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GI/Nutrition > Test 2 > Flashcards

Test 2 Flashcards

1
Q

What’s the #1 cause of extrahepatic obstruction? What most often brings this about?

A

large duct obstrution is #1 cause of extrahepatic obstruction; LDO is most commonly caused by gallstones

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2
Q

What causes hereditary tyrosinemia?

A

deficiency of fumarylacteoacetate hydrolase (FAH)

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3
Q

Describe the inflammation associated with ulcerative colitis.

A

crypt accesses with neutrophils

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4
Q

How does pregnancy related cholestasis present?

A

•Presents with intolerable pruritus (worse in soles and palms and at night) and elevation in serum bile acids

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5
Q

Which liver cells play an important role in the development of fibrosis?

A

stellate cells; when activated, they make collagen= fibrosis

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6
Q

Primary sclerosing cholangitis causes destruction of which ducts?

A

extra- and intrahepatic ducts of all sizes

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7
Q

Use of which antibiotic in particular predisposes to C. difficile infection?

A

clindamycin (First Aid also says ampicillin)

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8
Q

What should be considered for recurrent c. diff?

A

probiotic (first aid says fecal microbiota transplant)

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9
Q

What are the key pathologic features of Nonalcoholic Fatty Liver Disease & Non-alcoholic Steatohepatitis (NASH)?

A
  • ­Steatosis, often zone 3
  • ­Lobular inflammation, mixed but often neutrophils
  • ­Pericellular fibrosis and ballooning degeneration
    • ­Fibrosis around individual hepatocytes
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10
Q

results from surgical resection of a large portion of the small intestine

A

short bowel syndrome

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11
Q

What’s the clinical presentation of Crigler-Najjar Syndrome?

A

presents within first 3 days of life with persistant jaundice and unconjugated hyperbilirubinemia. Can lead to kernicterus= bilirubin deposition in brain= severe neuro damage

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12
Q

What’s the treatment for Gaucher disease?

A

IV recombinant glucocerebrosidase

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13
Q

At what point is alcoholic fatty liver irreversible?

A

when fibrosis develops

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14
Q

What are the typical laboratory findings of alcoholic hepatitis?

A
  • AST and ALT mildly elevated
    • AST>ALT (usually 2:1 pattern for alcohol)
  • markedly elevated bilirubin
  • very elevated WBC
  • elevated INR
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15
Q

What’s the main stay of treatment of colon cancer?

A

complete surgical resection

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16
Q

Describe the morphology of Clostridium difficile.

A

spore-forming, anaerobic, gram-positive bacillius

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17
Q

Iron deficiency anemia is common with colorectal cancer in which segment of the colon

A

right colon

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18
Q

What’s the best diagnostic test for ischemic colitis ?

A

sigmoidoscopy/ colonoscopy with biopsy

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19
Q

What WHVP, FHVP, AND HVPG values do you expect for presinusoidal liver disease?

A
  • WHVP normal
  • FHVP normal
  • HVPG normal
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20
Q

What is this an image of?

A

alcoholic hepatitis demonstrating both Mallory’s hyaline and fatty change

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21
Q

A hepatic venous pressure gradient (HVPG) of what predicts increased risk of death?

A

> or = to 16

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22
Q

What is this an image of? How can you tell?

A

autoimmune hepatitis; Portal and periportal inflammation (hepatitis) with prominence of plasma cells

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23
Q

What are the features of Peutz-Jeghers syndrome?

A

numerous hamartomatous polyps throughout GI tract along with hyperpigmented mouth, lips, hands, and genitalia

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24
Q

What’s the treatment for C. Difficile?

A

metronidazole or ORAL vancomycin

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25
Q

What’s an effective treatment for IBS-C (constipation)?

A

linaclotide and lubiprostone

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26
Q

How do you treat Wilson’s disease?

A
  • penacillamine to chelate copper
  • liver transplant in severe cases
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27
Q

In what patient population is IBD most prevalent?

A

middle-aged women

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28
Q

What’s the main enzyme responsible for metabolizing alcohol? What does it break it down to?

A

alcohol dehydrogenase (ADH) converts ethanol to acetaldehyde

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29
Q

What mutation is seen in ~50% of Peutz-Jeghers syndrome cases?

