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Flashcards in Exam 2 Deck (444):
1

why do people turn yellow with jaundice

due to disease product bile leaks into blood and patients look yellow

2

how heavy is liver

1.5 kg

3

what is glisson's capsule

thin CT capsule deep to mesothelium around the entire liver

4

blood supply to liver (2) and route in liver

1. hepatic artery from aorta - supplies 25% of blood - highly oxygenized

2. portal vein - supplies 75% of blood - poorly oxygenated, nutrient rich

they mix in sinusoids, drain into central veins in the middle of lobules, and then trains into hepatic veins into the iVC

5

components of portal triad

branch of portal vein, branch of hepatic artery bile duct

6

what's a portal lobule?

roughly triangular with central veins at three corners and portal triad in the middle - emphasizes production of bile

7

what's the hepatic acini lobulation structure

diamond shaped with central veins and two ends and portal triads at middle ends - emphasizes blood flow

zone 3 is closest to central vein - recieves least oxygenated blood
zone 1 is closest to portal triad, gets damaged first by toxins

8

what kind of epithelium does bile duct have

simple cuboidal

9

kupffer ceclls

fat, phagocytic cells lining hepatic sinusoids

10

ito cells

store vitamin A

11

space of disse

between endothelium and hepatic parechymal cels - only see on EM

12

gall bladder histology

1. mucosa (no muscularis mucosae) has foldings
2. tall columnar abosrptive cells NO GOBLET CELLS
3. inner thick circullar, variable outler long
4. in neck, some mucous secreting cells in submucosa
5. mostly serosal, but neck is retroperioteal - adventitia

13

capillaries in pancreas - where are they open and where are they closed

closed in exocrine (enzymes), open in endocrine (hormones)

14

alpha and beta cells - what do the produce and where do you see them in light microscope

alpha- glucagon
beta - insulin

alpha smaller darker and peripheral
beta larger lighter and central

15

centroacinar cells

cell between acinus and intercalated duct

16

names of ducts (and epithelium type) from acinus to end of pancreas (4)

1- intercalated ducts (centroacinar cells at tips)

2- intralobular (cuboidal)

3- interlobular (low columnar)

4- main pancreatic (low columnar)

17

is pancreas mostly endocrine or exocrine

exocrine

18

what stimulates pancreatic enzyme secretion and through what pathway (5)

Calcium mediated:
CCK
ACh
GRP

cAMP mediated:
VIP
Secretin

19

salivary versus pancreatic secretions - hypo hyper or iso osmotic

salivary is hypo, pancreatic is iso

20

what transporters maintain gradient to pump bicarb out of pancreas (3)

1. basolateral sodium bicarb co transporter
2. basolateral sodium potassium ATPase
3. apical CFTR chloride channel

21

phases of pancreatic secretion (4)

1. basal - 10% enzyme secretion into acini

2. cephalic - neural signals, thinking about eating, Ach from vagus, increases enzyme secretion 20%

3. gastric - also Ach release by vagus from neural signals strech receptors, only 5% enzyme secretion

4. intestinal - 70% of excretion - copious in response to chyme in small intestine - CCK, Secretin, Ach and VIP (enteropancreatic reflex)

22

at what pH is secretin released

below 4.5

23

what are the primary bile acids (2), secondary bile acids (2) and bile salts (2)

primary (after 7alpha hydroxylase from cholesterol):
cholic acid
chenodeoxycholic acid

secondary (after bacteria does 7alpha dehydroxylase):
deoxycholic acid (from cholic)
lithocholic acid (from cheno)

bile salts:
taurine
glycine

24

bile salt independent flow regulators (3)

1. increased in response to secretin
2. opposed by somatostatin
3. comprised of secretion of bicarb, absportion of Na and Cl

25

sodium dependent bile acid transporters - what do they transport into the cell?

1. IONIZED unconjugated/free
bile acids
2. conjugated bile acids (ionized or not)

26

how does gut talk to the liver?

bile acids increase in ileal lumen

acids bind nuclear receptor FXR in ileal enterocyte and dimerizes with RXR

downstream gene expression of FGF19 increases

FGF19 gets into blood stream to liver, which gets to hepatocyte

FGF19 then inhibits CYP7A1 which in turn shuts down synthesis of 7alpha hydroxylase - rate limiting step in bile acid synthesis

27

when does glucuronidation happen

secondary bile acids are not good to have around, so they get glucuronidated

28

why is poop brown

conjugated bilirubin from liver gets converted via bacteria to urobilinogen, then to stercobilinogen, and then to stercobilin which is brown

29

why is pee yellow

urobilinogen gets oxidized to urobilin which is yellow

30

how does bilirubin get into hepatocyte

via OATP

31

how does bilirubin get into bile

conjugated to glucuronic acid via general transport MRP

32

jaundice in infants

(UGT) UDP-glucuronyl transferase reduced in infants

33

hemolytic jaundice - what kind of bilirubin do you see

lots of unconjugated bilirubin

34

obstructive jaundice- what kind of bilirubin do you see

lots of conjugated bilirubin

35

where does ammonia come from? (3)

50% from colon - bacterial ureases and AA metabolism

40% from kidneys - glutamine metabolism

red from RBC and muscle

36

which is caudate and which is quadrate

quadrate = with gall bladder

37

cystic artery comes off of what, and where is it

right hepatic, in the triangle between common hepatic duct and cystic duct and liver

38

branches if iMA

left colic - to descending colon and up to splenic flexture - then meets up with marginal artery

sigmoid arteries - to sigmoid colon (2-4 arteries)

superior rectal artery

39

ligament of treitz - AKA, where is it, what does it come from

suspensory ligament of duodenum - holds up the 4th part of duodenum, under the pancreas - from right crus of diaphragm

40

what does left crus of diaphragm do

nothing special

41

what part of pancreas is intraperitoneal

tail next to spleen

42

what vessel is the neck of the pancreas laying over

SMA

43

what structures are posterior to the SMA

unctinate process of pancreas and duodenum

44

hepatic portal vein components

union of smv and splenic vein

45

inferior mesenteric vein dumps into where usually

splenic vein

46

in what part of the duodenum does bile enter into

2nd part

47

why do women get gallstones more than men

high estrogen states makes bile precipitate

48

why do you get referred pain

general somatic and visceral nerve fibers converge on same spinal neuron - brain gets confused where pain is actually coming from

49

extra GI manifestations of gallbladder obstruction

- scleral icterus, jaundice and yellowing frenulum
- abdominal tenderness (somatic localized or visceral diffuse pain)
- mass (distended gall bladder, neoplasm)

