Gastrointestinal Flashcards
(359 cards)
1
Q
In an immunocompromised person with odynophagia consider-
A
candidiasis
2
Q
dysphagia
A
difficulty swallowing
3
Q
odynophagia
A
pain with swallowing
4
Q
oropharyngeal dysphagia presentation and complications
A
issues initiating swallowing.
can cause aspiration of food into lungs. (coughing, choking, drooling)
5
Q
Etiology of oropharyngeal dysphagia
A
neurologic or muscular. stroke. parkinson. myesthenia gravis. prolonged intubation. Zenker diverticulum.
6
Q
oropharyngeal dysphagia is usually more of a problem with ______ than _____
A
liquids than solids
7
Q
Esophageal dysphagia
etiologies and presentation
A
obstruction caused by stricture, schatzki rings, carcinoma.
motility disorder- achalasia, scleroderma, esophageal spasm
8
Q
esophageal obstruction causes more of a problem with _____ than _____
A
solids than liquids
9
Q
Motility disorders cause issues with eating _____ and _____
A
solids AND liquids
10
Q
Diagnosis/work up for oropharyngeal dysphagia
A
- modified barium swallow (video flouroscopic swallow exam) sometimes EGD
11
Q
Diagnosis/work up for esophageal dysphagia
A
Initially EGD (can do pre EGD barium swallow) **esp if history of esophageal radiation and strictures
12
Q
Diagnosis of odynophagia?
A
EGD
13
Q
Should you ever perform manometry before EGD?
A
NO
14
Q
Candida esophagitis is an ___ defining illness
A
AIDS
15
Q
Name causes of infectious esophagitis
A
- candida albicans
- herpes simplex virus
- CMV
16
Q
Exam findings, upper EGD findings, Treatment for Candida albicans
A
Exam: oral thrush. can be scraped off
EGD: yellow, white plaques adherent to mucosa
Treatment: fluconazole PO
17
Q
Exam findings, upper EGD findings, Treatment for Herpes Simplex Virus
A
Exam: oral ulcers
EGD: small, deep ulcerations. +Tzank smear. multinucleated inclusions on biopsy
Treat: Acyclovir IV
18
Q
Exam findings, upper EGD findings, Treatment for CMV
A
exam: retinitis, colitis
EGD: large, superficial ulcerations. intranuclear and intracytoplasmic inclusions on biopsy
Treatment: Ganciclovir IV
19
Q
Diffuse distal esophageal spasm
A
motility disorder where normal peristalsis is interrupted by non-peristaltic contractions
20
Q
Presentation of esophageal spasms
A
heartburn, chest pain, dysphagia, odynophagia
21
Q
esophageal spasms are often precipitated by ingestion of? pain relieved by?
A
Hot or cold liquids.
Nitroglycerin provides relief
22
Q
Diagnosis of esophageal spasm?
A
EGD to rule out structural abnormalities
Barium swallow
Esophageal manometry:(DEFINITIVE TES)
23
Q
what will barium swallow show for patient with esophageal spasm?
A
Corkscrew-shaped esophagus
24
Q
What will esophageal manometry show for esophageal spasm?
A
DEFINITIVE TEST. high amplitude, simultaneous contractions in greater than 20% of swallow.
25
Corkscrew barium swallow
esophageal spasm
26
Birds beak sign on barium swallow
achalasia
27
Nodular mucosa and raised filling defect on barium swallow
barret esophagus and adenocarcinoma
28
musculature in upper 1/3 of esophagus is _____ while lower 2/3 is _______
skeletal, smooth
29
Treatment for esophageal spasm?
calcium channel blockers, TCAs, nitrates
30
treatment for severe incapacitating symptoms of spasm?
surgery (esophageal myotomy)
31
Achalasia
motility disorder of esophagus characterized by impaired relaxation of LES and loss of peristalsis in distal 2/3 esophagus
32
Cause of achalasia
degeneration of inhibitory neurons in myenteric (Auerbach) plexus
33
presentation of achalasia
Progressive dysphagia (solids + liquids), chest pain, regurg of undigested food, weight loss, nocturnal cough
34
what may mimic achalasia?
malignancy
35
Diagnosis of achalasia?
EGD to rule out structural disorders (mechanical obstruction)- especially cancer
initial test: barium swallow- dilation with a "bird beak" sign
Definitive test: manometry: increased resting LES pressure, incomplete LES relaxation with swallow, and decrease peristalsis in esophagus
36
Treatment for achalasia
short term: nitrates, ccb, endoscopic injection of botulinum toxin into LES
long term: pneumatic balloon dilation or surgical (Heller) myotomy.
37
Zenker diverticulum
cervical out-pouching through cricopharyngeus muscle (posterior-FALSE diverticulum)
38
presentation of Zenker diverticulum?
chest pain, dysphagia, halitosis, regurg of undigested food
39
Dx of Zenker:
barium swallow with outpouchings
40
Tx of Zenker:
Surgical excision of diverticulum if symptomatic. (myotomy of cricopharyngeus to relieve high pressure)
41
Most common type of esophageal cancer world-wide?
SCC
42
Most common type of esophageal cancer in U.S, Europe, Australia?
Adenocarcinoma
43
Risk factors for SCC?
Alcohol, tobacco use, nitrosamines
44
Adenocarcinoma risk factors?
Barett esophagus (columnar metaplasia of distal esophagus secondary to chronic GERD)
45
Presentation of esophageal cancer?
Progressive dysphagia. initially to solids. then to liquids. weight loss. odynophagia. GERD. GI bleed. Vomiting.
46
Why does esophageal cancer metastasize early?
Esophagus lacks a serosa
47
SCC occurs in _____ of esophagus. Adeno occurs in _____ of esophagus.
