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OMS III > IM Gastro > Flashcards

IM Gastro Flashcards

1
Q

Esophageal Disorders

A

dysphagia is the essential feature of the majority of esophageal disorders. dysphagia means difficulty swalllowing. Odynophagia is the proper term for pain while swallowing. both of these can lead to wieght loss (thus weight loss cannot be used to answer what is the most likely diagnosis question.

when severe esophageal disorders will aslo give anemia and hemepositive stool

when any of these alarm sx are present endoscopy should be performed to exclude cancer

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2
Q

alarm sx indicating endoscopy:

A

weight loss

blood in stool

anemia

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3
Q

Achalasia

definition/etiology

A

inability of the LES to relax due to a loss of the nerve plexus within the lower esophagus. etiology is not clear, aperistalsis of the esophageal body

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4
Q

Achalasia

what is the most likely dx

A

young pt (under 50)

progressive dysphagia to both solids and liquids at the same time

no association with alcohol and tobacco use

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5
Q

Achalasia

diagnostic tests

A

barium esophagram will show a birds beak as the esophagus comes down to a point

manometry is the most accurate test and will show a failure of the les to relax

xcr may show some abnormal widening of the esophagus, but cxr is neither very sensitive nor very specific

upper endoscopy shows normal mucosa in achalasion, however, endoscopy is useful in some pts to exclude malignancy

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6
Q

in the esophagus barium studies are acceptable to do first in most pts although

A

radiologic tests always lack the specifiticty of endoscopic procedures

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7
Q

in the esophagus what is diagnosed by biopsy

A

cancer and barrett esopahgus

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8
Q

Achalasia

treatment

A

cannot exactly b cured

nothing can restolr the normal function off the missing neurological control of the esophagus, all treatment is based on mechanical dilation

  1. pneumatic dilation: place an endoscope witht he ability to inflate a device that will enlarge the esophagus. effective in more than 80-80% of pts
  2. surgical sectioning or myotomy: can help to alleviate sx. surgery is more effective than pneumatic dilation and surgery
  3. botulinum toxin injection: this will relax the les but the effects will wear off in about 3-6 months, requiring reinjection
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9
Q

pneumatic dilation leads to peroration in how many pts?

A

less than 3%

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10
Q

Esophageal Cancer

What is the most likely dx

A

age 50 or older

dysphagia first for solids, followed later to syxphagia for liquids

association with prolonged alcohola nd tobaxxo use

more than 5-10 years of GERD sx

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11
Q

Esophageal Cancer

diagnostic tests

A
  1. endoscopy is indispensible, since only a biopsy can diagnonse cancer
  2. barium might be the best iniital test but no radiologic test can diagnose cancer
  3. ct and mri scans are not enough to diagnose esophageal cancer, they are used to determine the extent of spread intot he surrounding itssues
  4. PET scan is used to determine the contents of anatomic lesions if you are not certain whether they coitain cancer. PEt scan is often used to determine whether a cancer is resectable. lcoal disease is resectable and widely metastatic cancer is not
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12
Q

Esophageal Cancer

treatment

A
  1. no resection = no cure, resection is always the right thing to do
  2. chemotheraphy and radiation are sued in addition to surgical removal
  3. stent placement is sue dfor lesions that cannot be resected surgically just to keep the esophagus open for palliation and to improve dysphagia
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13
Q

for cancer thre radiologic test is

A

never the most accurate

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14
Q

the single word progressive (or from solids to liquieds is the most important clue to the diagnosis of

A

esophageal cancer

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15
Q

Esophageal spasm

A

the 2 forms of spastic disorders, diffuse esophageal spasm (DES) and nutcracker esophagus, are clinically indistinguishable. both present with the sudden onset of chest pain that is not related to exertion. therefore, at first it is impossible to distinguish them from some form of atypical oronary artery spasm or unstable angina. they can be precipitated by drinking cold liquieds. the case will describe sudden severe chest pain and the ekg and stres test will be normal

esophagram and endoscopy will be noraml

DES and nutcracker esophagus can be distingueished only by the most accurate test: manometry, which will show a different patter or abnoraml contraction in each of them

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16
Q

Esophageal spasm

treatment

A

esophageal spastic diorders are treated with ccb and nitrates this is similar to teh treatment of prinzmetal angina. PPis can improve a number of cases of spastic disease

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17
Q

Esophageal spasm

barium studes

A

can show a corkscrew appearance at the time of the spasm

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18
Q

Infectious Esophagitis

most common question

A

esophageal candidiasis in a person wtih AIDS

thrush does not need to be present in esophageal candidiasi

cmv andherpes can also cause esophageal infection over 90% in people with aids is candidiasis

trate empirically with fluconazole

if this doesnt work then do an endoscopy

iv amphotericin is used for confirmed candida not responding to fluconazole

nystatin only treats oral candida not esophageal

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19
Q

what pills cause esophagitis if prolonged contact

A

doxycycline, alendronate and KCl

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20
Q

dysphagia iwth HIV CD4<100

improvement with fluconazole

A

cointuen therapy and haart

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21
Q

dysphagia iwth HIV CD$<100

no improvement with fluconazole

A

perfrom upper endoscopy with biopsy

if there is large ulceration = cmv and treate with ganciclovir or foscarnet

if there is small ulcerations=HSV treat with acyclovir

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22
Q

rings and webs

A

schatzki ring and plummervinson syndrome both give dysphagia.

schatzki rings is often form acid reflux and is associated with hiatal hernia. this is a type of scarring or tightening (also called peptic stricture) of hte distal esophagus.

Plummer vinson syndrome is assocaited with iron dificiency anemia and can rarely transorm into squamous cell cancer. the iron difiicency is not caused by blood loss. Plummer-vinson is more proximal. rings are easiily detected on barium studies of the esophagus

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23
Q

schatzki ring on barium studies

A

distal narrowing of the esophagus

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24
Q

steakhouse syndrome

A

dysphagia from solid food associted with schatzki rings

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25
Q

schatzki rings is assocaited with

A

intermittent dysphagia and is tretaed with pneymatic dilation in an endoscopic procedure

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26
Q

Plummer vinson syndrome is treated with

A

iron replacement at first which may lead to resolution of the lesion

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27
Q

Zenker is associated with

A

bad smell and halitosis

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28
Q

Zenker Diverticulum

definition

A

outpocketing of the posterior pharygeal constrictor muscles

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29
Q

Zenker Diverticulum

sypmtoms

A

dysphagia

halitosis

regurgitation of food particles

can have aspiration pneymonia when the contents of the diverticulum end up in the lung

