Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

STEP2 > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

Common causes of viral gastroenteritis

A

Norwalk (cruise), Coxsackivirus (summer), Echovirus (summer), Adenovirus (conjunctivitis), Rotavirus (foul-smelling greenish diarrhea)

Mostly self- limited and they get better on their own

n/v/d/abd pain, cramping, myalgia, low-grade fever

Labs: no fecal white blood cells, viral cultures

Treatment: maintain hydration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Bacterial gastroenteritis: Bacillus cereus

A 
Bacillus cereus (fried, reheated rice)
vomiting within several hours of eating

Treatment: maintain hydration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Bacterial gastroenteritis: campylobacter jejuni

A

poultry
2nd most common food-borne bacterial GI infection
bloody or watery diarrhea

rare association with Guillain-Barre syndrome

Treatment: usually self- limiting, so try rehydration and maybe azithromycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Bacterial gastroenteritis: clostridium botulinum

A

honey, home- canned foods
n/v/d
flaccid paralysis
don’t allow children

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Bacterial gastroenteritis: C. Diff

A

antibiotic- induced suppression of normal colonic flora “superinfection”

watery or bloody diarrhea

pseudomembranous colitis

Treatment: metronidazole, vancomycin (oral, because Po stays in the GI tract)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Bacterial gastroenteritis: E. Coli (enterotoxigenic)

A

travelers’ diarrhea
contaminated food and water
watery diarrhea, vomiting, fever

Treatment: often self- limited, hydration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Bacterial gastroenteritis: E. Coli (enterohemorrhagic, O157:H7)

A 
undercooked ground beef 
bloody diarrhea
vomiting, fever ,abdominal pain
Hemolytic uremic syndrome
-thrombocytopenia
-hemolytic anemia
-acute renal failure

Treatment: hydration and supportive care

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Bacterial gastroenteritis: staph aureus

A

room-temperature food
it’s the premade toxins that make you sick

Vomiting within hours of eating
Diarrhea
treatment: hydration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Bacterial gastroenteritis: Salmonella

A 
Food-borne
-egg salad at picnic
-poulty, milk, fresh produce
-nausea, abd pain
-bloody diarrhea
-Treatment: hydration
The disease is usually self- limited

fluoroquinolones if immunocompromised or very ill

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Bacterial gastroenteritis: Shigella

A

food or water-borne
overcrowding
“bacterial dysentery”
fever, nausea/vomiting, severe bloody diarrhea, abdominal pain

HUS
Treatment: hydration
We do use antibiotics here:
fluoroquinolones (ciprofloxicin)
TMP-SMX
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Bacterial gastroenteritis: vibrio cholerate

A 
"rice water" diarrhea
seafood
abd pain, watery diarrhea, within 24 hours of eating
treatment- hydration
Tetracycline or doxycycline
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Bacterial gastroenteritis: Vibrio parahaemolyticus

A

seafood (oysters)
abd pain
watery diarrhea within 24 hours of eating
treatment: hydration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Bacterial gastroenteritis: yersinia

A

pork, produce, puppy feces
abd pain, bloody diarrhea, RLQ pain
Treatment: hydration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Parasitic and protozoan GI infections: giardia lamblia

A

surface water
greasy, foul- smelling diarrhea
abd pain, malaise
cysts and trophozoites in the stool

Treatment: metronidazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Parasitic and protozoan GI infections: entameoba histolytica

A

water-borne
areas of poor sanitation
mild to severe bloody diarrhea

abd pain
cysts and trophozoites in stool
liver abscess

Treatment: metronidazole, paromomycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Parasitic and protozoan GI infections: Cryptosporidium

A 
food or water-borne
immunocompromised patients
watery diarrhea, abd pain, malaise
acid fast stain- parasites in stool
Treatment- nitazoxanide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Parasitic and protozoan GI infections: trichonella

A

undercooked pork
fever, myalgias, periorbital edema
eosinophilia
CNS and cardiac symptoms also may occur

this is a bendy work
Treatment: albendazole, mebendazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Parasitic and protozoan GI infections: Taenia solium

A

undercooked pork
mild diarrhea
CNS symptoms

Call it “taeniasis” if the adult is carrying the tapeworm in the gut

If the person ingests eggs, then these lead to cyst formation in the muscles (cysticercosis) and brain (neurocysticercosis)

Treatment:
praziquantel (GI)
albendazole + corticosteroids (CNS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Food poisoning as a result of mayonnaise sitting out too long

A

staphylococcus aureus, salmonella

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Rice- water stools

A

vibrio cholerae, enterotoxigenic e. coli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

diarrhea transmitted from pet feces

A

yersinia enterocolitica

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

food poisoning resulting from reheated rice

A

bacillus cereus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

MCC “Traveler’s diarrhea”

A

enterotoxigenic e.coli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Diarrhea after a course of antibiotics

A

c. difficile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

diarrhea and recent ingestion of water from a stream

A

giardia lamblia

entamoeba histolytica

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

mild intestinal infection that can become neurocysticercosis

A

taenia solium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

food poisoning from undercooked hamburger

A

enterohemorrhagic e. coli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

diarrhea from seafood

A

vibrio species

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

bloody diarrhea from poultry

A

salmonella, campylobacter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

diarrhea and pink eye

A

adenovirus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

bloody diarrhea leading to liver abscess

A

entamoeba histolytica

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

diarrhea in an AIDS patient

A

cryptosporidium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

dehydrated child with greenish diarrhea in winter months

A

rotavirus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Treatment for entamoeba histolytica

A

metronidazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Treatment for giardia lamblia

A

metronidazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Treatment for salmonella

A

fluoroquinolones only if pt is immunocompromised or very ill

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Treatment for shigella

A

fluoroquinolones, TMP-SMX

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Treatment for campylobacter

A

erythromycin, but this is usually self- limited

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

How long does hepatitis last before we call it chronic?

A

6 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

risk factors for viral hepatitis

A

IV drug use
alcoholism
travel to developing countries
poor sanitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

history and physical consistent with hepatitis B

A 
asymptomatic
or
malaise, arthralgias, fatigue
nausea/vomiting
RUQ pain
jaundice, scleral icterus
hepatomegaly, splenomegaly
lymphadenopathy
Labs:
bilirubin
increased AST
increased ALT
(roughly equally elevated)
increased bilirubin
increased alk phos
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

hepatitis A diagnostic labs

A

Anti-HAV IgM abs
-present during illness

Anti-HAV IgG abs

  • after illness has resolved
  • present with vaccination
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

HBsAg

A

active disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

HBcAb

A

history of active disease
IgM rises early
IgG rises late

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

HBeAg

A

active viral replication, high transmissibility

HBeAb signifies low transmissibility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Hep A

characteristics of the virus

A

ssRNA
spread by fecal- oral route
food/shellfish

treatment: self-limited, supportive care

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Hep B

A

dsDNA
spread by blood, sexual contact

Treatment: hep B vaccine, IFN-gamma

Prevention: hep B vaccine

Complications: chronic hepatitis, cirrhosis, hepatocellular carcinoma
persistent carrier state
fulminant hepatic failure

Extrahepatic manifestations: polyarteritis nodosa (vasculitis of medium and small- sized arteries), glomerular disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

polyarteritis nodosa

A

vasculitis of medium and small- sized arteries

fever
weakness
rash
joint pain
erythematous nodules

associated with hep B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

glomerular disease

A

membranous nephropathy
rarely, membranoproliferative GN (hep B or hep C), proteinuria

adults>children

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Hep C

A

ssRNA
spread via blood
treat: IFN-alpha, ribavirin

there is no vaccine

complications: 
chronic hepatitis
cirrhosis, hepatocellular carcinoma, persistent carrier state
extrahepatic manifestations:
membranoproliferative GN
essential mixed cryoglobinemia
lymphoma
thyroiditis
porphyria cutanea tarda
lichen planus
DM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Hep D

A

disabled, requires co-existant hep B in order to be infectious

Treatment: IFN-alpha
prevention: Hep B vaccine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Hep E

A

spread by facal-oral route, contaminated waters

treatment: self- limited, supportive care
complications: pregnant women

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Sialolithiasis

A

obstructed salivary gland by a stone

swelling, pain with eating

Tx: warm compresses, massage, sour candy, surgery (remove the stones)

antibiotics if infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Sjogren syndrome

A

inflammatory disorder that can affect the salivary glands.
Dry mouth, dry eyes (sicca complex)
diminished secretions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is the most common neoplasm affecting the salivary glands

A

pleomorphic adenoma, benign

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

MC site for sialic neoplasm

A

parotid gland, which can also be a site of extra-pulmonary sarcoidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Dysphagia

A

difficulty or abnml swallowing
(oropharyngeal/transfer disfunction= difficulty initiating swallo)

(esophageal phase is the 2nd phase of the swallow)

Causes: achalasia, scleroderma, food impaction
peptid strictures, cancer, esophageal webs/rings, radiation- induced fibrosis, alkaline fluid-induced fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

odynophagia

A

pain with swallowing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Plummer Vinson triad

A

iron def
dysphagia
esoph web

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

feeling of food stuck in throat with swallowing (immediate discomfort)
cough
choking

A

Oropharyngeal dysfuntion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

delayed discomfort dysphagia

A

esophageal dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

dysphagia characterized by difficulty with solids

A

obstructive pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

dysphagia characterized by difficulty with solids and liquids

A

neuromuscular dysmotility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

diagnostic testing for dysphagia

A

BARIUM SWALLOW
esophagogastroduodenoscopy (EGD)
manometry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What anatomical structures in the GI tract are evaluated by the barium swallow?