SCC- upper and middle thirds. Adeno- lower 3rd
48
Diagnosis of esophageal cancer
Initial test: barium study: narrowing of esophagus with irregular border protruding into lumen
EDG with biopsy makes diagnosis:
CT and endoscopic ultrasound: staging cancer
49
treatment for esophageal cancer
chemo and surgical resection are 1st line treatment
50
treatment for cases of high grade barrett's?
resection may be required
51
Etiology of GERD?
most often from transient LES relaxation
| incompetent LES, gastroparesis, hiatal hernia
52
sour taste "water brash" or sensation of globus lump in throat?
GERD
53
Diagnosis of GERD
clinical diagnosis with empiric treatment first
54
when is EGD with biopsy performed for GERD patients
1. refractory symptoms to therapy
2. long standing GERD (rule out barrett and adeno)
3. blood in stool, weight loss, dysphagia, odynophagia, chest pain
55
Definitive test for GERD?
24 hour pH monitoring with impedance (only for uncertain diagnosis)
56
Treatment for GERD
lifestyle
mild intermittent: antacids
chronic/frequent: H2 antagonists (cimetidine, ranitidine) or PPIs (omeprazole, lansoprazole)
57
Treatment for severe, erosive GERD
PPI first. Nissen fundoplication
58
Complications of GERD
Erosive esophagitis, peptic stricure, aspiration pneumonia, upper GI bleed, Barrett esophagus
59
Hiatal hernia 3 types
1. sliding hiatal hernia (95%)
2. paraesophageal hiatal hernia (5%)
3. mixed hiatal hernia (rare)
60
Sliding hiatal hernia
GE junction and any portion of stomach above diaphragm. usually asymptomatic
61
Is GERD a result of presence of H.pylori?
NO. arises from relaxation of LES
62
Paraesophageal hiatal hernia
GE junction below diaphragm. fundus herniates into thorax. can cause strangulation
63
Sliding hiatal hernia presentation?
can be asymptomatic or GERD
64
Dx of hiatal hernia?
often indidental finding on CXR. barium swallow or EGD diagnosis
65
Tx sliding hiatal hernia
medical therapy and lifestyle mods to decrease GERD
66
Tx paraesophageal hernia
surgical gastropexy (attachment of stomach to rectal sheath and closure of hiatus
67
Acute gastritis
rapidly developing superficial lesions. often due to NSAID use, alcohol, H.pylori, stress from severe illness (burns, CNS injury)
68
Chronic gastritis Type A and Type B
Type A: (10%)- Occurs in fundus. due to autoantibodies to parietal cells (pernicious anemia).
Type B: (90%)- Antrum, caused by NSAIDs or H.pylori. often asymptomatic. but associated with increased risk of peptic ulcer disease and gastric cancer
69
Pernicious anemia associated with?
associated with other autoimmune disorders and increased risk of gastric adenocarcinoma
70
Type A related gastritis (autoantibodies to parietal cells) occurs in the ____ of stomach?
fundus
71
Does H.pylori infection always cause gastritis?
NO
72
Why is type A gastritis associated with pernicious anemia?
Auto-antibodies attack parietal cells. Parietal cells make intrinsic factor. Need intrinsic factor to absorb B12.
73
Curling ulcers
stress ulcers associated with burn injuries
| burn with curling iron
74
cushing ulcer
stress ulcer associated with CNS injury (TBI)
75
Treatment for PUD/Gastritis
Stop offending agents (NSAID, alcohol)
Antacids, sucralfate, H2 receptor blockers, PPIs
**Triple therapy (amoxicillin, clarithromycin, omeprazole) for H. Pylori infection
76
What should triple therapy for H.Pylori include if patient is allergic to penicillin?
Metronidazole, clarithromycin, omeprazole
Metro instead of amoxicillin
77
Are H. pylori antibodies a good measure of infection? why/why not?
NO. they stay (+) even when disease is cleared.
78
How to diagnose H. pylori?
Urea breath test
79
Test of cure for H. pylori?
repeat stool antigen
80
4 different tests for H. pylori
1. serology
2. urea breath test
3. stool antigen test
4. endoscopic biopsy
81
Who should get prophylactic PPIs?
Patients at risk for stress ulcer- ICU patients!
82
Krukenberg tumor
gastric adenocarcinoma that metastasizes to ovary
83
How does urea breath test work?
H.pylori urease converts urea to CO2 and ammonia. Test detect ammonia from urea metabolism.
84
sensitivity and specificity of serology IgG testing for h.pylori?
high sensitivity. lower specificity
85
sensitivity specificity for for urea breath test?
high specificity. lower sensitivity. PPIs can cause false negatives.
86
stool antigen test for H. pylori
detects H. pylori antigen in stool. high specificity and high sensitivity. cost-effective initial test for H.pylori**
87
Gold standard diagnosis for H.pylori or gastritis?
endoscopic biopsy.
88
Malt Lymphoma
rare gastric tumor that presents in patients with chronic H.pylori infection.
89
how to cure malt lymphoma
only malignancy that can be cured with antibiotics. treat with triple therapy. (amox, clarithromycin, omeprazole)
90
Virchow node.
enlargement of left supraclavicular node. often indicative of gastric cancer.
91
most common GI cancer?
adenocarcinoma (common in Korea and Japan)
92
Risk factors for GI adenocarcinoma
Diet high in nitrites, salt, low in fresh veggies (antioxidants). H.pylori. Chronic gastritis
93
presentation of gastric cancer
indigestion, loss of appetite early
| late- weight loss, upper GI bleed, abd pain
94
Dx gastric cancer:
upper endoscopy with biopsy (definitive)
95
Tx: gastric cancer
surgical resection. most patients present with late stage, incurable disease.