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30
Q

Zenker Diverticulum

diagnostic tests/treatment

A

barium studes

surgery there i sno medical therapy

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31
Q

do not answer what with zenkers

A

ng tube or upper endoscopy these can cause perforation

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32
Q

Scleroderma

A

mechanical immobitlity of the esophagus

present with sx of reflux and have a clear hx of sclerodermaor progressive systemic sclerossis

manometry shows decrased les pressure from inability to clos the LES

management is with ppis

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33
Q

manometry is the answer for

A

achalasia

spasm

scleroderma

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34
Q

Mallor-Weiss Tear

A

presents with upper gi bleeding after severe vomiting or retching,

repeated retching is followed by hematemsisi of bright red blood or by black stool

doe snot present with dysphagia

there is no specific thearpy and it will resolve spontaneously

severe cases are managed with an injection of epinephrine to stop bleeding or the use of electrocautery

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35
Q

boerhaave syndrome

A

full thickness tear

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36
Q

mallory-weiss is what type of tear?

A

nonpenetrating tear of only the mucosa

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37
Q

Epigastric pain

Definition

A

common, occuring in as much as 25% of the population at some point in their lives.

tenderness which is increased pain on palpation or pressure in the epigastric area, is far less common

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38
Q

Epigastric pain

endoscopy

A

the only way to get a precise diagnosis

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39
Q

Epigastric pain

diagnostic test

A

endoscopy is the only way to truly know the etiology from ulcer dz

radiology and barium are modest in accuracy but you cannot do a biopsy

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40
Q

Epigastric pain

What is the most likely dx

pain worse with good

A

gastric ulcer

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41
Q

Epigastric pain

What is the most likely dx

pain better with food

A

duodenal ulcer

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42
Q

Epigastric pain

What is the most likely dx

weight loss

A

cancer, gastric ulcer

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43
Q

Epigastric pain

What is the most likely dx

tenderness

A

pancreatitis

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44
Q

Epigastric pain

What is the most likely dx

bad taste, cough, hoarse

A

gerd

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45
Q

Epigastric pain

What is the most likely dx

diabetes, bloating

A

gastroparesis

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46
Q

Epigastric pain

What is the most likely dx

nothing

A

non-ulcer dyspepsia

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47
Q

Epigastric pain

treatment

A

PPO are always a good place to start

h2 blockers are not as effective but still work in 70% of pts

liquid antacids have roughly the same efficacy as H2 blockers

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48
Q

Epigastric pain

treatment

misoprostol

A

is always the wrong answer

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49
Q

RUQ pain

A

cholecystitis
biliary colic
cholangitis
perforated duodenal ulcer

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50
Q

LUQ pain

A

splenic rupture

IBS-splenic flexure syndrome

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51
Q

RLQ pain

A

appi
ovarian torsion
ectopic pregnancy
cecal diverticulitis

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52
Q

LLQ pain

A

sigmoid volvulus
sigmoid diverticulitis
ovarian torsion
ectopic pregnancy

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53
Q

Midepigastrium pain

A

pancreatitis
aortic dissection
peptic ulcer disease

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54
Q

GERD

definition/etiology

A

the inappropriate relaxation of the les, resulting in acidic contents of the stomach coming up into the esophagus

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55
Q

GERD

sx are worsened by

A

nicotine

alcohol

caffeine

chocolate

peppermint

late-night meals

obesity

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56
Q

GERD

what is the most likely dx

A

epigastric burning pain radiating up into the chest

pt also complains of sore thorat, bad taste in the mouth (metallic), hoarseness, or cough

do not need these extra sx to diagnose with gerd

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57
Q

there are no unique findings in GERD

A

it is a sx complex

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58
Q

GERD

diagnostic tests

A

most often diagnosed based on pt hx.

can do 24 hr Ph monitoring

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59
Q

when is endoscopy indicated with GERD

A

signs of obstruction such as dysphagia or odynophagia

weight loss

anemia or heme-positive stools

more than 5-10 years of sxto exclude barrett esophagus

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60
Q

What might GERD show on endoscopy

A

reness, erosions, ulcerations, strictures, or Barrett esophagus

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61
Q

GERD

treatment for all pts

A

lowe wieght if obese

avoid alcohol, nicotine, caffeine, chocolate, and peppermint

avoid eating at night before sleep (w/in 3 hours of bedtime)

elevate head 6 to 8 inches

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62
Q

GERD

treatment

mild or intermittent sx

A

liquid antacids or H2 blockers

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63
Q

GERD

treatment

persistent sx or erosive esophagitis

A

ppis

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64
Q

GERD

treatment

treatment of those not responsive to medical therapy

A

5% dont respond to treatment

surgical correction to tighten the LES
nissen fundoplication - warapping the stomach around the lower esophageal sphincter
endocinch - using a scope to place a suture around the LES to tighten it
local heat or radiation of LES to cause scarring

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65
Q

endoscopy will show nothing where there is only

A

pyrosis (heartburn)

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66
Q

Barrett Esophagus

A

long-standing GERD leads to histologic changes in the lower esophagus with columnar metaplasia

columnar metaplasia needs at least 5 years of reglux to develop.

there are no unique physical findings or lab tests

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67
Q

Barrett Esophagus

Diagnostic Tests/Treatment

A

biopsy is the only way to be certainof th epresence of Barrett esophagus and/or dyspepsi, this is indispensible bc the biopsy drives therapy. columnar metaplasia with intestinal features has the greatest risk of transforming into esophageal cancer

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68
Q

Management of Barrett’s Alone

A

PPi’s and rescope every 2-3 years

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69
Q

management of low grade dysplasia in Barrett Esophagus

A

PPi’s and rescope every 6-12 months

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70
Q

management of high-grade dysplasia in Barrett Esophagus

A

ablation with endoscopy: photodynamic therapy, radiofrequency ablation, endoscopic mucosal resection

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71
Q

what percentage of pts with barretts progress to esophageal cancer

A

0.5% each year

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72
Q

Gastritis

defintion

A

inflammation or erosion of the gastric lining that is sometimes called gastropathy

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73
Q

Gastritis is caused by

A 
alcohol
NSAIDS
H. Pylori
Portal htn
stress like burns, trauma, sepsis, and multiorgan failure (uremia)
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74
Q

atrophic gastritis is associated with

A

B12 defiiciency

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75
Q

Gastritis

what is the most likely dx

A

often presents with gi bleeding w/o pain. severe, erosive gastritis can present with epigastric pain. nsaids or alcoholism in the hx is a clue

cannot answer this question from the hx and physical alone

can present with any degree of bleeding from mild “coffe ground emesis” to large volume of vomiting red blood , to black stool (melena)