A

esophagus, LES, stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What anatomical structures in the GI tract are evaluated by the gastric emptying study?

A

stomach, pyloric sphincter, duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What anatomical structures in the GI tract are evaluated by the small bowel follow through (SBFT)

A

stomach to terminal ileum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What anatomical structures in the GI tract are evaluated by the barium enema?

A

appendix to rectum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

complications of NG tube

A

esophageal reflux

pressure necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

complications of percutaneous endoscopic gastrostomy (PEG) tube

A

feeding tube directly into the stomach, can occur at the bedside with proper equipment

open gastrostomy allows the same outcome but with a bigger incision, better for longterm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

complications of gastrostomy tube

A

patient may yank the tube

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

complications total parenteral nutrition (TPN)

A 
nutrition into the veins. 
prefer to use the gut
biostasis
acalculous cholecystitis
venous line is a potential site for infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

laparascopy

A

visualization of the peritoneal cavity using a laparoscope

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

laparotomy or celiotomy

A

surgical incision into the abdominal cavity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

ectomy

A

surgical removal or something

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

achalasia

A

neuromuscular disorder of the esophagus
impaired peristalsis
decreased lower esophageal (LES) relaxation
most commonly affects people 25-60 years old

secondary causes:
Chagas disease
neoplasms
scleroderma

H and P:
gradually progressive dysphagia of solids and liquids
regurgitation
cough
aspiration
heartburn
weightloss

Diagnostics:
Manometry shows increased LES pressure
Incomplete LES relaxation and decreased peristalsis

Barium swallow shows “bird’s beak” sign

Treatment goal is to lower LES pressure
pneumatic dilation
myotomy (open up the muscle)
botulinum toxin injections
nitrates
dihydropyridine CCBs

Order an EGD to rule out malignancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Diffuse esophageal spasm

A

neuromuscular disorder
non-peristaltic contractions of the lower esophagus

H and P:
chest pain
dysphagia for liquids and solids

diagnostic testing: “cork screw” pattern on barium swallow

non-peristaltic contractions on manometry

Treatment:
CCBs, TCAs, nitrates relieve pain but worsen reflux

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Zenker diverticulum

A

outpouching of upper posterior esophagus caused by smooth muscle weakness

immediately above the UES

H and P:
bad breath
difficulty initiating swallowing
regurgitation of food several days after eating
occasional dysphagia
feeling of aspiration

Radiology: barium swallow shows
outpouching of the esophagys

complications:aspiration
squamous cell carcinoma

perforation may occur with endoscopy

Treatment:
crichopharyngeal myotomy
diverticulectomy via external neck incision

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Traction diverticulum- where in the esophagus is it found?

A

between UES and LES

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Where is the epiphrenic diverticulum found

A

above the LES

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

GERD

A

Caused by a lower esophageal sphincter that transiently and intermittently relaxes

Stomach contents reflux back into the esophagus

Risk factors:
obesity
hiatal hernia
pregnancy
scleroderma
H and P:
burning chest pain 30-90 minutes after eating
sour taste in mouth
regurgitation
dysphagia
nausea
cough

symptoms worsened by consumption of alcohol or fatty foods, or after lying down

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

GERD- diagnostic testing

A

upper endoscopy with biopsy to evaluate for reflux or other causes
ambulatory pH monitoring to confirm acid reflux
manometry can be used to monitor for dysphagia due to neuromuscular dysfunction
CXR to assess for neoplasm
barium swallow can show peptic stricture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

GERD treatment

A

elevation of the head of the bed
weight loss- avoid carbonated bevereges
dietary modifications

Antacids:
calcium carbonate
aluminum hydroxide
milk of magnesia
these neutralize stomach acid quickly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

H2 blockers

A

Famotidine, ranitidine, cimetidine

These should be used on select occasions in patients who do not respond to antacids. They should be used in anticipation of reflux (delayed onset of action, longer duration of action).

Reversibly block H2 receptors to inhibit gastric acid secretion

Side effects: 
headache
diarrhea
thrombocytopenia
gynecomastia and impotence (cimetidine)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Proton-pump inhibitors (PPIs)

A

omeprazole, lansoprazole

given to patients who don’t response well to H2 blockers

well-tolerated, but block CYP450 enzymes
irreversibly inhibit the parietal cell proton pump (H/K ATPase) to block gastric acid secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Promotility agents in GERD

A

metoclopramide is an example, no longer recommended for GERD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

GERD treatments that are safe in pregnancy

A

antacids, PPIs, H2 blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

How do we treat refractory GERD?

A

Nissen fundoplification

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

GERD complications

A 
Esophageal ulceration
Esophageal stricture
Barrett esophagus
Adenocarcinoma
Reflux- induced asthma
Laryngeal disorders
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Esophageal cancer: 2 major types

A

Squamous cell carcinoma (more common worldwide)

Adenocarcinoma (more common in the US, less common worldwide)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Barrett’s esophagus

A

intestinal metaplasia of the distal esophagus secondary to chronic GERD

increases risk of adenocarcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Risk factors for esophageal cancer

A 
alcohol
tobacco
chronic GERD
obesity (adenocarcinoma)
nitrates
preserved meats
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

H and P for esophageal cancer

A 
progressive dysphagia
weight loss
odynophagia
reflux
GI bleeding
vomiting
weakness
cough, hoarseness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Esophageal cancer diagnostic studies

A

barium swallow
EGD (biopsy is what makes the diagnosis)

MRI, CT, PET scan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Esophageal cancer treatment

A

surgical resection
radiation and chemotherapy (non-operative and advanced cases)
neoadjuvant therapy to surgery
poor prognosis because it has often extended by the time it is diagnosed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Mallory- Weiss syndrome

A

longitudinal mucosal laceration in the distal esophagus and proximal stomach, minor injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Boerhaave syndrome

A

perforation or rupture in the distal esophagus, tears all layers of the esophagus; life-threatening

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

chest pains, uncoordinated contractions, corkscrew pattern on barium swallow

A

diffuse esophageal spasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

inability to relax the LES; bird’s beak on barium swallow

A

achalasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

bad breath, regurgitation of food eaten days ago

A

Zenker diverticulum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Common symptoms of GERD

A

persistent cough

heartburn

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Which is associated with ischemia- sliding hiatal hernia or paraesophageal hiatal hernia?

A

paraesophageal hiatal hernia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

What is gastritis

A

inflammation of the gastric mucosa, acute (erosive) or chronic (non-erosive), related to NSAIDs, alcohol, corrosive materials, h. pylori, stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Where is B12 absorbed?

A

terminal ileum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

How do we diagnose H. Pylori?

A

urea breath test
antral biopsy
serum h.pylori antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Gastritis treatment

A

stop alcohol or offending medications
H2 blocker or PPI
Vit B12 (type A)
Treat h. pylori (type B): PPI, clarythromycin, amoxicillin or metronidazole for 7-14 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Peptic ulcer disease: Gastric ulcer

A

Patients tend to be older,
H. pylori +
chronic NSAID users

25% if ulcers

pain occurs soon after eating due to acid produced to process food; eating worsens the pain and leads to n/v

normal or low gastric acid level

+/- high gastrin level

eating may cause n/v as well

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Peptic ulcer disease:duodenal ulcers

A

Patients:
younger
+H.Pylori

75% of ulcers

pain occurs 2-4 hours after eating

eating improves pain initially, but the pain then worsens

normal or low gastrin level
there may be nausea or vomiting

patient tends to be thinner than patients with other types of ulcers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

Ulcer associated with severe burn

A

Curling’s ulcer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

Ulcer associated with intracranial injuries

A

Cushing’s ulcers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

Zollinger- Ellison syndrome

A

increased gastrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

What findings on barium swallow are suggestive of cancer?

