alarm features (anemia, dysphagia, vomiting, weight loss), symptom relief with PPI therapy confirms which diagnosis.

A

GERD

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12
Q

what test to order if GERD symptoms refractory to empiric therapy with PPIs

A

Make sure patient is on bid dosing x 4-8w then Upper endoscopy; if normal, then choose ambulatory esophageal pH monitoring or impedance pH testing while taking a PPI for symptom–reflux correlation

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13
Q

next step if patient has Dysphagia, odynophagia, and weight loss

A

EGD to rule out malignancy

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14
Q

what should be the suggestion for a patient with GERD refractory to medical management or patients who have an excellent response to a PPI but do not want long-term medical therapy.

A

antireflux surgery

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15
Q

what testing should be done prior to surgery

A

Patients should undergo pH monitoring to demonstrate true reflux with symptom correlation and manometry to rule out a
motility disorder before surgery

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16
Q

what is barretts esophagus

A

a premalignant condition caused by longstanding GERD

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17
Q

Barrett screening

A

Screen MEN only aged >50 years with GERD symptoms for more than 5 years and additional risk factors (nocturnal reflux symptoms,
hiatal hernia, elevated BMI, tobacco use, and intra-abdominal distribution of fat)

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18
Q

how is barrett diagnosed

A

columnar epithelium above the normally located GE junction. Lowgrade or high-grade dysplasia in biopsy specimens should be confirmed by an expert pathologist.

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19
Q

tx for barretts based on dysplasia

A

No dysplasia- PPI

low to high grade- ablation

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20
Q

surveillance for barretts

A

In patients with BE and no dysplasia, surveillance examinations should occur at intervals no more frequent than 3 to 5 years.

More frequent intervals of every 6 to 12 months are indicated in patients with BE and low-grade dysplasia who do not choose endoscopic ablation

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21
Q

most common infectious cause of candidiasis

A

Candida albicans is the most common infectious cause, followed by CMV and HSV

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22
Q

pills that cause esophagitis

A

tetracyclines, NSAIDs, potassium chloride, iron, and alendronate

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23
Q

how do young patients with eosinophilic esophagitis present

A

extreme dysphagia and food impaction.

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24
Q

endoscopy findings in EE

A

w mucosal furrowing, stacked circular rings, white specks, and mucosal friability.
Endoscopic biopsies show marked infiltration with eosinophils.

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25
Q

after endoscopy next step in EE

A

Evaluation of EE includes an 8-week trial of a PPI; clinical response to the PPI trial indicates GERD-associated eosinophilia rather than EE.

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26
Q 
TX for 
Esophageal Candidiasis 
HSV esophagitis 
CMV esophagitis 
EE
and Pill induced
A
  • fluconazole or itraconazole for esophageal candidiasis
  • acyclovir, famciclovir, or valacyclovir for HSV esophagitis
  • ganciclovir and/or foscarnet for CMV esophagitis
  • swallowed fluticasone or budesonide for EE
  • supportive care for pill esophagitis
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27
Q

symptoms of PUD

A

dyspepsia or epigastric burning, early satiety, nausea, and postprandial belching or bloating

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28
Q

most common cause of pud

A

Helicobacter pylori infection or NSAID use.

All patients with PUD should be tested for H. pylori infection regardless of NSAID use

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29
Q

complications of PUD

A

Penetration is characterized by a gradual increase in the severity and frequency of abdominal pain, with pancreatitis as a common presentation.

  • Perforation is characterized by severe, sudden abdominal pain that is often associated with shock and peritoneal signs.
  • Outlet obstruction is characterized by nausea, vomiting, and/or early satiety and a succussion splash.
  • Bleeding is characterized by hematemesis, melena, or hematochezia (see Upper GI Bleeding)
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30
Q

general approach for patients aged <60 years with dyspepsia without alarm symptoms, including anemia, dysphagia, persistent vomiting, or
weight loss

A

use the “test-and-treat” approach for H. pylori without initially performing upper endoscopy.

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31
Q

when can false positives occur in h. pylori

A

recently took antibiotics, bismuth-containing compounds, or PPIs; these drugs should be stopped before testing
(28 days for antibiotics, 2 weeks for PPIs) or histologic assessment for H. pylori should be performed.

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32
Q

treatment for h. pylori

A
  • If resistance to clarithromycin is unlikely, use clarithromycin-based triple therapy.
  • If resistance to clarithromycin is probable, use bismuth quadruple therapy.