A

loss of function mutations of STK11 gene. B/c it’s only seen in 50% of cases, absence of this mutation doesn’t rule out Peutz-Jeghers syndrome

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30
Q

What is the toxic biproduct of acetaminophen? What is it normally inhibited by?

A

NAPQI which is typically taken care of (not allowed to have toxic effects) by glutathione

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31
Q

What’s the treatment for autoimmune hepatitis?

A

corticosteroids and azathioprine

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32
Q

Fulminant hepatic failure is acute liver failure with encephalopathy within 2-3 weeks of hepatic dysfunction. What causes it?

A

viral hepatitis or drugs (acetaminophen most common)

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33
Q

What is used to treat hepatic encephalopathy?

A

lactulose; if it’s refractory or intolerant to lactulose, add rifaximin

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34
Q

What are the triad of findings in Reye’s syndrome?

A
  • encephalopathy
  • microvesicular fatty change in liver
  • transaminase elevation
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35
Q

What’s the only major carbohydrate malabsorption?

A

lactase deficiency

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36
Q

What are some clinical signs of portal hypertension?

A

ascites

congestive splenomegaly

esophageal varices

hemorrhoids

caput medusae

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37
Q

What’s the most common genotype for wild type alpha 1 antitrypsin? What percentage of normal ciruculating alpha 1 antitrypsin is present in these individuals?

A
  • PiMM
  • 100%
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38
Q

What’s the best method of diagnosis for primary sclerosing cholangitis?

A

cholangiography. Large duct strictures lead to beads in a row (or pearl necklace) appearance

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39
Q

Describe the gross appearance of tissue effected by Crohn disease.

A

cobblestone mucosa, creeping fat, and strictures (‘string-sign’ on imaging)

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40
Q

What’s the common presentation of patients with ischemic colitis?

A

sudden abdominal pain and bright red blood in stool

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41
Q

What’s the best confirmatory test of cholestasis (Any condition in which the flow of bile from the liver stops or slows)?

A

5’-nucleotidase

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42
Q

•Majority of patients with clinically significant HH are:

A

–C282Y/C282Y homozygotes or

–C282Y/H63D compound heterozygotes

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43
Q

Celiac disease is associated with which HLA types (first aid)?

A

HLA-DQ2 HLA-DQ8

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44
Q
  1. When do symptoms of hemochromatosis usually present?
  2. Which sex is most often effected?
  3. What can exacerbate symptoms?
A
  1. fourth decade
  2. males b/c female menses reduces iron overload
  3. chronic alcohol ingestion or hep C infection
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45
Q

What’s the phenobarbital response in Crigler-Najjar Syndrome patients?

A

it will not have an effect on bilirubin levels

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46
Q

Which race is particular suceptible to NAFLD? which race seems to be protected?

A

Increased risk in hispanic pts.

decreased risk in black pts.

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47
Q

Primary sclerosing cholangitis is commonly seen with _____.

A

Inflammatory bowel disease (70% of cases coexist with ulcerative colitis)

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48
Q

What’s the treatment for celiac disease?

A

eliminate dietary gluten

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49
Q

what is Reye’s syndrome assoicated with ?

A

•Associated with aspirin administration to children with acute viral infections (chickenpox and influenza)

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50
Q

A protracted course of Primary sclerosing cholangitis can lead to the development of which real bad disease?

A

10-15% develop cholangiocarcinoma

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51
Q

What’s the main treatment for pregnancy related cholestasis?

A

Delivery; also ursodeoxycholic acid, cholestryamine, and vitamin K if fat soluble vitamin deficiency develops

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52
Q

How is alcohol abuse defined?

A

engaging in harmful use of alcohol with negative consequences (negative social and health consequences)

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53
Q

Describe the gross appearance of tissue effected by ulcerative colitis.

A

pseudopolyps. Loss of haustra (‘lead pipe’ sign on imaging)

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54
Q

Mutations in which gene are associated with Hereditary Hemochromatosis ? On which chromosome is this gene?

A

HFE gene; chromosome 6

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55
Q

Primary sclerosing cholangitis is more prevalent in which sex?

A

males

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56
Q

How do stimulant laxatives work?

A

Stimulate colonic motility to help produce defecation

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57
Q

What are the risk factors for Nonalcoholic Fatty Liver Disease & Non-alcoholic Steatohepatitis (NASH)?

