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Flashcards in Gastroenterology Deck (284):
1

Common causes of viral gastroenteritis

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

2

Bacterial gastroenteritis: Bacillus cereus

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

Treatment: maintain hydration

3

Bacterial gastroenteritis: campylobacter jejuni

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

4

Bacterial gastroenteritis: clostridium botulinum

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

5

Bacterial gastroenteritis: C. Diff

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)

6

Bacterial gastroenteritis: E. Coli (enterotoxigenic)

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

Treatment: often self- limited, hydration

7

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

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

Treatment: hydration and supportive care

8

Bacterial gastroenteritis: staph aureus

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

Vomiting within hours of eating
Diarrhea
treatment: hydration

9

Bacterial gastroenteritis: Salmonella

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

10

Bacterial gastroenteritis: Shigella

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

11

Bacterial gastroenteritis: vibrio cholerate

"rice water" diarrhea
seafood
abd pain, watery diarrhea, within 24 hours of eating
treatment- hydration
Tetracycline or doxycycline

12

Bacterial gastroenteritis: Vibrio parahaemolyticus

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

13

Bacterial gastroenteritis: yersinia

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

14

Parasitic and protozoan GI infections: giardia lamblia

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

Treatment: metronidazole

15

Parasitic and protozoan GI infections: entameoba histolytica

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

abd pain
cysts and trophozoites in stool
liver abscess

Treatment: metronidazole, paromomycin

16

Parasitic and protozoan GI infections: Cryptosporidium

food or water-borne
immunocompromised patients
watery diarrhea, abd pain, malaise
acid fast stain- parasites in stool
Treatment- nitazoxanide

17

Parasitic and protozoan GI infections: trichonella

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

this is a bendy work
Treatment: albendazole, mebendazole

18

Parasitic and protozoan GI infections: Taenia solium

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)

19

Food poisoning as a result of mayonnaise sitting out too long

staphylococcus aureus, salmonella

20

Rice- water stools

vibrio cholerae, enterotoxigenic e. coli

21

diarrhea transmitted from pet feces

yersinia enterocolitica

22

food poisoning resulting from reheated rice

bacillus cereus

23

MCC "Traveler's diarrhea"

enterotoxigenic e.coli

24

Diarrhea after a course of antibiotics

c. difficile

25

diarrhea and recent ingestion of water from a stream

giardia lamblia
entamoeba histolytica

26

mild intestinal infection that can become neurocysticercosis

taenia solium

27

food poisoning from undercooked hamburger

enterohemorrhagic e. coli

28

diarrhea from seafood

vibrio species

29

bloody diarrhea from poultry

salmonella, campylobacter

30

diarrhea and pink eye

adenovirus

31

bloody diarrhea leading to liver abscess

entamoeba histolytica

32

diarrhea in an AIDS patient

cryptosporidium

33

dehydrated child with greenish diarrhea in winter months

rotavirus

34

Treatment for entamoeba histolytica

metronidazole

35

Treatment for giardia lamblia

metronidazole

36

Treatment for salmonella

fluoroquinolones only if pt is immunocompromised or very ill

37

Treatment for shigella

fluoroquinolones, TMP-SMX

38

Treatment for campylobacter

erythromycin, but this is usually self- limited

39

How long does hepatitis last before we call it chronic?