A

abnormal appearing mucosal folds in the region near the ulcer

Mass near ulcer

Irregular filling defects in ulcer base

Biopsy 4 quadrants around the ulcer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

Treat a peptic ulcer

A
  1. rule out active bleeding: CBC, EGD, Stool guiac
  2. decrease gastric acid levels
    PPI
    H2 antagonist
  3. protect mucosa
    Sucralfate
    Bismuth subsalicylate
    Misoprostol
  4. Treat H. Pylori: PPI, Amoxicilin or metronidazole, clarithromycin
  5. Surgery
    -perforation repair
    -parietal cell vagotomy
    -antrectomy
  6. COX2 inhibitors (still have some gastric side effects)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

complications of peptic ulcer

A

hemorrhage
perforation
lymphoproliferative disease

115
Q

Zollinger-Ellison syndrome

A

gastrin- producing tumor in the duodenum or pancreas

refractory PUD
abdominal pain
n/v
indigestion
diarrhea
steatorrhea
other endocrine abnormalities
  1. Labs:
    fasting gastrin level (>1000)
    secretin stimulation test (secretin induces a steep rise in gastrin levels in patients who do have ZE)
  2. Radiology
    CT or MRI to look for the tumor
    Endoscopic ultrasound to look for small pancreatic tumors
    Somatostatin receptor scintigraphy can localize tumors
    Angiography can be used to look for the tumor if it is hypervascular
  3. Treatment:
    Surgical resection
    PPI (stop before gastrin testing to get an accurate reading)
    H2 antagonist
    Octreotide
    If you must pick between PPI and octreotide, then pick PPI
116
Q

Gastric cancer subtypes

A
  1. ulcerating (this is why we biopsy the area around all gastric ulcers)
  2. polypoid
  3. superficial spreading
  4. linitis plastica, involving all layers of the stomach
117
Q

Gastric cancer risk factors

A 
H. Pylori
Family history
Japanese person living in Japan
Tobacco use
Alcohol use
Vit C deficiency
Preserved foods (nitrosamines)
Males>females
118
Q

Gastric cancer H and P

A

weight loss, anorexia, early satiety
vomiting, dysphagia, epigastric pain
left supraclavicular node: Virchow’s node
periumbilcal node (Sister Mary Joseph node)

Labs:
increased CEA

Radiology: barium swallow
EGD to visualize ulcers

Treatment:
subtotal gastrectomy in the distal third
Total gastrectomy for lesions in the middle or upper part of the stomach

Adjuvant chemotherapy and radiation

Prognosis >70% if early detection

119
Q

Surgical therapy for obesity

A

malabsorption and restriction
sustained weightloss- 30-50%
reduction or cure of DM, HTN, OSA, mortality overall

depression and suicide increase in the first year after surgery, so pre-opping is extensive

120
Q

complications of surgical therapy for obesity

A 
nutritional deficiencies
iron
b12
folate 
thiamine
vit D
GERD
Dumping syndrome: bloating, swelling, steatorrhea, diarrhea
121
Q

Most effective treatment of a duodenal ulcer not due to cancer?

A

H. Pylori triple therapy

PPI
Amoxicillin
Clarithromycin (metronidazole if pt allergic to clarithromycin)

122
Q

Subtotal gastrectomy

A

subtotal if cancer in the distal 1/3 of the stomach: subtotal gastrectomy

Total gastrectomy if cancer in the middle or upper stomach

add on adjuvant chemo and radiation as needed

123
Q

Branching rods, oral infection, what bacteria is this?

A

actinomyces israelii

124
Q

How does malabsorption present?

A

weight loss, bloating, diarrhea, steatorrhea, glossitis, dermatitis (zinc deficiency), edema (protein malabsorption)

125
Q

Where is ethanol absorbed?

A

stomach

126
Q

Celiac sprue

A

reduced absorptive capacity from duodenum and jejunum
Labs:anti-tissue transglutaminase antibody
antiendomysial antibody
antigliadin ab no longer considered reliable

definitive diagnosis via biopsy of duodenum +/- jejunum looking for blunting of the villi

H and P:
FTT, bloating, abnormal stools
diarrhea, steatorrhea, weight loss

5% of Down syndrome patients have this

Associated with dermatitis herpetiformis

Treatment:
removal of gluten (wheat, barley, rye) from the diet

Refractory disease may require corticosteroids

127
Q

Tropical sprue

A

similar presentation to celiac sprue, but the autoantibody tests would be negative and removing gluten from the diet will not have any benefits

occurs in patients who have spent time in the tropics, may present years after leaving the tropics

Megaloblastic anemia

Treatment: folic acid replacement
tetracycline, sulfa drugs

128
Q

Lactose intolerance

A

lactase deficiency
lactose goes straight to the colon when it is not metabolized, drawing water into the colon, causing osmotic diarrhea

flatulence, bloating, abdominal pain, diarrhea

Treatment: remove lactose from the diet and supplement calcium

129
Q

Whipple disease

A

bacterial infection with tropheryma whipplei

RF:white, european ancestry

H and P: abdominal pain
diarrhea
weight loss
arthralgia
wasting
endocarditis
pleural effusions
abdominal distention from ascites or adenopathy
vision abnormalities
dementia

Labs:
jejunal biopsy- foamy macrophages on PAS stain, villous atrophy
PCR

Treatment:
1. IV ceftriaxone
2. TMP-SMX
continue treatment for 12 months to prevent relapse

130
Q

Sudan stain

A

if you suspect fat malabsorption
bacterial overgrowth
pancreatic insufficiency

131
Q

D-xylose

A

if you suspect carbohydrate malabsorption

PO radiolabelled D-xylose, then
blood and urine are tested. Low levels suggest impaired carb absorption (poor absorption)
Pancreatic insufficiency would be expected to show normal levels of D-xylose

Meanwhile, normal sudan stain but high D-xylose might indicate lactase deficiency

132
Q

Schilling test

A

B12 malabsorption

Stage 1: give radiolabeled B12 by itself and see if it is absorbed by detecting it in the urine or the serum

If it is present in high amounts, malabsorption may be due to absent IF or diminished terminal ileum absorption

Stage 2: B12 is administered with intrinsic factor
If B12 is absorbed in the second stage, then IF is probably the problem

If B12 is not absorbed in the second stage, then the problem is likely the terminal ileum, or maybe the problem is bacterial overgrowth

antibiotics or pancreatic enzymes are given in some versions of the Schilling test to further characterize the cause of malabsorption

133
Q

Acute diarrhea

A
134
Q

chronic diarrhea

A
  1. inflammatory
    - autoimmune disorders
    - Crohn disease
    - Ulcerative colitis
    - Chronic infection
  2. fatty
    - pancreatic insufficiency
    - Whipple disease
  3. watery
    -osmotic
    celiac sprue
    tropical sprue
    lactose intolerance
    excess sorbitol
    lactulose
    milk of magnesia
-secretory
irritable bowel syndrome
laxative abuse
enterotoxic bacteria
hormone-mediated (VIPomas, gastrinomas, medullary thyroid cancer, carcinoid tumors)

treatment:ileum resection
history and physical:
FOBT, CBC, metabolic panel, lactose- restricted diet
sudan stain, D-xylose test, stool electrolytes
osmotic gap125= osmotic

colonoscopy with possible biopsy (malignancy, inflammatory bowel disease?)

135
Q

The formula for stool osmotic gap

A

290-2(Na+K)= stool osmotic gap

136
Q

Pediatric diarrhea

A

infection

  • rotavirus (winter)
  • adenovirus (plus conjunctivitis)

antibiotic use
-macrolides

immunosuppression

137
Q

What is the cut-off in osmotic gap for secretory diarrhea

A
138
Q

What is the cut-off in osmotic gap for osmotic diarrhea

A

> 125

139
Q

Which tumors can cause diarrhea due to hormone excess

A

carcinoid tumor
VIPoma
gastrinoma
medullary thyroid cancer

140
Q

most common food-borne bacterial GI infections in the US

A

campylobacter

salmonella

141
Q

IBS

A

idiopathic, women more than men, related to stress

abdominal pain
diarrhea
constipation
bloating
nausea
mild abdominal tenderness
urinary frequency
urinary urgency
symptoms of fibromyalgia
142
Q

What are the Rome diagnostic criteria for IBS?

