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GI Flashcards

1
Q

what is the most common finding in patients with GERD

A

Hiatal hernia

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2
Q

what food decrease LES tone and cause GERD

A

tobacco, coffee, spicy foods,alcohol, fatty foods, chocolate

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3
Q

what are the clinical features of GERD

A 
heart burn after eating
retrosternal chest pain
regurgitation
odynophagia
cough, hoarsness, hiccuping
worse when lying down after meals
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4
Q

what is the gold standard for diagnosing GERD

A

24 hour pH monitoring

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5
Q

what is the test of choice for GERD

A

endoscopy with biopsy not necessary for typical uncomplicated cased
mostly used in refractory to treatment or dysphagia or GI bleeding

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6
Q

what complications can occur from GERD

A 
Erosive esophagitis
peptic stricture
Esophageal ulcer
Barretts esophagus 
Recurrent pneumonia
dental erosions
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7
Q

what is the initial treatment for GERD

A

behavior modification
-Diet avoid fatty foods, coffee, alcohol, orange juice, chocolate, large meal before bed
Antacids after meals (Ca, Al, Mg)

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8
Q

what should you used after behavior modification

A

add an H2 blocker which can be used instead of or in addition to antacids
H2 blockers stop acid production

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9
Q

what should you use after failed H2 blocker

A

PPI like omperazole

PPI’s work by inhibiting H+/K+ ATPase enzyme of the gastric parietal cells

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10
Q

what should be added if a PPI does not work

A

a promotility ages such as metoclopramide

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11
Q

if a pro-motility agent doesn’t work then what

A

add combo therapy of H2 plus promotility agent

or PPI and promotility

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12
Q

what surgery is done for resistant cases of GERD

A

nissen fundoplication

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13
Q

who gets infectious esophagitis?

A

immunocompromised patients

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14
Q

how do you work up patients with infectious esophagitis?

A

H&P with EGD

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15
Q

what is the treatment for candida

A

fluconazole

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16
Q

what is the treatment for deep esophageal ulcers

A

acyclovir to treat HSV

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17
Q

How do you treat shallow ulcers in the esophagus

A

ganciclovir for CMV treatment

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18
Q

what are the two types of esophageal neoplasms

A

squamous cell carcinoma

adenocarcinoma

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19
Q

squamous cell carinoma of the esophagus is common in what ethnicity

A

African Americans

occurs in mid to upper third of esophagus

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20
Q

what are risk factors for squamous cell cancer

A

tobacco and alcohol use, betel nuts, ingestion of hot foods and beverages
HPV, achalasia

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21
Q

adenocarcinoma of the esophagus is common in what ethnicity

A

caucasians

occurs in the distal third of esophagus

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22
Q

what is the risk factors for adenocarcinmoa

A

GERD, Barrett’s esophagus, alcohol and tobacco

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23
Q

what are symptoms of esophageal cancer

A 
dysphagia intially solids only then progression to liquids
weight loss
anorexia
odynophagia
hematemesis
aspiration pneumonia
chest pain
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24
Q

how is esophageal cancer diagnosed?

A

upper endoscopy with biopsy and brush cytology

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25
Q

what is the treatment of esophageal cancer

A

palliation is the goal in most patients because the disease is usually advanced at presentation
Esophagectomy can be curative i patients with 0,1 or 2A

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26
Q

what is achalasia

A

acquired motility disorder of esophageal smooth muscle in which the lower esophageal sphincter fail to completely relax with swallowing and abnormal peristalsis

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27
Q

what is the absolute criteria for achalasia diagnosis

A

incomplete relaxation of the LES

aperistalsis of esophagus

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28
Q

what are the clinical feature of achalasia

A

dysphagia
Equal trouble swallowing solids and liquids
Patients eat slowly and drink lots of water to wash down food
Regurgitation
Chest pain
weight loss
recurrent pulmonary aspirations

