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final Flashcards

1
Q

Where does jaundice first appear?

A

conjunctiva of eyes

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2
Q

what other symptom is jaundice classicaly associated with?

A

pruritis

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3
Q

T/F: carotenemia does not affect the conjunctiva

A

TRUE

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4
Q

what are the 2 most common causes of hepatocellular jaundice?

A

viral hepatitis and alcoholic cirrhosis

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5
Q

what are 2 examples of obstructive jaundice?

A

gallstone/gallbladder dz and pancreatic cancer involving pancreatic head

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6
Q

what leads to the so-called “painless jaundice”?

A

pancreatic cancer involving pancreatic head

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7
Q

what does increased bilirubin levels from excessive breakdown of RBCs cause?

A

hemolytic jaundice

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8
Q

what is the most common cause of acute liver failure?

A

drug related hepatotoxicity (about 50%). Acetominophen = 40% of cases

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9
Q

what are the tests that assess liver function?

A

albumin and total serum protein, PT time, bilirubin

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10
Q

what usually causes chronic liver dz to be suspected?

A

when one of complications occur

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11
Q

T/F: a lack of symptoms for chronic liver dz usually means a benign cause

A

false - lack of sx is no assurance of benign cause

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12
Q

What are the classic symptoms of chronic liver dz?

A

fatigue, flu-like symptoms, diffuse RUQ or abdominal discomfort

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13
Q

What occurs in the icteric phase of chronic liver dz?

A

accumulation of bilirubin in blood and tissues => jaundice. Common sx = pruritis, dark urine, light stools

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14
Q

what percentage of pts with Acute liver failure die?

A

28%

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15
Q

what are 3 common signs of chronic liver dz?

A

spider telangiectasia, palmar erythema, dupuytrens contracture

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16
Q

what are 3 complications of chronic liver dz?

A

portal HTN, esophageal varices, increased risk of primary liver cancer (hepatocellular carcinoma)

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17
Q

how does the liver react to chronic injury?

A

steatosis, fibrosis, and/or cirrhosis

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18
Q

describe hepatic steatosis

A

fatty liver w/o inflammation. Lipid accumulation in liver of >5% of livers weight

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19
Q

what is the livers most common response to injury?

A

steatosis

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20
Q

what is the most common form of hepatic steatosis?

A

macrovesicular steatosis

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21
Q

what is macrovesicular steatosis classically assoc. with?

A

obesity, type II DM, alcoholism

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22
Q

what is the most common discovery on physical exam of pt w/ macrovesicular steatosis?

A

non-tender hepatomegaly in an obese, alcoholic, or diabetic pt

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23
Q

what is the “two-hit model?”

A

possible complications of steatosis - steatosis makes liver sensitive to a second hit from pro-inflammatory molecules

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24
Q

what are the almost universal findings in pts with nonalcoholic fatty liver dz (NAFLD)?

A

insulin resistance/metabolic syndrome/syndrome x

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25
Q

describe steatohepatitis

A

fatty liver WITH inflammation. Usually presents with chronic unexplained elevations in amino transferase

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26
Q

T/F: fibrosis is synonymous with cirrhosis

A

false - fibrosis is NOT necessarily synonymous with cirrhosis

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27
Q

what is the predominant clinical reflection of hepatic fibrosis?

A

portal hypertension

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28
Q

is cirrhosis reversible?

A

cirrhosis is usually IRREVERSIBLE

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29
Q

what are the common causes of cirrhosis in the western world?

A

alcoholic liver dz and chronic hep c

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30
Q

how many drinks per day have been assoc w/ cirrhosis in women?

A

2-3/day

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31
Q

how many drinks per day have been assoc w/ cirrhosis in men?

A

3-4/day

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32
Q

what is the only test that can directly confirm a dx of cirrhosis?

A

percutaneous liver biopsy

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33
Q

what is the cause of hep A?

A

fecal oral contamination

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34
Q

what is the cause of hep B?

A

infected blood or infected blood-bearing fluids

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35
Q

what is the cause of hep C?