A

recurrent abdominal pain/discomfort at least 3 days per month in the last 3 months associated with at least 2 of the following:
1. relief with defecation
2. onset associated with a change in frequency of stool
3. onset associated with a change in form of stool
important to rule out other causes

143
Q

What are the subtypes of IBS?

A

IBS with diarrhea
IBS with constipation
Mixed IBS
IBS unsubtyped

144
Q

What symptoms are NOT c/w IBS alone?

A 
anorexia
weight loss
malnutrition
progressively worsening pain
pain that prevents sleep
rectal bleeding
145
Q

What lab findings are NOT consistent with IBS alone?

A

electrolyte disturbances
anemia
increased inflammatory markers

146
Q

What imaging is helpful in ruling out other diagnoses when you are considering IBS?

A

abdominal x-ray
abdominal CT
barium studies

147
Q

Treatment for IBS

A 
physician assurance
no higher rate of malignancy
goal is to improve symptoms
eat a high-fiber diet
avoid gas-producing foods
avoid lactose and gluten

possible psychotherapy

Constipation predominant:
fiber and hydration, polyethylene glycol

Diarrhea predominant:
anti-diarrheals
TCAs
SSRIs

Treat abd pain and bloating with
antispasmodics
antidepressants

funtional disorder

148
Q

IBD

A

inflammatory disease

Crohn
Ulcerative colitis

149
Q

Crohn symptoms

A

fatigue
abdominal pain
weight loss
watery diarrhea

PE: 
fever
RLQ abdominal mass
Abdominal tenderness
Perianal fissures and fistulas
Oral ulcers
Features:
transmural inflammation
skip lesions
most commonly affects the distal ileum
"gum to bum"

Imaging:
Transmural inflammation and strictures
String sign (not much lumen in some areas)
Skipped areas of bowel

  1. Barium study with small bowel follow-through
  2. Colonoscopy: granulomas, colonic ulcers
Complications:
malabsorption
fissures
fistulas
strictures
obstruction
abscess formation

Treatment for Crohn disease:

  1. steroids +/- abx for acute exacerbations
  2. azathioprine or mercaptopurine> methotrexate
  3. anti-TNF-alpha agents (infliximab, adalimumab)

Medical management preferred over surgical resection, as surgery is not curative

distal ileum classically involved
mouth to anus with multiple skip areas in between
entire thickness of bowel wall is affected

150
Q

distinguishing features of Crohn disease

GIFTS

A

distal ileum classically involved
mouth to anus with multiple skip areas in between
entire thickness of bowel wall is affected

Granulomas
Ileum
Fistula and fissures 
Transmural
Skip lesions
151
Q

Ulcerative colitis

A 
fatigue
abdominal pain
diarrhea
weight loss
fecal urgency
tenesmus
incontinence
bloody diarrhea
PE:
fever
abdominal tenderness
gross blood on rectal exam
orthostatic hypotension
tachycardia

continuous disease of the colon
perianal inflammation
Colonoscopy would show continuous involvement, pseudopolyps, friable mucosa

barium enema would show lead pipe colon, colonic shortening

Complications: hemorrhage, toxic megacolon, perforation

Longterm complications: strictures leading to obstruction
and dysplasia leading to colon cancer

Treatment: topical treatment with suppositories and enema preferred to oral treatment

start with aminosalicylate (mesalamine), then move on to oral glucocorticoids, immunosuppressive agents, supplemental iron

Total colectomy is curative as long as there is no dysplasia

152
Q

Extraintestinal manifestations of IBD

A 
arthritis
ankylosing spondylitis
erythema nodosum
pyoderma gangernosum
uveitis
primary sclerosing cholangitis
153
Q

Serologic markers for IBD

A

ASCA:anti-saccharomyces cerevisiae abs often positive in Crohn

pANCA- perinuclear anti-neutrophil cytoplasmic antibodies, often positive with UC

154
Q

Bowel obstruction- common causes

A

Adhesions (from previous surgeries ~75% of cases)
Bulge- incarcerated hernia (second most common cause)
Cancer (most commonly metastatic colorectal cancer)

Other less common causes:
volvulus, intussusception, Crohn disease, gallstone ileus, bezoar (organic sediment gets impacted in the small bowel), bowel wall hematoma from trauma, inflammatory stricture, congenital malformation, radiation enteritis

155
Q

What are the classic signs and symptoms of SBO?

A

abdominal pain and tenderness
n/v
+/- recent flatus/ small BM
hyperactive high- pitched bowel sounds

diagnosis: dilated loops of small bowel proximal to the obstruction seen on plain film abdominal series or CT scan of the abdomen

156
Q

What is the treatment for SBO?

A

NPO, IV fluids, monitor electrolytes, Foley catheter to monitor urine output

NG tube to low intermittent wall suction (LIWS) especially if the patient has severe intermittent nausea and vomiting

Partial obstruction might just need bowel rest

Complete might need surgery

Hospital observation with frequent reassessments +/- repeat CT scan

Avoid pain medication if possible, which may interfere with identification of disease worsening, but treat pain

Surgery (laparotomy and lysis of adhesions) if:
no improvement in 12-24 hours
complete SBO
suspected, impending, or ongoing strangulation

157
Q

What is the most common benign small bowel tumor?

A

leiomyoma

158
Q

WHat is the most common malignant small bowel tumor?

A

carcinoid

159
Q

Large bowel obstruction common causes:

A

neoplasm
adhesions
volvulus
diverticulitis

radiology:
bowel distention proximal to the obstruction

treatment:
NPO, maintain hydration, colonoscopy, surgery if necessary

160
Q

ischemic colitis

A

ischemia of the colon secondary to vascular compromise

embolus
bowel obstruction
hypotension
medication
surgery

RF: diabetes, atherosclerosis, PVD, lupus

presents with 
acute abdominal pain
bloody diarrhea
vomiting
mild abdominal tenderness
pain out of proportion to exam

Barium enema- thumbprint sign 2/2 diffuse submucosal changes from localized bleeding

Sigmoidoscopy- bloody and edematous mucosa

CT- air within the bowel wall- pneumotosis coli, maybe bowel- wall thickening

Treatment: IV fluids, bowel rest, antibiotics, surgical resection of necrotic bowel

Complications: high mortality rate if irreversible damage

161
Q

Appendicitis

A

inflammation with possible perforation of appendix

common clinically

lymphoid hyperplasia, more often seen in children

fibroid bands, fecalith

H and P:
dull periumbilical pain that migrates to the RLQ
n/v/anorexia

Tenderness at McBurney’s Point (2/3 of the way between umbilicus and ASIS)

Rebound tenderness due to peritoneal irritation

Psoas sign- pain on passive extension

Rovsing sign- RLQ pain with LLQ palpation

Obturator sign- RLQ pain on passive internal rotation

Severe pain, distention, rebound tenderness, rigidity, guarding, high fever, hypotension, shock

Labs: CBC with left-shift
UA- increased WBC, cystitis, UTI

162
Q

What radiological studies can be used to diagnose appendicitis?

A

CT scan with oral contrast
CT scan with rectal contrast +/- IV contrast
CT scan without contrast (fast, higher rate of false neg, but better than no CT scan)
Plain radiograph for fecolith
Ultrasound for pelvic pathology in women

Don’t wait so long for imaging that the appendix perforates

163
Q

Treatment for appendicitis

A

Pain control: Morphine or meperidine PCA

Antibiotic administration for mild to moderate inpatient:

  • Ampicillin/sulbactam (Unasyn)
  • Piperacillin/tazobactam (Zosyn)
  • Ticarcillin/clavulanate (Timentin)
  • Levofloxacin + metronidazole
  • Ciprofloxacin + metronidazole

Antibiotic administration for severe ICU patient:

  • Ampicillin + levofloxacin + metronidazole
  • Imipenem/cilastatin (Primaxin)
  • Meropenem

If presentation within 24-72 hours of symptom onset, then proceed with surgical removal of appendix by laparoscopy or open appendectomy

If symptoms present for more than 5 days and pain is specifically in the RLQ, then antibiotics, IVF, bowel rest–> interval appendectomy about 8 weeks later

If abscess on CT scan, then percutaneous drainage (interventional radiology)

164
Q

Ileus

A

paralytic obstruction of small bowel secondary to decreased peristalsis

infection, ischemia, recent surgery, DM

typically less than 5 days. small bowel recovers first (

165
Q

Gallstone ileus

A

gallstone impacted in ileum after passing through biliary-enteric fistula

subacute, episodic obstruction in elderly woman with vague, recurrent abdominal pain and vomiting that recurs as the stone repeatedly lodges and dislodges