50

murphy's sign

acute cholecystitis -

51

cullen's sign and grey-turner

flank, peri-umbilical ecchymosis/ bleeding
- hemmorhhagic pancreatitis

52

boas sign

irritation heightened sensation in scapular region - referred pain T6-T8

53

rebound tenderness

peritoneal inflammation

54

lab data for gallbladder obstruction (3)

total and direct bilirubin (Extrahepatic obstrution)

gamma glutamyl transpepeitase (Extrahepatic)

amylase rises earlier in pancreatitis, lipase rises later

55

is normal gallbladder hypo or hyper echoic

hypo, hyper would indicate stones (stones also have shadows behind)

56

acute cholecystitis on US (2)

obstruction causes contraction and thickening of the wall

increased bile density - super saturated

57

fat stranding on CT - what does it indicate

haziness - indicates inflammation

58

HIDA scan

hepatobiliary iminodiacetic acid - tracer attaches to anywhere with bile. want to see if it's emptying completely

59

cystic duct obstruction
lab values

normal LFTs and normal pancreatic enzymes

60

when do you get gangrenous changes in gallbadder

if you let acute cholecystitis go on too long

61

what oxidation state of iron can cross through membranes

+2

62

what oxidation state is stored as ferritin

+3

63

which oxidation state of iron is more dangerous

+2

64

how do you go from transferrin outisde of cell to iron inside cell

transferrin receptor is endocytosed, acidified, transerrin releases +3 iron, which is reduced to +2, transported out of endosome and used, any extra is stored as +3 in ferritin

65

heme biosynthesis steps (feedback and rate limiting) (4)

1. glycine +succinyl-CoA makes 5ALA (via 5ALA synthase - rate limiting step in LIVER) feedback inhibition by hemin (+3 oxidized heme) and lead (replaces zinc cofactor)

2. 2 molecules of 5ALA get converted to porphobilinogen via 5ALA dehydratase

3. 4 molecules of porhobilinogen get converted to uro-porphyrinogen 3 somewhat spontaenously

4. Uro-porphyrinogen 3 then becomes protoporhyrin 9 - and ferrochelatase inserts iron into ring structure and makes heme (rate limiting in RBCs, inhibited by lead)

66

what does 5ALA synthase do and what do you get if it's deficient

makes 5ALA from glycine and succinyl co-a

get X-linked sideroblastic anemia

67

what does ALA dehydratase do and what do you get if it's deficient

takes 2 ALA and makes porphobilinogen

get ALA dehydratase deficient porphyria

68

what does PGB deaminase do and what do you get if it's deficient

takes 4 porphobiliogen into hydroxymethylblaine

get acute intermittent porphyria

69

what does uroporphyrinogen 3 synthase do and what do you get if it's deficient

takes hydroxymethylblaine and makes uroporphyrinogen 3

get congenital erythropoetic porphyria

70

what does uroporphryinogen decarboxylase do and what do you get if it's deficient

takes uroporphyrinogen 3 and makes coproporphyrinogen 3

get porphyria cutanea tarda

71

what does coporporhyrinogen oxidase do and what do you get if it's deficient

takes coproporphyrinogen 3 and makes protoporphyringoen 9

get hereditary coproporphyria

72

what does protoporhyrinogen oxidase do and what do you get if it's deficient

takes protoporphyrinogen 9 and makes protoporphyrin 9

get variegate porphyria

73

what does ferrochelatase do and what do you get if it's deficient

adds iron to protoporphryin 9 and makes heme b

get erythropoetic protoporphyria

74

which steps in heme biosynthesis happen in mitochondria

first and last 3:

enzymes:
1. 5ALA synthase
2. coproporphyrinogen oxidase
3. protoporphyringen oxidase
4. ferrocheletase

75

what happens with water, sunlight and conjugated double bonds

make free radicals - peroxides etc.

76

what kinds of porphyria are considered acute (3)

1. acute intermittent
2. variegate
3. hereditary coproporphyria

77

what are symptoms of acute porphyria (5)

1. ab pain
2. purple skin rashes
3. red urine
4. muscle weakness
5. psychotic episodes

inducible expression

78

what kinds of porphyria are considered chronic (3)

1. congenital erythropoeitic porphyria
2. porphyria cutanea tarda
3. veriegate porphyria

79

chronic porphyria symptoms (4)

1. derm issues (light sensitive, blistering)
2. red urine, blue urine
3. werewolf syndrome - fine hair body-wide, light sensitive
4. vampire syndrome - red fluorescent teeth and gums, light sensitivity AND can't eat garlic for GI issues

80

tx for acute porphyria

hemin - feedback inhibition of ALA synthase

81

what oxygenation state likes to bind to cyanide

+3 - methemoglobin

82

what helps RBCs off load more oxygen

rapaport luebering shunt - stabilizes deoxygenated state

83

Glucose 6 phospate dehydrogenase deficiency

quinine generates free radicals - causes hemolytic anemia

84

what mechanisms are in place to reduce organ damage with hemolysis (2)

haptoglobin - complexes with hemoglobin from lysed RBCs to protect kidney filtration

hemopexin - binds free heme or hemin to generate free radicals

85

what oxygen state is the iron in hemin

+3

86

what happens to hemoglobin in macrophage, once RBC is internalized?

hemoglobin gets broken down into hemin and globin

hemin gets converted to biliverdin via heme oxygenase with NADPH (produces CO)

biliverdin gets converted to bilirubin via biliverdin reductase and NADPH

87

structural difference between biliverdin and bilirubin

verdin is green - has double bonds, is linear, modestly soluble - can interact with water

rubin - 4 single bonds, can rotate and fold back on itself - not soluble, needs to be transported via albumin to the liver to get glucuronidated to make it soluble

88

what's the enzyme that's deficient in neonates

glucuronosyl transferase

89

why does phototherapy work for neonatal jaundice

light (blue especially) converts unconjugated bilirubin into isomeric form (bilverdin) the the liver can kick to bile

90

van den bergh reaction equation

total bilirubin (indirect reacting) - conjugated bilirubin (direct reacting) = unconjugated bilirubin

91

stellate cells - where are they, what do they do

in spce of disse, store vitamin A in quiescent state, activated cells become myofibroblasts that make collagen - for scar formation in liver damage

92

what proteins does the liver make (2)

albumin and most clotting factors

93

when does jaundice become visible

when bilirubin is 2x normal in adults, or 5x normal in neonates

94

halflife of bilirubin-dicluronide, vs bilirubin and biliprotein

biliprotein halflife is 20 days versus 1 day for bili-diglucuronide

95

how to measure direct and indirect

direct measures conjugated - turns serum blue - how much blue, then accellerant is added, and then you measure the rest - then get total