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76
Q

there are no unique physical findings for

A

gastritis

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77
Q

Volume of bleeding in coffee-ground emesis

A

5-10 ml

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78
Q

Volume of bleeding in heme (guaiac positive) stool

A

5-10 ml

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79
Q

Volume of bleeding in melena

A

50-100 ml

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80
Q

Gastritis

Diagnostic Tests

A

only upper endoscopy can definitively diagnose erosive gastritis

although anemia ay occur there are not specific blood tests

upper GI radiology is not specific enough

Capsule endoscopy is not appropriate for upper GI bleeding if endoscopy is one of the choices

test for h pylori

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81
Q

Gastritis Treatment

A

treat with PPI’s before any of the other gerd treatments. sucralfate is the wrong answer

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82
Q

stress ulcer phophylaxid is indicated in

A

mechanical ventilation

burns

head trauma

coagulopathy

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83
Q

H Pylori Testing

endoscopic biopsy

A

the most accurate of all the tests

requires an invasive procedure such as endoscopy

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84
Q

H Pylori Testing

Serology

A

inexpensive, easily exluded infection if it is negative, no complications or procedures required

lacks specificity, a positive test does not easily tell the difference between current and precious infection

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85
Q

H Pylori Testing

Urea C13 and C14 breath testing

A

positive only in active infection, noninvasive

requires expensive equipment in office

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86
Q

H Pylori Testing

h pylori stool antigen

A

positive only in active infection, noninvasive

requires stool sample

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87
Q

Peptic Ulcer Disease

Definition

A

the term peptic ulcer disease refers to both duodenal ulcer and gastric ulcer disease. they cannot be distinguished definitively without endoscopy. The name is a misnomer based on the mistaken belief that they were caused by the protein digesting enzyme pepsin

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88
Q

Peptic Ulcer Disease

etiology

A

commonly caused by H Pylori.

NSAIDS are the second most common cause bc of their effect inhibiting the production of the protective mucus barrier in the stomach. they inhibit prostaglandins and prostaglandins produce the mucus

burns

head trauma

crohn disease

gastric cancer

gastrinoma (ZES)

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89
Q

nsaids produce more of what than pain

A

bleeding

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90
Q

alcohol and tobacco do what with ulcers

A

they dont cause them they delay their healing

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91
Q

Peptic Ulcer Disease

presentation/wht is the most likely diagnosis

A

pud presents with recurrent epidosed of epigastric pain that is described as dull, sore, and gnawing. although the most common cause of upper GI bleeding is pud, the majority of those with ulcers do not bleed. Tenderness and vomiting are unusual

cannot answer pud as the most likely dx based on symptoms alone

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92
Q

duodenal ulcer disease is mor often improved with

A

eating

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93
Q

gastric ulcer diseaseis more often worsened with

A

eating, so it is associated with weight loss

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94
Q

you cannot definitively diagnose what without endoscopy

A

DU, DU, gastritis and non-ulcer dyspepsia

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95
Q

there is no way to diagnose pud without

A

endoscopy or barium studies

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96
Q

Peptic Ulcer Disease

diagnostic tests

A

upper endoscopy is the most accurate test

radiologic testing such as an upper gi series can detect ulcers but cannot detect the presence of either cancer or H Pylor

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97
Q

H. Pylori Testing in Peptic Ulcer Disease

A

in those who are to undergo endoscopy, there is no point in doing noninvasive testing such as serology, breath testing, or stool antigen detection methods.

biopsy is the most accurate test H pylori

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98
Q

endoscopy is the only method of detecting

A

gastric cancer, it is present in 4% of people with Gastric ulcers and in 0% of people with Duodenal ulcers

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99
Q

Peptic Ulcer Disease

Treatment

A

responds to PPis in over 95% of cases, but will recure unless H pylori is eradicated in those infected

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100
Q

what percentage of Duodenal ulcers are associated with h Pylori

A

80 to 90%

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101
Q

what percentage of Gatric ulcers are associated with h pylori

A

50-70%

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102
Q

therapy of h pylori

A

ppi with clarithromycin and amoxicillin is best initial, if penicillin allergy than do metro instead

if pt doesnt respond to this then metronidazole and tetracycline can be used as alternate abs

adding bismuth to a change of abs may aid in resolution of treatment of resistant ulcers

retest with breath test to confirm cure of h pylori 30-60 days after therapy

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103
Q

treatment of refractory ulcers

A

if the initial therapy does not resolve the DU then detecting persistent h pylor and switchingthe abs to meto and tetra is appropriate.

for those with gu a repeat endoscopy is done to exclude cancer as a reason for not getting better

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104
Q

test for cure of h pylori after treatment with

A

stool antigen or breath test

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105
Q

Ulcer treatment failure most often stems from

A

nonadherence to meds

alcohol

tobacco

nsaids

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106
Q

Gastric ulcers

overview

A

the omst improtant reason to scop a pt is to exclude gu as a cause of the pain bc of the possibility of cancer

only way to exclude cancer is with biopsy

you can test for h pylori noninvasively but there is no way to exclude cancer noninvasively

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107
Q

Diff of GU and DU

A

Gu pain is worsened with food

Gu is biopsied

gu has cancer in 4% of pts

repeating the endoscopy to confirm healing is standard iwth GU

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108
Q

Non Ulcer Dyspepsia

Definition

A

epigastric pain that has no identified etiology

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109
Q

Non Ulcer Dyspepsia

diagnosis

A

can only be diagnosed after endoscopy

under 45 treat first, over 55 do scope to exclude cancer, in the middle it is unclear on what to do

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110
Q

Non Ulcer Dyspepsia

presentation

A

the pain can be identicalto gasgritis, pud, gasric cancer, or reflux disease

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111
Q

Non Ulcer Dyspepsia

treatment

A

if pt is under 45 treat empirically with antisecretory therapy such as ppis and scope only if it doesnt resolve

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112
Q

scope pts with dyspepsia if

A

pt is over 55 years old

alarm sx are present (dysphagia, weight loss, anemia)

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113
Q

most common cause of epigastric pain

A

Non Ulcer Dyspepsia

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114
Q

Non Ulcer Dyspepsia and h pylori

A

not associated but if origanal treatment with ppis doesnt resolve then try and treat h pylori

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115
Q

Non Ulcer Dyspepsia is epigastric pain with

A

a normal endoscopy

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116
Q

Gastrinoma (ZES)

what is the most likely diagnosis

A

look for a pt with ulcers that are:

large (>1-2 cm)

recurrent after h pylori eradication

distal in the duodenum

multiple

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117
Q

how many pts with an ulcer have a gastrinoma?