96
<90% of duodenal ulcers and 70% of gastric ulcers are caused by?
H.pylori
97
Other risk factors for PUD
alcohol, NSAID, tobacco
98
Presentation of acute perf caused by PUD
rigid abdomen, rebound tenderness, guarding (do upright KUB- show free air under diaphragm)
99
In recurrent or refractory cases of PUD, check serum ______ to screen for?
gastrin, Zollinger-Ellison syndrome
100
if Xray shows no perf, but high clinical suspicion of PUD perf, order?
CT
101
How to rule out/in active bleeding with PUD?
serial hematocrits, rectal vault exam, NG lavage. Monitor BP and treat with IV hydration, blood transfusion, IV PPIs. Perform urgent EGD to control suspected bleeding.
102
Parietal cell vagotomy should be performed
with severe cases of PUD refractory to medical therapy
103
After a meal pain from Gastric ulcer is ________ while pain from Duodenal ulcer is _______
Gastric ulcer - Greater
Duodenal ulcer- Decreased
104
Should all gastric ulcers be biopsied? why/why not?
YES. rule out malignancy
105
What is a major complication of gastric ulcer?
Hemorrhage
106
What gastric ulcers are most likely to cause hemorrhage? why?
Posterior gastric ulcers that erode into the gastroduodenal artery
107
Other complications of gastric ulcer?
perforation, gastric outlet obstruction, intractable vomiting
108
What can you give patients who require NSAID therapy for arthritis to help with PUD? why?
Misoprostol- PGE1 analogue -> increases production and secretion of gastric mucous barrier and decreases gastric acid production.
109
Zollinger-Ellison syndrome?
Rare condition characterized by gastrin producing tumor in duodenum or pancreas.
110
Gastrinomas are associated with what syndrome 20% of the time?
MEN 1
111
how to diagnose ZE syndrome?
fasting serum gastrin levels elevated and increased gastrin levels with the administration of secretin. (CT scan to stage the disease)
112
Tx of ZE:
moderate to high dose PPI
| Surgical resection of gastrinoma after CT or octreotide scan to identify carcinoid tumors
113
ZE syndrome components
1. hypercalcemia (MEN 1)
2. Epigastric pain (peptic ulcer)
3. Diarrhea (mucosal damage and pancreas enzyme inactivation leading to malabsorption)
114
Diarrhea definition
production of >200g feces/day along with increased frequency or liquidity of stool.
115
most common subtypes of diarrhea
1. malabsorption/maldigestive/osmotic
2. secretory
3. inflammatory/infectious
4. increased motility
116
Normal stool osmotic gap?
50-100
117
Stool osmotic gap equation
stool osmotic gap = 290 - 2(Stool Na + stool K)
118
Acute diarrhea definition and common etiology
< 2 weeks, usually infectious and self-limited
119
Common causes of pediatric diarrhea
rotavirus, norwalk, enterovirus
120
Chronic diarrhea definition and common causes
>4 weeks. insidious onset.
| Secretory, Malabsorption, Inflammatory/Infectious, Increase motility
121
Secretory diarrhea examples
Carcinoid tumor, VIPoma (VIP increases intestinal water and electrolyte secretion)
122
Malabsoption diarrhea ex:
bacterial overgrowth, pancreatic insufficiency, mucosal damage, lactose intolerance, celiac disease, laxative abuse, post-surgical short bowel
123
inflammatory diarrhea ex:
IBD
124
Increased motility diarrhea ex:
IBS
125
Cryptosporidium and Isospora are associated with chronic diarrhea in _____ patients
HIV/AIDS
126
Organisms that cause bloody diarrhea include
1. salmonella
2. shigella
3. e.coli (EHEC)
4. campylobacter
127
Organisms that cause watery diarrhea include
1. vibrio cholera
2. rotavirus
3. e.coli (ETEC)
4. Cryptosporidium
5. Giardia
6. Norovirus
128
When are studies needed for acute diarrhea?
high fever, bloody diarrhea, lasting > 4-5 days diarrhea
129
Additional studies for chronic diarrhea
1. stool analysis (leukocytes, culture, c.diff, ova and parasite)
2. sigmoidoscopy (only if with bloody diarrhea and unknown cause)
130
Low osmotic gap diarrhea <50
Secretory diarrhea (increase secretion or inhibition of water absorption) (cholera, e.coli, VIPoma, gastrinoma, medullary cancer of thyroid
131
High osmotic gap diarrhea >100
osmotic diarrhea (osmotically active compounds draw in water) (celiac, whipple disease, pancreatic insufficiency, laxative abuse)
132
Whipple Disease
CAN of Chocolate WHIP cream
C-cardiovascular
A-arthralgia
N-neurologic
Chocolate (diarrhea)
AND Osmotic diarrhea
133
History, Exam, Test Results, Treatment: campylobacter
History: most common cause of bacterial diarrhea (ingesting contaminated food/water). affects young kids and young adults. lasts 7-10 days.
Exam/Tests: Bloody diarrhea. Fecal RBC/Fecal WBC
Treatment: rule out IBD, rule out appendicitis. Supportive treatment then ciprofox or azithromycin if needed
134
History, Exam, Test Results, Treatment: C.diff
history: recent treatment with abx (penicillin, quinolone, clinda). hospitalized adult patients.
exam: fecal RBC/WBC. fever, abd pain, systemic tox
Dx: c.diff toxin. sigmoidoscopy with psuedomembrane.