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29
Q

how is achalasia diagnosed

A

Manometry to confirm the diagnosis
barium swallow will show narrowing of distal esophagus (birds beak) and a large dilated esophagus proximal to narrowing
Upper GI to rule out secondary causes of achalasia

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30
Q

what is the treatment of achalasia

A 
chew food to consistency of pea soup
sleep elevated
dicyclomine
sublingual nitro, CCB's
Botulism injections of esophagus
forceful dilations
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31
Q

what is esophageal spasm

A

spontaneous contraction of the esophageal body

Nomal LES

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32
Q

how is esophageal spasm diagnosed

A

esophageal manometry

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33
Q

Tx for esophageal spasm

A

Nitrates or CCB

possible TCA

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34
Q

what is zenkers diverticulum

A

outpuching of posterior hypopharynx

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35
Q

signs/sypmtoms of zenkers diverticulum

A

dysphagia
regurgitation
cough
halitosis

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36
Q

how is zenkers diagnosed

A

barium swallow

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37
Q

what is a mallory weiss tear

A

mucosal tear at GE junction leads to bleeding

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38
Q

what is Boerhaave’s syndrome

A

esophageal rupture that is full thickness, patient’s appear sick
happens after vomiting and there is excruciating pain

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39
Q

presentation for esophageal perforation

A 
history specific
hematemesis
chest pain
dyspnea
tachypnea
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40
Q

what is the treatment of a mallory weiss tear

A

90% stop bleeding without treatment
treatment is surgery or angiographic emcolization if bleeding continues
acid suppression to promote healing

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41
Q

what is the etiology of esophageal varices

A

portal HTN and cirrhosis

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42
Q

what is the presentation of esophageal varicies

A

usually profuse hematesis which is life threatening

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43
Q

how are esophageal varices treated

A

hemodynamic support
IV fluids and vasopressors and immediate control of bleeding
Endoscopy and octreotide are preferred therapy

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44
Q

what is the etiology of esophageal strictures

A

complications of GERD, autoimmune disease, infectious, caustic ingestion, congenital, med induced, radiation

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45
Q

how does esophageal strictures present

A

usually progressive dysphagia of solids may progress to liquids

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46
Q

how are stricture worked up

A

Barium esophagram, EGD

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47
Q

what is the treatment of a stricture

A

dilation and stent placement

unless malignant then it needs to be resected

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48
Q

what causes peptic ulcer disease

A 
H pylori
NSAIDS
Hypersecretion states like Zollinger Ellison Syndrome
Also
Smoking
alcohol and coffee Stress
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49
Q

what is PUD

A

any ulcer of the upper digestive tract eg gastric or duodenal ulcer

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50
Q

what is the most common cause of PUD

A

H pylori

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51
Q

What are risk factors for gastric cancer

A

H pylori or gastric ulcers

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52
Q

features of PUD/Gastritis or Duodenitis

A

described as burning or gnawing that radiates to the back or LUQ
Hematemesis or melana
N/V

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53
Q

How will a duodenal ulcer feel when you eat food

A

improves with food

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54
Q

how will food affect a gastric ulcer

A

it typically worsens which leads to anorexia and weight loss

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55
Q

what are complications of ulcers

A

bleeding
perforation
Obstruction from scarring
malignancy

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56
Q

how is PUD diagnosed

A

Endoscopy is most accurate
essential in gastric ulcers to rule out malignancy
preferred with acute or severe bleeding

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57
Q

How is H pylori diagnosed

A

Biopsy is gold standard
Urease breath test is most convenient test and is 95% specific and sensitive
Serology of antibodies to H pylori

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58
Q

what is the treatment for PUD caused by H. Pylori

A

Amoxicillin and Clarithromycin plus PPI
or metronidazole for 14 days
OR
Bismuth subsalicylate plus tetracycline, metronidazole and PPI for 7 days

