1
Q
causes of oropharyngeal dysphagia
A
muscular or neurologic disorders, most commonly stroke, Parkinson disease, ALS, MG, and muscular dystrophy
2
Q
what test to rule out oropharyngeal disease
A
videofluroscopy
3
Q
signs of zenker diverticulum
A
present with regurgitation of undigested food, gurgling sound in the chest, and severe halitosis.
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
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
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
7
Q
does achalasia affect solid, liquids or both and common presenting symptom
A
both
presents with nonacidic regurgitation of undigested food
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
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
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.
11
Q
a patient without alarm features (anemia, dysphagia, vomiting, weight loss), symptom relief with PPI therapy confirms which diagnosis.
A
GERD
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
13
Q
next step if patient has Dysphagia, odynophagia, and weight loss
A
EGD to rule out malignancy
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
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
16
Q
what is barretts esophagus
A
a premalignant condition caused by longstanding GERD
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)
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.
19
Q
tx for barretts based on dysplasia
A
No dysplasia- PPI
low to high grade- ablation
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
21
Q
most common infectious cause of candidiasis
A
Candida albicans is the most common infectious cause, followed by CMV and HSV
22
Q
pills that cause esophagitis
A
tetracyclines, NSAIDs, potassium chloride, iron, and alendronate
23
Q
how do young patients with eosinophilic esophagitis present
A
extreme dysphagia and food impaction.
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.
25
after endoscopy next step in EE
Evaluation of EE includes an 8-week trial of a PPI; clinical response to the PPI trial indicates GERD-associated eosinophilia rather than EE.
26
```
TX for
Esophageal Candidiasis
HSV esophagitis
CMV esophagitis
EE
and Pill induced
```
* 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
27
symptoms of PUD
dyspepsia or epigastric burning, early satiety, nausea, and postprandial belching or bloating
28
most common cause of pud
Helicobacter pylori infection or NSAID use.
| All patients with PUD should be tested for H. pylori infection regardless of NSAID use
29
complications of PUD
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)
30
general approach for patients aged <60 years with dyspepsia without alarm symptoms, including anemia, dysphagia, persistent vomiting, or
weight loss
use the “test-and-treat” approach for H. pylori without initially performing upper endoscopy.
31
when can false positives occur in h. pylori
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.
32
treatment for h. pylori
* 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.
33
how to determine h. pylori eradication
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
34
causes of gastroparesis
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.
35
testing for gastroparesis
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.
36
how can acute hyperglycemia impair testing
• Patients with diabetes mellitus should have a blood glucose level <275 mg/dL during testing because marked
hyperglycemia can acutely impair gastric emptying.
37
tx for gastroparesis
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.
38
what are some serious complications reglan
Dystonia and parkinsonian-like tardive dyskinesia
| stop drug immediately effects may not be reversible
39
major complications of roux en y
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
40
common complications of gastrectomy
* anastomotic leaks and strictures
* marginal/anastomotic ulcers
* delayed gastric emptying
* dumping syndrome
* fat malabsorption
41
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
dumping syndrome
Treat with small frequent feedings and low-carbohydrate meals
42
If you see Loose stools and malabsorption following bypass surgery think
Choose blind loop syndrome (SIBO)
| Treat with antibiotics and nutritional supplements
43
if you see Abdominal pain, bloating, difficulty belching following fundoplication think
Choose gas-bloat syndrome
| Treat with diet modification; most treatments are untested
44
imagining for pacreatitis
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.
45
rf for severe pancreatitis
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).
46
when do you feed in pancreatitis
| and is enteral or tpn better in severe pancreatitis
when symptoms improve
| enteral > tpn
47
diagnostic critera for chronic pancreatitis
history of pain, recurrent attacks of pancreatitis, weight loss
• pancreatic calcifications on imaging
• ductal dilation or inflammatory masses
• exocrine pancreatic insufficiency (steatorrhea)
• diabetes
48
how do patients with autoimmune pancreatitis present
obstructive jaundice
49
Type 1 AIP presentation
lder men and is associated with pancreatitis, Sjögren syndrome, PSC, bile duct strictures, autoimmune
thyroiditis, and interstitial nephritis. Serum IgG4 level is increased.