96

prehepatic - what kind of bilirubinemia do you get

increased all uncojugated

97

hepatic- what kind of bilirubinemia do you get

elevated in both - prevents unconjugated from excreting and conjugated from being conjugated

98

post-hepatic - what kind of bilirubinemia do you get

at first, you have increase of conjugated, but then you start to see increases in conjugated too - cause hepatocyte damage eventually

99

cause of pre-hepaitc hyerbilirubinemia

1. hemolysis, transfusion

2. decreased albumin-bilirubin binding

3. decreased hepatocyte internalization

last two affect neonates - physiologic jaundice, can lead to kernicterus - treat with UV light or phenobarb

100

parenchymal causes of hyperbilirubinemia (5)

high unconj:
1. Gilberts
2. Crigler-Najjar type 1

both:
3. Cirgler-Najjar type 2

more conj than unconj:
4. cirrhosis
5. hepatitis

101

enzymes that indicate bile stasis (2)

1. alk phos (7 day half-life)

2. gamma-glutamyl transferase (26 day half-life) - indirect marker of alcohol abstinence

if both are increased, indicates damage to cannalicular membranes. if just alk phos, could be bone, placenta etc.

102

decrease in albumin might mean acute or chronic liver problem

chronic - half life is 20 days

103

increased prothrombin time indicates what kind of liver problem

in acute, severe liver injury - half life is 6 hours (depends on vitamin K - give vitamin K to see if it resolves)

104

liver transaminase half-lives

cytosolic ALT is 48hours

cytosolic AST is 8 hours

mithochondrial AST is 10 days

lactate dehydrogenase - 4-6hours

105

acute, abrupt liver injury - which transaminase is higher

AST is higher, much more of it in liver cell than ALT

106

lower grade and sustained liver injury - which transaminase is higher

ALT is higher - longer half life

107

alcohol-related liver injury - which transaminase is higher

AST is higher than ALT - alcohol inhibits ALT synthesis

108

injury versus function enzymes

bilirubin, albumin and PT are liver fucntion

AST and ALT and alk phos are mark of injury

109

congeintal anolomalies in gall bladder (6)

1. sometimes under left lobe
2. cysts and 3. diverticulae
4. septate gallbladder, multpile gallbladders
5. heterotopia - normal tissue in abnormal location- pancreatic tissue in wall of gallbladder
6. hypoplasia

110

cholesterolosis

red-tinged with yellow stippling- foamy macrophages with cholesterol esters deposited in lamina propria

111

composition difference between cholesterol and pigmented stones

cholesterol has more than 50% cholesterol component

112

different risk factors for choletsterol stones

high fat, age, female gender, pregnancy, obesity, bile stasis

113

risk factors for pigmented stones

heredity
helolytic syndrome
biliary infectinos
GI diseases - chrohn's etc.

114

what do you see in gross for acute cholecystitis? (3)

1. hemorrhage
2. edema
3. mucosal ulceration

115

what do you see in histo for acute cholecystitis

1. fibrin exudate
2. neutrophils
3. hemorrhage that can extend through wall and be necrosis

116

chronic cholecystitis gross findings (1)

thickening of wall

117

chronic cholecystitis histo findings (5)

1. Rokitansky-Aschoff sinuses (look like diverticuli)
2. SM hypertrophy
3. lymphocytic infiltrate
4. granulomas +/-
5. hyperplastic or metaplastic epithelium

118

follicular cholecystits findings and associations (3)

lymph follicles in gallbladder, associated iwth primary sclerosing cholangitis, typhoid and gram neg bacterial infection

119

xanthogranulomatous cholecystitis findings (5)

1. foamy macrophages
2. cholesterol clefts
3. extruded bile
4. multinucleated giant cells and neutrophils
5. thickening of wall with yellow-brown nodules

120

hyalinizing cholecystitis findings and associations (1)

1. replacement of gallbladder wall by hyalinized fibrosis
2. associated with occult adenocarcinoma

121

gallbladder tumors (4)

1. benign (adenomyoma)
2. polyps (cholesterol non-neoplastic, adenoma papillary neoplasms)
3. epithelial dysplasia (biliary intraepithelial neoplasia)
4. malignant adenocarcinoma

122

where/when are adenocarcinomas usually found

in fundus and body more so than the neck in older female with stones, esp in south america

123

What parts of the pancreas come from which embryological structures "buds"

ventral bud (from hepatic duct) - forms posterior/inferior head and uncinate process

dorsal bud (From foregut) - forms body, tail and anterior head

124

congenital pancreatic disorders (4)

1. annular pancreas around 2nd part of duodenum
2. divisum - failure of duct fusion (2 ducts) associated with cancers
3. heterotopic pancreas (tissue from pancreas in stomach, duodenum, jejunum)
4. metabolic disorders

125

acute pancreatitis gross/histo findings (4)

1. interstitial edema
2. hemorrhage
3. necrosis (and fat necrosis)
4. pancreatic pseudocysts

126

chronic pancreatitis findings gross and histo (3)

1. loss of parenchyma - replaced by fibrosis and fat tissue
2. chronic inflammation around lobules and ducts (sparing islets)
3. can mimic a pancreatic mass

127

causes of chronic pancreatitis (6)

1. genetic (CFTR)
2. toxic (calc, lipid, alcohol, smoking, hydrocarbons, drugs -thiazides)
3. obstruction
4. autoimmune
5. infectious
6. other (radiation, post-transplant)

128

pseudocyst composition

no epithelial lining, fillled with turbid, blood tinged fluid = necrotic debris, inflammation, hemorrhage, walled off by fibrosis sometimes

129

pancreatic tumors (4)

most are malignant and solid:
1. ductal adenocarcinoma
2. neuroendocrine tumors
3. anaplastic carcinoma
4. acinar cell carcionma

130

panIN

less than 5mm
dysplasia in cysts in pancreas - benign pancreas

grade by low and high - becomes more papillary and enlarged nuclei that lose polarity

131

pancreatic neuroendocrine tumor types and grading

"functional" - have clinical presentation (insulinoma - fainted, irregular heart rate)
"non functional" - no clinical presentation (usually found more advanced)

grading (3) based on mitotic count and IHC

132

anaplastic carcinoma characteritsics (4)

undifferentiated, large eosinophilic cells
rare
poor porgnosis

133

acinar cell carcinoma characteristics (3)

1. metastatic at presentation
2. syndrome of lipase hypersecretion - polyarthralgias, fat necrosis, peripheral eosinophilia
3. sheet of acinar cells

134

serous cystadenoma characteristics (4)

1. benign neoplasm (but may metastasize)
2. central stellate scar with surrounding cysts
3. cysts lined by cuboidal epithelium
4. associated with VHL gene mutation