6 months

40

risk factors for viral hepatitis

IV drug use
alcoholism
travel to developing countries
poor sanitation

41

history and physical consistent with hepatitis B

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

42

hepatitis A diagnostic labs

Anti-HAV IgM abs
-present during illness

Anti-HAV IgG abs
-after illness has resolved
-present with vaccination

43

HBsAg

active disease

44

HBcAb

history of active disease
IgM rises early
IgG rises late

45

HBeAg

active viral replication, high transmissibility

HBeAb signifies low transmissibility

46

Hep A
characteristics of the virus

ssRNA
spread by fecal- oral route
food/shellfish

treatment: self-limited, supportive care

47

Hep B

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

48

polyarteritis nodosa

vasculitis of medium and small- sized arteries

fever
weakness
rash
joint pain
erythematous nodules

associated with hep B

49

glomerular disease

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

adults>children

50

Hep C

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

51

Hep D

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

Treatment: IFN-alpha
prevention: Hep B vaccine

52

Hep E

spread by facal-oral route, contaminated waters

treatment: self- limited, supportive care

complications: pregnant women

53

Sialolithiasis

obstructed salivary gland by a stone

swelling, pain with eating

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

antibiotics if infection

54

Sjogren syndrome

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

55

What is the most common neoplasm affecting the salivary glands

pleomorphic adenoma, benign

56

MC site for sialic neoplasm

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

57

Dysphagia

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

58

odynophagia

pain with swallowing

59

Plummer Vinson triad

iron def
dysphagia
esoph web

60

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

Oropharyngeal dysfuntion

61

delayed discomfort dysphagia

esophageal dysfunction

62

dysphagia characterized by difficulty with solids

obstructive pathology

63

dysphagia characterized by difficulty with solids and liquids

neuromuscular dysmotility

64

diagnostic testing for dysphagia

BARIUM SWALLOW
esophagogastroduodenoscopy (EGD)
manometry

65

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

esophagus, LES, stomach

66

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

stomach, pyloric sphincter, duodenum

67

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

stomach to terminal ileum

68

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

appendix to rectum

69

complications of NG tube

esophageal reflux
pressure necrosis

70

complications of percutaneous endoscopic gastrostomy (PEG) tube

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

71

complications of gastrostomy tube

patient may yank the tube

72

complications total parenteral nutrition (TPN)

nutrition into the veins.
prefer to use the gut
biostasis
acalculous cholecystitis
venous line is a potential site for infection

73

laparascopy

visualization of the peritoneal cavity using a laparoscope

74

laparotomy or celiotomy

surgical incision into the abdominal cavity

75

ectomy

surgical removal or something

76

achalasia

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

77

Diffuse esophageal spasm

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

78

Zenker diverticulum

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

79

Traction diverticulum- where in the esophagus is it found?

between UES and LES

80

Where is the epiphrenic diverticulum found

above the LES

81

GERD

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

82

GERD- diagnostic testing

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

83

GERD treatment

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

84

H2 blockers

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)

85

Proton-pump inhibitors (PPIs)

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

86

Promotility agents in GERD

metoclopramide is an example, no longer recommended for GERD

87

GERD treatments that are safe in pregnancy

antacids, PPIs, H2 blockers

88

How do we treat refractory GERD?

Nissen fundoplification

89

GERD complications

Esophageal ulceration
Esophageal stricture
Barrett esophagus
Adenocarcinoma
Reflux- induced asthma
Laryngeal disorders

90

Esophageal cancer: 2 major types

Squamous cell carcinoma (more common worldwide)
Adenocarcinoma (more common in the US, less common worldwide)

91

Barrett's esophagus

intestinal metaplasia of the distal esophagus secondary to chronic GERD

increases risk of adenocarcinoma

92

Risk factors for esophageal cancer

alcohol
tobacco
chronic GERD
obesity (adenocarcinoma)
nitrates
preserved meats

93

H and P for esophageal cancer

progressive dysphagia
weight loss
odynophagia
reflux
GI bleeding
vomiting
weakness
cough, hoarseness

94

Esophageal cancer diagnostic studies

barium swallow
EGD (biopsy is what makes the diagnosis)

MRI, CT, PET scan

95

Esophageal cancer treatment

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

96

Mallory- Weiss syndrome

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

97

Boerhaave syndrome

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

98

chest pains, uncoordinated contractions, corkscrew pattern on barium swallow

diffuse esophageal spasm

99

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

achalasia

100

bad breath, regurgitation of food eaten days ago

Zenker diverticulum

101

Common symptoms of GERD

persistent cough
heartburn

102

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

paraesophageal hiatal hernia

103

What is gastritis

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

104

Where is B12 absorbed?

terminal ileum

105

How do we diagnose H. Pylori?

urea breath test
antral biopsy
serum h.pylori antibodies

106

Gastritis treatment

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

107

Peptic ulcer disease: Gastric ulcer

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

108

Peptic ulcer disease:duodenal ulcers

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

109

Ulcer associated with severe burn

Curling's ulcer

110

Ulcer associated with intracranial injuries

Cushing's ulcers

111

Zollinger- Ellison syndrome

increased gastrin

112

What findings on barium swallow are suggestive of cancer?

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

113

Treat a peptic ulcer

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)

114

complications of peptic ulcer

hemorrhage
perforation
lymphoproliferative disease

115

Zollinger-Ellison syndrome

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

Gastric cancer subtypes

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

Gastric cancer risk factors

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

118

Gastric cancer H and P

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

Surgical therapy for obesity

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

complications of surgical therapy for obesity

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

121

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

H. Pylori triple therapy

PPI
Amoxicillin
Clarithromycin (metronidazole if pt allergic to clarithromycin)

122

Subtotal gastrectomy

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

Branching rods, oral infection, what bacteria is this?

actinomyces israelii

124

How does malabsorption present?

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

125

Where is ethanol absorbed?

stomach

126

Celiac sprue

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

Tropical sprue

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

Lactose intolerance

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

Whipple disease

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

Sudan stain

if you suspect fat malabsorption
bacterial overgrowth
pancreatic insufficiency

131

D-xylose

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

Schilling test

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

Acute diarrhea

134

chronic diarrhea

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

The formula for stool osmotic gap

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

136

Pediatric diarrhea

infection
-rotavirus (winter)
-adenovirus (plus conjunctivitis)

antibiotic use
-macrolides

immunosuppression

137

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

138

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

>125

139

Which tumors can cause diarrhea due to hormone excess

carcinoid tumor
VIPoma
gastrinoma
medullary thyroid cancer

140

most common food-borne bacterial GI infections in the US

campylobacter
salmonella

141

IBS

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

What are the Rome diagnostic criteria for IBS?