A

less than 1%

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118
Q

Gastrinoma (ZES)

Diagnostic testing

A

once endoscopy confirms the presence of an ulcer, the most accurate diagnostic test is:

 High gastrin levels off antisecretory therapy (PPI's or H2 blockers)
 high gastrin levels despite a high gastric acid output
 persistent high gastrin elvels depsite injecting secretin

any one of these three, always a funtional test looking at the response to secretin

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119
Q

Gastrinoma (ZES)

imaging

A

most important issue is to exclude mets. ct and mri of the abdomen have poor sensitivity but are done first, neg mri or ct does not exclude mets

somatostain receptor scintigraphy (nuclear octreotide scan) is combined with endoscopic ultrasound to exclude mets. do these if the Ct and MRI are normal

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120
Q

Gastrinoma is often associated with diarrhea

A

bc acid inactivates lipase

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121
Q

hypercalcemia is the clue for

A

multiple endocrine neoplaisa from hyperparathyroidism

122
Q

Gastrinoma is associated with a massive increase in the number of

A

somatostatin receptors in the abdomen

123
Q

Gastrinoma (ZES)

treatment

A

local disease is removed surgically. mets is unresectable and is treated with lifelong ppis to block acid production

124
Q

Diabetic Gastroparesis

definition/etiology

A

long standing diabetes leads to gastric dysmotility. distention of the sotmach and intestines is normally the most immportant stimulant to motility

gastroparesis is an autonomic neuropathy leading to dysmotility

dysmotility is from the inability to sense stretch in the GI tract

125
Q

Diabetic Gastroparesis

what is the most likely dx

A

look for a diabetic pt with chronic abdominal discomfort, bloating, and constipation. also anorexia, nausea, vomiting, and early satiety

126
Q

Diabetic Gastroparesis

most accurate test

A

nuclear gastric emptying study

127
Q

Diabetic Gastroparesis

treatment

A

erythromycin and metoclopromide increase gi motility

128
Q

fluids when bp is low

A

lr and ns is better than d5

129
Q

GI bleeding

most improtant thing to do first

A

if it is severe you want to fluid resuscitate first

130
Q

upper GI bleeding

etiology

A

ulcer disease is the most common

gastritis

esophagitis

duodenitis

cancer

varices

131
Q

lower GI bleeding

etiology

A

diverticulosis is the most common

angiodysplasia (arteriovenous malformation)

polyps or cancer

ibd

hemorrhoids

upper gi bleed with rapid transit from high volume

132
Q

what is the most important initial management for GI bleeding

A

assessing bp

133
Q

GI bleeding

physical findings

A

orthostasis
more than a 10 point rise in pulse when going from lying down to sitting or
systolic blood pressure drop of 20 points of more when sitting up

134
Q

Severity of blood loss on hemodynamics

A

orthostasis: 12-20% blood loss

pulse >100 per minute: 30% loss

Systolic BP < 100 mm Hg: 30% loss

135
Q

Variceal bleeding

overview

A

only form of gi bleeding where physical examination helps determine etiology

the presence of the signs of liver disease helps establish dx

136
Q

Variceal bleeding is suspected when the case describes

A

vomiting blood w/or w/o black stool

spider agniomata and caput medusa

splenomegaly

palmar erythema

asterixix

137
Q

GI bleeding

acute bleeding

A

it is far more important to replace fluids anc check the hematocrit, platelet count, and coagulation like pt or inr than it is to do endoscopy

138
Q

initial manegament of GI bleeding is

A

not based on the etiology but on the severity

139
Q

nasogastric tube with GI bleeding

A

ten percent of those with red blood fromt he rectum have high-volume upper gi bleeding with rapid transit time. ng tube can rapidly identify upper gi bleeding and hence, who needs upper endoscopy for banding before colonoscopy. the sensitivity of ng tube is 70%. if you see bile in the aspirate then you know the ng tube aspirate really is fully sensitive

if the stool is black in a person with cirrhosis but there is no hematemesis, an ng tube showing red blood may tell you to use octreotide for varices and arrange urgent endoscopy for possible banding of varices

140
Q

role of ng tube in GI bleeding if you are going to do egd

A

limited role and probably dont do

141
Q

80% of GI bleeding will stop spontaneously if

A

the fluid resuscitation is adequate. most pts die of inadequate fluid resuscitation

142
Q

GI bleeding diagnostic tests

nuclear bleeding scan

A

endoscopy unrevealing in a msasive acute hemorrhage, this test lacks accuracy

143
Q

GI bleeding diagnostic tests

angiography

A

specific vessel or site of bleeding needs to be idnetified prior to surgery or emoblization of the vessel, used only in massive nonresponsive bleeding

144
Q

GI bleeding diagnostic tests

capsule endoscopy

A

small bowel bleeding, upper and lower endoscopy do not show the etiology

145
Q

GI bleeding diagnostic tests

Ct or MRI of abdomen

A

not useful in GI bleeding

146
Q

GI bleeding diagnostic tests

ekg, lactate level

A

shows ischemia in severe bleeding

147
Q

GI bleeding diagnostic tests

treatment (8)

A
  1. fluid replacement with high volumes (1-2 L an hour) of saline or LR in those with acute severe bleeding
  2. packed rbc if the hematocrit is below 30 in those who are older or suffer from coronary artery disease, if the pt is young, transfusion may not be needed until the hematocrit is very low (under20-25
  3. FFP if the pt or inr is elevated and active bleeding is occurring
  4. platelets if the count is below 50000 and there is bleeding
  5. octreotide for variceal bleeding
  6. endoscopy to determine the diagnosis and administer some treatment (band varices, cauterize ulcers, inject epinephrine into bleeding gastric vessels)
  7. IV PPI for upper GI bleeding
  8. surgery to remove the site of bleeding if gluids, blood, platelets, and plasma will not control the bleeding
148
Q

when do you transfuse platelets in a spontaneous bleed (not GI)

A

below 10000-20000

149
Q

Esophageal and gastric varices what do you do in addition to fluids blood platelets and plasma (5)