135

solid pseudopapillary neoplasm - characteristics (4)

1. seen in young females
2. well circumscribed mass with solid and necrotic parts
3. on histo - papillary with fibrovascular cores
4. associated with beta catenin gene mutation (CTNNB1)

136

mucinous cystic neoplasm (4)

1. more freqently in females
2. mucious material and epithelium
3. wall looks like ovary (spindled stroma)
4. associated with KRAS and secondary mutations later

137

intraductal papillary mucinous neoplasm findings (4)

1. more in men
2. mucinous materal and epithelium
3. are associated with pancreatic duct
4. KRAS and/or GNAS mutations

138

what do mets to the pancreas look like

multiple (intrinsic tumors tend to be solitary) well circumscribed masses

139

are cholesterol stones seen on xray?

no - low calcium

140

what kind of bilirubin is in pigmented stone

unconjugated

141

do you see pigmented stones on xray?

yes

142

which kind of stones are infectious

brown pigmented stones (E. coli)

143

what kind of stones are seen in hemolysis and sickle cell

black pigmented stones

144

why does rapid weight loss result in gall stones

lipids go down, so abnormal composition in bile - get bound to calcium and form stones

145

charcot's triad

RUQ pain, fever, jaundice

146

reynolds pentad

charcot's triad plus sepsis and mental status changes

147

how big is ileocecal valve - aka what size stones will cause obstruction

15mm

148

when do you intervene in sphincter of oddi dysfunction

you need to have at least either abnormal liver enzymes or abnormal biliary imaging, biliary type pain is not sufficient

149

causes of acute pancreatitis (6)

1. stones
2. alcohol
3. trauma
4. post-op
5. meds (steroids, estrogens, HIV meds, antibiotics)
6. high triglycerides (over 1000) and calcium

150

what can kill you with acute pancreatitis (2)

ARDS
splenic artery rupture

151

what 2 out of 3 things do you need to indicate acute pancreatitis

1. ab pain
2. CT findings
3. abnormal lab work (increased lipase and amylase)

152

how bad does chronic pancreatitis have to get to cause steatorrhea and fat malabsorption?

have to burn through 90% of exocrine function

153

fecal elastase indication

if low, then it indicates poor exocrine pancreas function

154

how does chronic pancreatitis sx work (peustow's, frey, whipple)

slice pancreas like a sausage, put part of the intestines in there - decreased ductal pressure

155

how likely are people with chronic pancreatitis to get cancer

4x more likely

156

primary biliary cholangitis associations/patient demographic

1. 30-65 age
2. female predominance
3. associated with thyroid and autoimmne

157

primary biliary cholangitis physical exam and symptoms (8)

1. pruritis
2. fatigue
3. hyperpigmentation
4. xanthelasma (deposits on eyelids)
5. dry eye and mouth (sicca syndrome)
6. jaundice
7. excoriations from itching
8. hepatosplenomegaly

158

what do you do when someone has elevated alk phos

elevated ggtp and 5nt - indicate liver

if liver, go over drug list, AMA (primary biliary cholangitis) ACE (sarcoidosis) RUQ US

159

primary biliary cholangitis lab findings (5)

1. elevated alk phos
2. AMA pos (95%)
3. ANA pos (70%)
4. elevated IgM
5. elevated cholesterol and lipids

160

histo findings for primary biliary cholangitis (3)

1. "florrid" interlobular duct lesions - inflammation around duct (plasma cells, macrophages, eosinophils)
2. granulomas if present are highly indicative
3. eventual fibrosis which leads to cirrhosis

161

treatment for primary biliary cholangitis (2)

ursodeoxycholic acid - which increases bile flow and decreases toxic/hydrophobic bile acids by replacing with more hydrophilic and antinflammatory bile acids

cholestyramine for pruritis (bile acid sequestrants)

162

primary sclerosing cholangitis associations/patient demographics (4)

1. mean age 41
2. 70% male
3. 80% have UC
4. maybe bacterial infection

163

what size ducts are affecting in primary sclerosing cholangitis

medium and large (as opposed to biliary cholangitis - which is interlobular and small ducts)

164

symptoms of primary sclerosing cholangitis (5)

1. RUQ pain
2. fatigue
3. pruritis
4. fevers, chills, night sweats
5. jaundice

165

lab findings in primary sclerosing cholangitis (3)

1. elevated alk phos
2. high IgG4 (steroid responsive) and IgM levels
3. P-ANCA positive

166

imaging findings for primary sclerosing cholangitis (3)

1. bile duct wall thickening and focal dilations
2. beaded appearance of bile duct (short strictures)
3. later, see obliterated ducts with strictures - "pruned tree" appearance

167

histo findings for pirmary sclerosing cholangitis

fibrous obliteration of small bile ducts - onion skinning pattern

168

treatment for primary sclerosing cholangitis

ursodeoxycholic acid - possible, not shown

management of symptoms and liver transplant (recurrence happens often at 5 years)

169

immune-mediated pattern of liver disease - timing of rise of enzymes

slow to rise over several weeks, plateaus and slowly resolves. usually prothrombin time is normal

170

direct toxic pattern - timing of enzymes

pulse injury - marked release in liver enzymes at once (AST higher at first), falls precipitously

171

alcohol related pattern - timing of enzymes

flat - inhibit the synthesis of enzymes to some extent

172

acute viral heptatis histology findings

red swollen liver
1. infiltrate in portal tract and in parenchyma
2. necrosis
3. drop out and apoptotic bodies

173

unpredictable drug reaction liver injury

parenchymal hepatitis that looks a lot like viral hepatitis

174

predictable drug reaction liver injury

see necrosis in zone 3 - looks like ischemia

175

alcohol hepatitis injury pattern

sudden acute liver fat accumulation and inflammation in zone 3 with BALLOON CELLS empty looking cells, and cells with fat globules, some have intermediate fillament aggregations in them (MALLORY BODIES)

176

ascending cholangitis on histology (5)

1. hepatocytes with feathery degeneration (xanthomatous degeneration)
2. bile infarcts/plugs
3. bile lakes
4. ductular proliferation
5. neutrophils

177

causes of chronic hepatitis (3)

1- viral (hep B and C)
2- autoimmune
3- drug-related

178

causes of metabolic chronic liver injury (3)

1- hemachromatosis
2- Wilson's disease
3- antitrypsin deficiency

179

causes of vascular chronic liver injury

1. venous outflow obstruction (Budd-Chiari)
2. CHF and ischemic necrosis

180

examples of chronic cholestatic syndromes (3)

1. partial extrahepatic obstruction
2. primary biliary cirrhosis
3. primary sclerosing cholangitis

181

clinical definition of chronic hepatitis (2)