Average time from symptom onset to hospitalization- 5 days

166
Q

Volvulus

A

abnormal rotation of bowel
obstruction, ischemia

double bubble sign on xray
due to air trapped both distal and proximal to the volvulus

barium enema may show bird’s beak at distal volvulus as well

Treatment:
sigmoidoscopy, colonoscopy for decompression, contra-indicated if gangrene due to risk of perforation

If the bowel is gangrenous or sigmoid/colonoscopy is unsuccessful, then laparoscopic resection of the affected colon and colostomy

Once corrected, the recurrence in 40-60% of patients can be prevented with one of the following:

  • mesosigmoidopexy
  • resection with primary anastomosis
  • Hartmann’s procedure (proximal colostomy + stapling but not removal of the distal segment)
167
Q

Diverticulosis

A

outpouchings, may erode and cause bleeding, may become inflammed and infected

RF: low- fiber, high fat diet
being older

H and P:
occasional cramping
bloating
flatulence
irregular defecation
painless rectal bleeding

MCC lower GI bleed in patients > 40 yo

Mild LLQ pain relieved with defecation

Radiology: irregular outpouchings
Colonoscopy can also visualize diverticulosis

Treatment: do not limit seeds, nuts, popcorn

Complications: diverticulitis, GI bleeds

168
Q

Diverticulis

A

infection of diverticulum that can lead to necrosis or perforation

H and P:
LLQ pain
older patient
fever

Labs: increased WBC count with or without left shift

CT scan: increased soft- tissue density in the affected area due to inflammation. You will see bowel wall thickening, and possible abscess formation

Treatment: outpatient
bowel rest
fluoroquinolone + metronidazole

TMP-SMX + metronidazole
Amoxicillin- clavulanic acid

169
Q

When is inpatient admission for diverticulitis treatment indicated?

A 
elderly
immunocompromised
significant comorbidities
high fever with significant leukocytosis
unable to tolerate oral intake
170
Q

What are the steps in inpatient management of diverticulitis

A
  1. IV fluids
  2. broad- spectrum empiric antibiotics (similar to appendicitis)
  3. If there are signs of peritonitis (guarding, tenderness), then sent the patient for emergency exploration through midline incision
171
Q

What are the complications of diverticulitis?

A

Colonic abscesses
fistulas
sepsis

172
Q

Hemorrhoids

A

dilated veins
internal- superior rectal veins, above the pectinate line, painless

external- inferior rectal veins, painful if thrombosed

sigmoidoscopy
colonoscopy
anoscopy

Anal exam for fistulas, lesions

Treatment: warm baths, high fiber diet, avoid prolonged straining, sclerotherapy, ligation, surgical excision

173
Q

Anal fissure

A

spasm of rectal sphincter may result

treatment:
1. stool softeners + hydration
2. topical nitroglycerin
3. diltiazem, nifedipine, bethanechol
4. botulinum toxin injection
5. sphincterotomy, which carries 10-30% risk of incontinence

174
Q

Anorectal abscess

A

infection of anal crypts, hair follicles
H and P:
throbbing rectal pain, fever, tenderness on DRE

Treatment:
Antibiotics
I and D

175
Q

Rectal fistula (aka fistula in ano)

A

A tract between rectum and adjacent structures from unknown cause or 2/2 ischemic bowel

H an P:
mild pain during defecation
visible site draining pus

Treatment:
fistulotomy

176
Q

Pilonidal disease

A

1 or more curaneous tracts in the midline gluteal cleft

H and P:
asymptomatic
painful cysts
abscesses

Treatment:
I and D
Sterile packing with changing
Surgical closure of sinus tract

177
Q

Carcinoid tumors

common sources, sites, features

A

serotonin-secreting tumor, mc arising from ileum, bronchopulmonary tree, appendix, rectum

MC GI site is the small i (ileum)

H and P:
asymptomatic, because the serotonin gets processed in the liver

abdominal pain

Be FDR
Bronchospasm (10-20%)
Flushing (85%)
Diarrhea (80%)
Right- sided valvular disease/murmurs

Treatment:
Somatostatin analog octreotide helps shut down serotonin

Other drugs that can be used for symptom relief:
cyproheptadine for diarrhea and/or anorexia

Albuterol and/or theophylline for asthma symptoms

Codeine and/or cholestyramine for diarrhea

If symptoms are refractory to octreotide, give IFN-alpha combined with ocretotide

Surgical resection in certain circumstances of isolated tumors

Valvular surgery for symptomatic carcinoid heart disease

Labs:
you might see an increase in urine 5-HIAA
increased serum serotonin

178
Q

The biggest risk factor for colon cancer

A

presence of colon polyps, especially the adenomatous ones

179
Q

Risk factors for developing colon cancer

A 
adenomatous colon polyps
hereditary polyposis syndromes
family history
previous colon cancer
ulcerative colitis and Crohn's disease
low fiber/ high-fat diet
alcohol
smoking 
diabetes
180
Q

Familial adenomatous polyposis

A

hundreds of polyps in the colon due to mutated APC gene
Treatment: prophylactic subtotal colectomy (this requires a colostomy bag, so wait until after high school)

If a patient has an APC gene mutation, you can start doing colonoscopies at a young age

181
Q

Gardner syndrome

A

APC mutation
colon polyps
osteomas
soft tissue tumors

182
Q

Turcot syndrome

A

APC gene mutation
colonic adenomas
CNS tumors

183
Q

Juveile polyposis

A

polyps in colon, small bowel, stomach

Hamartoma, which is an excess amount of normal tissue (not adenomas, so the polyps don’t become tumors, but they can be a source of GI bleeding)

184
Q

Peutz-Jeghers syndrome

A

Hamartomas in the GI tract

pigmented lesions on lips and oral mucosa

185
Q

Hereditary Non-polyposis Colorectal Cancer (HNPCC)

A

Colon cancer arising from normal- appearing mucosa
without forming polyps

Neoplasms form in the proximal colon (distal is more common)

186
Q

How does colon cancer present?

A

distal colon leads to change in bowel habits

left colon changes leads to thinned stool caliber
There may be hematochezia or melena
Iron deficiency anemia (right- sided cancer)
Weakness, fatigue
Weightloss

Labs:
positive stool guaiac test
anemia
increased CEA *not specific but can be used to monitor response to therapy/ recurrence

Radiology:
apple-core lesion seen on barium enema
colonoscopy
CT 
PET

Treatment:
take out the cancer and at least 12 nodes

187
Q

How do we stage colon cancer? what characterizes stages 3 and 4?

A

node involvement: stage III, involves chemotherapy

met’s beyond nodes: stage IV

188
Q

Colon cancer post- treatment surveillance

A

CEA every 3 months for 3 years
CT chest/abdomen/pelvis every year
Colonoscpoy at 1, 3, 5, years

189
Q

Colon cancer screening for avg risk patient

A

For the average patient, after age 50

  • fecal occult blood test annually with guiac (samples from 3 consecutive stools is ideal)
  • Colonoscopy every 10 years
  • or, flex sig, which goes up to the splenic flexure, with double- contrast barium enema to see proximal to the splenic flexure BOTH every 5 yrs
  • CT colonography is not currently used for screening because it does not have adequate sensitivity and specifiticy, followed by colonoscopy if anything is seen
  • screening should stop when a patient’s life expectancy is less than 5 years (or at age 75, whichever comes first)

Screen more frequently if you find polyps

190
Q

Disadvantages to flex sig

A

contrast enema requires that the patient take in contrast from above and below, and also tolerate air in the colon

Flex sig done without conscious sedation

Better visualization with colonoscopy than with flex sig

191
Q

Hematochezia- bright red blood in the stool

A

lower GI bleed
rapid or heavy bleed

could be an upper GI bleed if it is a severe upper GI bleed

192
Q

Melena- dark blood

A

upper GI or proximal small bowel blood

193
Q

Coffee ground emesis

A

blood that has been sitting in the stomach for some time

194
Q

Causes of upper GI bleed

A 
peptic ulcer disease
Mallory- Weiss tears
esophagitis
esophageal varices
gastritis
195
Q

Causes of lower GI bleed

A

Diverticular disease (most common cause of lower GI bleed in anyone over 40yo)
Neoplasms
Ulcerative colitis
Mesenteric ischemia
AV malformations
Hemorrhoids
Meckel diverticulum (bleeding 2/2 acid secretion into the ileum)

196
Q

imaging of choice for lower GI bleed

A

colonoscopy

197
Q

imaging of choice for upper GI bleed

A

EGD

198
Q

Where does the EGD end

A

duodenum

199
Q

Where does a colonoscopy stop?