A
  • ­Metabolic syndrome
    • ­Obesity
    • ­Type 2 diabetes
    • ­Hyperlipidemia
  • ­Amiodarone – anti-arrhythmic
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58
Q

What causes Hepatoerythropoietic porphyria (HEP)? what is seen on it’s liver histology that makes it unqiue?

A

defects in both uroporphyrinogen decarboxylase (UROD) genes

  • characteristic needles seen in liver
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59
Q

What complications of short bowel syndrome do you need to be on the lookout for?

A

-bile salt diarrhea -kidney stones (oxalate stones) -cholesterol gall stones

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60
Q

What are xanthomas?

A

collection of cholesterol; white plaque like lesion (often seen under eye but can be other places)

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61
Q

What are the 2 main causes of predictable (dose dependent) drug induced liver injury (DILI)?

A

acetaminophen

chemo

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62
Q

Organs are assigned to patients based on what?

A
  1. patient blood type
  2. MELD score
  3. area of the country of the transplant center
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63
Q

putting nutrition inside the gut (i.e. nasal tube to stomach/intestines)

A

enteral nutrition

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64
Q

Gilbert syndrome patients would have what response to phenobarbitol?

A

lowers bilirubin levels

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65
Q

What WHVP, FHVP, AND HVPG values do you expect for sinusoidal liver disease?

A
  • WHVP= elevated
  • FHVP= normal
  • HVPG= elevated
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66
Q

What is hepatocellular pattern of injury in drug induced liver injury associated with?

A

–Involves elevation of transaminases (AST/ALT)

•May be dramatic (>1000)

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67
Q

Besides having 100s to 1000s of polyps in familial adenomatous polyposis (FAP), what’s the big concern?

A

100% progress to colorectal cancer before age 30

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68
Q

What causes cholestasis?

A

results from impaired bile formation and bile flow that causes accumulation of bile pigment in the hepatic parenchyma.

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69
Q

Non-alcohol fatty liver disease is highly associated with metabolic symptoms. Name a few.

A

–Central obesity

–Hypertriglyceridemia*

–Hypertension

–Impaired glucose tolerance

–Low HDL concentration*

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70
Q

What does this image show?

A

biliary atreasia; an absence of visualization of the common hepatic duct and the intrahepatic bile ducts.

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71
Q

What’s the genetic defect in Wilson’s disease?

A

•Genetic defect on Chromosome 13 (ATP7B gene) involving transmembrane copper-transporting ATPase, located on the hepatocytes canalicular membrane

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72
Q

putting nutrition beside intestines (i.e. IV nutrition)

A

parenteral nutrition

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73
Q

What drug therapy should be used for recurrent c. diff colitis?

A

repeating metronidzale or vancomycin or, adding fidaxomicin

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74
Q

What are hemorrhoids?

A

Dilations of the veins of the internal or external hemorrhoidal plexus in the rectum and anus

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75
Q

How much alcohol is needed to cause fatty liver?

A

•Fatty liver develops in about 90% of individuals who drink >60g/day of EtOH (~4-5 beers)

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76
Q

What’s the best treatment for NAFLD?

A

weight loss

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77
Q

What’s the clinical presentation of Wilson’s disease?

A

•Clinical presentation: extremely variable

–acute or chronic liver disease

–Mild behavioral changes- frank psychosis

–Kayser-Fleischer rings: copper deposits in cornea

–Rarely presents with fulminant hepatitis with rapid downhill clinical course

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78
Q

What’s the gold standard for testing for C. Difficile?

A

PCR toxin gene detection or screening + PCR

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79
Q

What causes small intestinal bacterial overgrowth?

A

due to alterations of the small bowel:

  • Function (stasis) i.e. gastroparesis, enteroparesis
  • Anatomy (postoperative)
  • Diameter (short bowel)
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80
Q

What temporary malabsorption problem is common after any gastroenteritis?

A

transient lactase deficiency

81
Q

What’s the most clinically significant HFE gene mutation?

A

C282Y

82
Q

Solitary rectal ulcer syndrome is an example of an inflammatory polyp. What’s the triad associated with it?

A

1) rectal bleeding 2) mucus discharge 3) inflammatory lesion at the anterior rectal wall

83
Q

90% of patients with primary biliary cirrhosis display _____.