ALT or AST >1.5X (ALT usually higher except for end stage and alcohol)
4-6 mo duration

182

histology of chronic viral hepatitis

zone 1 lymphocytic infiltrate and necrosis. more so in portal tract than parenycmal

183

top 3 causes of liver disease

1. hep B and C
2. alcohol
3. non-alcoholic (getting greater)

184

what is erosion of "limiting plate" on histo and when do you see it

limiting plate is boundary of portal triad - in chronic hepatitis you erode that limiting plate - interface hepatitis

activity grade = how much necrosis do you see

185

fibrous stages in chronic hepatitis

1. enlarged portain tract
2-3. bridges of fibrosis - portal to portal tract
4. cirrhosis encircling fibrosis around regenerative nodules of hepatocytes

186

clues to distinguish chronic hepatitis causes (3)

classic for viral is GROUND GLASS HEPATOCYTE - excess of surface antigen in endoplasmic reticulum - hep B

autoimmune - PLASMA CELLS

drug tox - EOSINOPHILS

187

who gets autoimmune hepatitis

mostly European females, bimodal age distribution, half have extrahepatic autoimmune disease

188

diagnosis of autoimmune heptatitis - tests (3)

ANA (67%)
SMA (87%)
liver biposy (plasma cells)

189

tx for autoimmune hepatitis

steroid

190

what do you see with chronic ischemic fibrosis

chronic centrilobular fibrosis (zone 3)

191

risk factors for chronic liver ischemic/vascular congestion/necrosis

Budd Chiari:
1. young woman - oral contraceptives or pregnancy, and other hypercoaguable states
2. hepatocellular carcinoma
3. right heart failure- cor pulmonale

192

gross characteristic of chronic vascular congestion/necrosis/ischemia

NUTMEG LIVER - congestion and dilation in sinusoids

193

treatment for budd-chiari (3)

1. antithormbotics if quick enough
2. management of ascites
3. TIPS stent to relieve pressure

194

alpha-antitrypsin deficiency also causes

emphysema

195

genes involved in hereditary hemochromatosis

C282Y

H63D gene

196

extrahepatic manifestations of hereditary hemochromatosis (4)

1. cardiomyopathy
2. skin and pancreas - bronze diabetes
3. degenerative arthritis (does not resolve with tx)
4. low libido (pituitary - hypogonadism)

197

histo - hereditary hemochromatois

iron accumulation IN HEPATOCYTES (not just macrophages)
golden brown on H&E
can do prussion blue stain for positive

198

gene related to wilson's

ATP7B

199

when do you start to see copper in extrahepatic tissue

when liver is overwhelmed - probably already cirrhotic

can see movement disorders, RBC hemolysis, renal tubular acidosis, cornea

200

what's the best diagnostic test for wilsons

24hr urine copper excretion test is good

liver biopsy is gold standard

201

copper accumulation in histo

Rhodanine stain - red granules

202

alpha-antitrypsin deficiency gene

protease inhibitor PiZZ

203

histo finding for alpha antitrypsin

PAS diastase resistant red granules

204

difference between steatohepatitis and fatty liver disease

steatohepatitis has inflammatory component - worse- cause chronic damage

205

nonalcoholic steatohepatitis findings (lab)

ALT>AST (opposite for alcohol)
20% lead on to cirrhosis

206

treatment for nonalcoholic steatohepatitis

vitamin E
weight loss and diabetic control

207

steatohepatitis gross presentation

"micronodular" cirrhosis (nodules less than 0.5cm

208

difference between forms of steatohepatitis on histo

mostly the same, but non-alcoholic has more lymphocytes, not so many neutrophils (as opposed to alcohol)

209

flroid duct associated iwth what

PBC

210

onion skin fibrosis of ducts associated with

PSC

211

how to make diagnosis of PSC

imaging

212

what about hepatocytes and sinusoids changes in cancer

hepatocytes are 1-2 cells thick so that every hepatocyte has access to sinusoid, even in cirrhosis, if that's disturbed then that indicates cancer

213

chronic cholestasis extrahepatic manifestations

pruritic rash
xanthelasma (on eyes)
xanthomata (on hands )

214

hepcidin role

normal hepcidin works to endocytose ferroportin transporters, thus decreases iron absorption

abnormal hepcidin (caused by HFE gene mutation) doesn't downregulate iron absoprtion, thus allowing for too much iron into the cells

215

lab values/test for hemochromatosis (2)

1. iron/TIBC >45%
2. ferritin >200 in men and 150 in women

if any of those are positive then do genetic screening (for H63D and C282Y)

216

goal of phlebotomy in hemochromatosis

get ferritin less than 50

217

what should people with hemochromatosis NOT do (3)

1. take iron supplements
2. drink alcohol
3. get cirrhotic - higher chance of cancer

218

patient presents with mental status changes, hemolysis and increased liver enzymes

Wilson's

219

why does Wilson's lead to hemolysis

copper damages RVC cell membrane

220

what lab values/tests do you look for in wilsons

low ceruloplasmin (ceruloplasmin bound to copper does not show up - meaning there's a lot of copper)

urine 24hour commer excretion

221

tx for wilson's (3)

Chelation:
D-penicillamine (EXCEPT in mental status change)
Trientine (in mental status changes)

oral zinc - decreases copper stores, and dietary modification

222

patient presents with RUQ tenderness, elevated liver enzymes, and hyperinflated lungs

alpha 1 antitrypsin deficiency

223

dx for alpha 1 antirtyprsin (2)

blood test for levels and function of antitrypsin protein

liver biopsy

224

tx for alpha 1 antirtyprsin (1)

AAT replacement for lung injury. liver injury is non-reversible - eventually will need transplant

225

what BMI is morbid obesity

over 40

226

swollen smooth liver can be seen with (2)

edema
fat

227

what test is less useful in people with morbid obesity

NAFLD fibrosis score calculator

228

where does collagen get laid down in fatty liver

perisinusoidal - in SPACE OF DISSE

229

where is scar in steatohepatitis and cirrhosis

steato = centrilobular
cirrhosis - encircling hepatocytes

230

drinks/week risk factors for alcoholic liver disease

14/week for women
21/week for males

231

"metabolic syndrome" risk factors for non alcoholic fatty liver disease (5)

1. fasting glucose >100
2. obesity
3. triglycerids >150
4. BP over 130/85
5. HDL <40 in men and 50 in women

232

pathogenesis of non alcoholic fatty liver disease and steatohepatitis

in insulin resistance:
- decreased adiponectin (which, with the help of PPAR gamma, normally decreases lipid synthesis)
- triglycerides accumulate in liver
- SECOND HIT from microbiome - generates free radicals, stimulates inflammation

233

pioglitazone recommendation and adverse

recommeneded for NASH, but everyone gains weight on it

234

vitamin E adverse

in men is linked to prostate cancer

235

patient presents with jaundice, arthralgia, amenorrhea, fever for 4months. takes OCP. elevated liver enzymes, ANA and ASMA

Autoimmune hepatitis

236

what immune cell is predominant in the infiltrate in autoimmune hepatitis

T cells (also plamsa cells)

237

type 1 autoimmune hepatitis demographics and antibodies

(80% of AIH cases)
female, young
ANA and/or SMA
commonly associated with other autoimmune diseases (thyroid, UC)

238

type 2 AIH demographics and antibodies

anti LKM1 and/or anti LC1 or LKM3

mostly children
other immune diseases
progresssion to cirrhosis is common

239

which Ig levels are abnormal in AIH?