A

terminal ileum

200
Q

What can you do to visualize the part of intestine that lies between duodenum and terminal ileum?

A

capsule endoscopy, which sends pictures to a received

201
Q

Tagged RBC scan

A

tagged technetium helps localize bowel bleed to quadrant, helpful for intermittent bleeds

202
Q

Relevant radiology for GI bleeds

A

EGD- upper GI bleeds
Colonoscopy- lower GI bleeds
Capsule endoscopy
Tagged RBC scan
Angiography- would miss an intermittent bleed
Meckel scan- just for Meckel diverticulum

203
Q

Management steps for GI bleed

A
  1. H and P
  2. Continuous monitoring of vital signs
  3. obtain IV access with 2 large bore IVs (18 gauge in both arms) or central line
    4, Volume and rescuscitation with NS or LR as needed
  4. type and cross 2 U PRBC
  5. Labs:CBC, coags (guaiac stool if necessary, to confirm blood)

Treat and determine the cause

  1. NG tube to rule out massive upper GI bleed
  2. If colonoscopy is nondiagnostic and not feasible (too much active bleeding may obscure visualization), and bleeding persists, then radionucleotide scan and/or angiogram
204
Q

How does history of colon cancer in a first degree relative affect screening?

A

Start at 40 years of age, or 10 years before the age the relative was diagnosed- whichever comes first

205
Q

The 3 most common causes of acute pancreatitis

A

gallstones
chronic alcohol use
idiopathic

206
Q

acute PANCREATITIS causes

A 
hyperParathyroidism
Alcohol
Neoplasm (backed up enzymes)
Cholelithiasis
Rx (drugs- HIV drugs and sulfa drugs)
ERCP (backflow)
Abdominal surgery
hyerTriglyceridemia
Infection (mumps)
Trauma
Idiopathic 
Scorpion sting

pathophysiology:leakage of pancreatic enzymes into surrounding tissue

increased serum lipase and amylase on labs, though these are not prognostic indicators. Lipase is more specific than amylase

207
Q

Ranson criteria

A 
total 11 values
5, assessed at admission at GA LAW
Glucose >200mg/dK
AST>250 IU/L
LDH> 350 IU/L
Age>55 yo
WBC> 16,000/mL

6 assessed after 48 hours:
CALvin and HOBBeS

Calcium10%
pO2 4mg/dL
BUN increase >5mg/dL
Sequestration of fluid > 6L

0-2: 0-3% mortality
3-5: 11-15% mortality
6-11: > 40% mortality

208
Q

H and P findings c/w acute pancreatitis

A 
acute epigastric pain
n/v
Cullen sign: periumbilical ecchymosis
Grey Turner sign: ecchymosis of flank
Tachycardia
Hypotension
Shock- the pt may need fluids

Check labs for Ranson criteria and for elevated amylase

Upright AXR may show Sentinel loop (dilated loop of bowel)

  • elevated hemidiaphragm
  • the right colon may be distended until you get to the pancreas “colon cut-off” sign
  • pleural effusion

CT scan is most sensitive:
-enlarged, inflamed pancreas
-pseudocyst
US-gallstone

209
Q

Treat pancreatitis

A

aggressive hydration
NPO
NGT to suction
correct electrolytes
opioids for pain control
morphine causes sphincter of Odi to spasm (meperidine is therefore preferred)
NJ tube for feeding (nasojejunum, so as not to stim the stomach)
TPN
prophylactic abx
debridement
cholecystectomy if they have gallstones causes pancreatitis
ERCP (remove the stones, or this can cause pain, so weight risk and benefits)

210
Q

Complications of acute pancreatitis

A 
pancreatic abscess
pseudocyst
pancreatic necrosis
fistulas
renal failure
chronic pancreatitis
hemorrhage
shock 
DIC
sepsis
respiratory failure

treat patients before they get quick

211
Q

Chronic pancreatitis causes

A

almost always due to alcoholism

recurrent

212
Q

Chronic pancreatitis signs and symptoms

A 
recurrent epigastric pain
steatorrhea
weight loss
nausea
constipation

Labs: mildly increased amylase and lipase
low fecal elastase (most specific and sensitive test for chronic pancreatitis)

Xrays and CTs:
pancreatic calcifications
enlarged pancreas
pseudocyst
MR-CP pancreatic duct
213
Q

Chronic pancreatitis treatment

A 
stop alcohol use
stop smoking
opioids
pancreatic enzymes
vitamin supplements
small, low-fat meals
surgical repair of ductal damage
214
Q

Complications of chronic pancreatitis

A 
ductal obstruction
pseudocyst
malnutrition
glucose intolerance
pancreatic cancer
215
Q

Pancreatic pseudocyst- what is it?

A

enzyme-rich fluids contained in a sac of inflamed membranous tissue

lined with granulation tissue and fibrous tissue, filled with pancreatic juice

usually asymptomatic
incidental finding
epigastric pain
fever

Labs: elevated WBC and amylase

On aspiration, the cyst contents also hold a lot of amylase

216
Q

Treatment of pancreatic pseudocyst

A

often resolves on its own
drain for diagnosis
debridement or percutaneous drainage if the cyst persists over 4 weeks

217
Q

Pancreatic pseudocyst complications

A

rupture
abscess
hemorrhage
pseudoaneurysm (digests vessels so that they bleed into the cyst)

218
Q

Exocrine pancreatic cancer

A

The most common kind
adenocarcinoma
usually in the head of the pancreas, where the bulk of pancreatic tissues lies

Risk factors:
chronic pancreaitis
diabetes
family history
tobacco use
high- fat diet
male>female
obesity
sedentary lifestyle
abdominal pain with radiation to the back
anorexia
nausea/vomiting
weight loss
jaundice
Signs and symtoms:
palpable, nontender gallbladder
-courvoisier sign
-splenomegaly
-palpable deep abdominal mass

Pancreatic adenocarcinoma tumor markers
CEA
CA 19-9

increased bilirubin and increased phosphatase with biliary obstruction

CT abdomen: mass at the head of the pancreas will be visible
ERCP to locate

Endoscopic ultrasound

Treatment:

  1. resection (whipple procedure)
  2. adjuvant chemotherapy
  3. pancreatic enzymes
  4. stenting (this would be a palliative measure)

Pancreatic adenocarcinoma- complications:
death, with 1 yr survival less than 2%

Trousseau syndrome: migratory thrombophlebitis classically associated with pancreatic adenocarcinoma

219
Q

Trousseau syndrome

A

migratory thrombophlebitis classically associated with pancreatic adenocarcinoma

220
Q

Gastrinoma- stomach tumor

A

Gastrin- secreting glandular tumors that cause Zollinger- Ellison syndrome

221
Q

Insulinoma

A

insulin-secreting beta-cell tumor that causes hypoglycemia

Labs: increased fasting insulin
elevated C-peptide (produced when the insulin is made)

CT or US can help, but these tumors are often difficult to locate

Treatment: surgical resection
Diazoxide, which reduces insulin release
Octreotide

222
Q

Glucagonoma

A

glucagon- secreting alpha-cell tumor that causes hyperglycemia

Elevated glucagon, presents with refractory diabetes

may present with necrolytic migratory erythemarash, erythematous plaques on the face, perineum, extremities

Treatment: surgical resection if you can localize the tumor

  • surgical resection
  • octreotide
  • IFNalpha
  • embolization

Frequently malignant

223
Q

Necrolytic migratory erythema

A

uncommon presentation of glucagonoma

rash, erythematous plaques on the face, perineum, extremities

224
Q

VIPoma

A

tumor that produces vaso-active intestinal peptide, which leads to watery diarrhea

usually non-beta islet cells

labs: increased serum VIP
high stool osmolality

Treatment: 
hydration and electrolyte replacement
surgical resection
steroids
chemotherapy
octreotide
embolization
225
Q

Risk factors for cholelithiasis

A 
fat
fertile
female
forty
family history
Also, 
OCP use
TPN
rapid weightloss

most gallstones are made of cholesterol, calcium, and bilirubin

H and P:
pain worse after fatty meals, which cause the gallbladder to contract
n/v
indigestion
flatulence
RUQ tenderness to palpation

Dx: see gallstones on ultrasound
cholesterol stones don’t show up on xray or CT; bile stones might

Tx:
low-fat diet
bile salts
lithotripsy
cholecystectomy

complications:
more stones
cholecytitis
pancreatitis

226
Q

acute cholycystitis

A

inflammation of the gallbladder

Usually, a gallstone obstructs the cystic duct, leading to infection and inflammation behind the obstruction

227
Q

Acalculous choecystitis

A

patients on TPN
critically ill patients
inflammation, without obstruction

228
Q

Murphy sign

A

inspiration stopped by pain when you put your hand over the RUQ

positive test consistent with cholecystitis

229
Q

H and P c/w cholecystitis

A 
RUQ radiating to back
n/v
fever
palpable gallbladder
\+Murphy sign

Labs:
increased WBC
increased bilirubin and alk phos

Radiology
Ultrasound: gallstones, thickened gallbladder wall, sludge in the gallbladder, sonographic Murphy sign (Murphy sign elicited with an ultrasound probe), HIDA scan (detects obstruction of the cystic duct)

230
Q

What is a HIDA scan (cholescintigraphy)?