A
  1. octreotide (somatostatin) decreases portal pressure
  2. banding performed by endoscopy obliterates esophageal varices
  3. transjugular intrahepatic portosystemic shunting (TIPS) is used to decrease protal pressure in those who are not controlled by octreotide and banding.
  4. propranolol or nadolol is used to prevent subsequent episodes of bleeding. beta blockers such as propranolol will not do naything for the current episode of bleeding
  5. antibiotics to prevent SBP with ascites
150
Q

scleropathy is never the right answer if

A

banding is technically possible

151
Q

Antibiotic associated diarrhea

A

clindamycin has the highest incidency of antibiotic associated diarrhea and cdiff but any ab can cause diarrhea.

blood and white cells may be present in the stool

usually presents everal days or week safter the start of abs.

best initial test is a stool cdiff toxin test or PCR

metro is the best initial therapy then vanco if no repsonse or fidaxomicin

152
Q

recurrent cdiff treat with

A

metro, if it was susceptible before

only use iv metro if pt cant take orally

153
Q

when do you give iv vancomycin for ab associated diarrhea

A

never, bc it wont pass the bowel wall

154
Q

diarrhea causing malabsorption

A

celiac disease is one of the most common types of malabsorption and can present as an adult.

chornic pancreatitis has a very similar presentation with fat malabsorption

rare causes or fat malabsorption are tropical sprue and whipple disease

all of these present with steatorrhea which is oily freasy floating and foul smelling stool

155
Q

all forms of fat malabsoprtion present with deificency of

A

adek

156
Q

Vit D deficiency manifestation

A

hypocalcemia, osteoporosis

157
Q

Vit K deficiency manifestation

A

bleeding, easy bruising

158
Q

Vit B12 deficiency manifestation

A

anemia, hypersegmented neutrophils, neuropathy

159
Q

fat malabsorption presents with

A

weight loss

160
Q

b12 needs an intact what to be absorbed

A

bowel wall and pancreatic enzymes

161
Q

what can clinically distinguish between celiac disease and topical sprue

A

nothing

162
Q

what percentage of celiac disease people have dermatitis herpetiformis

A

100%

163
Q

whipple disease

presents with

A

diarrhea

arthralgias

ocular findings

neurologic abnormalities (dementia and seizures)

fever

lymphadenopathy

164
Q

treat whipple disease with

A

ceftriaxone followed by bactrim

165
Q

main distinctions between celiac disease and chronic pancreatitis

A

iron deficiency bc it needs an intact bowel wall but no pancreatic enzymes to be absorbed

166
Q

Celiac disease testing unique tests

A

ant-tissue tanglutaminase (first test)

antiendomysial antibody

IgA antigliadin antibody

167
Q

Most accurate diagnostic test for celiac disease

A

small bowel biopsy that shows flattening of the villi

168
Q

most accurate diagnostic testing for whipple disease and topic sprue

A

bowel wall biopsy showing the specific organisms

169
Q

bowel biopsy is essential in celiac disease to exclude

A

lymphoma

170
Q

chronic pancreatitis

specific diagnostic tests

A

abdominal xray: 50% to 60% snesitive for calcification of the pancreas

abodminal CT: 80% to 90% sensitiive for pancreatic calcifications

secretin stimulation testing: this is the mos taccurate diagnostic test. place a nasogastric tube, an unaffected pancreas will release a large colume of bicarbonaste-rixh fluids after the iv injection of secretin

171
Q

rice and wine are safe in

A

celiac disease

172
Q

treatment for chronic pancreatitis

A

enzyme replacement

173
Q

treatment for celiac disease

A

avoid gluten-containing foods such as wheat, oats, rye, or barley

174
Q

treatment for whipple disease

A

ceftriaxone, bactrim

175
Q

treatment for topical sprue

A

bactrim, tetracyline

176
Q

d-xylose test

A

old test to dinstinguesh pancreatitis from bowel wall abnormalities, it will be normal in pancreatic disorders

177
Q

carcinoid syndrome

presentation

A

presents with intermiittent diarrhea in assocation w/

flusshing

wheezing

cardiac abnormalities of the right side of the heart

178
Q

carcinoid syndrome

testing and therapy

A

urinary 5hydroxyindoleacetic acid (5HIAA) test

octreatide, synthetic somatostain used to control diarrhea

179
Q

Lactose intolerance

A

no wiegh tloss is associated with lactose intolerance bc lastose is only one of several sugars to absorb

doe snot alther the absorption of any other nutrients to there is no defiicency in calories

vitamons are absorbed onramally

stoll osmolality is increased

usual way to make the diagnosis is simply remove all milk containing products form diet, and wait to see if sx go away

can still eat yogurt but no other milk products

can use oral lactase replacement

180
Q

Lactose intolerance

A

no wiegh tloss is associated with lactose intolerance bc lastose is only one of several sugars to absorb

doe snot alther the absorption of any other nutrients to there is no defiicency in calories

vitamons are absorbed onramally

stoll osmolality is increased

usual way to make the diagnosis is simply remove all milk containing products form diet, and wait to see if sx go away

can still eat yogurt but no other milk products

can use oral lactase replacement

181
Q

irritable bowel syndrome

definition

A

a pain syndrome that can have diarrhea, constipation, or both. there is no specific diangostic test and it is a diagnosis of exclusion in assocation with a complex of sx.

182
Q

ibs is not associated with

A

weight loss, pain does not mean malabsorption

or

blood or white cells in the stool

183
Q

pain of IBS is

A

relieved by a bowel movement

less a tnight

relieved by a change in bowel habits such as diarrhea

184
Q

irritable bowel syndrome

treatment

A

fiber

antispasmodics: hyoscyamine or dicyclomine

tca or ssris

antimotility agents like loperamide for diarrhea

lubiprostone (cholride channel activator that increases bowel movement frequency). linaclostide also treats the contipation that is predominant in IBS

185
Q

IBD

definition/presentation

A

idiopathic disorder that presents with diarrhea, blood in stool, weight loss, and fever.

186
Q

both crohn disease and ulcerative colitis have extraintestinal manifestation that can ve identical in both diseases

A

arthralgias
uveitis, iritis
skin manifestation (erythema nodosum, pyoderma gangenosum)
scleorising cholangitis (more frequent in uc)

187
Q

IBD can turn into

A

colon cancer. the risk is related to the duration of involvement of the colon. CD that involves the colon has the same risk of colon cancer as UC

188
Q

Erythemia nodosum is an indicator

A

of diseasea activity

189
Q

Crohn Disease

A

skip lesions

tranmural granulomas

fistulas and abscesses

masses an obstruction

perianal disease

190
Q

Ulcerative Colitis

A

curable by surgery

entirely mucosal

no fistulas or abscesses

no obsrtuction

no perianal disease

191
Q

When should colon cancer screeing occur in a pt with IBD

A

after 8 to 10 years of colonic involvement, with colonoscopy every 1 to 2 years

192
Q

IBD

Antibody diagnostic testing

A

ANCA positive in UC

ASCA positive in CD

193
Q

IBD

diagnostic testing

A

endoscopy is the most accurate test when the disease can be reached by the scope.