A

infected blood or infected blood-bearing fluids

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36
Q

why is hep c considered very dangerous?

A

slow spreading, clinically “silent”

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37
Q

what percentage of hep C pts can “clear the virus” from their blood?

A

20%

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38
Q

are primary or secondary liver tumors more common?

A

secondary 40x more common

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39
Q

what is the most common site of metastasis in those who die from neoplasms?

A

liver

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40
Q

what finding strongly suggests a liver tumor?

A

a bruit or friction rub over the liver

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41
Q

what is biliary colic?

A

pain assoc w/ transient obstruction of cystic duct. Very symptomatic stage of gallstone dz

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42
Q

what is cholelithiasis?

A

presence of gallstones in gall bladder

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43
Q

what is pain assoc w/ prolonged obstruction of cystic duct?

A

cholecystitis

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44
Q

what is it called when there is a stone in the common duct?

A

choledocholelithiasis

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45
Q

what is the term that describes obstruction/inflammation of the biliary or hepatic ducts?

A

cholangitis

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46
Q

are gallstones more common in men or women?

A

women

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47
Q

what are the primary bile acids?

A

cholate and chenodeoxycholate

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48
Q

what kind of bile acids tend to be more hydrophilic?

A

primary bile acids

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49
Q

what are the secondary bile acids?

A

deoxycholate and lithocholate

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50
Q

what kind of bile acids tend to be more hydrophobic?

A

secondary bile acids

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51
Q

what accelerates the formation of cholesterol gall stones and has been linked to prolonged small intestine transit time?

A

increased deoxycholate levels

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52
Q

what is the only significant mechanism for the elimination of excess cholesterol?

A

synthesis of bile acids and their subsequent excretion in the feces

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53
Q

an increase in what bile acid might impair gall bladder emptying?

A

deoxycholate

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54
Q

during fasting, what percentage of hepatic bile passes directly to the duodenum?

A

25%

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55
Q

describe the gall bladder “contractions”

A

small, slow, and somewhat random changes in basal tone

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56
Q

where is the sphincter of Oddi located?

A

duodenum

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57
Q

T/F: gallbladder contraction alone exerts enough force to fully open the sphincter of Oddi

A

False - it does NOT exert enough force to open the sphincter

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58
Q

what does CCK cause to happen to the sphincter?

A

relaxation of the sphincter as the gall bladder contracts

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59
Q

after hepatic bile is concentrated, how much of gall bladder bile is water?

A

90%

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60
Q

what does an increased concentration of cholesterol or mucin cause?

A

impaired emptying of gall bladder

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61
Q

what percentage of gallstones in the us are cholesterol based?

A

75-80%

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62
Q

where do cholesterol stones most often form?

A

gall bladder

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63
Q

what are black pigment stones assoc with?

A

hemolytic conditions

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64
Q

what are brown pigment stones assoc with?

A

infection of gall bladder

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65
Q

what are the 4 stages of formation of cholesterol gall stones?

A
  1. cholesterol supersaturation 2. poss. Formation of biliary sludge 3. microlithiasis 4. “mature” stones
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66
Q

in a pt that is not obese and has normal serum cholesterol levels, is it possible to have cholesterol based gall stones?

A

yes

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67
Q

what is a common symptom of a pt w/ multiple/faceted stones?

A

pt complaining of back pain

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68
Q

what are the non modifiable risk factors for cholesterol gall stones?

A

increasing age, female gender (exposure to estrogen), genetic factors (American Indian tribes, Hispanic populations w/ strong American Indian influence)

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69
Q

what is the first and foremost cause of cholesterol supersaturation?

A

obesity (decrease BMI and serum triglyceride levels)

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70
Q

how do most pts with gallstones present?

A

asymptomatic - gallstones don’t leave gallbladder

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71
Q

how is Dx of gallstone dz usually made?

A

Hx of convincing attack and visualization of gallstones in gall bladder

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72
Q

how sensitive is US in detecting gallstones in the gall bladder?

A

95%

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73
Q

is it easier to detect gallstones via US when they are in or out of the gall bladder?