A

technectium- labeled hepatic iminodiacetic acid given IV, taken up by hepatocytes, excreted into bile for visualization of gallbladder

Inability to visualize the gallbladder with this test indicates cystic duct obstruction, usually from acute cholecystitis or an obstructing stone

231
Q

How do we treat cholecystitis?

A

hydration
antibiotics
wait 24-48 hours, then proceed to cholecystectomy

Use ERCP to inject solvent if you can’t stabilize the patient for surgery

232
Q

Cholangitis

A

infection of the bile duct, usually due to bile duct obstruction

RUQ pain, chills, jaundice, fever (Charcot triad)

Labs: biliary obstruction
increase AST, ALD, amyplase
increased WBC count
increased bilirubin
increased alk phos

Radiology: ultrasound ok, HIDA scan is preferred test (HIDA accumulates in the liver, and then depending on where the obstruction is, it might fill the gallbladder, or fill the gallbladder and not be able to empty)

Treatment: 
hydration
IV antibiotics
endoscopic biliary drainage
delayed cholecystectomy
233
Q

Charcot triad- cholangitis

A

RUQ pain
jaundice
fever

cholangitis until proven otherwise

234
Q

Reynolds pentad, cholangitis

A

Charcot triad (RUQ pain, fever, jaundice) + AMS and hypotension or shock

235
Q

Gallbladder cancer

A

Adenocarcinoma of the gallbladder

a/w cholilithiasis, biliary tract disease, chronic infection

poor prognosis
Symptoms:
pain
jaundice
palpable gallbladder

Labs:
elevated bilirubin
elevated alk phos

Porcelain (calcified) gallbladder, while more suggestive of chronic cholecystitis, is cancer 10-30% of the time.

Treatment: 
cholecystecomy
lynph node dissection
removal of adjacent hepatic tissue
radiation and chemo
236
Q

Why do we always do cholecystecomy on porcelain gallbladder?

A

Porcelain (calcified) gallbladder, while more suggestive of chronic cholecystitis, is cancer 10-30% of the time.

237
Q

Primary biliary cirrhosis

A
  • autoimmune disease that destroys the intrahepatic bile ducts (cholesterol, bile acids)
  • more common in women
  • associated with autoimmune diseases
238
Q

What physical exam and lab findings would lead you to suspect primary biliary cirrhosis as a diagnosis?

A

Usually women (95% of patients) between ages 30-65

Fatigue and pruritis are the most common presenting symptoms

  • excessive daytime somnolence
  • pruritis often starts during pregnancy and then not relieved postpartum
  • patients are often initially referred to a dermatologist for pruritis and excoriations are common

Skin changes:

  • hyperpigmentation due to melanin deposition, xerosis, dermatographism (wheal where you write on them)
  • xanthelasma (cholesterol- filled plaques on the medial aspects of the eyelids bilaterally and/or xanthomata

Hepatomegaly that progressively worsens +/- splenomegaly

Malabsorption and steatorrhea from less bile acid secretion

In late stages, cirrhosis, jaundice, ascites, edema, portal hypertension

Labs:

Elevated alk phos, elevated GGT, elevated direct and indirect bilirubin (in late disease), elevated cholesterol

Elevated serum antimitochondrial antibodies (AMA), in >95% of patients: qhallmark finding of PBC

Elevated antinuclear antibodies (ANA) in 70%

Associated conditions: osteoporosis, osteomalacia, other autoimmune disorders (thyroiditis/hypothyroid, sicca syndrome, scleroderma, Sjogren syndrome, arthritis, Raynaud)

Treatment:
 Ursodeoxycholic acid (UDCA), delays disease progression and enhances survival. The only approved therapy for PBC

Definitive treatment is liver transplantation

239
Q

What laboratory finding is a hallmark of primary biliary cirrhosis?

A

Elevated serum antimitochondrial antibodies (AMA)

240
Q

Primary sclerosing cholangitis

A

progressive destruction of intrahepatic and extrahepatic bile ducts, leading to fibrosis and cirrhosis.

Presents with fatigue, pruritis, hepatomegaly, xanthomas, maybe jaundice if severe

UNLIKE PBC
PSC is more common in men
Associated with ulcerative colitis

Labs: negative ANA
often with + p-ANCA

ERCP shows “beads on a string”

Treatment: transplant

Associated with increased risk of cholangiocarcinoma

241
Q

What condition is associated with cholangiocarcinoma?

A

primary sclerosing cholangitis is associated with cholangiocarcinoma, which is cancer of the bile duct

242
Q

What are some of the possible etiologies of secondary (as opposed to primary) sclerosing cholangitis?

A
  • intraductal biliary stones
  • surgical trauma or blunt abdominal trauma to the biliary tree
  • drugs (IV chemotherapy)
  • recurrent pancreaitis
  • autoimmune pancreatitis
  • AIDs cholangiopathy
243
Q

Gilbert disease

A
  • mild deficiency of UDPGT
  • mild jaundice following fasting, exercise, stress
  • increased indirect bilirubin (
244
Q

Crigler-Najjar syndrome type 1

A 
autosomal recessive
-severe deficiency of UDPGT
present in infancy
-persistent jaundice
-kernicterus

Icreased indirect bilirubin (>5mg/dL)

fatal if untreated

  • phototherapy
  • plasmapheresis
  • liver transplantation
245
Q

Crigler-Najjar syndrome type 2

A

Mildly decreased UDPGT

Mildly elevated indirect bilirubin

Treatment- phenobarbital,
Note, phenobarbital will induce cytochrome p450 as well as production of UDPGT

246
Q

Deep palpation of RUQ leads to arrest of inspiration due to pain

A

Murphy sign

Cholecystitis

247
Q

Charcot triad (fever, jaundice, RUQ pain), hypotension, AMS

A

Reynold’s pentad

Cholangitis

248
Q

RLQ pain on passive extension of the hip

A

psoas sign

appendicitis

249
Q

RLQ pain on passive internal rotation of the flexed hip

A

obturator sign

appendicitis

250
Q

LUQ pain and referred left shoulder pain

A

Kehr’s sign

splenic rupture

251
Q

Ecchymosis of skin overlying the flank

A

acute pancreatitis

252
Q

Ecchymosis of the skin overlying the periumbilical area

A

Cullen sign

acute pancreaitis

253
Q

What are the major stages of liver change due to chronic alcohol use

A
  1. hepatic steatosis (Reversible early on)
  2. steatohepatitis (fat and inflammation)
  3. cirrhosis
254
Q

nonalcoholic steatohepatitis (NASH)

A

mcc: obesity, DM hyperlipidemia, insulin resistance

insulin resistance leads to excess lipid accumulation in the liver

can progress to cirrhosis, lead to hcc, or worsen hep C progression

suspect NASH if chronically elevated LFTs

Diagnose NASH with liver US, CT scan, or MRI

Magnetic resonance spectroscopy (MRS) is the gold standard
liver biopsy can also make the diagnosis, and can be used to identify those at risk for disease progression

Treatment:

  1. avoid all alcohol
  2. weight loss: most likely beneficial, but no proven benefit
  3. Control any diabetes aggressively to keep HbA1C
255
Q

symptoms and signs of alcoholic liver disease

A 
anorexia
n/v
abd tenderness
ascites
splenomegaly

lab: elevated ALT, AST, GGT
unless the liver is so far gone that it doesn’t make enzymes anymore
look for AST>ALT by 2:1 or more

Also, elevated alk phos and bilirubin

Low albumin, prolonged PT and PTT, low triglycerides, LDL, HDL
increased WBC

256
Q

Treat alcoholic liver disease

A 
stop alcohol use
thiamine
folate
high caloric intake
liver transplant (eligible after sober 6 months)
257
Q

Cirrhosis

A 
alcohol
Hep B and C
bile duct obstruction, chronic cholestasis- PBC, PSC
hemochromatosis
Wilson disease 
A1AT deficiency
Non-alcoholic steatohepatitis
autoimmune hepatitis
258
Q

What do hepatocytes do?