For CD in the small bowel barium studies will detect the lesions.

when the diganosis is still unclear serologic testing may be helpful. All IBD is associated with anemia

194
Q

IBD Treatment

A

acute exacerbation of disease are treated with steroid, prednisone or budesonide.

chornic maintenance of remission is with 5-asa derivatives such as mesalamine. ASacol (mesalamine) is used for UC and Pentasa (mesalamine ) for CD. Rowasa (mesalamine) is for UC largely limited to the rectum.

azathiprine and 6 mercaptopurin are used to wean pts off of streoids. whent he disease is so severe that sevvere recurrences develop as the stroids are stopped.

everyone needs calcium and Vit D

perianal CD is treated with cipro and metro

fistulae and severe disease unresponsive to other agnets is treated iwth antitumor necrosis factor (TNF agents such as infliximab. surgery is done for fistulae only if hter eis no response to anti-TNF agents

neither form of IBD is routinely trated with surgery, UC can be cured however with colectom. In CD, surgery is used exclusively for bowel obstruction bc it will recure at the site of surgery

195
Q

Budesonide is a stroid speicific for IBD

A

first pass effect is good for EBD treatment

196
Q

Diverticulosis

A

outpocketings of the colon are so common on a standard meat-filled diet as to be expected in those above 65 to 70 years of age.

vegetarianins rarely develop diverticulosis

asymptomatic most of the time, may present iwth llq abdominal pain, constipation, bleeding, and sometimes infection (diverticulitis)

197
Q

Diverticulosis

Testing

A

most accurate is colonoscopy

barium studies are acceptable but no as accurate

198
Q

Diverticulosis

treatment

A

bran

psyllium, methylcellulose and increased dietary fiber are used to decrease the rate of proggresion and complications

199
Q

Diverticulitis

Most likely diagnosis

A

on older pt with:

llq pain and tnederness
fever
leukocytosis
palpable mass sometimes occurs

(nausea constiaption and bleeding can occur but are nonspecific

200
Q

Diverticulitis

best initial test

A

CT Scan

201
Q

dangerous tets in Diverticulitis

A

colonoscopy and barium enema bc of the increased risk of perforation. infection weakens the colonic wall

202
Q

Diverticulitis

treatment

A

abs that will cover e coli and anaerobes that are present in the bowel

cipro with metro

or

augmentin
ticarcillin/clavulanate or piperacillin/tazobactam
erapenem (carbapenems)

203
Q

Diverticulitis

when is surgery the answer

A 
no response to medical therapy
frequent recurrences of infection
perforation
fistula
abscess
strictures
obstruction
204
Q

pt with acute diverticulitis should not be

A

fed

205
Q

Diverticulitis

who is more likely to get surgery

A

yougner pts bc they will have more recurrences

206
Q

does diverticulities disappear

A

no

207
Q

95% of colon cancer deaths are preventable with

A

screening

208
Q

when is virtual colonoscopy the right answer

A

never

209
Q

colonoscopy testing frequency

routine testing

A

pts should have a colonoscopy q 10 years beginning at age 50

210
Q

colonoscopy testing frequency with a fx hx of colon cancer

single family member

A

begin 10 years earlier than the age at which the faimly member devloped thier cancer or age 40, whichever is younger.

repeat the scope q 5 years if the family member is under age 60

211
Q

colonoscopy testing frequency with a fx hx of colon cancer

3 family members, 2 generations, i premature (before 50)

A

hereditary nonpolyposis colon cancer syndrome (HNPCC). comprises these factors .

start screening at age 25 q 1 to 2 years

212
Q

colonoscopy testing frequency with a fx hx of colon cancer

familial adenomatous polyposis (FAP)

A

FAP is defined as the presence of thousands of polyps with an abnormal genetic test known as the adenomatous polypossi coli (APC) test.

start scrrning iwth sigmoidoscopy at age 12 every year

213
Q

colonoscopy testing frequency with a fx hx of colon cancer

Previous adenomatous polyp

A

pt whould have a colonsocopy q 3 to 5 years

214
Q

colonoscopy testing frequency with a fx hx of colon cancer

previous hx of colon cancer

A

pt should ahve colonsocopy at 1 year after resection, then at 3 years, then every 5 years

215
Q

Peutz-jeghers syndrome

A

characterized by multipole hamartomatous polyps in association wiht:

melanotic spots on the lips and skin

increased frequency of breats cancer

increaes gonadal and pancreatic ancer

do not increases frequency of colonosopies

216
Q

gardner syndrome

A

colon cancer in association with

osteomas

dsmoid tumors

other soft tissue tumors

217
Q

turcot syndrome

A

colon cancer in assocaition with

CNS malignnacy

218
Q

juvenile polyposis

A

colon cancer in association with

mulitple hamartomatous polyps

219
Q

what syndromes do not requre increased coloncoscopy screenings

A

peutz jeghers

gadner

turcot

juvenile

220
Q

what percentage of colon cancers occur proximal to rectum and sigmoid colon

A

40%

they will be missed by sigmoidoscopy

221
Q

Acute pancreatitis

definition/etiology

A

acute inflammation of the pancreas

over 90% caused by alcoholism and cholelithiasis

222
Q

less common causes of Acute pancreatitis

A

trauma

hypertriglyceridemia

hypercalcemia

infection

Drug toxicity (pentamidine, didanosine, azathioprine, estrogens)

drug allergy ( sulfas like lasix and hctz

Ductal obstruction, endoscopic retrograde cholangiopancretography, cystic fibrosis

scorpion sting

223
Q

Acute pancreatitis

presentation/what is the most likely dx

A

acute epigasting pain and tnederness and nausea/vomiting=pancreatitis

insevere causes there is also hypotension and fever

224
Q

pancreatitis poem

A

a stone
a stricture
a tumor
an obstruction

225
Q

tip about pancreatitis and cholecystitis pain

A

pnacreas pain goes straight back like a spear

gallbladder pain around the side to the back

226
Q

worst prognosis with pancreatitis

A

low calcium, severe damage decreases lipase production and release leading to fat malabsorption in the gut. calcium binds with fat (saponofies) in the bowel, leading to calcium malabsorption. althorugh amylase and lipase are elveated in pancreittis theres no correlation betweent he ehight of these enzyme levels and disease severity.