A

more difficult when they have left gall bladder

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74
Q

how long does it take stones to make it through the cystic duct?

A

30 min - 6 hrs

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75
Q

What will you find on physical exam of a pt with biliary “colic”?

A

nothing

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76
Q

what is the most common disorder resulting from gallstones?

A

biliary “colic”

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77
Q

how long does a biliary colic attack last?

A

30-60 mins, up to 6 hrs

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78
Q

what is the second most common disorder resulting from gallstones?

A

acute cholecystitis

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79
Q

which attacks last longer, acute cholecystitis or biliary colic?

A

acute cholecystitis - lasts >6 hrs (12-18 hrs)

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80
Q

how often is Murphys sign present in acute cholecystitis?

A

60%

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81
Q

where does pain from biliary colic classically refer?

A

RUQ, R shoulder

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82
Q

what type of pain does biliary colic create?

A

visceral

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83
Q

what type of pain does acute cholecystitis create?

A

parietal

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84
Q

what are the characteristics of a large gall stone?

A

20-25 mm, rarely leaves gall bladder

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85
Q

what are large gall stones likely to cause?

A

gall bladder empyema (infection) and result in biliary tract fistula

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86
Q

why is a large gall stone sx profile atypical?

A

do not cause Hx of “convincing” attack

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87
Q

what can choledocholelithiasis lead to?

A

liver damage and jaundice

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88
Q

what can microlithiasis greatly increase the risk of?

A

gallstone pancreatitis

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89
Q

what does gall bladder hydrops/mucocele do?

A

inhibits emptying of gall bladder

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90
Q

what has gall bladder sx in the absence of stones?

A

sphincter of oddi syndrome/biliary dyskinesia

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91
Q

what is carnetts used to assess?

A

chronic and unremitting abdominal pain

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92
Q

what is considered the gold standard for dx’ing chronic cholelithiasis?

A

ultrasound (95% sensitive for detecting gallstones IN gall bladder)

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93
Q

what is the sensitivity of ultrasound in detecting stones in the common duct?

A

50%

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94
Q

what is defined as “attempted auto digestion of the pancreas?”

A

acute pancreatitis

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95
Q

what is defined as “permanent structural changes often associated w/ chronic alcoholism”?

A

chronic pancreatitis

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96
Q

T/F: pancreatic cancer is often untreatable by the time it is dx’ed

A

TRUE

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97
Q

is the pancreas retroperitoneal or within peritoneum?

A

retroperitoneal

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98
Q

describe the pain from the pancreas

A

visceral and poorly localized

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99
Q

how does the pancreas normally feel on palpation?

A

soft and pliable

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100
Q

what does chronic pancreatitis lead to?

A

deposition of CT in pancreatic acini and ductules

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101
Q

what leads to the deposition of ectopic fat in the pancreas?

A

high fat diet or obesity

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102
Q

what happens to ectopic fat during episodes of pancreatic inflammation?

A

can become necrotic (activated proteases and lipases try to digest phospholipids in cell walls)

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103
Q

what is a classic axiom when referring to the pancreas?

A

“no stimulation, no secretion”

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104
Q

How much does eating or thinking about eating stimulate pancreatic enzyme production?

A

up to 70% of max capacity

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105
Q

what occurs during an acute alcoholic episode?

A

pancreas temporarily ceases fxn

106
Q

what happens to the pancreas during chronic alcoholism?

A

becomes hypersecretory

107
Q

how much alcohol does it take to mess up the pancreas?

A

nobody knows

108
Q

what is the problem that occurs involving zymogen granules in the pancreas?

A

can cause premature activation of proenzymes in the pancreas

109
Q

what is the classic pain referral for inflammation of the pancreatic head?

A

the back

110
Q

what is the classic pain referral for inflammation of the pancreatic body?

A

to the back and/or left flank

111
Q

what is the classic pain referral for inflammation of the pancreatic tail?

A

left flank

112
Q

what specific clinical feature allows the clinician to definitively dx pancreatitis?

A

none

113
Q

is acute pancreatitis reversible?