A

conjugate bilirubin
synthesize proteins
metabolize toxins

259
Q

What hand finding is associated with alcoholic cirrhosis?

A

Dupuytren contracture

260
Q

How to treat cirrhosis:

A

stop all alcohol even if it isn’t the main problem
lactulose to trap ammonia in the gut
rifaximin to kill of ammonia- producing gut bacteria
liver transplant

261
Q

What are signs and symptoms of Budd- Chiari syndrome, and how does it usually present?

A

thrombosis and occlusion of the hepatic vein or intrahepatic/suprahepatic portion of the IVC

presentation: ascites (84%)
hepatomegaly (76%)
jaundice

acute presentation: acute RUQ pain and hepatomegaly
rapid development of jaundice and ASCITES

subacute or chronic presentation gradual development of ascietes, LE edema, cirrhosis, portal hypertension over a few months

eventual development of liver failure and hepatic encephalopathy

Best initial diagnostic test: US

Gold standard test: hepatic venography

262
Q

How do you diagnose Budd- Chiari?

A

Best initial diagnostic test: US

Gold standard test: hepatic venography

263
Q

How do we treat Budd-Chiari syndrome?

A 
Thrombolytics to dissolve the clot)
Diuretics
Anticoagulation
Angioplasty
Shunting
264
Q

Where do varices form, subsequent to portal hypertension?

A

These varices form due to the need for bypassing blood vessels, around the portal venous system (forming where portal venous system interfaces with the systemic circulation)

  1. esophageal varices
  2. hemorrhoids
  3. caput medusae
  4. renal varices
  5. paravertebral varices
265
Q

Serum- ascites albumin gradient (SAAG)

subtract!

A

measure albumin in the ascites
measure the albumin in the serum

SAAG= serum alb- ascites albumin

266
Q

Significance of SAAG> 1.1

A 
portal hypertension (low albumin in the ascites)
cirrhosis
alcoholic hepatitis
heart failure/ constrictive pericarditis
massive hepatic metastases
Budd- chiari syndrome
267
Q

Significance of SAAG

A

ascites not due to portal hypertension (high albumin in the ascietes, or low serum albumin)
high albumin in the ascites
-peritoneal carcinomatosis (ovarian cancer)
-peritoneal tuberculosis
-pancreatitis
-serositis

low serum albumin
-nephrotic syndrome

268
Q

What if you have high albumin and high LDH on paracentesis?

A

consider cancer as a cause of ascites

do a workup for cancer if this is the case

269
Q

What if you have elevated WBC on paracentesis?

high WBC
high protein
low glucose
LDH higher in ascites than serum

A

consider spontaneous bacterial peritonitis

270
Q

What is the treatment for spontaneous bacterial peritonitis (SBP)?

A
  1. Cefotaxime, ceftriazone, or other third- generation cephalosporin for at least 5 days to cover for gut bacteria (E. coli, klebsiella, and enterococcus), staph, and strep
  2. Give IV albumin because it maintains plasma volume, preserves renal function, and reduces renal impairment and mortality
271
Q

How do we treat portal hypertension?

A
  1. salt restriction and diuretics (spironolactone and furosemide combined each morning)
  2. beta blockers to reduce risk of bleeding (propanolol, nadolol)
  3. vasopressin or sclerotherapy
  4. hepatic shunting
  5. TIPs procedure (trans-jugular intra-hepatic port-caval shunt) which channels through liver to shunt blood from portal to systemic systems. This increases risk of hepatoencephalopathy while relieving varices
272
Q

Hereditary hemochromatosis

A

AR
excess iron absorption, which then gets deposited in the liver, heart, pituitary

H and P:
abdominal pain
polydipsia
polyuria
arthralgias
lethargy
bronze hue of the skin
hepatomegaly
testicular atrophy/impotence related to infiltration of the pituitary
dilated> restrictive cardiomyopathy

Labs: increased iron, increased ferritin, increased transferrin saturation, increased AST, ALT

Bx will help determine extent of damage

Tx:

  • phlebotomy weekly until iron levels normalize
  • avoid excess alcohol consumption
  • deferoxamine

Complications:

  • cirrhosis
  • hcc
  • CHF
  • diabetes
  • hypopituitarism
273
Q

Wilson disease

A

impaired copper secretion
Copper in the brain can yield depression, personality changes, loss of coordination, Parkinsonian-like symptoms like tremor
dysphagia

Copper in the liver:
jaundice
hepatomegaly
cirrhosis

Copper in the cornea:
Kayser- Fleischer rings

Labs: decreased serum ceruloplasmin (binds copper and transports it in the blood)
UNlikely to be Wilson if pt >40

Labs:

  • decreased serum ceruloplasmin
  • increased urinary copper
  • increased AST and ALT
  • liver biopsy with increased copper deposits

Treatment:
trientine and penicillamine as copper chelators
zinc supplements
restrict dietary copper

Vitamin B6 supplements
Liver transplant

complications: fulminant hepatic failure, cirrhosis

274
Q

Alpha1- antitrypsin deficiency

A

panacinar emphysema
liver disease- mutated form of alpha1- antitrypsin, which polymerizes and accumulates in liver cells, toxic to hepatocytes

Co-dominant disorder (homozygous confers early emphysema; heterozygotes might not get lung disease unless they smoke)

labs:
increased AST and ALT

PFTs: obstructive disease
emphysema

Tx: liver transplant, lung transplant if severe

275
Q

Autoimmune hepatitis

A

Autoimmune inflammation of the liver
More common in women than men
Often asymptomatic/subclinical, may result in cirrhosis

2 clinically similar sybtypes:
Type 1 (classic): associated with +ANA and anti-smooth muscle antibodies (ASMA)

Type 2- associated with antibodies against liver- kidney- microsomal (LKM) antibodies or liver cytosol antigens

Treat with glucocorticoids

or glucocorticoids + azathioprine (immunosuppressant)

276
Q

+ANA and anti-smooth muscle antibodies (ASMA)

A

Type 1 autoimmune hepatitis

277
Q

anti- liver- kidney- microsomal (LKM) antibodies or liver cytosol antigens

A

type 2 autoimmune hepatitis

278
Q

Benign hepatic neoplasms

A

hepatic adenomas
focal nodular hyperplasia
hemangiomas
hepatic cysts

These benign liver growths are more common in women who use OCP

Asx unless they get really big, usually found incidentally and don’t need to be treated
Can cause RUQ fullness

279
Q

Hepatic adenoma

A

most often in women ages 20-44 (OCP years)

risk factors: OCP use, anabolic steroids, glycogen storage diseases types I and III

symptoms: +/- RUQ pain, usually asx

10% with malignant transformation

Treatment: discontinue the OCP, serial imaging and AFP, +/- resection (especially if >5cm)

280
Q

What should you do if you see a suspicious liver mass on CT?

A

CT chest/abd/pelvis, since mets are much more common than primary liver tumors

Consider colonoscopy if the patient is at risk or at screening age

281
Q

Hepatocellular carcinoma

A

malignant tumor of hepatic parenchyma

risk factors:
hepatitis B
hepatitis C
cirrhosis
aflatoxin (corn, nuts)
History and physical:
RUQ abdominal pain
weight loss
malaise
anorexia
diarrhea
jaundice
hepatomegaly
bruit over the liver
ascites

Labs:
increased AST, ALT
increased alk phos and bilirubin
increased alpha-fetoprotein

complications: hemorrhage, so biopsy is risky

Treatment: 
surgical resection
chemotherapy
transplant
radiofrequency ablation and chemoembolization if the tumor is unresectable

Complications contd..
liver failure
Budd-Chiari
portal vein obstruction

Paraneoplastic syndromes associated with hcc:

  1. hypoglycemia
  2. excessive RBC production -increased erythropoietin
  3. refractory watery diarrhea
  4. hypercalcemia
  5. various skin lesions
282
Q

Erythropoietin increase may be explained by…

Potentially Really High Hematocrit

A

Pheochromocytoma
Renal Cell Carcinoma
Hemangioblastoma
HCC

283
Q

What’s the most widely-used screening test for hemochromotosis?

A

Ferritin (high)

284
Q

What lab value do you look for with WIlson disease?

A

serum ceruloplasmin (low)

STEP2 (34 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions