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
2
Q
alarm sx indicating endoscopy:
A
weight loss
blood in stool
anemia
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
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
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
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
7
Q
in the esophagus what is diagnosed by biopsy
A
cancer and barrett esopahgus
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
- 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
- surgical sectioning or myotomy: can help to alleviate sx. surgery is more effective than pneumatic dilation and surgery
- botulinum toxin injection: this will relax the les but the effects will wear off in about 3-6 months, requiring reinjection
9
Q
pneumatic dilation leads to peroration in how many pts?
A
less than 3%
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
11
Q
Esophageal Cancer
diagnostic tests
A
- endoscopy is indispensible, since only a biopsy can diagnonse cancer
- barium might be the best iniital test but no radiologic test can diagnose cancer
- ct and mri scans are not enough to diagnose esophageal cancer, they are used to determine the extent of spread intot he surrounding itssues
- 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
12
Q
Esophageal Cancer
treatment
A
- no resection = no cure, resection is always the right thing to do
- chemotheraphy and radiation are sued in addition to surgical removal
- stent placement is sue dfor lesions that cannot be resected surgically just to keep the esophagus open for palliation and to improve dysphagia
13
Q
for cancer thre radiologic test is
A
never the most accurate
14
Q
the single word progressive (or from solids to liquieds is the most important clue to the diagnosis of
A
esophageal cancer
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
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
17
Q
Esophageal spasm
barium studes
A
can show a corkscrew appearance at the time of the spasm
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
19
Q
what pills cause esophagitis if prolonged contact
A
doxycycline, alendronate and KCl
20
Q
dysphagia iwth HIV CD4<100
improvement with fluconazole
A
cointuen therapy and haart
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
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
23
Q
schatzki ring on barium studies
A
distal narrowing of the esophagus
24
Q
steakhouse syndrome
A
dysphagia from solid food associted with schatzki rings
25
schatzki rings is assocaited with
intermittent dysphagia and is tretaed with pneymatic dilation in an endoscopic procedure
26
Plummer vinson syndrome is treated with
iron replacement at first which may lead to resolution of the lesion
27
Zenker is associated with
bad smell and halitosis
28
Zenker Diverticulum
definition
outpocketing of the posterior pharygeal constrictor muscles
29
Zenker Diverticulum
sypmtoms
dysphagia
halitosis
regurgitation of food particles
can have aspiration pneymonia when the contents of the diverticulum end up in the lung
30
Zenker Diverticulum
diagnostic tests/treatment
barium studes
surgery there i sno medical therapy
31
do not answer what with zenkers
ng tube or upper endoscopy these can cause perforation
32
Scleroderma
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
33
manometry is the answer for
achalasia
spasm
scleroderma
34
Mallor-Weiss Tear
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
35
boerhaave syndrome
full thickness tear
36
mallory-weiss is what type of tear?
nonpenetrating tear of only the mucosa
37
Epigastric pain
Definition
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
38
Epigastric pain
endoscopy
the only way to get a precise diagnosis
39
Epigastric pain
diagnostic test
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
40
Epigastric pain
What is the most likely dx
pain worse with good
gastric ulcer
41
Epigastric pain
What is the most likely dx
pain better with food
duodenal ulcer
42
Epigastric pain
What is the most likely dx
weight loss
cancer, gastric ulcer
43
Epigastric pain
What is the most likely dx
tenderness
pancreatitis
44
Epigastric pain
What is the most likely dx
bad taste, cough, hoarse
gerd
45
Epigastric pain
What is the most likely dx
diabetes, bloating
gastroparesis
46
Epigastric pain
What is the most likely dx
nothing
non-ulcer dyspepsia
47
Epigastric pain
treatment
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
48
Epigastric pain
treatment
misoprostol
is always the wrong answer
49
RUQ pain
cholecystitis
biliary colic
cholangitis
perforated duodenal ulcer
50
LUQ pain
splenic rupture
| IBS-splenic flexure syndrome
51
RLQ pain
appi
ovarian torsion
ectopic pregnancy
cecal diverticulitis
52
LLQ pain
sigmoid volvulus
sigmoid diverticulitis
ovarian torsion
ectopic pregnancy
53
Midepigastrium pain
pancreatitis
aortic dissection
peptic ulcer disease
54
GERD
definition/etiology
the inappropriate relaxation of the les, resulting in acidic contents of the stomach coming up into the esophagus
55
GERD
sx are worsened by
nicotine
alcohol
caffeine
chocolate
peppermint
late-night meals
obesity
56
GERD
what is the most likely dx
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
57
there are no unique findings in GERD
it is a sx complex
58
GERD
diagnostic tests
most often diagnosed based on pt hx.