A

potentially

114
Q

how many cases of acute pancreatitis involve gall stones?

A

about 40%

115
Q

how many cases of acute pancreatitis are d/t alcohol abuse?

A

35%

116
Q

how many cases of acute pancreatitis are idiopathic?

A

10%

117
Q

what is the most common type of acute pancreatitis?

A

edematous pancreatitis

118
Q

how many cases of acute pancreatitis are severe?

A

24%

119
Q

what is the mortality rate of hemorrhagic pancreatitis?

A

50-85%

120
Q

what will you see with hemorrhagic pancreatitis?

A

cullens sign, grey-turner sign

121
Q

what is the cardinal symptom of acute pancreatitis?

A

epigastric pain of sudden onset, usually lasts >1 day

122
Q

what is the characteristic patient postion in cases of pancreatitis?

A

thoracolumbar spinal flexion

123
Q

T/F: overt rebound tenderness is a common finding with acute pancreatitis

A

false - uncommon

124
Q

how does the degree of amylase/lipase elevation correlate with the severity of pancreatitis?

A

it doesn’t correlate

125
Q

what are 3 common complications of acute pancreatitis?

A

mortality, pancreatic necrosis, pseudocyst

126
Q

what are the characteristics of chronic pancreatitis?

A

self perpetuating, mostly irreversible, and leads to structural changes w/in pancreas

127
Q

what are the structural changes that occur during chronic pancreatitis?

A

fibrotic tissue/calcium deposition in pancreas

128
Q

what are the pathological hallmarks of chronic pancreatitis?

A

chronic inflammation, glandular atrophy, ductal changes, fibrosis

129
Q

what are the causes of chronic pancreatitis?

A

metabolic, excessive alcohol, idiopathic, ductal obstruction

130
Q

what is the most common cause of chronic pancreatitis?

A

alcohol consumption (60%)

131
Q

what percentage of alcoholics develop chronic pancreatitis?

A

<10%

132
Q

what are the 2 common causes of chronic pancreatitis d/t ductal obstruction?

A

congenital anomalies, blunt abdominal trauma

133
Q

what is the cardinal symptom of chronic pancreatitis?

A

intermittent and unpredictable attacks of severe epigastric pain

134
Q

what 2 things signify the “end of the road” for chronic pancreatitis pts?

A

malabsorption and steatorrhea (at least 90% of function is lost) - IRREVERSIBLE

135
Q

what is the overall 5 yr survival rate of pancreatic cancer?

A

<5%

136
Q

what percentage of pancreatic cancers develop in the pancreatic head?

A

about 75%

137
Q

what percentage of pancreatic cancers develop in the pancreatic tail?

A

5-10%

138
Q

what percentage of pancreatic cancers develop in the pancreatic body?

A

15-20%

139
Q

what is the only know risk factor for pancreatic carcinoma?

A

age (median 65-69)

140
Q

what is the clinical presentation for pancreatic cancer?

A

gradual onset of nonspecific symptoms, abdominal/back pain, significant weight loss, mild-moderate mid epigastric tenderness, “mild” jaundice

141
Q

what is the most common presenting sx in pancreatic cancer?

A

abdominal/back pain

142
Q

what is the classic association for “painless” jaundice?

A

pancreatic cancer (d/t common duct obstruction because of pancreatic head involvement)

143
Q

what is the most common intestinal cause of lower abdominal pain in the western world?

A

irritable bowel syndrome

144
Q

when do sx of IBS often present?

A

before age 30

145
Q

what are the diagnostic criteria for IBS?

A

at least 3 mos of recurrent abdominal pain/discomfort associated with 2 or more of: improvement w defecation, change in stool frequency, change in stool form or appearance

146
Q

what are the 2 cluster groups of the majority of the pts with IBS?

A

diarrhea cluster and constipation cluster

147
Q

which subset of IBS is known as spastic colon?

A

constipation predominant (dry hard stools)

148
Q

which subset of IBS is known as painless diarrhea or nervous diarrhea?

A

diarrhea predominant

149
Q

which subset of IBS alternates constipation and diarrhea?