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59
Q

what is the treatment of Gastritis/duodenitis

A

H2 blockers or PPI

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60
Q

what causes gastritis

A

inflammation of gastric mucosa caused by NSAIDS/Aspirin, H pylori, alcohol

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61
Q

how is gastritis treated

A

empiric therapy with H2 or PPI and stopping NSAIDS

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62
Q

the majority of gastric cancer are what kind

A

adenocarcinomas

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63
Q

which gastric cancer has the most favorable prognosis

A

superficial spreading

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64
Q

what are risk factors for gastric cancer

A 
atrophic gastritis 
adenomatous gastric polyps
H. Pylori infection
Post antrectomy
Pernicious anemia
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65
Q

what is Virchows node

A

metastsis to superclavicular node

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66
Q

what is sister mary josephs node

A

metastasis to the periumbilical lymph node

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67
Q

what are the clinical features of gastric cancer

A

abdominal pain and unexplained weight loss
reduced appetite, anorexia, dyspepsia,
N/V, anemia, melena guaiac positive

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68
Q

how is gastric cancer diagnosed

A

endoscopy with multiple biopsies

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69
Q

what is the treatment for gastric cancer

A

surgical resection with wide margins and extended lymph node dissection

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70
Q

what is zollinger-Ellison syndrome

A

is a condition which one or more tumors form in your pancreas or upper part of small intestines
The gastrinomas secrete large amount of gastrin which causes excessive acid production which leads to PUD

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71
Q

how is zollinger ellison syndrome diagnosed

A

blood is analyzed to see whether you have elevated gastrin levels
they can do a secretin injection test
EGD

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72
Q

treatment of zollinger ellison syndrome

A

PPI and possible surgical resection

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73
Q

what is the most common extra-nodal site for non-hodgkins lymphoma

A

the stomach lymph nodes

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74
Q

who get pyloric stenosis

A

infants

male more than females

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75
Q

what is pyloric stenosis

A

hypertrophy of the pyloric muscle

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76
Q

what are the symptoms of pyloric stenosis

A

projectile nonbilious vomiting

weight loss and dehydration

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77
Q

what will you find on exam in a patient with pyloric stenosis

A

olive shaped mass in epigastrum

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78
Q

what is the treatment for pyloric stenosis

A

pylorotomy

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79
Q

how is pyloric stenosis diagnosed

A

barium swallow will show delayed emptying and string of pearls
or ultrasonography

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80
Q

what is cholelithiasis

A

stones in the gallbladder

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81
Q

what are the three types of stones

A

cholesterol stones most common which are yellow to green

pigment stones associated with hemolysis and sickle cell or alcoholic cirrhosis
mixed

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82
Q

what is a common symptom of cholecystitis

A

Pain in typically located in RUQ or epigastrium
Pain happens usually after eating and at night
radiates to subscapular
N/V anorexia
Murphys signs is pathognomonic
low grade fever and hypoactive bowel sounds

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83
Q

how is cholecystitis diagnosed

A

RUQ ultrasound will show thickened gallbladder wall, pericholecystic fluid, distended gallbladder and stones
Use HIDA scan when ultrasound is inconclusive

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84
Q

what does a positive HIDA scan mean

A

gallbladder was not visualized

if its not visualized after 4 hours diagnosis of acute cholecystits

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85
Q

what is the treatment

for acute cholecystitis

A

IV fluids, Bowel Rest, analgesics and correct electrolyte abnormalities
Cholecystectomy for pts with symptomatic stones

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86
Q

what is biliary colic

A

when stones in the gallbladder block the cystic duct and the gall bladder contracts and it usually only lasts a few minutes

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87
Q

what is acute cholecystitis

A

obstruction of the cystic duct (not infection) causes inflammation of the gallbladder wall