can do 24 hr Ph monitoring
59
when is endoscopy indicated with GERD
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
60
What might GERD show on endoscopy
reness, erosions, ulcerations, strictures, or Barrett esophagus
61
GERD
treatment for all pts
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
62
GERD
treatment
mild or intermittent sx
liquid antacids or H2 blockers
63
GERD
treatment
persistent sx or erosive esophagitis
ppis
64
GERD
treatment
treatment of those not responsive to medical therapy
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
65
endoscopy will show nothing where there is only
pyrosis (heartburn)
66
Barrett Esophagus
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
67
Barrett Esophagus
Diagnostic Tests/Treatment
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
68
Management of Barrett's Alone
PPi's and rescope every 2-3 years
69
management of low grade dysplasia in Barrett Esophagus
PPi's and rescope every 6-12 months
70
management of high-grade dysplasia in Barrett Esophagus
ablation with endoscopy: photodynamic therapy, radiofrequency ablation, endoscopic mucosal resection
71
what percentage of pts with barretts progress to esophageal cancer
0.5% each year
72
Gastritis
defintion
inflammation or erosion of the gastric lining that is sometimes called gastropathy
73
Gastritis is caused by
```
alcohol
NSAIDS
H. Pylori
Portal htn
stress like burns, trauma, sepsis, and multiorgan failure (uremia)
```
74
atrophic gastritis is associated with
B12 defiiciency
75
Gastritis
what is the most likely dx
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)
76
there are no unique physical findings for
gastritis
77
Volume of bleeding in coffee-ground emesis
5-10 ml
78
Volume of bleeding in heme (guaiac positive) stool
5-10 ml
79
Volume of bleeding in melena
50-100 ml
80
Gastritis
Diagnostic Tests
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
81
Gastritis Treatment
treat with PPI's before any of the other gerd treatments. sucralfate is the wrong answer
82
stress ulcer phophylaxid is indicated in
mechanical ventilation
burns
head trauma
coagulopathy
83
H Pylori Testing
endoscopic biopsy
the most accurate of all the tests
requires an invasive procedure such as endoscopy
84
H Pylori Testing
Serology
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
85
H Pylori Testing
Urea C13 and C14 breath testing
positive only in active infection, noninvasive
requires expensive equipment in office
86
H Pylori Testing
h pylori stool antigen
positive only in active infection, noninvasive
requires stool sample
87
Peptic Ulcer Disease
Definition
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
88
Peptic Ulcer Disease
etiology
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)
89
nsaids produce more of what than pain
bleeding
90
alcohol and tobacco do what with ulcers
they dont cause them they delay their healing
91
Peptic Ulcer Disease
presentation/wht is the most likely diagnosis
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
92
duodenal ulcer disease is mor often improved with
eating
93
gastric ulcer diseaseis more often worsened with
eating, so it is associated with weight loss
94
you cannot definitively diagnose what without endoscopy
DU, DU, gastritis and non-ulcer dyspepsia
95
there is no way to diagnose pud without
endoscopy or barium studies
96
Peptic Ulcer Disease
diagnostic tests
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
97
H. Pylori Testing in Peptic Ulcer Disease
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
98
endoscopy is the only method of detecting
gastric cancer, it is present in 4% of people with Gastric ulcers and in 0% of people with Duodenal ulcers
99
Peptic Ulcer Disease
Treatment
responds to PPis in over 95% of cases, but will recure unless H pylori is eradicated in those infected
100
what percentage of Duodenal ulcers are associated with h Pylori
80 to 90%
101
what percentage of Gatric ulcers are associated with h pylori
50-70%
102
therapy of h pylori
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
103
treatment of refractory ulcers
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
104
test for cure of h pylori after treatment with
stool antigen or breath test
105
Ulcer treatment failure most often stems from
nonadherence to meds
alcohol
tobacco
nsaids
106
Gastric ulcers
overview
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
107
Diff of GU and DU
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
108
Non Ulcer Dyspepsia
Definition
epigastric pain that has no identified etiology
109
Non Ulcer Dyspepsia
diagnosis
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
110
Non Ulcer Dyspepsia
presentation
the pain can be identicalto gasgritis, pud, gasric cancer, or reflux disease
111
Non Ulcer Dyspepsia
treatment
if pt is under 45 treat empirically with antisecretory therapy such as ppis and scope only if it doesnt resolve
112
scope pts with dyspepsia if
pt is over 55 years old
alarm sx are present (dysphagia, weight loss, anemia)
113
most common cause of epigastric pain
Non Ulcer Dyspepsia
114
Non Ulcer Dyspepsia and h pylori
not associated but if origanal treatment with ppis doesnt resolve then try and treat h pylori
115
Non Ulcer Dyspepsia is epigastric pain with
a normal endoscopy
116
Gastrinoma (ZES)
what is the most likely diagnosis
look for a pt with ulcers that are:
large (>1-2 cm)
recurrent after h pylori eradication
distal in the duodenum
multiple
117
how many pts with an ulcer have a gastrinoma?