A

alternating IBS (classic IBS)

150
Q

which subset of IBS presents with cramping abdominal pain that is relieved by passing gas/bowel movement?

A

pain predominant IBS

151
Q

what often accompanies the feces in painless diarrhea?

A

visible mucus

152
Q

T/F: nocturnal diarrhea is a prominent feature of IBS

A

false - is not a prominent feature (does not wake you from sleep)

153
Q

what are the IBS red flags?

A

weight loss, positive FOBT, anemia, fever, nocturnal symptoms, first onset in elderly

154
Q

where is the pain most likely located in an IBS pt?

A

LLQ (localized to sigmoid colon)

155
Q

where could palpation of the sigmoid colon cause pain referral to?

A

rectum and anus

156
Q

does IBS or functional constipation present with abdominal discomfort?

A

IBS

157
Q

what can secondary constipation be caused by?

A

medications and supplements

158
Q

what has constipation classically been linked to?

A

dehydration, lack of adequate dietary fiber, and/or physical inactivity

159
Q

what are the insoluble fiber bulking agents?

A

methylcellulose maltodextrin, xanthan gum

160
Q

what are the soluble fiber bulking agents?

A

psyllium, bran, calcium polycarbophil, etc

161
Q

how is abdominal pain in IBS affected by soluble and insoluble fiber?

A

pain not reduced with either fiber

162
Q

for how long should you avoid using anti-diarrheal medications, and why?

A

avoid for first 24 hrs - diarrhea helps rid body of infection

163
Q

what are defined as “pulsion herniations of the colon wall”?

A

diverticula

164
Q

what is the long term result of diverticula?

A

long term IBS

165
Q

what has diverticula been assoc. with?

A

low fiber diet

166
Q

where do diverticula most commonly occur?

A

sigmoid colon

167
Q

what are the symptoms of diverticulosis that overlap w/ IBS?

A

pain (usually colicky), bloating sensation, changes in bowel habits, fullness or tenderness

168
Q

how does classic diverticulitis present?

A

acute constant abdominal pain, usually in LLQ, fever and leukocytosis, nausea/vomiting, constipation and/or diarrhea, localized w/ poss. Guarding

169
Q

what are 2 of the complications of diverticulosis th/ require surgical consultation?

A

fistula and bowel obstruction

170
Q

where is the classic “home” of the appendix?

A

McBurneys point (2/3 of distance from umbilicus to ASIS)

171
Q

what is acute appendicitis initiated by?

A

obstruction of the vermiform appendix

172
Q

in children with acute appendicitis, what can the obstruction be caused by?

A

lymphoid hyperplasia, or fecoliths

173
Q

what is the normal orientation and location of appendix?

A

close proximity to abdominal wall, between 4 and 6 o’clock

174
Q

what is the most common abdominal surgical emergency?

A

appendicitis

175
Q

when does appendicitis most often occur?

A

b/t ages of 10 and 30

176
Q

how long is the clinical course of acute appendicitis?

A

12-48 hrs (gangrene and perforation can occur w/in 36 hrs)

177
Q

what are the most effective and practical dx modalities for acute appendicitis?

A

routine hx and physical exam

178
Q

what is stage 1 of classic appendicitis?

A

early inflammation of the appendix

179
Q

where does the pain refer to in stage 1 of appendicitis?

A

vague pain that refers to umbilicus or epigastrium

180
Q

what is stage 2 of classic appendicitis?

A

distension of the appendix

181
Q

what type of pain is there in stage 2 of appendicitis?

A

constant colicky ache in area of RLQ

182
Q

what is a big clue for appendicitis (in regards to pain)?

A

MOVES from umbilicus to RLQ in stage 2

183
Q

what makes the pain worse in stage 2 of appendicitis?

A

walking or coughing

184
Q

what msl findings will be present on physical exam in stage 2 of appendicitis?

A

right rectus abdominis more tense on palpation than left

185
Q

what is stage 3 of classic appendicitis?

A

inflammation reaches the serosa

186
Q

describe the pain in stage 3 of appendicitis?