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

What are the subtypes of IBS?

IBS with diarrhea
IBS with constipation
Mixed IBS
IBS unsubtyped

144

What symptoms are NOT c/w IBS alone?

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

145

What lab findings are NOT consistent with IBS alone?

electrolyte disturbances
anemia
increased inflammatory markers

146

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

abdominal x-ray
abdominal CT
barium studies

147

Treatment for IBS

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

IBD

inflammatory disease

Crohn
Ulcerative colitis

149

Crohn symptoms

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

distinguishing features of Crohn disease

GIFTS

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

Ulcerative colitis

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

Extraintestinal manifestations of IBD

arthritis
ankylosing spondylitis
erythema nodosum
pyoderma gangernosum
uveitis
primary sclerosing cholangitis

153

Serologic markers for IBD

ASCA:anti-saccharomyces cerevisiae abs often positive in Crohn

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

154

Bowel obstruction- common causes

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

What are the classic signs and symptoms of SBO?

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

What is the treatment for SBO?

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

What is the most common benign small bowel tumor?

leiomyoma

158

WHat is the most common malignant small bowel tumor?

carcinoid

159

Large bowel obstruction common causes:

neoplasm
adhesions
volvulus
diverticulitis

radiology:
bowel distention proximal to the obstruction

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

160

ischemic colitis

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

Appendicitis

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

What radiological studies can be used to diagnose appendicitis?

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

Treatment for appendicitis

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

Ileus

paralytic obstruction of small bowel secondary to decreased peristalsis

infection, ischemia, recent surgery, DM

typically less than 5 days. small bowel recovers first (

165

Gallstone ileus

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

Volvulus

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

Diverticulosis

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

Diverticulis

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

When is inpatient admission for diverticulitis treatment indicated?

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

170

What are the steps in inpatient management of diverticulitis

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

What are the complications of diverticulitis?

Colonic abscesses
fistulas
sepsis

172

Hemorrhoids

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

Anal fissure

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

Anorectal abscess

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

Treatment:
Antibiotics
I and D

175

Rectal fistula (aka fistula in ano)

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

Pilonidal disease

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

Carcinoid tumors

common sources, sites, features

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

The biggest risk factor for colon cancer

presence of colon polyps, especially the adenomatous ones

179

Risk factors for developing colon cancer

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

Familial adenomatous polyposis

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

Gardner syndrome

APC mutation
colon polyps
osteomas
soft tissue tumors

182

Turcot syndrome

APC gene mutation
colonic adenomas
CNS tumors

183

Juveile polyposis

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

Peutz-Jeghers syndrome

Hamartomas in the GI tract
pigmented lesions on lips and oral mucosa

185

Hereditary Non-polyposis Colorectal Cancer (HNPCC)

Colon cancer arising from normal- appearing mucosa
without forming polyps

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

186

How does colon cancer present?

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

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

node involvement: stage III, involves chemotherapy

met's beyond nodes: stage IV

188

Colon cancer post- treatment surveillance

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

189

Colon cancer screening for avg risk patient

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

Disadvantages to flex sig

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

Hematochezia- bright red blood in the stool

lower GI bleed
rapid or heavy bleed

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

192

Melena- dark blood

upper GI or proximal small bowel blood

193

Coffee ground emesis

blood that has been sitting in the stomach for some time

194

Causes of upper GI bleed

peptic ulcer disease
Mallory- Weiss tears
esophagitis
esophageal varices
gastritis

195

Causes of lower GI bleed

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

imaging of choice for lower GI bleed

colonoscopy

197

imaging of choice for upper GI bleed

EGD

198

Where does the EGD end

duodenum

199

Where does a colonoscopy stop?

terminal ileum

200

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

capsule endoscopy, which sends pictures to a received

201

Tagged RBC scan

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

202

Relevant radiology for GI bleeds

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

Management steps for GI bleed

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
5. type and cross 2 U PRBC
6. Labs:CBC, coags (guaiac stool if necessary, to confirm blood)

Treat and determine the cause
7. NG tube to rule out massive upper GI bleed
8. If colonoscopy is nondiagnostic and not feasible (too much active bleeding may obscure visualization), and bleeding persists, then radionucleotide scan and/or angiogram

204

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

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

205

The 3 most common causes of acute pancreatitis

gallstones
chronic alcohol use
idiopathic

206

acute PANCREATITIS causes

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

Ranson criteria

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

H and P findings c/w acute pancreatitis

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

Treat pancreatitis

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

Complications of acute pancreatitis

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

treat patients before they get quick

211

Chronic pancreatitis causes

almost always due to alcoholism
recurrent

212

Chronic pancreatitis signs and symptoms

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

Chronic pancreatitis treatment

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

214

Complications of chronic pancreatitis

ductal obstruction
pseudocyst
malnutrition
glucose intolerance
pancreatic cancer

215

Pancreatic pseudocyst- what is it?