Tx: stop antibiotics. PO metronidazole (mild)
PO vanc (mod-severe)
IV metro +/- rectal vanc if ILEUS
135
History, Exam, Test Results, Treatment: Entamoeba Histolytica
hx: travel in develop countries (food/water)
incubation can be 3 months. severe abd pain and fever.
dx: endoscopy with flask shaped ulcers
Tx: metronidazole
136
History, Exam, Test Results, Treatment: E.coli O157H7
hx: ingestion of raw meat. affects kids and elderly. lasts 5-10 days. severe abd pain, low fever, vomiting.
137
History, Exam, Test Results, Treatment: Salmonella
hx: ingestion of contaminated poultry, egg. young children and elderly. 2-5 days. prodromal HA, fever, myalgia, abd pain
tx: fluids! oral quinolone or TMP-SMX
138
History, Exam, Test Results, Treatment: Shigella
hx: extremely contagious. fecal oral. young children and hospitalized. can cause febrile seizures in the young.
tx: TMP-SMX to decrease person/person spread.
139
What should you watch for as severe complication of C.diff infection?
toxic megacolon
140
Flask shaped ulcers on endoscopy?
entamoeba histolytica
141
Treating entameoba histolytica with steroids can lead to?
fatal perforation
142
what is a complication of entamoeba histolytica
chronic amebic colitis (mimics IBD)
143
potential complication of E.coli- particularly in children?
HUS
144
What e.coli treatment increases risk of HUS?
Antibiotics or antidiarrheal therapy (SO DONT GIVE)
145
What is a major concern for salmonella
SEPSIS. 5-10% become bacteremic.
146
What patients are at particular risk if they contract salmonella?
sickle cell patients. invasive disease leading to osteomyelitis is more common
147
Antidiarrheal agents
loperamide, bismuth salicylate
148
Tropical sprue
malabsorption, tropical regions, abnormal flattening of villi, inflammation of lining of small intestine,
(typically 30 degrees north or south of equator)
149
Celiac disease is associated with which rash?
dermatitis herpetiformis
150
Carb malabsorption will present with?
frequent, loose, watery stool
151
fat mal absorption
pale, foul smelling, bulky stool associated with flatus, bloating, weight loss, nutritional deficiency and fatigue
152
Lactase
brush border enzyme that metabolizes lactose into glucose and galactose
153
transiet lactose intolerance can occur after
acute gastroenteritis
154
presentation of lactose intolerance
bloating, flatulence, cramping, watery diarrhea following milk ingestion
155
hydrogen breath test shows ____ in lactose intolerant individuals
Increased hydrogen following ingestion of lactose
156
Carcinoid syndrome
metastasis of carcinoid tumors- most commonly arise in ileum or appendix and produce serotonin.
157
Why dont carcinoid tumors cause symptoms until they metastasize?
because serotonin secreted hormones go first pass through the liver.
158
presentation of carcinoid tumor
cutaneous flushing, diarrhea, abd cramp, wheezing, right sided cardiac valve lesions
159
patients with carcinoid syndrome develop _____ deficiency because tryptophan is metabolized into _______
niacin
serotonin
160
Dx of carcinoid syndrome
high urine levels of 5-HIAA. CT and octreotide scans used to localize tumor
161
Tx for carcinoid tumor
octreotide and surgical resection
162
Classic presentation of Pellagra
```
4 D's:
Diarrhea
Dementia
Dermatitis
Death
```
163
Rome III diagnostic criteria
diagnosis of IBS:
At least 3 days in 3 months of episodic abd discomfort that is (1. relieved by defecation) 2. associated with change in stool frequency/consistency 3. associated with change in stool appearance
-exclude organic disorders with CBC, TSH, electrolytes, stool culture, abdominal film, barium contrast, colonoscopy with biopsy
164
Increased incidence of ______ disease in IBS patients
celiac
165
Partial SBO
continued flatus, no stool
166
Obstipation
no flatus or stool. complete SBO
167
most common cause of SBO in adults? kids?
adults: stricture/adhesions
kids: hernia
168
presentation of SBO
crampy abd pain at 4-5 min intervals. vomiting. distension, tenderness, high pitched tinkles and peristaltic rushes- hyperactive BS on exam.
169
Complications of SBO
ischemic necrosis, bowel rupture
170
Fever, hypotension, rebound tenderness, tachy and history of SBO- worry about?
ischemic necrosis or bowel rupture
171
Pellagra is deficiency in?
vitamin B3- niacin
172
Why niacin deficiency with carcinoid syndrome?
Carcinoid tumors produce serotonin. Tryptophan is used to make serotonin and also niacin. So much tryptophan goes into serotonin production that niacin levels fall and cause the 4 D's of pellagra.
173
Gallstone ileus
form of SBO that occurs when gallstone lodges in ileocecal valve
174
Diagnosis of SBO - INITIAL TEST
abd films showing stepladder pattern of dilated small bowel loops with air-fluid levels and small amount of gas in colon
175
Definitive test for SBO?
CT of abdomen (evaluate for etiology of SBO)
176
leukocytosis may be present with SBO if there is?
ischemia or necrosis of bowel
177
Lab test with SBO often show
dehydration and metabolic alkalosis
178
Lactic acidosis is a prognostic sign with SBO as it means?
ischemic bowel may be present
179
Treatment of SBO
partial obstruction?
complete obstruction?