227
Q

does pain intensity correlate with the degree of organ damage

A

no bc it is subjective

228
Q

CRP

A

has no definite correlation with severity in any disease

229
Q

Acute pancreatitis

diagnostic tests

A

best initial test is amylase and lipase

most specific test is CT scan

230
Q

Acute pancreatitis

disease severity

A

strongly correlates with the degree of necrosis seen on Ct scanning. needle biopsy is indispensible in determineng the presence of infection in those who have extensive necrosis

231
Q

what is extensive necrosis in Acute pancreatitis

A

greater than 30%

232
Q

Acute pancreatitis laboratory tests

A

cbc show leukocytosis, drop in hematocrit over time with rehydration

elevated ldh and ast

hypoxie, hypocalcemia

elevated urinary trypsinogen activation pepetide

233
Q

Acute pancreatitis

imaging

A

ct or mir scna are best, these also detet pseudocysts

mrcp is usueful in determing the etiology of the disease (stones, stricture, tumorr) mrcp is diagnostic, ERCP is for therapy

plain film shows a sentinel loop of bowel (air-filled piece of small bowel in the luq)

us has very poor accuracy, overlying bowel blockes precise imaging

234
Q

Acute pancreatitis

treatment

A

npo

iv hydration at very high volume

analgesia

ppis decrease pancreatic stimulation from acid entering the duodenum

235
Q

Acute pancreatitis

treatment with more than 30% necrosis

A

add as like imipenem or meropenem they may decrease mortality by decreasing the devlopment of infected, necrotic pancreatitis

needle biopsy to confirm infection

236
Q

pseudocyst Acute pancreatitis treamtnet

A

drained with a needle if enlarging or painful

237
Q

ERCP with Acute pancreatitis is used to

A

remove obstructing stones and dilate strictures

place stents

238
Q

Acute pancreatitis

abdominal CT

A

always perfomr with IV and oral contrast to better define and outline abdominal structures

239
Q

infected, necrotic pancretitis should

A

be resected with with surgical debridement to prevent ARDS and death

240
Q

Liver disease

all forms of chornic Liver disease can produce

A

ascites

coagulopathy (all clotting factors except VIII are made in liver)

asterixis and encephalopathy

hypoalbuminemia and edema

spider angiomata and palmar erythema

portal htn leading to varices

thrombocytopenia from splenic sequstration

renal insufficiency (hepatorenal syndrome)

hepatopulmonary syndrome

241
Q

Ascites

paracentesis should be performed if there is

A

new-onset acites

abdominal pain and tenderness

fever

242
Q

Ascites

etiology

A

portal htn from cirrhosis fi there is an low albumin level in the fluid

the differenceor graident between the serum and scites is also called the serum ascites albumin gradient (SAAG). if the SAAg is above 1.1 it is highly suggestive of protal htn

243
Q

SAAG less <1.1 g/dl

A

infection (except SBP)
cancer
nephrotic syndrome

244
Q

SAAg greater >1.1g/dl

A

portal htn
chf
hepatic vein thrombosis
constrictive pericariditis

245
Q

Spontaneous bacterial peritonitis

definition and etiology

A

infection without a perofration of the bowel, we dont know how the baterial gets there. E Coli is the most common organism. anaerobes are rarely the cause. pneumococcus causes it for some reason.

246
Q

Spontaneous bacterial peritonitis

diagnostic tests

A

best initial test: cell count with more than 250 neutrophils is when we start therapy

ldh is too nonspecific

247
Q

Spontaneous bacterial peritonitis

treatment

A

cefotaxime or ceftriaxone

248
Q

Spontaneous bacterial peritonitis

recurring

A

it frequently recurs. when the ascites fluid albumin level is quite low, prophylactic norlfoxacin or bactrim is sued to prevent SBP. all pts need lifelong prophylaxis for recurrence

249
Q

all variceal bleeding with ascites needs

A

Spontaneous bacterial peritonitis prophylaxis

250
Q

anyone with Spontaneous bacterial peritonitis needs

A

lifelong prophylaxis

251
Q

Cirrhosis treatment of ascites and edema

A

sprionolcatone and other diuretics, serial paracentesis for large-volume ascites

252
Q

Cirrhosis treatment of coagulopathy and thromocytopenia

A

FFP and/platelets only if bleeding occurs

253
Q

Cirrhosis treatment of encephalopathy

A

lactulose and rifaximin

254
Q

Cirrhosis treatment of hypoalbuminemia

A

no specific therapy

255
Q

Cirrhosis treatment of spider angiomata and palmar erythema

A

no specific therapy

256
Q

Cirrhosis treatment of varices

A

propanolol and banding via endoscopy

257
Q

Cirrhosis treatment of hepatorenal syndrome

A

somatostating (octreotide), midodrine

258
Q

Cirrhosis treatment of hepatopulmonary syndrome

A

no specific therapy

259
Q

Hepatopulmonary syndrome

A

htis is lung disease and hypoxia entirely on the basis of liver failure. look for orthodeoxia, which is hypoxia upon sitting upright. there is no specific therapy

260
Q

Specific causes of cirrhosis

A

alcoholic liver disease

primary biliary cirrhosis

primary sclerosing cholangitis

alpha 1antitrypsin deficiency

hemochromatosis

Chronic hepatitis b and c

wilson disease

autoimmune hepatitis

nonalcoholic steatohepatitis (NASH) or nonalcoholic Fatty Liver Disease

261
Q

Alcoholic liver disease

A

diagnosis of exclusion

no specific ltherapy

most accurate test is liver biopsy

alcohol and all drugsgive greater elevation in ASt compared to ALT

262
Q

viral hepatitis ast and alt

A

alt is higher

263
Q

binge drinking give a sudden rise in

A

GGTP

264
Q

Primary Biliary cirrhosis

most likely diagnosis

A

women in 40s or 50s

fatigue and itching

normal bilirubin with elevated alk phos

265
Q

unique features of PBC are

A

xanthelasma/xanthoma

osteoporosis

266
Q

PBC diagnostic tests and treatment

A

liver biopsy is the most acurate test

most accurate blood test is the antimitochonidrial antibody

bilirubin and IgM levels do not elevate untilt he disease is very fare advanced

treate with ursodeoxycholic acid

267
Q

Priary Sclerosing cholangitis

presentation

A

over 80% occurs in IBD

pruritis

elevated alk pho and GGTP as well as elevated bilirbuin level

can look psc and bilirubin can be normal in early disease

268
Q

PSC tests

A

most accurate test is MRCP and ERCP that shows beading, anrrowing, or strictures in the biliary system. MRCP is generally done bc there is no therapuetic need for ERCP. you can diagnose PSC from a biopsy if it was done for other reasons, but biopsy is not essential for establishing the diagnosis