IgG is high

240

histo of AIH (2)

interface hepatitis (zone1 and triad)

plasma cells, lymphocytes

241

tx for AIH (3)

corticosteroids
azathioprine
6MP

242

phase 1 and 2 reaction enzymes and "zones" for drug metabolism

phase 1 cyt p450 (in zone3 - O2 depleted areas)

phase 2 glutathione (in zone1 - O2 rich areas)

243

R value

ratio of ALT/Alk phos:

greater than 5 = hepato
less than 2 = cholestasis

244

high INR means what

can't clot quickly enough

245

what kind of pathology does amox/calv cause

intrahepatic cholestasis

246

are NSAIDS predicatable or unpredictable

unpredictable

247

hepatic encephalopathy causes (4)

alteration of CNS due to hepatic insufficiency triggered by increased nitrogen, increased ammonia - encephalopathy

causes:
- infection
- upper GI bleed
- constipations
- electrolyte abnormalities

248

west-haven criteria/staging

for hepatic encephalopathy
stage 0-4:

- stage 0 have impoaried psychomotor testing
- stage 1 short attention, mild asterixis
- stage 2 - lethargic, asterixis
- stage 3 - will around
- stage 4 - comatose

249

how to dx hepatic encephalopathy

don't take ammonia level - might not represent brain levels

diagnosis of exclusion and clinical, eps with known cirrhosis

250

tx for hepatic encephalopathy (2)

1. lactulose - facilitates ammonia to ammonium, less absorbed

2. rifaximin - reduce bacterial production of ammonia

AVOID BENZOS

251

3 main mechanisms of ascites

1. portal htn
2. low albumin
3. peritoneal diseases - TB, cancer

252

serum ascietes albumin gradient (SAAG) - how do you get it, what is significant

subract ascitic fluid albumin from serum albumin:

normally less than 1.1
if more than 1.1 - 97% chance they have portal hypertension (albumin is large, can't cross barrier - stays high in serum)

253

if someone has ascites and is febrile, what are you thinking, and how can you tell if you're right

spontaneous bacterial peritonitis - do culture for PMN count>250

254

what causes spontaneous bacterial peritonitis

increased intestinal permeability, gut flora overgrowth - bacteria can translocate and colonize mesenteric lymph nodes and the fluid

255

tx for spontaneous bacterial peritonitis

life-long antibiotics

256

at what pressure gradient (between wedge hepatic and free hepatic venous) do you get worried at

10% - risk for variceal hemorrhage

257

red wale marking or white nipple sign - what is it, what does it indicate

red wale - vein very close to the surface,
white nipple - fibrin clot on varices (in esophagus) makes you very worried about hemorrhages

258

what is primary preventative treamtnet for esophageal variceal hemmorage (BEFORE bleed) (2)

non selective beta blockers (propranolol, nadolol)

banding if BB not tolerated

259

what is acute management of variceal hemmorage (4)

1. volume, coag and hemodynamic stability recussitation
2. intubate
3. octreotide
4. antibiotics

260

if acute management of variceal hemmorhage does not work, what do you do next (2)

1. tamponade iwth balloon
2. TIPS (in portal system) shunt surgery

261

what does AFP (alpha fetal protein) elevation indicate (2)

chronic heptatitis (hep B with or without cirrhosis)

can indicate hepatocellular carcinoma when it's over 250

262

how do you dx hepatocellular carcinoma

triple phase CT (arterial phase, portal phase, venous phase - will see WASHED OUT venous phase
increased intesity during arterial phase

if no classic CT or lab values, then do biopsy

263

tx for HCC

liver transplant
(only a candidate if you have 1 tumor less than 5cm or less than 3 tumors less than 3cm)

local ablation, chemoembolization

264

surveillance for HCC

ultrasounds every 6 months for all patients with cirrhosis, or chronic hep B (africans younger, then asians, and family hx of HCC)

265

hepatorenal syndrome type 1

rapid decline in renal function (doubling of creat in less than 2 weeks)

266

hepatorenal syndrome type 2

less rapid - may be manged in outpatient

267

tx for hepatorenal syndrome

IV albumin, octreotide, midodrine
only as bridge to liver transplant (necessary)

268

how do dx hepatorenal syndrome (3)

1. cirrhosis WITH ascites
2. serum creat >1.5
3. no response to volume expansion with albumin

269

non-specific stigmata of chronic liver disease 94)

1. palmar erythema
2. clubbing
3. spider angiomata
4. gynecomastia

increase in female estrogenic hormones and nitric oxide

270

portal hypertension cause classifications

prehepatic (portal vein thrombosis)

hepatic (cirrhosis, shistosoma)

posthepatic (budd-chiare, CHF)

271

what's a dangerous hepatic wedge pressure

over 12 - usually means cirrhosis

272

"compensatory" hypothesis for ascites

lymphatics weep, pressure pushes by hydrostatic pressure into peritoneal space, liver not making enough albumin, so not keeping osmotic pressure in vascualr space

273

"overflow" hypothesis for ascietes

primary renal retention - senses displacement of fluid into peritoneal space as hypovolemia - increases renin and aldosterone - sodium retention. makes more peritoneal fluid

274

what drugs do you stop if patient has ascites

NSAIDS and renal-toxic drugs like aminoglycodie antibiotics

275

tx for ascites (3)

diuretics: spironolactone and furosemide (watch for hypovolemic shock)

large volume pericentesis (not more than 4-5L)

with concurrent albumin infusion

276

when someone has really really bad breath, what do you think they might have, what substance makes the smell

hepatic encephalopathy , breath caused by mercaptor

277

child's pugh score

broad score of severit of cirrhosis using 5 parameters:
1. encephalopathey
2. ascites
3. high bilirubin
4. low albumin
5. decrased prothrombin ratio

A = normal paraeters (40mo)
B = 1-2 abnormal parameters (32mo)
C = more than 2 (8mo)