1. give fluids
partial: supportive care. NPO status, NG suction, IV hydration, correction of electrolytes, foley cath to monitor fluid status, pain management (avoid opioids and anticholinergics as they slow GI motility)
complete: exploratory laparotomy indicated in compete SBO, ischemic necrosis, refractory SBO
180
Ileus
loss of peristalsis without structural obstruction
181
Risk factors for ileus
recent surgery/GI procedures, severe medical illness, immobility, hypokalemia, other electrolyte abnml, hypothyroid, DM, meds slowing GI
182
presentation and PE for Ileus
constant abd discomfort, n/v, absence of gas and BM
Exam: hypoactive BS. diffuse tenderness, abd distension. rectal exam needed to rule out fecal impaction
183
Dx of ileus
Distended loop of small and large bowel with air in colon and rectum (compared to SBO)
CT- definitive test
184
Tx:
stop anti GI motility agents, bowel rest, NG suction/parenteral feeds as needed, hydrate and replete electrolytes as needed
185
Mesenteric Ischemia most common causes
1. embolism
2. acute arterial occlusion from thrombosis
3. atherosclerosis
4. arterial vasospasm
5. venous thrombosis
6. shock
186
Emboli as cause of Mes Isch
most common to come from heart (afib, stasis due to decreased EF are risk factors)
187
Arterial occlusion from thrombosis as cause of Mes Isch most common to occur where? greatest risk factor?
occurs in proximal SMA
| atherosclerosis
188
presentation of mesenteric ischemia
severe abd pain out of proportion to physical exam (n/v/diarrhea/bloody stool) and prior episodes of abd pain post eating (intestinal angina)
189
Diagnosis of mesenteric ischemia
| initial test
CXR and CT- reveal bowel wall edema "THUMBPRINTING" and air within bowel wall "PNEUMATOSIS INTESTINALIS"
190
Definitive test for diagnosis mes ischemia
Mesenteric/CT angiography: gold standard for diagnosis of arterial occlusive disease
191
Conventional angio allow for ______ for mes ischemia
therapeutic intervention of thrombosis/embolism
192
```
Treatment of mes ischemia
for all:
for acute thrombosis/embolism:
for venous thrombosis:
for infarcted bowel:
```
for all: fluid resuscitation, broad spectrum abx
acute thrombus/embolism: anticoag and laparotomy or angioplasty
venous thrombosis: anticoag
infarcted bowel: surg resection
193
complications of mes ischemia
sepsis/shock, multisystem organ failure, death
194
most common cause of acute lower GI bleeding in patients > 40 years of age?
Diverticulosis
195
Diverticula
moist common where?
outpouching of mucosa and submucosa (FALSE diverticula)
Sigmoid colon
196
diverticulitis
inflammation and generally microperf of diverticula 2ndary to a fecolith impaction
197
should you perform sigmoidoscopy in initial stage of diverticulitis?
no! risk of perf
198
iron def in elderly is ____ until proven otherwise
colon cancer
199
compare SBO/LBO history
SBO-copious emesis!
| LBO- pain less intense than SBO. less n/v than SBO but typically feculent
200
compare exam SBO/LBO
Both: high-pitched tinkly bowel sounds
and later complete absence of BS
SBO: surgical scars/hernias
201
etiology of SBO/LBO
SBO: hernia, adhesions from surg, volvulus, intussuception, gallstone ileus, foreign body, crohn, CF, hematoma, neoplasm
LBO: colon cancer!, diverticulitis, volvulus, fecal impactin, benign tumor (always assume colon cancer until proven otherwise)
202
Ogilvie syndrome
pseudo-obstruction
203
Water contrast enema should be done when?
to help diagnose LBO- if perf is suspected
204
treatment for LBO
obstruction can be relieved with gastrografin enema, colonoscopy, rectal tube but surgery is usually required. ischemic colon requires partial colectomy with diverting colostomy.
205
Patient found to have aortic endocarditis with strep bovis. what is next diagnostic step?
colonscopy! association between strep bovis and colon cancer.
206
ulcerative colitis or crohn disease more likely to get colon cancer?
ulcerative colitis
207
rank adenomatous polyps from most concerning to least
villious > tubular; sessile > pedunculated
208
Treatment for colon cancer
surgical resection. adjuvant chemo when lymph node +
209
how do you track colon cancer recurrence?
CEA levels, colonoscopy, LFTs, CXR, abdominal CT
210
Ischemic colitis usually affects what location?
left colon. watershed area at splenic flexure
211
risk factor for ischemic colitis?
atherosclerosis
212
presentation of iscemic colitis
crampy lower abd pain followed by bloody diarrhea after meals or exertion in heat. fever and peritoneal signs suggest bowel necrosis
213
Initial test for diagnosis of ischemic colitis
CT scan with contrast (thickened bowel wall and atherosclerosis0
214
Colonscopy for ischemic colitis will show
pale bowel wall with petechial bleeding
215
If first degree relative with colon cancer, how does screening change?
Colonscopy every 5 years starting at age 40 or every 5 years starting 10 year prior to affected family member at their time of diagnosis
216
Screening for colon cancer if you have ulcerative colitis?
colonoscopy every 1-2 years starting 8-10 years after diagnosis
217
Tx for ischemic colitis
supportive therapy with bowel rest, IV fluids, broad spectrum abx
surgical resection for infarction, fulminant colitis, obstruction
218
One unit of packed RBCs increases Hgb by? Hct by?
Hgb by 1. Hct by 3-4.
219
How to diagnose upper GI bleed?
NG tube and lavage (can be - in 15% upper GI bleeds)
endoscopy is definitive diagnosis
220
How to diagnose lower GI bleed?
Rule out upper GI hemorrhage with NG lavage if brisk.