50
Type 2 AIP presentation
Type II AIP is associated with chronic pancreatitis and IBD and less likely to include elevated IgG4 levels
51
tx for AIP
prednisone
52
what should you think about in a young patient with chronic pancreatitis
CF
53
how long should you wait before getting culture on acute diarrhea
1 w
54
Acute diarrhea that mimicks appendicitis and crohn's disease
Yersinia enterocolitica
55
acute diarrhea most common in aids patient's
. Cryptosporidiosis
56
when should you give abx in patients for acute diarrhea
diarrhea lasting >7 days or with symptoms of fever, abdominal pain, or hematochezia
57
do you give abx for ehec diarrhea
NO
58
what should you do if a patient with chronic diarrhea has a negative colonoscopy
48- to 72-hour stool collection with analysis of fat content. Fat excretion >14 g/d is
diagnostic of steatorrhea
59
differential for steatorhea
```
malabsorption disorders (e.g.,
celiac disease), bacterial overgrowth, and pancreatic insufficiency
```
60
what is the osmotic gap in osmotic diarrhea
gap>100
61
what is the osmotic gap in secretory diarrhea
gap <50
62
how can you tell facticious diarrhea based on osmolarity
y <250 mOsm/kg H2O suggests factitious diarrhea associated with chronic laxative abuse or
adding water to the stool
63
osmotic diarrhea character vs secretary diarrhea character
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
Diarrhea mainly in women aged 45-60 years, unrelated to food intake (nocturnal diarrhea), normal colonoscopy
microscopic colitis
65
Nocturnal diarrhea and diabetes mellitus or SSc
SIBO
66
Severe secretory diarrhea and flushing
Carcinoid syndrome; obtain test for 24-hour urinary excretion of 5-HIAA
67
next step if you see History of IBS and iron deficiency anemia
Diagnose celiac disease.
Obtain IgA anti-tTG antibody assay and small bowel biopsy if
positive.
Order a gluten-free diet.
68
next step if you see Chronic pancreatitis, hyperglycemia, history of pancreatic
resection, CF
Diagnose pancreatic insufficiency.
Obtain test for excess fecal fat and x-rays for pancreatic
calcifications.
Treat with pancreatic enzyme replacement therapy.
69
next step if you see Previous surgery, small bowel diverticulosis, dysmotility (SSc or
diabetes mellitus), combination of vitamin B12 deficiency and elevated folate level
Diagnose bacterial overgrowth.
| Order empiric trial of antibiotics or hydrogen breath test.
70
next step if you see History of resection of <100 cm of distal ileum, with voluminous
diarrhea, weight loss, and malnutrition
Diagnose short-bowel syndrome with bile acid enteropathy.
| Order empiric trial of cholestyramine.
71
next step if you see diarrhea wih Arthralgia; fever; neurologic, ocular, or cardiac disease
Diagnose Whipple disease.
Select small bowel biopsy and PCR for Tropheryma whippelii.
Order antibiotics for 12 months
72
next step if you see Travel to India or Puerto Rico, malabsorption, weight loss, malaise,
folate or vitamin B12 deficiency, steatorrhea
Diagnose tropical sprue.
Order a small bowel biopsy.
Treat with a sulfonamide or tetracycline and folic acid.
73
Prolonged traveler’s diarrhea, diarrhea after a camping trip,
outbreak in a day-care center
Diagnose giardiasis.
Identify Giardia parasites or Giardia antigen in the stool.
Treat with metronidazole.
74
skin lesion in celiac disease
pruritic papulovesicular rash on the extensor surfaces (dermatitis herpetiformis;
75
celiac is associated with what other disease
Type 1 diabetes mellitus and autoimmune thyroid (patients with celiac have trouble with consuming thyroid hormone.
76
patient who are noncompliant with gluten free diet in celiac can be susceptible to what disease state
small bowel lymphoma
77
what can cause a false negative on celiac screening
doing gluten free prior to testing or IgA deficiency
78
UC or Crohn's: Mucosal edema, erythema, and loss of the vascular pattern,
granularity, friability, ulceration, and bleeding
UC
79
UC or Crohn's: Altered crypt architecture with shortened, branched crypts and
crypt abscesses
UC
80
UC or Crohn's: Diarrhea (prominent), tenesmus, urgency hematochezia, weight
loss, and fever
UC
81
UC or Crohn's: Linear, stellate, or serpiginous ulcerations with “skip” areas of
inflammation involving entire GI tract
Crohn
82
UC or Crohn's: Granulomas are characteristic but are often not found. Transmural
involvement.
Crohn
83
UC or Crohn's: Abdominal pain (prominent), diarrhea, inflammatory masses,
fever, weight loss, intestinal strictures and fistula (to skin, bladder,
vagina, or enteric-enteric)
Crohns
84
IBD screening
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
what drugs have been implicated in microscopic colitis
NSAIDs, PPIs, and SSRIs
86
Tx for microscopic colitis
antidiarrheal for mild cases or else use budesinide
87
are patient's with microscopic colitis at an increase risk for colon cancer
no
88
what colon changes can happen with senna
melanosis coli.
89
step wise tx for chronic constipation
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
tx for pain associated with ibs
tricyclic antidepressants (preferred in IBS-D) and SSRIs (preferred in IBS-C) for abdominal pain
91
tx if ibs-c doesnt respond to peg
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
tx options for ibs-d
* loperamide for IBS-D
* eluxadoline for abdominal pain and stool consistency in IBS-D
* rifaximin for global symptoms associated with IBS-D
93
how does a diverticular bleed occur
rupture of an artery that has penetrated a diverticulum, is typically painless, and usually
stops without therapy
94
if clinical symptoms are high enough do you need imaging for diverticulitis
no
95
tx of diverticulitis
select a clear-liquid diet and a 7- to 10-day course of antibiotics, such as ciprofloxacin and
metronidazole.
96
risk of having recurrent diverticular disease
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
causes of embolism vs thrombis in acute mesenteric ischemia
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
how are nonocculsive mesenteric ischemia caused by
low flow states ie HF hypotension sepsis
99
disease and imaging for Poorly localized severe abdominal pain, often out of proportion to physical findings; peritoneal signs
signify infarction
AMI,CT angio
100
disease and imaging for Postprandial abdominal pain, fear of eating, and
weight loss; often, signs and symptoms of
atherosclerosis in other vascular beds
chronic mesenteric ischemia
| CTA, selective angiography, or MRA
101
disease and imaging for LLQ abdominal pain and self-limited bloody diarrhea
Ichemic colitis
| Colonoscopy: patchy segmental ulcerations
102
what can you see on xray in ischemic colitis
thumbprinting esp in the transverse colon
103
Tx for AMI with peritoneal signs
Urgent laparotomy
Resection of necrotic bowel
Embolectomy or thrombectomy and surgical revascularization
104
Tx for AMI without peritoneal signs
Angiography
Surgical embolectomy or intra-arterial thrombolysis
Intra-arterial papaverine for nonocclusive mesenteric ischemia
105
Tx for chronic mesenteric ischemia
Surgical reconstruction or angioplasty with stenting
106
Tx for Ischemic colitis
Supportive care with IV fluids and bowel rest
107
Diagnose Gilbert disease
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
hep A treatment to those who have come in contact
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
vaccine schedule for healthy travelers for hep 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
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
one dose of the vaccine and immune globulin.
111
postexposure prophylaxis after needle-stick injury and for sexual and household contacts of patients with HBV. is
Hepatitis B vaccine plus HBIG
112
Hep B immune tolerant phase
a normal ALT
| level despite a positive HBeAg and very high HBV DNA level
113
Hep B inactive carrier stage is characterized by
a normal ALT level and an HBV DNA level <20,000 U/mL
114
Hep B immune active and immune escape phase
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
Acute hepatitis B;
occasionally reactivation of
chronic hepatitis B serology
```
HBsAg +
Anti-HBs
IgM anti-HBc +
IgG anti-HBc
HBeAg +
Anti-HBe
HBV DNA, U/mL >20K
```
116
Hep B Resolved previous infection serology
```
HBsAg
Anti-HBs +
IgM anti-HBc
IgG anti-HBc +
HBeAg
Anti-HBe +/-
HBV DNA, U/mL - undetected
```
117
Hep B Immunity from previous
| vaccination serology
```
HBsAg
Anti-HBs +
IgM anti-HBc
IgG anti-HBc
HBeAg
Anti-HBe
HBV DNA, U/mL- undetected
```
118
hep b False-positive or resolved
| previous infection serology
```
HBsAg
Anti-HBs
IgM anti-HBc
IgG anti-HBc +
HBeAg
Anti-HBe
HBV DNA, U/mL- undetected
```
119
Chronic hepatitis B inactive
| carrier state serology
```
HBsAg +
Anti-HBs
IgM anti-HBc
IgG anti-HBc +
HBeAg
Anti-HBe +
HBV DNA, U/mL- <20K
```
120
HBeAg-positive chronic
| hepatitis B serology
```
HBsAg +
Anti-HBs
IgM anti-HBc
IgG anti-HBc +
HBeAg +
Anti-HBe
HBV DNA, U/mL- >20K
```
121
HBeAg-negative chronic
| hepatitis B serology
```
HBsAg +
Anti-HBs
IgM anti-HBc
IgG anti-HBc +
HBeAg
Anti-HBe +
HBV DNA, U/mL- <10K
```
122
treatment for hep b is indicated for
* 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
tx medication for hep b
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
tx for hiv and hep b not on art therapy
emtricitabine-tenofovir is typically used
| as part of ART
125
HCC surveillance in Hep B indicated for patients with
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
hep c screening
Universal screening is recommended for persons born between 1945 and 1965.
127
test for hep c when you have a patient with
chronic liver disease, as well as patients with vasculitis, cryoglobulinemia, GN, and porphyria
cutanea tarda
128
HCC surveillance in HCV pts
HCV rarely causes HCC in the absence of cirrhosis. Patients with cirrhosis should undergo sonography surveillance for HCC
every 6 months
129
HCV tx
• 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
diagnosis of autoimmune hepatitis
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
autoimmune demographics
women 20-40yo
132
other conditions with autoimmune hepatitis
thyroiditis, ulcerative colitis, or
| synovitis
133
tx for AIH
considered for treatment with
| glucocorticoids and azathioprine. Relapse occurs after stopping treatment in most patients
134
symptoms of hemochromotosis
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
testing for Hemochromotosis
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
tx for hemochromotosis
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
Screening for hemochromotosis
in first degree relatives
138
HCC screening for hemochromotosis
Screen for HCC with ultrasonography in patients with cirrhosis every 6 months.
139
diagnosis of NASH
* mild elevations of aminotransferase levels
* risk factors for NAFLD (diabetes, obesity, and hyperlipidemia)
* hyperechoic pattern on ultrasonography or low-density parenchyma on CT
140
diagnostic triad of PBC
* a cholestatic liver profile
* positive antimitochondrial antibody titer
* granulomatous inflammation centered on the septal bile duct
141
vitamin deficiency in PBC
fat-soluble vitamin deficiencies and osteoporosis or osteomalacia.
142
imaging in PBC
biliary ultrasound exclude extrahepatic bile duct obstruction.
143
tx for PBC
Ursodeoxycholic acid is the primary therapeutic agen
144
PSC is
a chronic cholestatic liver disease of unknown cause characterized by progressive bile duct destruction and biliary cirrhosis.
IBD
145
PSC classic features
pruritus or jaundice
• elevated serum alkaline phosphatase level
• elevated total bilirubin level
• modestly elevated AST and ALT levels
146
what disease do people with psc have
ibd (UC)
147
testing for PSC
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
Demographics comparison for PBC vs PSC
PBC Women aged 40-60 years
| PSC Men aged 20-30 years
149
Pathology difference PBC Vs PSC
PBC Cholestatic liver disease of small bile ducts
| PSC Cholestatic liver disease of medium and large bile ducts
150
Associated conditions PBC vs PSC
PBC other autoimmune disease
| PSC IBD
151
Clinical findings PBC vs pSC
PBC positive antimitochondrial antibody
| PSC sting of beads on MRCP vs ERCP
152
Treatment PBC vs PSC
PBC Ursodeoxycholic acid
PSC Endoscopic therapy for extrahepatic dominant strictures
Liver transplantation
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