less than 1%
118
Gastrinoma (ZES)
Diagnostic testing
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
119
Gastrinoma (ZES)
imaging
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
120
Gastrinoma is often associated with diarrhea
bc acid inactivates lipase
121
hypercalcemia is the clue for
multiple endocrine neoplaisa from hyperparathyroidism
122
Gastrinoma is associated with a massive increase in the number of
somatostatin receptors in the abdomen
123
Gastrinoma (ZES)
treatment
local disease is removed surgically. mets is unresectable and is treated with lifelong ppis to block acid production
124
Diabetic Gastroparesis
definition/etiology
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
Diabetic Gastroparesis
what is the most likely dx
look for a diabetic pt with chronic abdominal discomfort, bloating, and constipation. also anorexia, nausea, vomiting, and early satiety
126
Diabetic Gastroparesis
most accurate test
nuclear gastric emptying study
127
Diabetic Gastroparesis
treatment
erythromycin and metoclopromide increase gi motility
128
fluids when bp is low
lr and ns is better than d5
129
GI bleeding
most improtant thing to do first
if it is severe you want to fluid resuscitate first
130
upper GI bleeding
etiology
ulcer disease is the most common
gastritis
esophagitis
duodenitis
cancer
varices
131
lower GI bleeding
etiology
diverticulosis is the most common
angiodysplasia (arteriovenous malformation)
polyps or cancer
ibd
hemorrhoids
upper gi bleed with rapid transit from high volume
132
what is the most important initial management for GI bleeding
assessing bp
133
GI bleeding
physical findings
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
Severity of blood loss on hemodynamics
orthostasis: 12-20% blood loss
pulse >100 per minute: 30% loss
Systolic BP < 100 mm Hg: 30% loss
135
Variceal bleeding
overview
only form of gi bleeding where physical examination helps determine etiology
the presence of the signs of liver disease helps establish dx
136
Variceal bleeding is suspected when the case describes
vomiting blood w/or w/o black stool
spider agniomata and caput medusa
splenomegaly
palmar erythema
asterixix
137
GI bleeding
acute bleeding
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
initial manegament of GI bleeding is
not based on the etiology but on the severity
139
nasogastric tube with GI bleeding
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
role of ng tube in GI bleeding if you are going to do egd
limited role and probably dont do
141
80% of GI bleeding will stop spontaneously if
the fluid resuscitation is adequate. most pts die of inadequate fluid resuscitation
142
GI bleeding diagnostic tests
nuclear bleeding scan
endoscopy unrevealing in a msasive acute hemorrhage, this test lacks accuracy
143
GI bleeding diagnostic tests
angiography
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
GI bleeding diagnostic tests
capsule endoscopy
small bowel bleeding, upper and lower endoscopy do not show the etiology
145
GI bleeding diagnostic tests
Ct or MRI of abdomen
not useful in GI bleeding
146
GI bleeding diagnostic tests
ekg, lactate level
shows ischemia in severe bleeding
147
GI bleeding diagnostic tests
treatment (8)
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
when do you transfuse platelets in a spontaneous bleed (not GI)
below 10000-20000
149
Esophageal and gastric varices what do you do in addition to fluids blood platelets and plasma (5)
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
scleropathy is never the right answer if
banding is technically possible
151
Antibiotic associated diarrhea
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
recurrent cdiff treat with
metro, if it was susceptible before
only use iv metro if pt cant take orally
153
when do you give iv vancomycin for ab associated diarrhea
never, bc it wont pass the bowel wall
154
diarrhea causing malabsorption
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
all forms of fat malabsoprtion present with deificency of
adek
156
Vit D deficiency manifestation
hypocalcemia, osteoporosis
157
Vit K deficiency manifestation
bleeding, easy bruising
158
Vit B12 deficiency manifestation
anemia, hypersegmented neutrophils, neuropathy
159
fat malabsorption presents with
weight loss
160
b12 needs an intact what to be absorbed
bowel wall and pancreatic enzymes
161
what can clinically distinguish between celiac disease and topical sprue
nothing
162
what percentage of celiac disease people have dermatitis herpetiformis
100%
163
whipple disease
presents with
diarrhea
arthralgias
ocular findings
neurologic abnormalities (dementia and seizures)
fever
lymphadenopathy
164
treat whipple disease with
ceftriaxone followed by bactrim
165
main distinctions between celiac disease and chronic pancreatitis