Anoscopy/Sigmoid for patients < 45 with small amount of bleeding
Colonscopy if stable
Ateriography or ex-lap if unstable
221
Initial management of GI bleed
Protect airway (intubation may be needed), stabilize patient with IV fluids and packed RBCs (hct may be normal early on)
222
Inguinal hernia
protrusion of abdominal contents (usually small I) into inguinal region through a weakness or defect in abdominal wall (direct or indirect)
223
Direct hernias lie _____ and indirect hernias lie _____ to inferior epigastric vessels
MDs Dont LIE
224
Hesselbach triangle is an area bounded by?
inguinal ligament, inferior epigastric artery, rectus abdominus
225
Indirect hernia location
Lateral to epigastric vessels. through both external and internal rings.
226
indirect hernia etiology
patent processus vaginalis
227
what is more common- indirect or direct hernia?
indirect!
228
direct hernia location
medial to epigastric vessels. herniation through floor of hesselbach triangle
229
etiology of direct hernia?
mechanical breakdown in transversalis fascia resulting from age
230
femoral hernia location
herniation below inguinal ligament through femoral canal, below and lateral to pubic tubercle
231
etiology of femoral hernia
increased intra abdominal pressure, weakened pelvic floor (more common in women)
232
primary sclerosing cholangitis is associated with?
ulcerative colitis and crohns
233
Pseudopolyps on colonscopy are found in?
ulcerative colitis
234
diagnosis of chrons requires
upper GI series with small bowel follow through
235
colonoscopy of crohns may show
stellate ulcers, strictures, "cobblestoning" and "skip lesions" and "creeping fat" during laparotomy
236
Treatment for UC
5-ASA agents (sulfasalazine, mesalamine) topical or oral corticosteroid for flare ups
immunomodulators (azathioprine) or biologics (infliximab) for refractory or mod disase
237
treatment for crohns
5 ASA agents (mesalamine sulfasalazine)
steroid for flare
biologics (infliximab)
238
black pigmented gall stones result from
hemolysis
239
brown pigmented gall stones result from
infection
240
most gallstones are precipitations of cholesterol and are not _______
radioopaque
241
Labs in cholelithiasis
normal total bili, alk phos, serum amylase
242
treatment for symptomatic cholelithiasis
elective cholecystecomy
243
Labs in cholecystitis
increased WBC, normal t.bili, alk phos, amylase
244
diagnosis of cholecystitis
US, HIDA scan
245
If patient is too ill to undergo cholecystectomy when they have cholecystitis what do you do?
transcutaneous drainage of gall bladder
246
cholelithiasis
transient stone in cystic duct
247
cholecystitis
inflammation of gallbladder due to stone occluding cystic duct
248
choledocholithiasis
stone in CBD (jaundice, RUQ pain)
249
labs for choledocholithiasis
normal or increased WBC.
Increased t.bili
Increased alk phos
possible increased amylase/lipase
250
cholangitis
infection of CBD usually due to stone in CBD
251
Presentation of cholangitis
charcot triad: RUQ pain, fever, jaundice
| Reynolds pentad: shock and altered mental status
252
labs for cholangitis
increased WBC, total bili, alk phos
253
diagnosis and management of cholangitis
clinical dilation confirmed by biliary dilation on imaging or ERCP (ERCP also therapeutic). surgery if patient toxic
254
choledocolithiasis management
ERCP to remove stone followed by cholecystectomy.
255
Findings on ultrasound to diagnose cholecystitis
Stone in gall bladder, bile sludge, pericholecystic fluid, thickened gall bladder wall, gas in wall of gall bladder, ultrasonic murphys sign
256
When ultrasound is equivocal for cholecystitis next step?
HIDA scan
257
treatment for cholecystitis
broad spectrum antibiotics and IV fluids
| cholecystectomy
258
Treatment for acute cholangitis
patients often need ICU admission for monitoring, hydration, BP support, broad spec abx
259
Patients with acute suppurative cholangitis require emergent _____
bile duct decompression via ERCP sphincterotomy, percutaneous transhepatic drainage, open decompression
260
subacute SBO in elderly woman is classic for?
gallstone ileus
261
CXR with characteristics of SBO and pneumobilia (gas in biliary tree) is specific for?
gallstone ileus
262
In patients with gallstone ileus, upper GI barium contrast images will demonstrate _______
no contrast in the colon
263
Tx of gallstone ileus
laparotomy with stone extraction. closure of fistula. cholecystectomy
264
What percent of hep C patients will develop chronic Hep C?
70-80%
265
Most common causes of acute hepatitis?
HAV, HBV, HCV, HDV, HEV and drugs (alcohol, acetaminophen, INH, methyldopa)
266
Fulminant hepatitis
Acute liver failure. Liver injury with INR > 1.5 and hepatic encephalopathy and patient has no signs of underlying chronic liver disease
267
Most common causes of chronic hepatitis?
HCV, HBV (world-wide), alcohol, autoimmue, Wilson disease, Hemochromatosis, A1AT
268
If you have increased alk phos and bili without ducatal dilation of CBD what should you think about?
intrahepatic cholestatsis due to medications, post-op complications, sepsis
269
How does acute hepatitis initially present?
nonspecific viral prodrome (malaise, fever, joint pain, fatigue, URI, n/v, changes in bowels)
Next jaundice and RUQ tenderness
270
Self-limited acute phase viral hepatitis?
HAV and HEV
271
Presentation of chronic hepatitis
can be asymptomatic. may also cause fatigue and muscle/joint pain. jaundice and compications of portal htn (hepatic encephalopathy, ascites, esophageal varices)
272
Diagnosis of acute hepatitis
Labs reveal markedly elevated ALT and AST and bili/alk phos
273
Diagnosis of chronic hepatitis
ALT and AST are mildly elevated or can be normal low.
274
What pathology should you think about with isolated unconjugated hyperbilirubinemia?