A

well localized to RLQ, localized when coughing or on light percussion

187
Q

what is the typical posture for appendicitis?

A

lying on left side with right hip flexed

188
Q

what are 2 red flags that are suggestive of acute appendicitis?

A

abdominal pain and FEVER (esp in children), abdominal pain and VOMITING (esp in adults)

189
Q

what is the sequence of 4 findings that is a strong indicator of acute appendicitis?

A
  1. poorly localized pain around umbilicus 2. pain “migrates” from umbilicus to become poorly localized in RLQ 3. pain becomes well localized in RLQ 4. muscular rigidity in RLQ
190
Q

4 somewhat reliable exam procedures for dx’ing appendicitis?

A

direct percussion, indirect percussion (Rovsings sign), rebound tenderness, psoas sign

191
Q

what type of appendicitis will present with a positive psoas sign?

A

retrocolic/retrocecal

192
Q

what type of appendicitis will present with a positive obturator sign?

A

pelvic

193
Q

how do elderly pts with appendicitis typically present?

A

minimal, vague symptoms

194
Q

what is increased intestinal permeability aka?

A

leaky gut syndrome

195
Q

what causes leaky gut syndrome?

A

loosening junctions between cells, allows unwanted molecules to pass through mucosa => immune response => inflammation

196
Q

what is a desmosome?

A

cadherin “adhesion” protein

197
Q

What are the two main clinical entities of inflammatory bowel dz (IBD)?

A

ulcerative colitis and crohn’s dz

198
Q

T/F: many of the mucosal changes seen in pts w/ IBD are nonspecific in nature

A

TRUE

199
Q

Which is associated w/ nocturnal symptoms - IBS or IBD?

A

IBD

200
Q

which is associated w/ weight loss - IBS or IBD?

A

IBD

201
Q

which is associated w/ blood in the stool - IBS or IBD?

A

IBD

202
Q

which is associated w/ signs of inflammation - IBS or IBD?

A

IBD

203
Q

which race is more likely to have IBD?

A

caucasians 4x more likely

204
Q

T/F: IBD is curable

A

false - can be managed but not cured

205
Q

What is the name of the IBD support group?

A

Crohns and Colitis Foundation of America (CCFA)

206
Q

What single clinical finding is used to absolutely differentiate IBS from IBD?

A

none

207
Q

How long is ulcerative colitis subclinical?

A

9-18 mos

208
Q

How long is crohns dz subclinical?

A

24-60 mos

209
Q

what are 3 common complications of ulcerative colitis?

A

toxic megacolon, colon cancer, superimposed infection

210
Q

what are 4 common complications of crohns dz?

A

malnutrition, anemia, abscesses, colon cancer

211
Q

what is the peak age range for ulcerative colitis?

A

15-35 (SAME AS IBS!)

212
Q

Which is more common - ulcerative colitis or crohns dz?

A

ulcerative colitis slightly more common

213
Q

Where does ulcerative colitis start?

A

the rectum (“always”)

214
Q

What part of the GI tract is ulcerative colitis confined to in 50% of cases?

A

recto-sigmoid area

215
Q

Describe the inflammation in ulcerative colitis

A

uniform and continuous

216
Q

what happens to the lymphoid follicles in ulcerative colitis?

A

hyperplasia

217
Q

what is the end result of ulcerative colitis?

A

pseudopolyps

218
Q

Do the symptoms of ulcerative colitis come on gradually or acutely?

A

abrupt onset

219
Q

What are 5 common clinical features of ulcerative colitis?

A

diarrhea, rectal bleeding, rectal urgency, tenesmus, abdominal pain/tenderness

220
Q

what is tenesmus?

A

feeling of incomplete defecation

221
Q

What is the chief symptom of mild ulcerative colitis?

A

rectal bleeding (mistaken for hemorrhoids)

222
Q

what is the chief symptom of moderate ulcerative colitis?

A

severe diarrhea (often w/ blood in it)

223
Q

what is the peak age range for crohns dz?

A

10-30 (SAME AS IBS!)