When first-line therapy fails, a salvage regimen should avoid previously used antibiotics.

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33
Q

how to determine h. pylori eradication

A

Follow-up noninvasive testing to document H. pylori eradication should be performed at least 4 weeks after completion of therapy in any patient with a positive H. pylori test result.

Follow-up upper endoscopy for gastric ulcers is indicated only if the patient remains symptomatic after treatment, the cause is uncertain, or biopsies were not performed during initial upper endoscopy

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34
Q

causes of gastroparesis

A

systemic sclerosis, diabetes mellitus, hypothyroidism, administration of anticholinergic agents, and narcotics. A viral cause is suggested by rapid onset of gastroparesis after a presumed viral infection.

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35
Q

testing for gastroparesis

A

acute sx: upper endoscopy is the initial study to rule out pyloric channel obstruction caused by PUD

chronic sx: or negative findings on upper endoscopy should undergo a nuclear medicine solid-phase gastric emptying study.

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36
Q

how can acute hyperglycemia impair testing

A

• Patients with diabetes mellitus should have a blood glucose level <275 mg/dL during testing because marked
hyperglycemia can acutely impair gastric emptying.

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37
Q

tx for gastroparesis

A

Specific dietary recommendations include small low-fat meals consumed four to five times per day.

Use IV erythromycin for acute gastroparesis and metoclopramide for chronic gastroparesis.

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38
Q

what are some serious complications reglan

A

Dystonia and parkinsonian-like tardive dyskinesia

stop drug immediately effects may not be reversible

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39
Q

major complications of roux en y

A

cholelithiasis, nephrolithiasis (resulting from increased urinary oxalate excretion), dumping syndrome, anastomotic stricture or ulceration, small-bowel obstruction, and gastrogastric
fistula.

SIBO can occur as well

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40
Q

common complications of gastrectomy

A
  • anastomotic leaks and strictures
  • marginal/anastomotic ulcers
  • delayed gastric emptying
  • dumping syndrome
  • fat malabsorption
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41
Q

if you see Abdominal cramps, nausea, and loose stools 15 minutes after eating followed within 90 minutes by lightheadedness, diaphoresis, and tachycardia following gastric resection or bypass surgery think

A

dumping syndrome

Treat with small frequent feedings and low-carbohydrate meals

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42
Q

If you see Loose stools and malabsorption following bypass surgery think

A

Choose blind loop syndrome (SIBO)

Treat with antibiotics and nutritional supplements

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43
Q

if you see Abdominal pain, bloating, difficulty belching following fundoplication think

A

Choose gas-bloat syndrome

Treat with diet modification; most treatments are untested

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44
Q

imagining for pacreatitis

A

All patients with acute pancreatitis require abdominal ultrasonography to evaluate the biliary tract for obstruction.
CT of the abdomen is indicated if the pancreatitis is severe, lasts longer than 48 hours, or complications are suspected.

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45
Q

rf for severe pancreatitis

A

age >55 years, medical comorbidities, BMI >30, SIRS, signs of hypovolemia (serum BUN
level >20 mg/dL and rising, hematocrit >44%, or elevated serum creatinine).

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46
Q

when do you feed in pancreatitis

and is enteral or tpn better in severe pancreatitis

A

when symptoms improve

enteral > tpn

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47
Q

diagnostic critera for chronic pancreatitis

A

history of pain, recurrent attacks of pancreatitis, weight loss
• pancreatic calcifications on imaging
• ductal dilation or inflammatory masses
• exocrine pancreatic insufficiency (steatorrhea)
• diabetes

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48
Q

how do patients with autoimmune pancreatitis present

A

obstructive jaundice

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49
Q

Type 1 AIP presentation

A

lder men and is associated with pancreatitis, Sjögren syndrome, PSC, bile duct strictures, autoimmune
thyroiditis, and interstitial nephritis. Serum IgG4 level is increased.