Overproduction- hemolytic anemia
Defective conjugation - Gilbert (<5)
Crigler-Najjar
275
Pathology for elevated conjugated bili?
defective excretion from liver - Dubin Johnson and Rotor syndrome
276
Transmission of HAV and HEV
fecal-oral
277
Transmission of HBV, HCV, HDV
Body fluid
278
Which hepatitis can cause a more severe co-infection with HBV? And is actually dependent on HBV surface antigens
HDV
279
Which type of Hep has a high mortality rate in preg women and may become chronic in immunosuppressed patients?
HEV
280
What type of Hep is most likely to lead to fulminant hepatic failure? What type of Hep is most likely to become chronic?
Hep B ; Hep C
281
Diagnostic studies for work up of acute hepatitis?
Viral hep serologies
Autoimmune hepatitis
Hemochromatosis
Wilson disease
282
Autoimmune hepatitis lab studies
(+ ANA and anti-smooth muscle antibodies (type 1). anti liver-kidney microsomal-1 antibodies and anti liver cytosol antibodies (type 2). also elevated serum IgG and p-ANCA
283
Hemochromotosis labs will show
elevated ferritin and transferrin saturation > 50%. Liver biopsy with high hepatic iron index.
284
Wilson disease
decrease ceruplasmin, increase urine copper, keyser-fleischer rings. liver biopsy if uncertain about diagnosis
285
Sequela of chronic hep?
cirrhosis, portal htn, liver failure, hepatocellular carcinoma
286
treatment of acute hep B
generally supportive. may require antivirals
287
Chronic hepatitis treatment of HBV
Tenofovir and entecavir
288
Chronic HCV treatment
meds and treatment vary based on genotype, cirrhosis status, history of prior treatment
(either 2 direct acting antivirals or 1 DAA plus ribavirin) Interferon is used occasionally.
289
Definitive treatment for patients with end stage liver failure?
Liver transplant
290
Cirrhosis
bridging fibrosis and nodular regeneration resulting from chronic hepatic injury
291
most common causes of liver cirrhosis?
alcohol, chronic HCV, non-alcoholic steatohepatitis (causes can be intrahepatic or extrahepatic)
292
Extrahepatic causes of cirrhosis
biliary tract disease (primary biliary cirrhosis, primary sclerosing cholangitis)
293
posthepatic causes of cirrhosis
right sided heart failure, constrictive pericarditis, budd chiari syndrome
294
budd chiari syndrome
hepatic vein thrombosis 2ndary to hypercoagulability
295
How is SBP diagnosed?
>250 PMNs in ascitic fluid
296
Diagnosis of cirrhosis
synthetic dysfunction tests: decreased albumin, elevated PT/INR, elevated bili
portal htn: thrombocytopenia (2ndary to hypersplenism sequestration in liver and decreased thrombopoetin production), varices, ascites (paracentesis)
297
Definitive test for cirrhosis?
biopsy showing bridging fibrosis and nodular regeneration
298
How do you determine the etiology of ascites?
SAAG = serum albumin - ascites albumin
299
Etiologies for SAAG > 1.1
Portal htn:
Presinusoidal: splenic or portal vein thrombosis, schistosomiasis, mass effect.
Sinusoidal: cirrhosis
Postsinusoidal: RHF, budd-chiari, constrictive pericarditis
300
Etilogies for SAAG < 1.1
Nephrotic syndrome
TB
Malignancy (ovarian cancer)
301
Presentation and treatment of SBP
fever, abd pain, chills, nausea, vomiting
tx: IV abx (3rd gen cephalosporin)
IV albumin, prophylaxis with fluoroquinolone to prevent recurrence. SBP- poor 1 year prognosis
302
hepatorenal syndrome
acute prerenal failure in setting of severe liver disease. due to splanchinic vasodilation and reduced blood flow to kidneys. Urine Na will be less than 10mEq/L
303
Treatment for hepatorenal syndrome?
trial of volume repletion and rule out other causes of renal failure. can use octreotide to decrease splanchnic vasodilation and midodrine to increase blood pressure. may need dialysis. poor prognosis. liver transplant is curative
304
Surveillance and treatment of esophageal varices
EGD surveillance in cirrhosis patients
Med prophylaxis with B-blockers or endoscopic band ligation
for acute bleeding: EGD with band ligation or sclerotherapy. Urgent TIPS procedure if refractory
305
For acute bleeding due to coagulopathy what should you give?
FFP.
306
Will vit K correct coagulopathy?
NO
307
Primary sclerosing cholangitis is strongly associated with?
Ulcerative colitis
308
primary sclerosing cholangitis
idiopathic disorder- progressive inflammation and fibrosis strictures of extrahepatic and intrahepatic bile ducts. usually presents in young men with UC
309
Primary sclerosing cholangitis patients are at increased risk for?
cholangiocarcinoma
310
How do patients with primary sclerosing cholangitis present?
Jaundice, prutitis, fatigue
311
diagnosis of primary sclerosing cholangitis?
Alk phos, bili elevated. MRCP/ERCP shows bile duct strictures and dilatations "beads on a string"
312
Liver biopsy of primary sclerosing cholangitis reveals?
"onion skinning"
313
all newly diagnosed primary sclerosing cholagitis patients should have what other test?
colonoscopy to assess for IBD
314
treatment for PSC
dilation and stenting of biliary strictures with ERCP
| Liver transplant is definitive treatment
315
Primary biliary cirrhosis. presents in?
autoimmune disease characterized by destruction of intrahepatic bile ducts. most commonly found in middle-aged women with other autoimmune conditions
316
how do patients with PBC present?
progressive jaundice, pruritis, fat soluble vitamin deficiencies (ADEK)
317
Diagnosis of PBC
Lab: elevated alk phos, elevated bili, + antimitochondrial antibody, elevated cholesterol
318
Tx of PBC:
Ursodeoxycholic acid (slow progression of disease)
Cholestyramine for pruritis
liver transplant- definitive
319
PBC affects _____ ducts while PSC affects _____ and ______ ducts.