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88
Q

what are signs of biliary tract obstruction

A 
elevated alkaline phosphatases (ALP) increased GGT
Elevated conjugated bilirubin
Jaundice
pruitis
clay colored stool and dark urine
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89
Q

what is choledocholithiasis

A

stone in the CBD

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90
Q

what are clinical features of choledocholithiasis

A

RUQ or epigastric pain, and jaundice

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91
Q

what labs will be abnormal

A

total direct and indirect are elevated as well as ALK-P

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92
Q

What does a RUQ ultrasound show with choledocholithiasis

A

usually the initial study but not as sensitive for choledocholithiasis

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93
Q

what is the gold standard for diagnosis for choledocolithiasis

A

ERCP

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94
Q

what is the treatment of choledocolithiasis

A

ERCP with sphincterotomy, stone extraction and stent placement

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95
Q

what is cholangitis

A

infection of biliary tract secondary to obstruction which leads to biliary stasis and bacterial over growth

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96
Q

what types of obstructions cause cholangitis

A

60% of the time its due to choledocholithiaisis can also be due to neoplasms, post op strictures

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97
Q

what are the clinical features of cholangitis

A

Charcot’s triad
Fever, RUQ pain, jaundice
Renoylds pentad is
Fever, RUQ pain, jaundice, altered mental status and shock

98
Q

what should you do for patients who have cholangitis

A

Blood cultures
IV fluids
IV Abx and decompress CBD when pt is stable

99
Q

What are Lab findings with Cholangitis

A

hyperbilirubinemia, leukocytosis and elevated transaminases

100
Q

what is used to make definitive diagnosis of cholangitis

A

ERCP or PTC

101
Q

what is cirrhosis

A

liver disease characterized by fibrosis, disruption of the liver architecture and widespread nodules in the liver

102
Q

what does the destruction of the liver due to cirrhosis cause

A

decreased blood flow through the liver causing portal HTN

Hepatocellular failure which leads to decreased albumin synthesis and clotting factors

103
Q

what is the most common cause of cirrhosis?

A

Alcoholic liver disease

104
Q

what is the second most common cause of cirrhosis

A

Hep B and C infections

105
Q

what are other causes of cirrhosis

A 
Drugs- acetaminophen
Autoimmune hepatitis
Primary biliary cirrhosis
Hemachromatosis
Alpha1 antitrypsin deficiency
106
Q

what are features of cirrhosis

A 
Portal HTN
Varicies esophageal or gastric (caput medusa)
Ascities
gynecomastia
hemorrhoids 
hematemesis, melena
Palmar erythema 
hypoalbuminemia
107
Q

what is primary sclerosing cholangitis

A

chronic thickening of bile duct walls unknown etiology

Associated with IBD and UC

108
Q

what is primary sclerosing cholangitis associated with for cancers?

A

cholangiocarcinoma

109
Q

what are the features of PSC

A

fatigue, maliase,jaundice, pruritis and weight loss

110
Q

what is the treatment of PSC

A

Urosdiol

Liver transplant

111
Q

what is the treatment of cirrhosis

A

bed rest, low sodium diet and diuretics (furosemide and sprionolactone)
beta blockers
therapeutic paracentesis if tense ascities
TIPS transjugular intrahepatic portosystemic shunt

112
Q

what is hepatic encephalopathy

A

toxic metabolites mainly ammonia is thought to be the main one accumulate in the brain

113
Q

clinical features of hepatic encephalopathy

A

decreased mental function, poor concentration and stupor or coma
Asterixis
rigidity and hyperreflexia
musty breath

114
Q

what is the treatment for hepatic encephalopathy

A

Lactulose
Neomycin
Limit protein to 30-40 g/day

115
Q

what is hepatorenal syndrome

A

indicates endstage liver disease

progressive renal failure in advance liver disease secondary to renal hypoperfusion

116
Q

what are the clinical features of hepatorenal syndrome

A

azotemia, olgiouria, hyponatermia, hypotension

117
Q

what is the treatment for hepatorenal syndrome

A

liver transplant is the only cure

118
Q

what is spontaneous bacterial peritonitis?