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50
Q

Type 2 AIP presentation

A

Type II AIP is associated with chronic pancreatitis and IBD and less likely to include elevated IgG4 levels

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51
Q

tx for AIP

A

prednisone

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52
Q

what should you think about in a young patient with chronic pancreatitis

A

CF

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53
Q

how long should you wait before getting culture on acute diarrhea

A

1 w

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54
Q

Acute diarrhea that mimicks appendicitis and crohn’s disease

A

Yersinia enterocolitica

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55
Q

acute diarrhea most common in aids patient’s

A

. Cryptosporidiosis

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56
Q

when should you give abx in patients for acute diarrhea

A

diarrhea lasting >7 days or with symptoms of fever, abdominal pain, or hematochezia

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57
Q

do you give abx for ehec diarrhea

A

NO

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58
Q

what should you do if a patient with chronic diarrhea has a negative colonoscopy

A

48- to 72-hour stool collection with analysis of fat content. Fat excretion >14 g/d is
diagnostic of steatorrhea

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59
Q

differential for steatorhea

A 
malabsorption disorders (e.g.,
celiac disease), bacterial overgrowth, and pancreatic insufficiency
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60
Q

what is the osmotic gap in osmotic diarrhea

A

gap>100

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61
Q

what is the osmotic gap in secretory diarrhea

A

gap <50

62
Q

how can you tell facticious diarrhea based on osmolarity

A

y <250 mOsm/kg H2O suggests factitious diarrhea associated with chronic laxative abuse or
adding water to the stool

63
Q

osmotic diarrhea character vs secretary diarrhea character

A

Osmotic diarrhea is most commonly caused by lactase deficiency. Osmotic diarrhea is associated with eating, improves with fasting, and typically is not nocturnal.

Secretory diarrhea is characterized by large-volume, watery, nocturnal bowel movements and is unchanged by fasting

64
Q

Diarrhea mainly in women aged 45-60 years, unrelated to food intake (nocturnal diarrhea), normal colonoscopy

A

microscopic colitis

65
Q

Nocturnal diarrhea and diabetes mellitus or SSc

A

SIBO

66
Q

Severe secretory diarrhea and flushing

A

Carcinoid syndrome; obtain test for 24-hour urinary excretion of 5-HIAA

67
Q

next step if you see History of IBS and iron deficiency anemia

A

Diagnose celiac disease.
Obtain IgA anti-tTG antibody assay and small bowel biopsy if
positive.
Order a gluten-free diet.

68
Q

next step if you see Chronic pancreatitis, hyperglycemia, history of pancreatic
resection, CF

A

Diagnose pancreatic insufficiency.
Obtain test for excess fecal fat and x-rays for pancreatic
calcifications.
Treat with pancreatic enzyme replacement therapy.

69
Q

next step if you see Previous surgery, small bowel diverticulosis, dysmotility (SSc or
diabetes mellitus), combination of vitamin B12 deficiency and elevated folate level

A

Diagnose bacterial overgrowth.

Order empiric trial of antibiotics or hydrogen breath test.

70
Q

next step if you see History of resection of <100 cm of distal ileum, with voluminous
diarrhea, weight loss, and malnutrition

A

Diagnose short-bowel syndrome with bile acid enteropathy.

Order empiric trial of cholestyramine.

71
Q

next step if you see diarrhea wih Arthralgia; fever; neurologic, ocular, or cardiac disease

A

Diagnose Whipple disease.
Select small bowel biopsy and PCR for Tropheryma whippelii.
Order antibiotics for 12 months

72
Q

next step if you see Travel to India or Puerto Rico, malabsorption, weight loss, malaise,
folate or vitamin B12 deficiency, steatorrhea

A

Diagnose tropical sprue.
Order a small bowel biopsy.
Treat with a sulfonamide or tetracycline and folic acid.

73
Q

Prolonged traveler’s diarrhea, diarrhea after a camping trip,
outbreak in a day-care center

A

Diagnose giardiasis.
Identify Giardia parasites or Giardia antigen in the stool.
Treat with metronidazole.

74
Q

skin lesion in celiac disease

A

pruritic papulovesicular rash on the extensor surfaces (dermatitis herpetiformis;

75
Q

celiac is associated with what other disease

A

Type 1 diabetes mellitus and autoimmune thyroid (patients with celiac have trouble with consuming thyroid hormone.

76
Q

patient who are noncompliant with gluten free diet in celiac can be susceptible to what disease state

A

small bowel lymphoma

77
Q

what can cause a false negative on celiac screening

A

doing gluten free prior to testing or IgA deficiency

78
Q

UC or Crohn’s: Mucosal edema, erythema, and loss of the vascular pattern,
granularity, friability, ulceration, and bleeding

A

UC

79
Q

UC or Crohn’s: Altered crypt architecture with shortened, branched crypts and
crypt abscesses

A

UC

80
Q

UC or Crohn’s: Diarrhea (prominent), tenesmus, urgency hematochezia, weight
loss, and fever

A

UC

81
Q

UC or Crohn’s: Linear, stellate, or serpiginous ulcerations with “skip” areas of
inflammation involving entire GI tract

A

Crohn

82
Q

UC or Crohn’s: Granulomas are characteristic but are often not found. Transmural
involvement.