A

anti-mitochondrial antibodies (AMA’s)

84
Q

If given early enough, what can prevent some or all of the hepatic damage cause by acetaminophen overdose?

A

N-acetylcysteine (NAC)

85
Q

Autoimmune hapatitis is associated with increased frequency of which HLA types?

A

HLA-DR3

HLA-DR4

86
Q

What pharmacotherapy is used to treat esophageal varices and what’s the strategy behind it?

A

vasoconstrictors (beta blockers); -Decreases portal flow MORE SIGNIFICANTLY that the increase in portal resistance; so in end, you decrease portal pressure

87
Q

there are a lot of ways to classify esophageal varices. What’s the only one Duarte cares about us knowing?

A

small (<5mm)

large (>5mm)

88
Q

Whats causes sporadic porphyria cutanea tarda?

A

decreased uroporphyrinogen in hepatocytes

89
Q

What dermatological finding can sometimes be found in celiac disease patients?

A

dermatitis herptiformis

90
Q

What are some other names for acetaminophen we might encounter?

A

•Paracetamol, n-Acetyl-p-aminophenol (APAP)

91
Q

What’s the treatment for familial adenomatous polyposis (FAP)?

A

colectomy

92
Q

How does C. Diff toxin B work?

A

it’s a cytotoxin that causes cytoskeletal disruption via actin depolymerization

93
Q

What is a rectocele?

A

Abnormal protrusion of a portion of the rectum (usually the anterior wall) with attempted defecation

94
Q

What is used to prioritize patients for liver transplantation?

A

MELD score

95
Q

What WHVP, FHVP, AND HVPG values do you expect for postsinusoidal liver disease?

A
  • WHVP= elevated
  • FHVP= elevated
  • HVPG= normal
96
Q

The pathogenesis of Reye’s syndrome is unknown, but it involves:

A
  • Mitochondrial injury
  • disruption of the urea cycle
  • defective Beta-oxidation of fatty acids
97
Q

What are common presenting symptoms of Hereditary hemochromatosis ?​

A
  • fatigue
  • non-inflammatory osteoarthritis
  • hypogonadism
  • diabetes
  • skin bronzing
98
Q

What are the signs and symptoms of cholestasis?

A
  • Jaundice
  • pruritis
  • xanthomas
  • malabsorption (diarrhea, fat soluble vitmamin loss, steatorrhea)
  • high alkaline phosphatase
  • high GGT
99
Q

How is alcohol dependence defined?

A

drinking excessively with physical tolerance and withdrawal

100
Q

How do you treat hepatorenal syndrome?

A

albumin and vasoconstrictors

101
Q

What’s the most common lysosomal storage disease and what causes it?

A

Gaucher disease; deficiency in glucocerebrosidase (1q21)

102
Q

What are the possible treatments for biliary atresia?

A
  • liver transplant
  • if isolated involvement of common hepatic or right/left hepatic duct, then Kasai procedure (attach small intestine directly to the liver)
103
Q

What is the MELD score comprised of?

A

INR, serum creatinine, total bilirubin

MELD is much less subjective than CTP

104
Q

What percentage of the liver parenchyma usually has to be destroyed before you get liver failure?

A

80-90%

105
Q

What are the classic manifestations of celiac disease?

A

diarrhea and weight loss due to malabsorption

106
Q

Describe Crohn disease inflammation.

A

lymphoid aggregates with granulomas

107
Q

What’s the cause of short bowel syndrome?

A

inadequate mucosal surface area to perform adequate absorption

108
Q

Where is AST going to be primarily distributed?

A

primarily microsomal and peri-central (around central vein)

109
Q

What’s the most common hereditary hyperbilirubinemia? What gene is mutated in this syndrome?

A

Gilbert syndrome; good news is it has no clinical consequences

  • mutation in UGT1A1 which encodes bilirubin conjugating enzyme UDP glucuronosyltransferase
110
Q

What are the histological features of cholestasis?

A

bile plugs and bile staining of the hepatocytes

111
Q

What’s the inheritance pattern of familial adenomatous polyposis (FAP)?

A

autosomal dominant

112
Q

What’s the inheritance pattern of Hereditary Hemochromatosis?

A

autosomal recessive

113
Q

What’s the treatment for acute fatty liver of pregnancy?