A

infected ascitic fluid

occurs in patients with ascities by end stage liver disease

119
Q

what bacterial are responsible for SBP

A

e. coli
Klebsiella
Streptococcus pneumoniae

120
Q

what are symptoms of spontaneous bacterial peritonitis

A

abdominal pain, fever, vomiting, rebound tenderness,

121
Q

How is SBP diagnoes

A

paracentesis and examining fluid for WBC especially PMN
WBC>500
PMN>250

122
Q

what is the treatment for SBP

123
Q

how is cirrhosis treated

A

abstinence from alcohol and interferon for hep B and C
Avoid acetaminophen
Once cirrhosis develops goal is to manage complications
Liver transplant is the only cure

124
Q

what is primary biliary cirrhosis

A

cholestatic liver disease characterized by destruction of intrahepatic bile ducts

125
Q

what is the etiology of PBC

A

autoimmune and affects middle aged women

126
Q

what are the clinical features of PBC

A

fatigue, jaundice, pruritus, RUQ pain, xanthomata, Osteoporosis
Portal HTN

127
Q

how is PBC diagnosed

A

LFT’s and elevated ALK-p

positive AMA and a liver biopsy confirms diagnosis

128
Q

what is the most common benign liver tumor

A

cavernous hemangioma

129
Q

hepatocellular carcinoma accounts for what percent of liver cancer

A

80% althought they are rare in the US account for most deaths due to cancer world wide
High risk areas include africa and asia

130
Q

what type of hepatocellular carcinoma is associated with Hep B and C

A

nonfibrolamellar most common

131
Q

what are risk factors for hepatocelluar carcinoma

A 
cirrhosis especially in association with alcohol or hepatitis
Alpha 1 antitrypsyn deficiecny 
hemochromatosis, wilsons disease
Schistosomiasis
hepatic adenoma
cigarette smoking
132
Q

features of hepatocelluar carcinoma

A

abdominal pain
weight loss, anorexia, fatigue,
portal hypertension, jaundice
paraneoplastic syndromes- erythrocytosis, hypercalcemia, carinod syndrome

133
Q

how is hepatocellular carcinoma diagnosed

A

liver biopsy
Hep B&C serology, LFT and coags
US,CT,MRI is surgery is an option
Tumor marker elevation (AFP)

134
Q

what is the treatment for hepatocellular carcinoma

A

liver resection or liver transplant

135
Q

what is NASH

A

symiliar to alcoholic liver disease but patients have not history of alcohol use

136
Q

NASH is associated with

A

obesity, hyperlipidemia, DM

137
Q

what is the most common cause of hepatitis

138
Q

what is the second most common cause of hepatitis

A

toxins

Alcohol

139
Q

chronic hepatitis most often results from which hepatitis’s

A

B,C,D

but is often inherited disorders wilsons disease, alpha 1 antitrypsin deficiency

140
Q

How are hepatitis A&E transmitted

A

Fecal-Oral

141
Q

how are hepatitis B,C,D transmitted

A

blood or mucous membrane contact

142
Q

Clinical features of hepatitis

A

fatigue, malaise, nausea, abdominal discomfort

143
Q

what is the prognosis of Hep A&E

A

self limited and mild without long term sequalae

144
Q

when does a person get Hep D

A

only seen in patients with Heb B and associated with a more severe course

145
Q

Igm to Anti-HAV indicates what?

A

detects the onset of Hep A

146
Q

HAV IgG represents what

A

resolved hep A

147
Q

what does HBsAg mean

Hepatitis B surface antigen

A

current infection with HBV acute or chronic

148
Q

what does anti-HBs

anti-hepatitis B surface antigen

A

marker of immunity with HBV

149
Q

what does anti-HBc mean

Hep B core antibody

A

present between the disappearance of HBsAG and the appearance of anti-HBs indicating acute hepatitis

150
Q

what does HBeAg mean

Hepatitis B envelope antigen

A

indicates highly contagious HBV infection but anti-HBe antibodies indicate lower level of infection