A

Crohn

83
Q

UC or Crohn’s: Abdominal pain (prominent), diarrhea, inflammatory masses,
fever, weight loss, intestinal strictures and fistula (to skin, bladder,
vagina, or enteric-enteric)

A

Crohns

84
Q

IBD screening

A

Beginning 8 years after diagnosis, surveillance colonoscopy for colon cancer should be performed every 1 to 2 years for patients
with ulcerative pancolitis or Crohn disease involving most of the colon. If dysplasia is found, proctocolectomy is required.

85
Q

what drugs have been implicated in microscopic colitis

A

NSAIDs, PPIs, and SSRIs

86
Q

Tx for microscopic colitis

A

antidiarrheal for mild cases or else use budesinide

87
Q

are patient’s with microscopic colitis at an increase risk for colon cancer

A

no

88
Q

what colon changes can happen with senna

A

melanosis coli.

89
Q

step wise tx for chronic constipation

A

eliminate implicated medications, if possible
• increase physical activity and dietary fiber
• soluble fibers such as psyllium and methylcellulose
• surfactants such as docusate sodium or docusate calcium (most appropriate for very mild, intermittent constipation)
• osmotic laxatives include magnesium hydroxide, lactulose, sorbitol, and PEG 3350 (PEG is superior)
• stimulant laxatives such as anthraquinone, senna, and the diphenylmethanes (fastest-acting agents)
If chronic constipation does not respond to initial stepped approach, prosecretory agents, including lubiprostone and linaclotide,
are available by prescription.

90
Q

tx for pain associated with ibs

A

tricyclic antidepressants (preferred in IBS-D) and SSRIs (preferred in IBS-C) for abdominal pain

91
Q

tx if ibs-c doesnt respond to peg

A

lubiprostone (FDA approved for women with IBS-C) and linaclotide (guideline preferred; FDA approved for treatment of
IBS-C in adults) for IBS-C unresponsive to PEG

92
Q

tx options for ibs-d

A
  • loperamide for IBS-D
  • eluxadoline for abdominal pain and stool consistency in IBS-D
  • rifaximin for global symptoms associated with IBS-D
93
Q

how does a diverticular bleed occur

A

rupture of an artery that has penetrated a diverticulum, is typically painless, and usually
stops without therapy

94
Q

if clinical symptoms are high enough do you need imaging for diverticulitis

A

no

95
Q

tx of diverticulitis

A

select a clear-liquid diet and a 7- to 10-day course of antibiotics, such as ciprofloxacin and
metronidazole.

96
Q

risk of having recurrent diverticular disease

A

After recovering from acute diverticulitis, 30% of patients will have recurrent episodes. After a second episode, the risk of subsequent attacks increases to 50%, and surgical resection of the affected colon is indicated.

97
Q

causes of embolism vs thrombis in acute mesenteric ischemia

A

Embolism to the mesenteric arteries from AF or left ventricle thrombus causes 50% of AMI. Mesenteric arterial thrombosis is
usually caused by atherosclerotic disease.

98
Q

how are nonocculsive mesenteric ischemia caused by

A

low flow states ie HF hypotension sepsis

99
Q

disease and imaging for Poorly localized severe abdominal pain, often out of proportion to physical findings; peritoneal signs
signify infarction

A

AMI,CT angio

100
Q

disease and imaging for Postprandial abdominal pain, fear of eating, and
weight loss; often, signs and symptoms of
atherosclerosis in other vascular beds

A

chronic mesenteric ischemia

CTA, selective angiography, or MRA

101
Q

disease and imaging for LLQ abdominal pain and self-limited bloody diarrhea

A

Ichemic colitis

Colonoscopy: patchy segmental ulcerations

102
Q

what can you see on xray in ischemic colitis

A

thumbprinting esp in the transverse colon

103
Q

Tx for AMI with peritoneal signs

A

Urgent laparotomy
Resection of necrotic bowel
Embolectomy or thrombectomy and surgical revascularization

104
Q

Tx for AMI without peritoneal signs

A

Angiography
Surgical embolectomy or intra-arterial thrombolysis
Intra-arterial papaverine for nonocclusive mesenteric ischemia