A

it’s fatal to mother and baby and treatment is delivering the baby (ok b/c this occurs in 3rd trimester anyway)

114
Q

What is the most important predictor of outcome in colorectal cancer?

A

stage

115
Q

Describe the pathogenesis of colorectal cancer.

A

Loss of APC gene–> K-ras mutation –> loss of tumor suppressor p53

116
Q

What causes celiac disease?

A

an allergic reaction to dietary gluten in the intestines; results in immune mediated damage to the small intestinal epithelium

117
Q

What are the classic clinical findings of Budd-Chiari syndrome?

A
  • Hepatomegaly
  • Ascites
  • abdominal pain
  • varying degree of hepatic dysfunction
118
Q

How is hepatic venous pressure gradient (HVPG) calculated?

A

HVPG= WHVP - FHVP

normal is less than 5

WHVP= wedge hepatic pressure

FHVP= free hepatic pressure

119
Q

When doing a paracentesis, the serum-ascites albumin gradient (SAAG) is very important. How do you calculate it and how do you interpret your results?

A

SAAG= serum albumin concentration - ascites albumin concentration

greater than/or equal to 1.1 means the ascites was caused by elevatd hydrostatic pressure (cirrhosis or CHF)

less than that means the ascites was caused by an increased oncotic pressure (nephrotic syndrome or malignancy)

120
Q

What do you see high levels of in Dubin-Johnson syndrome?

A

conjugated bilirubinen

121
Q

Is it possible to recover from acute alcoholic hepatitis?

A

yes. if you quit drinking

122
Q

Cirrhosis is the end result of chronic liver disease. In western countries, what is the most common etiology?

A

alcohol

alcohol

booze

123
Q

Where is ALT going to be primarily distributed?

A

cytosolic; distributed throughout the liver

124
Q

What causes Dubin-Johnson syndrome?

A

•Mutation in ABBC2, which encodes multidrug resistance-associated protein 2 (MRP2)

–MRP is involved in the conjugation and transportation of bilirubin

–Absence of MRP2 in liver canaliculi, resulting in impaired secretion of conjugated bilirubin into bile

125
Q

What is cholestatic pattern of injury in drug induced liver injury associated with?

A

significant increases in alkaline phosphatase and bilirubin

126
Q

Which large class of drugs can cause cholestasis?

A

steroids

127
Q

What causes Crigler-Najjar Syndrome?

A

absent UDP -glucuronosyltransferase

128
Q

What’s the normal treatment for hereditary hemochromatosis? What if this doesn’t work?

A

phlebotomy; deferoxamine

129
Q

What is used to best estimate portal vein pressure?

A

hepatic venous pressure gradient (HVPG)

130
Q

What’s the unique pathology of Gaucher disease?

A

lipid laden macrophages resembling crumpled tissue paper

131
Q

What causes Budd-Chiari syndrome?

A

thrombosis of one or more major hepatic veins or IVC

132
Q

What’s the treatment for hereditary tyrosinemia?

A

–NTBC (drug that inhibits tyrosine metabolsim), low-tyrosine/low-phenylalanine diet; liver transplantation

133
Q

Describe the location of ulcerative colitis.

A

begins in rectum always and can extend proximally up to the cecum (only messes with colon); involvement in continuous

134
Q

What is used to check the ability of the liver’s reticuloendothelial system?

A

liver spleen scan

superbe, highly sensitive test for portal hypertension, even when esophageal varices are not yet present

135
Q

What’s the criteria for diagnosing IBS?

A

recurrent abdominal pain at least 3days/month associated with 2 or more of the following: -pain improves with defecation -change in stool frequency (diarrhea or constipation) -change in appearance of stool

136
Q

What’s the treatment for Reye’s syndrome?

A

supportive care

137
Q

In which part of the intestines is damage due to celiac disease most prominent?

A

duodenum

138
Q

There’s no treatment for Dubin-Johnson treatment. What should these patients avoid though?

A

estrogens

139
Q

How do osmotic laxatives work?

A

Act by increasing the osmolarity of the luminal contents, thereby keeping water in the lumen and softening the stool.

140
Q

What genetic mutations are connected with juvenile polyposis syndrome?

A

Mutations in TGF-beta pathway (SMAD4)

141
Q

What causes Lynch syndrome (Previously known as: Hereditary Non-Polyposis Colorectal Cancer (HNPCC))?