224
Q

describe the inflammatory process of crohns dz

A

non-specific, granulomatous

225
Q

which layers of the gut are affected by crohns dz?

A

all layers

226
Q

What happens to smaller ulcers in crohns dz?

A

may coalesce and form larger, linear ulcers

227
Q

what does fusion of larger ulcers lead to in crohns dz?

A

“cobblestoning” of mucosa

228
Q

what are “skip segments”?

A

discontinuous areas of involvement with crohns dz

229
Q

what is the “classic” age group for crohns dz?

A

late teens, early 20s

230
Q

do the symptoms of crohns dz come on gradually or acutely?

A

onset is insidious

231
Q

what are 3 classica clinical features of crohns dz?

A

abdominal pain, weight loss, diarrhea

232
Q

is diarrhea more likely to be bloody in ulcerative colitis or crohns dz?

A

ulcerative colitis

233
Q

what is crohns ileitis aka?

A

regional/terminal ileitis

234
Q

what are the sx of crohns ileits?

A

steady periumbilical pain made worse by eating, watery diarrhea, malabsorption/weight loss, fever, anemia

235
Q

what is crohns colitis aka?

A

granulomatous colitis

236
Q

what are the sx of crohns colitis?

A

crampy lower abdominal pain, incontinence, urgency, possible rectal bleeding

237
Q

what is crohns ileocolitis aka?

A

distal ileum and proximal colon colitis

238
Q

what are the sx of crohns ileocolitis?

A

mixed presentation of ileitis and colitis

239
Q

which type of colitis is most commonly mistaken for IBS?

A

granulomatous colitis

240
Q

what are the 2 articular manifestations of IBD?

A

peripheral arthritis and axial arthritis

241
Q

which type of arthritis tends to parallel the activity of the bowel dz?

A

peripheral arthritis

242
Q

is peripheral arthritis usually monoarticular or polyarticular?

A

monoarticular

243
Q

does peripheral arthritis more often involve upper limbs or lower limbs?

A

lower limbs

244
Q

what happens in peripheral arthritis with recurrence of IBD?

A

arthritis may “migrate” to another joint

245
Q

when does axial arthritis usually present in relation to the bowel dz?

A

tends to precede sx of bowel dz

246
Q

what are the 3 types of axial arthritis to be concerned about with IBD?

A

sacroiliits, spondyloarthritis, ankylosing spondylitis

247
Q

what 2 types of skin lesions are seen in 10-25% of IBD pts?

A

erythema nodosum, pyoderma gangrenosum

248
Q

what type of ocular lesions are seen in 3-11% of IBD pts?

A

acute iritis/anterior uveitis

249
Q

which type of IBD can cause sinus tracts/abscess formation?

A

crohns dz

250
Q

what percentage of recto-sigmoid cancers are in the early stages when discovered?

A

up to 90%

251
Q

what percentage of cancers found in the ascending colon are in the early stages when discovered?

A

fewer than 25%

252
Q

where are the majority of colon cancers?

A

recto-sigmoid area

253
Q

what do anemia and changes in bowel habits signify in pts w/ colon cancer?

A

associated with a worse prognosis

254
Q

what are the 3 classic sx of “left sided” colon cancer lesions?

A

hematochezia, constipation, alternating constipation/diarrhea (“paradoxical diarrhea”)

255
Q

what is hematochezia?

A

bright red blood in the stool

256
Q

what are the 3 classic sx of “right sided” colon cancer?

A

melena, diarrhea, anemia

257
Q

what is melena?

A

dark, tarry stools

258
Q

which “sided” colon cancer is associated with “napkin ring” tumors and “pencil-thin” stools?

A

“left sided” colon cancer

259
Q

what percentage of colon cancer is dx’ed in people w/ no known risk factors, including no family hx?

A

75%

260
Q

what percentage of people dx’ed with colon cancer are over 50?

A

90%

261
Q

what percentage of all colorectal cancer cases and deaths are thought to be preventable through screening tests?

A

90%

262
Q

what percentage of colorectal cancer is dx/ed in its early stages d/t low screening rates?

A

37%

Gastro (2 decks)

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