Intrahepatic ;
Intra and extra hepatic
320
Non-alcoholic fatty liver disease
steatosis of hepatocytes -> can progress to NASH -> liver fibrosis -> cirrhosis
321
Non-alc fatty liver disease is associated with?
Insulin resistance, metabolic syndrome
322
Tx for non-alc fatty liver?
weight loss, diet, exercise.
NASH: vitamin E and pioglitazone
323
Hepatocellular carcinoma Incidence
Risk factors in US/ Worldwide
One of most common cancers worldwide. Low incidence in US.
U.S risk factors: cirrhosis (alc, HCV, NASH) and chronic hep B even without cirrhosis.
WW: HBV and aflatoxins (in food sources)
324
Presentation of patients with hepatocellular carcinoma?
RUQ tenderness, abd distension, jaundice, easy bruisability, coagulopathy, enlargement of liver
325
Dx of hepatocellular carcinoma
mass on US or CT, abnml LFTs, significantly elevated AFP. Biopsy needed if uncertain about diagnosis.
326
Tx for hepatocellular carcinoma
Surgical: partial hepatectomy. orthotopic (liver removed and transplant placed in same place in body) liver transplant if only a few small tumors
327
Milan criteria
help decide treatment for hepatocellular carcinoma (single lesion <5cm or 3 lesions less than 3cm) - can perform orthotopic transplant
328
hemochromatosis
iron overload. hemosiderin accumulates in liver, pancreas islet cells, heart, adrenals, testes, pituitary.
329
primary hemochromatosis vs 2ndary
1: autosomal recessive disease characterized by mutations in HFE gene- result in excessive absorption of iron
2: patients receiving chronic transfusion therapy (sickle cell disease or alpha thalassemia)
330
how might patients with hemochromatosis present?
abd pain, DM, hypogonadism, arthropathy of MCP joints, heart failure, impotence, cirrhisis, bronze skin pigmentation, CHF, hepatomegaly, testicle atrophy
331
dx of hemochromatosis:
increase serum iron, percent saturation of iron and ferritin
decreased transferrin
liver biopsy, MRI, HFE genetic mutation screen
332
A transferrin saturation (serum iron / TIBC) > 45% is suggestive of?
iron overload
333
Tx hemochromatosis
weekly phlebotomy to normalize serum iron. Then maintenance phlebotomy every 2-4 months
Deferoxamine- iron chelating agent
334
Deferoxamine
iron chelating agent useful for iron toxicity or hemochromatosis
335
Wilson disease
AR disorder. defective Cu transport. Accumulation of Cu in Liver and brain. Occurs in patients < 30 yoa. 50% symptomatic by 15.
336
Presentation of wilson disease
hepatitis/cirrhosis, neuro dysfunction (ataxia, tremor), psych abnormalities (psychosis, anxiety, depression, maina)
337
PE of wilson disease
kayser-fleischer rings, jaundice, hepatomegaly, asterixis, choreiform movements, rigidity
338
Dx of wilson disease
Liver biopsy for uncertain diagnosis. low ceruloplasmin. elevated 24 hour urine Cu excretion.
339
Tx: wilson disease
penicillamine or trientine (copper chelators that increase urinary copper excretion)
dietary copper restriction: no shellfish, liver, legumes
340
hallmark finding in pancreatic cancer
non-tender, palpable gall bladder with jaundice
341
Insulinoma is associated with?
MEN type 1
342
hx of patient with insulinoma
hypoglycemia satisfying Whipple Triad
1. hypoglycemia on venipuncture
2. ass symp- sweating, palpitations, anxiety, tremor, HA, confusion
3. resolution of symp w/ correction of hypoglycemia
343
Dx of insulinoma
lab: elevated fasting serum insulin. elevated c-peptide
344
definitve test for insulinoma
72 hour fasting (profound or symptomatic hypoglycemia after fast)
345
What screen should you always do in patients presenting with hypoglycemia?
sulfonyurea abuse check
346
VIPoma
highly malignant tumors
| watery diarrhea, dehydration, muscle weakness, flushing
347
dx VIPoma
stool sample: low stool osmotic gap (secretory diarrhea)
Lab: high VIP, achlorhydria (gastrin inhibited by VIP), hyperglycemia, hypercacemia, hypokalemia
CT: localize tumor
348
Pancreatic cancer- most common type? most common location?
75% are adenocarcinoma in head of pancreas
349
risk factors for pancreatic cancer
smoking, chronic pancreatitis, first degree relative with panc cancer
350
presentation of panc cancer
abd pain radiating to back, obstructive jaundice, loss of appetite, n/v, weight loss, weakness, fatigue
usually asymptomatic so presents late in disease course
351
Courvoisier sign
non-tender palpable gallbladder- PANC CANCER
352
Trousseau sign
migratory thrombophlebitis
353
Diagnosis panc cancer
CT scan with contrast.
Endoscopic ultrasound plus/minus ERCP if nothing seen on CT
354
Tumor marker for pancreatic cancer that is neither sensitive nor specific?
CA 19-9
355
Grey Turner Sign
Flank bruising indicative of acute pancreatitis
356
Cullen Sign
periumbilical discoloration indicative of acute pancreatitis
357
Diagnosis of acute pancreatitis
elevated lipase, amylase. decreased calcium if severe.
358
"sentinel loop" or "colon cutoff sign"
signs on CXR- indicative of acute panc
359
Ranson criteria
predict mortality secondary to acute pancreatitis