278

meld score critea

for transplant list

uses creatining, bilirubin and INR

less than 10 score (going to survive more than 1 year) not on list. has to have less than 1 year survival

279

liver neoplasms - benign (2) and malignant

benign
1- hemangioma (most common liver neoplasm) cavernous type can be problematic
2- hepatic adenoma - related to females because of estrogen, fibrous capsule with normal hepatocytes but no portal tracts or veins. can grow and rupture

malignant - HCC

280

what viruses ONLY cause acute hepatitis (7)

1- hep A
2- hep E
3- EBV
4- CMV
5- HSV
6- VZV
7- yellow fever

281

what viruses cause BOTH acute and chronic hepatitis (3)

hep B
hep C
hep D

282

average incubation for acute hep A

30 days - infectious 1-2 weeks before symptoms present

283

labs for symptomatic acute hep A and E (2)

ALT>AST, over 1,000
elevated total bilirubin

284

types of hep E

5 types, 4 infect humans

GT1,2 have no animal reservoir and only fecal-oral transmission

GT3,4 is zoonotic - swine, deer, elk, bears, cattle (eating or bite from flea)

285

why do kids with Hep A or E have less severe symptoms than adults?

because the symptoms are a result of the immune response, not the virus itself

286

why is there a high mortality rate with hep E?

can get fulminant hepatitis if acquired during PREGNANCY (worse further along in pregnancy)

14-30% mortality rate in preg women

287

chronic hep E - what patients

transplant, chemo, HIV infected - rapid development of cirrhosis

288

definition of chronic viral hepatitis (timing)

hepatitis lasting longer than 3 months

289

hep B - when do infections occur

perinatal or early childhood

290

which of the hepatitis viruses are DNA

hep B

291

what antigens are specific for Hep B (3)

1. hep B surface antigen
2. hep B core antigen
3. hep B e antigen - marker of viral replication and infectivity

292

horizontal transmission of HBV (3)

1. needle sticks
2. sex
3. dialysis and transfusion

293

what can you do to reduce verticle transmission of Hep B?

give hep B immunogloblulin and vaccine to baby within 12 hours of birth

294

chronic hep B symptoms (4)

often nothing specific, but can have
1. cirrohsis symptoms
2. polyarteritis nodosa
3. glomerulonephritis
4. can go on to HCC because it integrates viral DNA (with or without cirrhosis)

295

HBV tx

tenofovir - nucleoside reverse transcriptase inhibitor - good because it's low resistance

296

hep D - who gets it

needs hep B for replication cycle

297

what causes symptoms of hep D

direct cytopathicity of virus - not from immune response like others

298

different classes of clinical preserntations of hep D (2)

can have coinfection:
- simultaneous hep B infection
- usually self-limiting

or

can have superinfection:
- acute D infection with chronic B infection
- get chronic D infection
- higher rates of liver failure, cirrhosis and cancer (worse than with B alone)

299

hep C viral characteristics (5)

1. flavivirus (like yellow fever)
2. infects only men and apes
3. very high replication rate
4. no proof-reading, so has high variablitly
5. uses membranous web for replication, does NOT integrate into DNA

300

what percentage of people with acute hepC progress to chronic

80-85%

301

what cofactors makes hepC infection worse and more likely to progress (4)

alcohol
HIV
male sex
older age

302

extra-hepatic manifestations of hep C (6)

1. cryoglobulinemia and assctd vasculitis
2. sjogren's
3. lymphoproliferative disorders
4. porphyria cutanea tarda
5. neuropathy
6. membranoproliferative glomeruloneprhtitis

303

fibroscan implication and use

for staging of liver disease

shear wave - faster it is the more scar you have

304

ribaviron mechanism of action

guanosine analog
inhibits viral RNA dependent polymerase, induces mutations in RNA

used for HCV

305

ribavirin adverse effect

hemolytic anemia

306

pegylated interferon mechanism of action

binds to membrane receptor and inhibits viral penetration, translation, transcription etc. ramps up immune system

(induces phagocytic activity of macrophages, prolieferation of cytotoxic T cells, and major histocompatibility complex antigens)

Hep C

307

pegylated intereron adverse effects

induces horrible flu-like symptoms

308

simeprevir mechanism of action

HCV protease inhibitor

used to treat HCV1

309

simeprevir adverse effects (3)

1- rash
2- photosensitiivity
3- drug-drug (p-glycoprotein transporter/cyp3A4 hinibitors)

(can have reactivation of HBV if co-infected)

310

sofosbuvir mechanism of action

RNA-dependent NS5B RNA polymerase inhibitor

has activity against all HCV genotypes and those resistant to PIs

311

sofosbuvir adverse effects (2)

1. not recommended for patients with severe renal dysfunction
2. drug-drug (P-gp induces like rifampin)

(can have reactivation of HBV if co-infected)

312

ledipasvir mechanism of action

inhibits NS5A protein which normally assembles the replisome

in combo with sofosbuvir = harvoni --> more effective

approved for HCV 1

313

ledpasvir adverse effects

no real toxicities by itself, but in combo with sofosbuvir can't take with renal dysfunction
(can have reactivation of HBV if co-infected)

314

benefits of most recent HCV txs (3)

approved for all genotypes of HCV

Zepatier can be used with renal impairment

cheaper

315

dx for acute hep A

IgM antibodies in first 3 months

316

what kind of bilirubin gets into urine to make it dark

conjugated

317

what's the cause of bruising in acute liver disease

decreased clotting factors

318

cause of small liver in acute case

hepatocyte drop out

319

how long does it take for albumin to get affected

20 days

320

viral has higher AST or ALT?

ALT (symptomatic 2-4 weeks post infection)

321

what zonality do you see in histo for acute viral hepatitis?

none - inflammation is througout

322

what zonality do you see in histo for chronic viral hepatitis?

zone 1 around portal tract

323

zonaity for balloon cells and mallory bodies

zone 3

324

what does pos AMA tell you

primary biliary sclerosis

325

what characteristic histo do you see for primary biliary sclerosis

florid duct lesion:
granulomatous infiltrate around intrahepatic bile ducts

326

what liver lab test is high for primary biliary sclerosis

alk phos

327

really really high alpha fetal protein indicates what

cancer

328

long term, what is still present in someone who had hep B in the past, versus someone who was vaccinnated

past infection:
1. HepB surface antibody
2. HepB core antibody

vaccination
1. just HepB surface antibody

329

what lab values do you need for chronic hep B

have surface ANTIGEN, e antigen (can be pos or neg), IgG pos, and HBV DNA persists