iron deficiency bc it needs an intact bowel wall but no pancreatic enzymes to be absorbed
166
Celiac disease testing unique tests
ant-tissue tanglutaminase (first test)
antiendomysial antibody
IgA antigliadin antibody
167
Most accurate diagnostic test for celiac disease
small bowel biopsy that shows flattening of the villi
168
most accurate diagnostic testing for whipple disease and topic sprue
bowel wall biopsy showing the specific organisms
169
bowel biopsy is essential in celiac disease to exclude
lymphoma
170
chronic pancreatitis
specific diagnostic tests
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
rice and wine are safe in
celiac disease
172
treatment for chronic pancreatitis
enzyme replacement
173
treatment for celiac disease
avoid gluten-containing foods such as wheat, oats, rye, or barley
174
treatment for whipple disease
ceftriaxone, bactrim
175
treatment for topical sprue
bactrim, tetracyline
176
d-xylose test
old test to dinstinguesh pancreatitis from bowel wall abnormalities, it will be normal in pancreatic disorders
177
carcinoid syndrome
presentation
presents with intermiittent diarrhea in assocation w/
flusshing
wheezing
cardiac abnormalities of the right side of the heart
178
carcinoid syndrome
testing and therapy
urinary 5hydroxyindoleacetic acid (5HIAA) test
octreatide, synthetic somatostain used to control diarrhea
179
Lactose intolerance
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
Lactose intolerance
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
irritable bowel syndrome
definition
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
ibs is not associated with
weight loss, pain does not mean malabsorption
or
blood or white cells in the stool
183
pain of IBS is
relieved by a bowel movement
less a tnight
relieved by a change in bowel habits such as diarrhea
184
irritable bowel syndrome
treatment
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
IBD
definition/presentation
idiopathic disorder that presents with diarrhea, blood in stool, weight loss, and fever.
186
both crohn disease and ulcerative colitis have extraintestinal manifestation that can ve identical in both diseases
arthralgias
uveitis, iritis
skin manifestation (erythema nodosum, pyoderma gangenosum)
scleorising cholangitis (more frequent in uc)
187
IBD can turn into
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
Erythemia nodosum is an indicator
of diseasea activity
189
Crohn Disease
skip lesions
tranmural granulomas
fistulas and abscesses
masses an obstruction
perianal disease
190
Ulcerative Colitis
curable by surgery
entirely mucosal
no fistulas or abscesses
no obsrtuction
no perianal disease
191
When should colon cancer screeing occur in a pt with IBD
after 8 to 10 years of colonic involvement, with colonoscopy every 1 to 2 years
192
IBD
Antibody diagnostic testing
ANCA positive in UC
ASCA positive in CD
193
IBD
diagnostic testing
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
IBD Treatment
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
Budesonide is a stroid speicific for IBD
first pass effect is good for EBD treatment
196
Diverticulosis
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
Diverticulosis
Testing
most accurate is colonoscopy
barium studies are acceptable but no as accurate
198
Diverticulosis
treatment
bran
| psyllium, methylcellulose and increased dietary fiber are used to decrease the rate of proggresion and complications
199
Diverticulitis
Most likely diagnosis
on older pt with:
llq pain and tnederness
fever
leukocytosis
palpable mass sometimes occurs
(nausea constiaption and bleeding can occur but are nonspecific
200
Diverticulitis
best initial test
CT Scan
201
dangerous tets in Diverticulitis
colonoscopy and barium enema bc of the increased risk of perforation. infection weakens the colonic wall
202
Diverticulitis
treatment
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
Diverticulitis
when is surgery the answer
```
no response to medical therapy
frequent recurrences of infection
perforation
fistula
abscess
strictures
obstruction
```
204
pt with acute diverticulitis should not be
fed
205
Diverticulitis
who is more likely to get surgery
yougner pts bc they will have more recurrences
206
does diverticulities disappear
no
207
95% of colon cancer deaths are preventable with
screening
208
when is virtual colonoscopy the right answer
never
209
colonoscopy testing frequency
routine testing
pts should have a colonoscopy q 10 years beginning at age 50
210
colonoscopy testing frequency with a fx hx of colon cancer
single family member
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
colonoscopy testing frequency with a fx hx of colon cancer
3 family members, 2 generations, i premature (before 50)
hereditary nonpolyposis colon cancer syndrome (HNPCC). comprises these factors .
start screening at age 25 q 1 to 2 years
212
colonoscopy testing frequency with a fx hx of colon cancer
familial adenomatous polyposis (FAP)
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
colonoscopy testing frequency with a fx hx of colon cancer
Previous adenomatous polyp
pt whould have a colonsocopy q 3 to 5 years
214
colonoscopy testing frequency with a fx hx of colon cancer
previous hx of colon cancer
pt should ahve colonsocopy at 1 year after resection, then at 3 years, then every 5 years
215
Peutz-jeghers syndrome
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
gardner syndrome
colon cancer in association with
osteomas
dsmoid tumors
other soft tissue tumors
217
turcot syndrome
colon cancer in assocaition with
CNS malignnacy
218
juvenile polyposis
colon cancer in association with
mulitple hamartomatous polyps
219
what syndromes do not requre increased coloncoscopy screenings
peutz jeghers
gadner
turcot
juvenile
220
what percentage of colon cancers occur proximal to rectum and sigmoid colon
40%
they will be missed by sigmoidoscopy
221
Acute pancreatitis
definition/etiology
acute inflammation of the pancreas
over 90% caused by alcoholism and cholelithiasis
222
less common causes of Acute pancreatitis
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
Acute pancreatitis
presentation/what is the most likely dx
acute epigasting pain and tnederness and nausea/vomiting=pancreatitis
insevere causes there is also hypotension and fever
224
pancreatitis poem
a stone
a stricture
a tumor
an obstruction
225
tip about pancreatitis and cholecystitis pain
pnacreas pain goes straight back like a spear
gallbladder pain around the side to the back
226
worst prognosis with pancreatitis
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
does pain intensity correlate with the degree of organ damage
no bc it is subjective
228
CRP
has no definite correlation with severity in any disease
229
Acute pancreatitis
diagnostic tests
best initial test is amylase and lipase
| most specific test is CT scan
230
Acute pancreatitis
| disease severity
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
what is extensive necrosis in Acute pancreatitis
greater than 30%
232
Acute pancreatitis laboratory tests
cbc show leukocytosis, drop in hematocrit over time with rehydration
elevated ldh and ast
hypoxie, hypocalcemia
elevated urinary trypsinogen activation pepetide
233
Acute pancreatitis
imaging
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
Acute pancreatitis
treatment
npo
iv hydration at very high volume
analgesia
ppis decrease pancreatic stimulation from acid entering the duodenum
235
Acute pancreatitis
treatment with more than 30% necrosis
add as like imipenem or meropenem they may decrease mortality by decreasing the devlopment of infected, necrotic pancreatitis
needle biopsy to confirm infection
236
pseudocyst Acute pancreatitis treamtnet
drained with a needle if enlarging or painful
237
ERCP with Acute pancreatitis is used to
remove obstructing stones and dilate strictures
place stents
238
Acute pancreatitis
abdominal CT
always perfomr with IV and oral contrast to better define and outline abdominal structures
239
infected, necrotic pancretitis should
be resected with with surgical debridement to prevent ARDS and death
240
Liver disease
all forms of chornic Liver disease can produce
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
Ascites
paracentesis should be performed if there is
new-onset acites
abdominal pain and tenderness
fever
242
Ascites
etiology
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
SAAG less <1.1 g/dl
infection (except SBP)
cancer
nephrotic syndrome
244
SAAg greater >1.1g/dl
portal htn
chf
hepatic vein thrombosis
constrictive pericariditis
245
Spontaneous bacterial peritonitis
definition and etiology
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
Spontaneous bacterial peritonitis
diagnostic tests
best initial test: cell count with more than 250 neutrophils is when we start therapy
ldh is too nonspecific
247
Spontaneous bacterial peritonitis
treatment
cefotaxime or ceftriaxone
248
Spontaneous bacterial peritonitis
recurring
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
all variceal bleeding with ascites needs
Spontaneous bacterial peritonitis prophylaxis
250
anyone with Spontaneous bacterial peritonitis needs
lifelong prophylaxis
251
Cirrhosis treatment of ascites and edema
sprionolcatone and other diuretics, serial paracentesis for large-volume ascites
252
Cirrhosis treatment of coagulopathy and thromocytopenia
FFP and/platelets only if bleeding occurs
253
Cirrhosis treatment of encephalopathy