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

Treatment of pancreatic pseudocyst

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

217

Pancreatic pseudocyst complications

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

218

Exocrine pancreatic cancer

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

Trousseau syndrome

migratory thrombophlebitis classically associated with pancreatic adenocarcinoma

220

Gastrinoma- stomach tumor

Gastrin- secreting glandular tumors that cause Zollinger- Ellison syndrome

221

Insulinoma

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

Glucagonoma

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

Necrolytic migratory erythema

uncommon presentation of glucagonoma
rash, erythematous plaques on the face, perineum, extremities

224

VIPoma

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

Risk factors for cholelithiasis

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

acute cholycystitis

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

227

Acalculous choecystitis

patients on TPN
critically ill patients
inflammation, without obstruction

228

Murphy sign

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

positive test consistent with cholecystitis

229

H and P c/w cholecystitis

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

What is a HIDA scan (cholescintigraphy)?

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

How do we treat cholecystitis?

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

Cholangitis

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

Charcot triad- cholangitis

RUQ pain
jaundice
fever

cholangitis until proven otherwise

234

Reynolds pentad, cholangitis

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

235

Gallbladder cancer

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

Why do we always do cholecystecomy on porcelain gallbladder?

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

237

Primary biliary cirrhosis

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

238

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

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

What laboratory finding is a hallmark of primary biliary cirrhosis?

Elevated serum antimitochondrial antibodies (AMA)

240

Primary sclerosing cholangitis

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

What condition is associated with cholangiocarcinoma?

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

242

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

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

243

Gilbert disease

-mild deficiency of UDPGT
-mild jaundice following fasting, exercise, stress
-increased indirect bilirubin (

244

Crigler-Najjar syndrome type 1

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

Crigler-Najjar syndrome type 2

Mildly decreased UDPGT

Mildly elevated indirect bilirubin

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

246

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

Murphy sign
Cholecystitis

247

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

Reynold's pentad
Cholangitis

248

RLQ pain on passive extension of the hip

psoas sign
appendicitis

249

RLQ pain on passive internal rotation of the flexed hip

obturator sign
appendicitis

250

LUQ pain and referred left shoulder pain

Kehr's sign

splenic rupture

251

Ecchymosis of skin overlying the flank

acute pancreatitis

252

Ecchymosis of the skin overlying the periumbilical area

Cullen sign
acute pancreaitis

253

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

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

254

nonalcoholic steatohepatitis (NASH)

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

symptoms and signs of alcoholic liver disease

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

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Treat alcoholic liver disease

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

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Cirrhosis

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

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What do hepatocytes do?

conjugate bilirubin
synthesize proteins
metabolize toxins

259

What hand finding is associated with alcoholic cirrhosis?

Dupuytren contracture

260

How to treat cirrhosis:

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

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

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

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How do you diagnose Budd- Chiari?

Best initial diagnostic test: US

Gold standard test: hepatic venography

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How do we treat Budd-Chiari syndrome?

Thrombolytics to dissolve the clot)
Diuretics
Anticoagulation
Angioplasty
Shunting

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Where do varices form, subsequent to portal hypertension?

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

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Serum- ascites albumin gradient (SAAG)

subtract!

measure albumin in the ascites
measure the albumin in the serum

SAAG= serum alb- ascites albumin

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Significance of SAAG> 1.1

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

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Significance of SAAG

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

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

consider cancer as a cause of ascites

do a workup for cancer if this is the case

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What if you have elevated WBC on paracentesis?

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

consider spontaneous bacterial peritonitis

270

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

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

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How do we treat portal hypertension?

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

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Hereditary hemochromatosis

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

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Wilson disease

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

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Alpha1- antitrypsin deficiency

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

Autoimmune hepatitis

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)

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+ANA and anti-smooth muscle antibodies (ASMA)

Type 1 autoimmune hepatitis

277

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

type 2 autoimmune hepatitis

278

Benign hepatic neoplasms

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

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Hepatic adenoma

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

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

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

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Hepatocellular carcinoma

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

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Erythropoietin increase may be explained by...

Potentially Really High Hematocrit

Pheochromocytoma
Renal Cell Carcinoma
Hemangioblastoma
HCC

283

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

Ferritin (high)

284

What lab value do you look for with WIlson disease?

serum ceruloplasmin (low)