A

inherited mutations in mismatch repair genes [MSH2 & MLH1]; this mismatch repair deficiency leads to microsatellite (repeated segments) instability

142
Q

What is dysbiosis?

A

defined as microbial imbalance inside the body

143
Q

Wilson’s disease is an _______ disorder of ____ metabolism.

A

autosomal recessive

copper

144
Q

What’s the treatment for primary biliary cirrhosis?

A

ursodeoxycholic acid greatly slows progress

145
Q

How does smoking effect Crohn disease?

A

smoking increases the risk for Crohn disease

146
Q

What’s the most important predictor of malignant progression in polyps?

A

size

147
Q

A hepatic venous pressure gradient (HVPG) of what is abnormal?

A

>5

148
Q

How does smoking effect ulcerative colitis?

A

smoking protects agains ulcerative colitis

149
Q

What are some decompensating events that would give a patient a ‘decompensated’ cirrohosis?

A

–Variceal hemorrhage

–Ascites

–Hepatic encephalopathy

–Jaundice

–Hepatocellular carcinoma

150
Q

What causes hereditary hemochromatosis?

A

a defect in regulation of intestinal absorption of dietary iron; excess iron deposits in organs and tissues, including liver, pancreas, and heart causing organ disfunction

151
Q

How is Biliary atresia defined?

A

Complete or partial obstruction of the lumen of the extrahepatic biliary tree within the first 3 months of life

  • Single most frequent cause of liver related death in childhood
152
Q

How do bulk forming agents work?

A

fiber supplements; Act by increasing stool bulk AND holding more water in the gut lumen

153
Q

What are the laboratory findings of autoimmune hepatitis?

A
  • ­Positive antinuclear antibody test and anti smooth muscle antibodies
  • ­Hypergammaglobulinemia
  • ­Increased transaminases – increased LFTs
154
Q

How is a diagnosis of small intestinal bacterial overgrowth made?

A

clinical suspicion after looking at risk factors

treat with cycled antibiotics

155
Q

How does C. diff toxin A work?

A

it’s an enterotoxin that binds to the brush border of the gut

156
Q

What will you find on liver biopsy that seals a Wilson’s disease diagnosis?

A

hepatic copper >250µg/ g dry weight (per gram of liver tissue)

157
Q

What can be found in the urine of patients with hereditary tyrosinemia that can be diagnostic?

A

high urinary succinylacetone

158
Q

Describe the location of Crohn disease.

A

can be anywhere from mouth to anus with skip lesions. spares the rectum. most common site is terminal ileum

159
Q

where do diverticula typically occur?

A

typically occur where arterial branches pass through the muscular layers to reach the submucosa

160
Q

Which amino acids are bile acids conjugated with?

A

glycine and taurine

161
Q

What’s the median survival for patients with compensated cirrhosis?

Decompensated cirrhosis?

A

10-12 yrs

<5 yrs

162
Q

How do stool softeners work?

A

Binds to stool and holds more water in the stool to make it softer

163
Q

What’s the test of choice for bile duct anatomy?

A

MRI with MRCP (Magnetic resonance cholangiopancreatography)

164
Q

What is this image of?

A

acetaminophen overdose; necrosis is centered around central veins

165
Q

Anti-TNF drugs are associated with increased risk of ______.

A

reactivation of latent TB infections

166
Q

What are the 2 cholesterol derived bile acids that get conjugated in the liver?

A

cholic acid and chenosdeoxy colic acid

167
Q

Autoimmune hepatitis most commonly occurs in ____.

A

women

168
Q

protein that is the main regulator of iron absorption

A

hepcidin; hepcidin lowers iron plasma levels–> deficiency causes iron overload

169
Q

How are protein losing enteropathies diagnosed?

A

fecal alpha-1 antitrypsin level (not normally found in stool)

170
Q

What’s the inheritance pattern of Peutz-Jeghers syndrome?

A

autosomal dominant

171
Q

What mutation causes familial adenomatous polyposis (FAP)?

A

mutation of APC tumor suppressor gene on chromosome 5q

172
Q

What are the gastrointestinal clinical presentation of cystic fibrosis?