151
Q

how can you tell when hep C is present

A

anti-HCV antibodies

152
Q

how is hep D detected

A

only happens when hep b and detected by anti-HDV antibodies

153
Q

how to tell if a person is Hep B carrier or is chronic infection

A

Both have positive HBsAg but in chronic infection there is elevated AST and ALT
hepatocelluar damage on biopsy

154
Q

his is hep A&E treated

A

supportive

155
Q

how is chronic HBV treated

A

Interferon

156
Q

how is chronic HCV treated

A

interferon and ribavirin

157
Q

what is pancreatitis

A

inflammation of the pancreas resulting from prematurely activated pancreatic digestive enzymes that induce autodigestion

158
Q

which type of pancreatitis will respond to supportive treatment

A

mild acute pancreatitis

159
Q

what are the most common causes of pancreatitis

A

alcohol or gallstones

can also be caused by post ERCP
Viral infection
post op
scorpion bites

160
Q

what are the clinical features of acute pancreatitis

A 
epigastric pain radiating to the back
N/V
leukocytosis
Fever/Peritonitis
severe hypovolemia, ARDS
161
Q

What labs will be abnormal in acute pancreatitis

A

serum amylase is the most common test but many condition cause hyperamylasemia
Levels need to be more than 5 times upper limits of normal
Serum lipase is more specific
LFT- to identify cause
Hyperglycemia,hypoxemia and leukocytosis

162
Q

how is pancreatitis diagnosed

A

CT scan

ERCP is used in severe gallstone pancreatitis with biliary obstruction

163
Q

what is the admission criteria for pancreatitis

A 
GA LAW
Glucose >200
Age>55
LDH>350
AST>250
WBC>16,000
falling Calcium
BUN Rising
164
Q

what is the treatment for acute pancreatitis

A

NPO-bowel rest
IV fluids
correct electrolyte abnormalities
Pain control

165
Q

what is cullens sign

A

periumbilical eccymoses from hemorrhagic pancreatitis

166
Q

what is grey turner sign

A

flank ecchymoses hemorrhagic pancreatitis

167
Q

what is fox’s sign

A

eccyhymosis of inguinal ligaments from hemorrhagic pancreatitis

168
Q

what is chronic pancreatitis

A

persistent or chronic inflammation of the pancreas with fibrotic tissue replacing pancreatic parenchyma and alteration of pancreatic ducts

169
Q

what is the most common cause of chronic pancreatitis

A

alcoholism

170
Q

what are the features of chronic pancreatitis

A

severe pain in epigastrium recurrent or persistent
N/V
aggravated by drinking episode

171
Q

how is chronic pancreatitis diagnosed

A

CT scan will show calcifications
ERCP is the gold standard
Lab studies not helpful

172
Q

treatment for chronic pancreatitis

A 
narcotics for pain management
NPO
Pancreatic enzymes and H2 blockers
Insulin 
alcohol abstinence 
surgery-whipple procedure
173
Q

what is the classic triad for pancreatic calcifications

A

steatorrhea, pancreatic calcifications, DM

Elevated fecal fat

174
Q

who gets pancreatic cancer

A

mostly elderly patients 75% >60yrs old

more common in african americans

175
Q

where is the most common location of pancreatic cancer

A

75% occur in the head

176
Q

what are risk factors for pancreatic cancer

A 
Smoking is most clearly established
chronic pancreatitis
DM
alcohol use
exposure to benzidine and b-naptthlamine
177
Q

what are clinical features of pancreatic cancer

A 
abdominal pain
jaundice
weight loss, anorexia
glucose intolerance
depression, fatigue
courvoisiers sign
178
Q

how is pancreatic cancer diagnosed

A

CT is the preferred test for diagnosis

Tumor markers CA19-9
CEA

179
Q

what is the treatment for pancreatic cancer

A

whipple procedure

180
Q

what is appendicitis?