269
Q

PSC treatment

A

cholestyramine or ursodeoxycholic acid

270
Q

PSc is the only cause of cirrhosis in which

A

a biopsy is not the most accurate test

271
Q

PSC does not improve or resolve with

A

resolution of the IBD. even after a colectomy in UC, the pt may still progress to needing a liver transplantation

272
Q

Alpha 1 antirypsin deficiency

A

look for comination of liver disease and emphysema (COPD) in a young pt under 40, who is a nonsmoker. they may throw in a family history of COPD at an early age. treat by replacing he enzyme. the most frequently asked question is “what is the most likely diagnosis?

273
Q

Hemochromatosis

definition

A

this is a genetic disorder leadint to overabsorption of iron in the duodenum, the mutation is C282y gene

men present earlier than women bc menstruation delays the onset of liver fibrosis and cirrhosis

274
Q

Hemochromatosis

presentation

A

look for a pt in his 50s with mild increases in AST and alkaline phosphatase and:

fatigue and joint pain (pseudogout)

ed in men and amenorrhea in women (from pituitary involvement)

skin darkening

diabetes

cardiomyopathy

275
Q

Hemochromatosis may be found on routin testing with

A

mildly abnomral lfts or iron levels

276
Q

with Hemochromatosis what bugs will you find

A

vibrio vulnificans, yersinia, and listeria infections occure bc they feed on iron

277
Q

Hemochromatosis

diagnostic tests

A

best initial test is iron tudes that show:
increase serum iron and ferritin

 decreased iron binding capacity

most accurate test is a liver biopsy for increased iron

ekg may show conduction defects and echo can show dilated or restrictive cardiomyopathy

mri will show increased iron in liver

278
Q

when is iron chelation therapy used in Hemochromatosis

A

cannot be managed with phlebotomy

are anemic and have hemochormatosis from overtransfusion such as thalassemia

279
Q

Hemochromatosis

treatment

A

phlebotomy is clearly the best therapy for those with aoverabsorption of iron

280
Q

liver fibrosis can resolve in Hemochromatosis if

A

phlebotomy is begun before cirrhosis develops

281
Q

Chronic Hepatitis B and C

overview

A

there are no specific physical findings to allow you to answer, what is the most likely diagnosis without blood testing

both chronic hepatitis b and c are associated with developing cirrhosis and liver cancer

both can be associated with polyarteritis nodosa

282
Q

Chronic Hepatitis B

diagnostic tests

A

surface antigen positive for longer than 6 months as a matter of definition.

most cases are e antigen positive as well. hep b dna level by pcr is the way to determine viral replication activity

biopsy to detect bridging necrosis no longer has any significant meaning

283
Q

Chronic Hepatitis C

diagnostic tests

A

in over 80% of pts with hepatitis C, the infection persists as chronic infection. since the acute viral illness is rarely felt with hep C, there is often no precise way to determine the time course of the infection

hep c pcr rna viral load is the most accurate way of determining disease activity.

284
Q

Acute hepatitis C is treated with

A

combination of ledipasvir and sofosbuvir. interferon, ribavirin, and either telaprevir or boceprevir are added when treatment fails

ribavirin and sofosbuvir can be used orally without interferon sometimes

285
Q

Chronic Hepatitis B and C

liver biopsy

A

determines the degree of inflammation and fibrosis. Biopsy can help you understand the urgency for treatment if fibrosis is present or worsening

286
Q

Chronic Hepatitis B

treatment

A

adefovir

lamivudine

telbivudine

entecavir

tenofovir

interferon

287
Q

Chronic Hepatitis B and C

how do you follow

A

with viral pcr load and objective is that you have an undetectable load

288
Q

Chronic Hepatits C

genotype 1

A

ledipasvir and sofosbuvir, both orally

289
Q

Chronic Hepatitis C

genotype 2 and 3

A

sofosbuvir and ribavirin orally

290
Q

which acute hepatitis is treated

A

C

291
Q

Adverse effects of interferon

A

arthralgieas, thrombocytopenia, deprssion, leukopenia

292
Q

Adverse effects of ribavirin

A

anemia

293
Q

Adverse effects of adefovir

A

renal dysfunction

294
Q

Adverse effects of lamivudine

A

none

295
Q

Wilson Disease

definition

A

abnormally decreased copper excretion from the body bc of a decrease in cerulopasmin, copper is not excreted and it builds up in the liver, kidney, rbcs, and nervous system

296
Q

Wilson Disease

what is the most likely diagnosis

A

cirrhosis and hpetaic insufficiency

neurological sx: psychosis, tremor, dysarthria, ataxia, or seizures

coombs negative hemolytic anemia

renal tubular acidosis or nephrolithiasis

297
Q

wilsons disease gives what type of cognitive issues

A

psychosis and delusions, not the encephalopathic features or delirium that you would get with any form of liver failure

298
Q

Wilson Disease

diagnostic tests

A

best initial test is a slit-lamp exam for kayser fleischer rings, a brownish ring around the eye from copper deposition (in the descemet membrane).

ceruloplasmin is usually low

liver biopsy is more sensitive and specific and will detect abrnoamlly increased hepatic copper

most accurate test is lookint an incrased amount of copper excretion ino the urin after giving penicillamine

299
Q

Wilson Disease

treatment

A

penicillamines will chelate copper and remove it form the body

zinc: interferes with intestinal copper absorption

Trientine: an alternate copper-chlating compund

300
Q

Autoimmune hepatitis

A

look for young women with signs of liver inflammation iwth a positive ana

more specific tests are liver kidney microsomal antibodies, hig gamma globuline (IGG), anti smooth muscle antibodies and antiliver kidney microsomal antibodies.

most accurate test is the liver biopsy

treate with prednisone and or azathioprine

301
Q

Nonalcoholic steatohepatitis

A

extremely common cause of mildly abnormaly liver function tests

biopsy is most accurate test and whos the microvesicular fatty depostis you would find in alcoholic liver disease

assocaited with: obesity, diabetes, hyperlipidemia, corticosteroid use

must exclude more serious liver disease, nothing to reverse it just treate the underlying causes

OMS III (21 decks)

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