A

•Gastrointestinal

–Meconium ileus (10%) at birth

–Pancreatitis and pancreatic insufficiency

–Malabsorption (Vit ADEK)

–Cirrhosis

173
Q

What are the 2 main clinical scores used in determining prognosis in cirrhosis?

A

–Child-Turcotte-Pugh (CTP) score

–Model for End-Stage Liver Disease (MELD) score

174
Q

What are markers of severe c. diff infection?

A

WBC>15,000; fever; dehydration

175
Q

How is neonatal cholestasis defined?

A

Prolonged conjugated hyperbilirubinemia > 14 days

176
Q

What’s the abnormal lab findings in Hereditary hemochromatosis ?

A

–Increased transferrin saturation

–Increased ferritin

–Elevated transaminases

  • The advanced stage of the disease is indicated when hepatic transaminase concentrations become elevated.
177
Q

Which macronutrient is most likely to have digestion and absorption problems?

A

fat

178
Q

Fatty liver is characterized by which steatosis?

A

microvesciular then macrovesicular steatosis

179
Q

Griffith’s point is a watershed area between the SMA and IMA that is particularly vulnerable to ischemic colitis. What area of the colon is this in?

A

splenic flexure (where transverse colon becomes descending colon)

180
Q

Primary biliary cirrhosis causes destruction of which ducts?

A

medium to small intrahepatic ducts

181
Q

What’s the most common genotype for clinically significant mutations of alpha-1 antitrypsin? What percentage of normal ciruculating alpha-1 antitrypsin is present in these individuals?

A
  • PiZZ
    • 10%
182
Q

What zone of the liver is effected by acetamenophen overdose?

A

zone 3 (closest to central vein)

183
Q

What is dyssynergia?

A

Impaired coordination between the muscles of the pelvic floor –Commonly involves failure of the external anal sphincter to relax with attempted defecation

184
Q

Primary biliary cirrhosis is more prevalent in which sex?

A

women

185
Q

What causes familial porphyria cutanea tarda?

A

inherited mutations in uroporphyrinogen decarboxylase (UROD)

186
Q

What serum marker is used as a major diagnostic tool for cholestatic and obstructive hepatobiliary disease?

A

alkaline phosphatase (ALP)

187
Q

What are the modifiable colorectal cancer risk factors?

A

tobacco, alcohol, physical inactivity, obesity, diet (high in red meats, low in fruits and veggies)

188
Q

How do you confirm a celiac diagnosis ?

A

-endoscopic biopsy of the small bowel -anti-tissue transglutaminase (tTG) antibodies -anti-endomysial antibodies

189
Q

What’s the histology of liver in patients with alpha-1 antitrypsin mutations?

A

•Hepatocytes contain round, cytoplasmic globular inclusions

  • PAS positive, diastase resistant
190
Q

What is steatosis?

A

abnormal accumulation of lipid (triglycerides) within hepatocytes

191
Q

What causes alcoholic hepatitis?

A

•Due to acetaldehyde (a major metabolite of ethanol) damage to hepatocytes

192
Q

How is the diagnosis of herediatry hemochromatosis confirmed?

A

genetic testing

–In the setting of clinical iron overload, a genetic testing showing an HH-associated mutation is diagnostic (C282Y/C282Y or C282Y/H63D)

193
Q

List some osmotic laxatives.

A
  • Milk of magnesia
  • Mineral oil
  • Sorbitol
  • Lactulose
  • Magnesium citrate
  • Phosphate-based enemas
  • Polyethylene glycol (Miralax)
194
Q

List the stimulant laxatives.

A
  • bisacodyl (Dulcolax)
  • senna

stimulate colonic motility to help produce defecation

195
Q

List some common bulk forming agents

A

Metamucil, Citrucel, Fibercon, Konsyl

fiber supplements; act by increasing stool bulk and holding more water

196
Q

List a common stool softener.

A

•Docusate

Binds to stool and holds more water in the stool to make it softer

  • Very mild in action
  • Works better as a preventive agent than in treating established constipation
197
Q

What is lubiprostone and how does it work?

A

Laxative; binds and opens chloride channels in the colon to increase water in the lumen

198
Q

What is linaclotide and how does it work?

A

•Activates guanylate cyclase to increase cGMP production, resulting in the opening of ion channels and allowing an increase in ions and water in the lumen

GI/Nutrition (4 decks)

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