A

lumen of the appendix is obstructed by hyperplasia of lymphoid or a fecalith

181
Q

what is the most common cause of appendicitis

182
Q

what age is the most common age for appendicitis

A

10-30 years of age

183
Q

what are the symptoms of appendicitis

A 
intermitten periumbilical or epigastric pain
pain at Mcburneys point
N/V, anorexia
Low grade fever
Psoas sign
184
Q

how is appendicitis diagnosed

185
Q

what is the treatment of appendicitis

A

appendectomy

Abx if perforation

186
Q

most colon cancers arise from what type of cells

187
Q

what do all patients with a positive FOBT need

A

colonoscopy

188
Q

what are risk factors for colon cancer

A 
age over 50
adenomatous polyps
villous adenomas
larger the size or greater number of polyps higher risk of cancer
prior Hx CRC
IBD
Both UC and Chrons increase risk but UC greater risk
Fam Hx 1st Degree relatives
Familial adenomatous polyposis
Gardners syndrom
Turcots syndrome
Peutz-Jegher
Lynch Syndrome
189
Q

clincial features of CRC

A 
melena, hematochezia, abdominal pain, iron deficiency anemia
Abdominal pain
Bowel obstruction
weight loss
blood in stool
190
Q

Signs of right sided tumors

A

occult blood in stool, iron deficiency anemia, melena

Triad of anemia weakness, RLQ mass

191
Q

signs of left sided tumor

A

obstruction
alternating constipation/ diarrhea
pencil stools
heamtochezia

192
Q

rectal cancer signs

A

heamtochezia
tenesmus
rectal mass

193
Q

what is the treatment of CRC

A

Surgery resection of tumor and regional lymphnodes

CEA level

194
Q

what is the surveillance for a person with CRC

A

stool guaiac test
annual CT scan of abdomen/pelvis and CXR up to 5 years
Colonoscopy at 1 year every 3 years
CEA levels

195
Q

what is the most common nonneoplastic polyp

A

hyperplastic/(metaplastic) polyps

hard to distinguish so often removed

196
Q

what are the three types of adenomas

A

Tubular which is the most common with the smallest risk of malignancy
Tubulovillous-intermediate risk
Villous- greatest risk

197
Q

what determines the malignant potential of a polyp

A

size- the larger greater risk of malignancy
histologic type
Atypia of cells
shape- sessile(more likely to be malignant) versus pedunculated on a stalk

198
Q

what is chrons disease

A

it is a chronic transmural inflammatory disease that can affect any part of the GI tract

199
Q

what is the hallmark location of chrons disease in the body

A

terminal ileum

200
Q

what does the pathology of chrons disease look like

A 
Skip lesions, discontinuous involvement 
Fistulae
Luminal strictures
noncaseating granuloma
Transmural thickening
201
Q

what are the clinical features of chrons

A 
diarrhea usually without blood
malabsorption 
abdominal pain in the RLQ
N/V
Fever malaise
Uveitis, Arthritis, Erythema nodosum, apthous ulcers
202
Q

how is chrons diagnosed

A

endoscopy with biopsy

203
Q

what are complications of chrons

A 
fistulae 
anorectal disease
SBO
Malignancy
Malabsorption
204
Q

what is the treatment for chrons

A

Sulfasalazine 5-ASA

205
Q

what is Ulcerative colitis

A

chronic inflammatory disease of the colon or rectal mucosa

206
Q

where is the most common site affected by colitis

A

the rectum

207
Q

what does the pathology of colitis look like

A

uninterrupted involvement of the rectum and colon NO SKIP lesions
PMN accru in the crypts of the colon

208
Q

what are the clinical features of colitis

A 
Blood diarrhea
abdominal pain
frequent but small bowel movenents
fever, anorexia, weight loss
tenesmus
Jaundice, arthritis
209
Q

what should you include in your work up of suspected colitis

A

stool cultures for ova and parasites
fecal leukocytes
Colonoscopy

210
Q

complications of UC

A 
iron deficiency anemia
hemorrhage
electrolyte abnormalities
Colon cancer
Sclerosing cholangitis
211
Q

what is the treatment for UC

A

systemic steroids for acute exacerbations

Sulfasalazine, Mesalamine

212
Q

what is IBS

A

combination of altered motility hypersensitivity to intestinal distention and psychological stress

213
Q

who is IBS more common in?