lactulose and rifaximin
254
Cirrhosis treatment of hypoalbuminemia
no specific therapy
255
Cirrhosis treatment of spider angiomata and palmar erythema
no specific therapy
256
Cirrhosis treatment of varices
propanolol and banding via endoscopy
257
Cirrhosis treatment of hepatorenal syndrome
somatostating (octreotide), midodrine
258
Cirrhosis treatment of hepatopulmonary syndrome
no specific therapy
259
Hepatopulmonary syndrome
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
Specific causes of cirrhosis
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
Alcoholic liver disease
diagnosis of exclusion
no specific ltherapy
most accurate test is liver biopsy
alcohol and all drugsgive greater elevation in ASt compared to ALT
262
viral hepatitis ast and alt
alt is higher
263
binge drinking give a sudden rise in
GGTP
264
Primary Biliary cirrhosis
most likely diagnosis
women in 40s or 50s
fatigue and itching
normal bilirubin with elevated alk phos
265
unique features of PBC are
xanthelasma/xanthoma
osteoporosis
266
PBC diagnostic tests and treatment
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
Priary Sclerosing cholangitis
presentation
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
PSC tests
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
PSC treatment
cholestyramine or ursodeoxycholic acid
270
PSc is the only cause of cirrhosis in which
a biopsy is not the most accurate test
271
PSC does not improve or resolve with
resolution of the IBD. even after a colectomy in UC, the pt may still progress to needing a liver transplantation
272
Alpha 1 antirypsin deficiency
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
Hemochromatosis
definition
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
Hemochromatosis
presentation
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
Hemochromatosis may be found on routin testing with
mildly abnomral lfts or iron levels
276
with Hemochromatosis what bugs will you find
vibrio vulnificans, yersinia, and listeria infections occure bc they feed on iron
277
Hemochromatosis
diagnostic tests
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
when is iron chelation therapy used in Hemochromatosis
cannot be managed with phlebotomy
are anemic and have hemochormatosis from overtransfusion such as thalassemia
279
Hemochromatosis
treatment
phlebotomy is clearly the best therapy for those with aoverabsorption of iron
280
liver fibrosis can resolve in Hemochromatosis if
phlebotomy is begun before cirrhosis develops
281
Chronic Hepatitis B and C
overview
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
Chronic Hepatitis B
diagnostic tests
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
Chronic Hepatitis C
diagnostic tests
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
Acute hepatitis C is treated with
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
Chronic Hepatitis B and C
liver biopsy
determines the degree of inflammation and fibrosis. Biopsy can help you understand the urgency for treatment if fibrosis is present or worsening
286
Chronic Hepatitis B
treatment
adefovir
lamivudine
telbivudine
entecavir
tenofovir
interferon
287
Chronic Hepatitis B and C
how do you follow
with viral pcr load and objective is that you have an undetectable load
288
Chronic Hepatits C
genotype 1
ledipasvir and sofosbuvir, both orally
289
Chronic Hepatitis C
genotype 2 and 3
sofosbuvir and ribavirin orally
290
which acute hepatitis is treated
C
291
Adverse effects of interferon
arthralgieas, thrombocytopenia, deprssion, leukopenia
292
Adverse effects of ribavirin
anemia
293
Adverse effects of adefovir
renal dysfunction
294
Adverse effects of lamivudine
none
295
Wilson Disease
definition
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
Wilson Disease
what is the most likely diagnosis
cirrhosis and hpetaic insufficiency
neurological sx: psychosis, tremor, dysarthria, ataxia, or seizures
coombs negative hemolytic anemia
renal tubular acidosis or nephrolithiasis
297
wilsons disease gives what type of cognitive issues
psychosis and delusions, not the encephalopathic features or delirium that you would get with any form of liver failure
298
Wilson Disease
diagnostic tests
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
Wilson Disease
treatment
penicillamines will chelate copper and remove it form the body
zinc: interferes with intestinal copper absorption
Trientine: an alternate copper-chlating compund
300
Autoimmune hepatitis
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
Nonalcoholic steatohepatitis
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