105
Q

Tx for chronic mesenteric ischemia

A

Surgical reconstruction or angioplasty with stenting

106
Q

Tx for Ischemic colitis

A

Supportive care with IV fluids and bowel rest

107
Q

Diagnose Gilbert disease

A

verify normal aminotransferase levels
and the absence of hemolysis.
• Patients with Gilbert disease usually have mild (<3 mg/dL) unconjugated bilirubin levels that increase with stress or
fasting

108
Q

hep A treatment to those who have come in contact

A

Immunization or immune globulin should be given within 2 weeks to household, sexual, and day-care contacts of patients with
hepatitis A or persons who ate foods contaminated with HAV

109
Q

vaccine schedule for healthy travelers for hep a

A

One dose of hepatitis A vaccine administered to travelers any time before departure provides protection for healthy persons aged
≤40 years. A second dose 6 to 12 months later is recommended.

110
Q

Vaccination for hep a in Older adults and those who are immunocompromised or have chronic liver disease and are departing in ≤2 weeks should receive

A

one dose of the vaccine and immune globulin.

111
Q

postexposure prophylaxis after needle-stick injury and for sexual and household contacts of patients with HBV. is

A

Hepatitis B vaccine plus HBIG

112
Q

Hep B immune tolerant phase

A

a normal ALT

level despite a positive HBeAg and very high HBV DNA level

113
Q

Hep B inactive carrier stage is characterized by

A

a normal ALT level and an HBV DNA level <20,000 U/mL

114
Q

Hep B immune active and immune escape phase

A

HBeAg-positive (immune active) or HBeAg-negative (immune escape) chronic HBV phases have an elevated ALT level and an HBV DNA level >10,000 U/mL

115
Q

Acute hepatitis B;
occasionally reactivation of
chronic hepatitis B serology

A 
HBsAg +
Anti-HBs
IgM anti-HBc +
IgG anti-HBc 
HBeAg +
Anti-HBe 
HBV DNA, U/mL >20K
116
Q

Hep B Resolved previous infection serology

A 
HBsAg 
Anti-HBs +
IgM anti-HBc 
IgG anti-HBc +
HBeAg 
Anti-HBe +/-
HBV DNA, U/mL - undetected
117
Q

Hep B Immunity from previous

vaccination serology

A 
HBsAg 
Anti-HBs +
IgM anti-HBc 
IgG anti-HBc 
HBeAg 
Anti-HBe 
HBV DNA, U/mL- undetected
118
Q

hep b False-positive or resolved

previous infection serology

A 
HBsAg 
Anti-HBs
IgM anti-HBc 
IgG anti-HBc + 
HBeAg 
Anti-HBe 
HBV DNA, U/mL- undetected
119
Q

Chronic hepatitis B inactive

carrier state serology

A 
HBsAg +
Anti-HBs
IgM anti-HBc 
IgG anti-HBc + 
HBeAg 
Anti-HBe +
HBV DNA, U/mL- <20K
120
Q

HBeAg-positive chronic

hepatitis B serology

A 
HBsAg +
Anti-HBs
IgM anti-HBc 
IgG anti-HBc + 
HBeAg +
Anti-HBe 
HBV DNA, U/mL- >20K
121
Q

HBeAg-negative chronic

hepatitis B serology

A 
HBsAg +
Anti-HBs
IgM anti-HBc 
IgG anti-HBc + 
HBeAg 
Anti-HBe +
HBV DNA, U/mL- <10K
122
Q

treatment for hep b is indicated for

A
  • acute liver failure or cirrhosis
  • infection in the immune-active phase (HBeAg positive, ALT ≥2 × ULN, HBV DNA ≥20,000 U/L)
  • infection in the reactivation phase (HBeAg-negative, ALT ≥2 × ULN, HBV DNA ≥2,000 U/L)
  • immunosuppression or planned immunosuppression
123
Q

tx medication for hep b

A

f entecavir or tenofovir (preferred). Pegylated interferon may be used for patients without cirrhosis
who have high ALT levels and relatively low HBV DNA levels or who are pregnant

124
Q

tx for hiv and hep b not on art therapy

A

emtricitabine-tenofovir is typically used

as part of ART

125
Q

HCC surveillance in Hep B indicated for patients with

A

cirrhosis
• Asian men >40 years and Asian women >50 years
• black patients >20 years
• elevated ALT level and HBV DNA levels >10,000 U/mL
• family history of HCC

126
Q

hep c screening

A

Universal screening is recommended for persons born between 1945 and 1965.