214
Q

how is IBS diagnosed

A

it is a diagnosis of exclusion

215
Q

what is intussusception

A

is invagination of the proximal segment of the bowel into the portion just distal to it
Occurs in 95% of children usually following viral infection
In adults its caused by a neoplasm

216
Q

clinical features of intussusception

A

colicky pain if stool is passed will contain blood and mucus (current jelly stools)
A sausage like mass may be felt on exam

217
Q

lab findings for Intussusception

A

for kid barium or air enema may be therapeutic and diagnostic

218
Q

how is intussusception diagnosed in adults

A

dont use barium

CT is best mean of establishing the diagnosis

219
Q

what is the treatment for intussusception

A

for kid barium or air enema

adults may require surgery

220
Q

what is diverticulosis

A

large outpouchings of the mucosa of in the colon

221
Q

what are laboratory findings with diverticulosis

A

occult blood in the stool and moderate leukocytosis
plain film to rule out free air
CT is warranted if patient does not respond to therapy

222
Q

what is the treatment for diverticulitis

A

low residue dies and broad spectrum Abx
Hospitalization for IV administration of IV Abx, bowel rest, pain meds, NG tube if ileus develops
Surgical management me be necessary in severe cases including peritonitis, large abscess
High Fiber diet

223
Q

clinical features of CMI are

A

abdominal angina with pain occuring 10 to 30 minutes after eating which is relieved somewhat by squatting or laying down

224
Q

how does AMI present

A

sudden angina with pain out of proportion to examination findings

225
Q

lab findings in AMI

A

Colonoscopy is the optimal test to evaluate for ischemia of the colon

226
Q

treatment for AMI

A

surgical revacularization

227
Q

what is toxic megacolon

A

extreme dilatation and immobility of the colon and represents a true emergency

228
Q

what causes toxic megacolon in kids

A

hirshsprungs disease

229
Q

what causes toxic megacolon in adults

A

UC, Chrons, psedomembranous colitis and shigella, campylobacter and clostridium

230
Q

clinical features of toxic mega colon

A

fever, prostration, severe cramps and abdominal distention

rigid abdomen and localized, diffuse or rebound tenderness

231
Q

what do the abdominal films show

A

colonic dilitation

232
Q

what is the treatment for toxic megacolon

A

decompression of the colon is required, in some cases a colostomy or even complete colonic resection

233
Q

what is celiac sprue

A

inflammation of the small bowel with the ingestion of gluten containing foods such as wheat, rye and barley leading to malabsorption

234
Q

how does celiac sprue present

A

diarrhea, steatorrhea, flatulence, weightloss, weakness, abdominal distention

235
Q

how is celiac disease diagnosed

A

IgA antiendomysial and antitissue transglutaminase antibodies
small bowel biopsy to confirm the diagnosis

236
Q

what is the treament for celiac disease

A

gluten free diet, refer patient to a nutrionist
possibly a lactose diet
supplement of B12, Iron, folic acid and Vitamin D

237
Q

what is a volvulus

A

twisting of any portion of the bowel on itself most commonly the sigmoid or cecal area

238
Q

clinical features of volvulus

A

cramping abdominal pain and distention with nausea, vomiting, and obstipation
abdominal tympany will be found on exam along with tachycardia, and fever

239
Q

how is volvulus confirmed

A

abdominal plain film which show colonic distention

240
Q

what is the treatment for volvulus

A

endoscopic decompression

surgical evaluation and treatment is required if volvulus fails to quickly resolve

PANCE (8 decks)

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