127
Q

test for hep c when you have a patient with

A

chronic liver disease, as well as patients with vasculitis, cryoglobulinemia, GN, and porphyria
cutanea tarda

128
Q

HCC surveillance in HCV pts

A

HCV rarely causes HCC in the absence of cirrhosis. Patients with cirrhosis should undergo sonography surveillance for HCC
every 6 months

129
Q

HCV tx

A

• sofosbuvir and ledipasvir (available as a combination
tablet)
• ombitasvir, paritaprevir, and ritonavir (available as a combination tablet) plus dasabuvir with or without ribavirin
• sofosbuvir and simeprevir with or without ribavirin
• glecaprevir-pibrentasvir or elbasvir-grasoprevir for
patients with end-stage kidney diseas

130
Q

diagnosis of autoimmune hepatitis

A

Aminotransferase levels range from mild elevations to >1000 U/L. IgG
levels are also elevated. Other findings include positive ANA and anti–smooth muscle antibody titers, positive p-ANCA, or antiLKM I antibody. Liver biopsy establishes the diagnosis.

131
Q

autoimmune demographics

A

women 20-40yo

132
Q

other conditions with autoimmune hepatitis

A

thyroiditis, ulcerative colitis, or

synovitis

133
Q

tx for AIH

A

considered for treatment with

glucocorticoids and azathioprine. Relapse occurs after stopping treatment in most patients

134
Q

symptoms of hemochromotosis

A

erectile dysfunction, fatigue, destructive arthropathy of the second and third MCP joints
characterized by distinctive hook-like osteophytes, and OA involving unusual joints, such as the shoulders, ankles, and
elbows

patients may have diabetes, HF, hyperpigmentation (skin bronzing), and panhypopituitarism

135
Q

testing for Hemochromotosis

A

fasting serum ferritin
>60% in men or >50% in women, and others suggest >55% for all patients.

C282Y homozygous or C282Y/
H63D compound heterozygous HFE genotypes are diagnostic of hemochromatosis.

136
Q

tx for hemochromotosis

A

Patients who are C282Y homozygous but have normal serum ferritin levels can be monitored without treatment.

Patients with an elevated ferritin level should be treated with phlebotomy

137
Q

Screening for hemochromotosis

A

in first degree relatives

138
Q

HCC screening for hemochromotosis

A

Screen for HCC with ultrasonography in patients with cirrhosis every 6 months.

139
Q

diagnosis of NASH

A
  • mild elevations of aminotransferase levels
  • risk factors for NAFLD (diabetes, obesity, and hyperlipidemia)
  • hyperechoic pattern on ultrasonography or low-density parenchyma on CT
140
Q

diagnostic triad of PBC

A
  • a cholestatic liver profile
  • positive antimitochondrial antibody titer
  • granulomatous inflammation centered on the septal bile duct
141
Q

vitamin deficiency in PBC

A

fat-soluble vitamin deficiencies and osteoporosis or osteomalacia.

142
Q

imaging in PBC

A

biliary ultrasound exclude extrahepatic bile duct obstruction.

143
Q

tx for PBC

A

Ursodeoxycholic acid is the primary therapeutic agen

144
Q

PSC is

A

a chronic cholestatic liver disease of unknown cause characterized by progressive bile duct destruction and biliary cirrhosis.

IBD

145
Q

PSC classic features

A

pruritus or jaundice
• elevated serum alkaline phosphatase level
• elevated total bilirubin level
• modestly elevated AST and ALT levels

146
Q

what disease do people with psc have

A

ibd (UC)

147
Q

testing for PSC

A

Abdominal ultrasonography is often the initial diagnostic study.
If intrahepatic biliary dilation is seen, MRCP or ERCP establishes the diagnosis (look for the “string of beads” pattern).

148
Q

Demographics comparison for PBC vs PSC

A

PBC Women aged 40-60 years

PSC Men aged 20-30 years

149
Q

Pathology difference PBC Vs PSC

A

PBC Cholestatic liver disease of small bile ducts

PSC Cholestatic liver disease of medium and large bile ducts

150
Q

Associated conditions PBC vs PSC

A

PBC other autoimmune disease

PSC IBD

151
Q

Clinical findings PBC vs pSC

A

PBC positive antimitochondrial antibody

PSC sting of beads on MRCP vs ERCP

152
Q

Treatment PBC vs PSC

A

PBC Ursodeoxycholic acid

PSC Endoscopic therapy for extrahepatic dominant strictures
Liver transplantation

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