CANNOT have sufrace antibody - that means you have immunity

330

what lab distinguishes chronic from acute hep B

acute has IgM and chronic has IgG

331

what weight/age is suspicious of poor growth

<5% on MORE THAN ONE occasion

332

what is hind milk and what is special about it

milk after feeding - higher proportion of fat - offer it in bottle after breastfeeding

333

how regularly should the baby feed

every 3 hours, for 20-30 minutes of active feeding

334

pyogenic liver abscess demographic and causes

middle-aged
- from biliary tree (cholangitis, stone)
- portal vein (diverticulitis, appendicitis, etc.)
- hepatic artery (endocarditis)
- penetrating trauma

335

deductive vs inductive vs abductiv reasoning

deductive (general hypothesis --> specific conclusion)

inductive (specific observations --> general conclusions)

abductive (incomplete observations --> likely explanation)

336

what causes narrowed pulse pressure (incr dec syst or dias)

increased diastolic

337

thromboelastograph (TEG) purpose

Tells about time, rate, quality of clotting

338

ATP and NADH and alcohol

ethoanol powers up ATP - increases ATP/ADP ratio and causes more reduced system (NADH/NAD ratio increases too)

favors SYNTHESIS and production of free radicals

339

how is ethanol produced in yeast

pyruvate --> acetaldehyde --> ethanol + co2 + NAD+

feedback inhibition --> why beer and wine have limited alcohol content

340

ehtanol metabolism in liver

alcohol --> (alcohol dehydrogenase) --> acetaldehyde --> (aledhyde dehydrogenase) --> acetate -->

341

MEOS system

electron transport system cyp2E1

alcohol --> acetaldehyde

produces FREE RADICALS

342

what percentage of alcohol goes through MEOS vs alcohol dehydrogenase system

20% through MEOS
80% through alcohol dehdyrogenase

alcohol dehydrogenase system maxes out at some point and then shunts to MEOS

343

what enzyme changes causes asian flush syndrome

increased ADH1 activity along with decreased ALDH2

344

which aldehyde dehydrogenase isoform localizes to mitochondria

ALDH2

345

which ADH has to do with retinol

ADH7

346

Which ADH has to do with alcohol metabolism

ADH1 dimers - alpha beta and gamma

347

which ADH isoforms has the highest/lowerst affinity for substrate

ADH1 beta1 - very low 0.05 - higher tolerance because alcohol doesn't build up

ADH1beta3 - very high 40 - alcohol builds up before it can be metabolized (seen more in native americans)

348

if you have a really active ADH and really inactive ALDH, what will happen

acetaldehyde is toxin and will build up if you consume alcohol

349

ecxess exposure to acetaldehyde can cause (3)

too much acetyl-CoA which makes KETONES andcan cause synthesis of triacylglyerols and cholesterol (FAT)

too much acetaldehyde causes FREE RADICALS

350

where is cyp2E1 found

inducible microsomal membrane based mini electron transport chain (MEOS)

converts alcohol to acetaldehyde and radicals

351

schiff bases and acetaldehyde

without NADPH alcetaldehyde reacts with lysine redicues to form unstable adduct of schiff base

352

VLDL in excess ehtanol systems

too much acetyl CoA buidlup and NADHPH/NADP ratio is high -- thus, under chronic conditions, VLDL isn't able to traffic all the fatty acids and trigclyerides outof liver -- causing accumulation and fibrotic lesions

353

gluconeogenesis, NADH and ethanol

excess NADH from ethanol metabolism drives pyruvate to lactate, all lactate (lactic acidosis) gets stuck in liver, blocks gluconeogenesis causing hypoglycermia

354

at what BAC does acetaldehyde dehydrogenase work and stop working

when BAC is less than 0.1% ADH works

above than, MEOS kicks in

355

disulfram mechanism

directly inhibits aldehyde dehydrogenase (ALDH) - accumulates acetaldehyde in system causing nausaea, vomitting, headache, and hypotension

356

what drugs have ethanol drug interactions that cause acetaldehyde accumulation (2)

metronidazole and some cephalosporins

hypoglycemics (sulfonylureas)

357

what are examples of p450 metabolized drugs that can have drug drug interactions with alcohol (5)

tricyclic antidepressnants
h1 antihistamines
OPIOIDS
BENZOs

358

whig drug drug interactions with chronic alcohol will cause induction of cyp2e1 and liver damage (1)

acetaminophen

give n-acetylcysteine

359

how many grams of ethanol is in a typical drink

15g

360

BAC calculation for one drink

15g in 50L (for a 150lb person) = 0.3 = 0.03%

361

how long does ADH metabolize asingle drink

1.5 - 2 hours

362

in non tolerant individual, what BAC can cause death (in absence of other drugs)

0.5% (BAC of greater than 500)

363

ethanol CNS effects (3)

enhance GABAa receptor (inhibitory neurotransmitter) - enhances receptor bidning, more negative membrane potential, less likely to fire --> CNS depression


also inhibit glutamate activation of NMDA - causing CNS depression


increases synaptic concentrations of dopamine and endogenous opiods in nucleus accumbens and ventral tegmental area -- leads to dependency and relapse

364

benzos and ethanol CNS effects

benzos and alcohol increase synergystic increased affinity for GABA and receptor causing increased CNS depression

365

two kinds of tolerance

1. MEOS enzyme induction


2. functional tolerance

366

3 ways that functional tolerance happens

reduction of CNS sensitivity to ethanol due to
- down reg of GABAa
- upreg of NMDA receptors
- up reg of voltage gated cA2+ channels

367

malabsorption of what vitamin causes unique syndrome in chronic alcoholics?

thiamine (B1)

368

Wernicke - Korakoff syndrome

associated with thiamin deficiency resulting in encephalopathy -- results from chronic alcoholism and malnutrition

presents with ataxia, confusion, memory loss, paralysis

369

where do lesions occur in wernicke-korsakoff

mammary bodies - repsonsible for spacial memory

370

teratogenic effects of alcohol

neurodegeneration and abberant neuronal and glial migration - sensitive in 1st and 3rd trimester

371

mild alcohol withrawl symptoms caused by what and treated by what (2)

caused by sympathetic nervous system, so can be treated by adrenergic drugs like CLONIDINE and peripherally acting PROPRANOLOL (non-selective)

372

Severe withdrawl symptoms caused by what, treated by what (2)

increased CNS excitation due to tolerance - neuradaptive changes are now upopposed - seizures

give tapered DIAZEPAM or other long acting BENZOs

373

how does disulfram work

purposefully inhibits acetaldehyde dehyrogenase - causing adverse reactions (nausaea, vomiting etc.) - associates alcohol consumption with adverse affects - behavior modification

374

Naltrexone mechanism

short circuit reward pathway

naltrexone - mu opionid receptor antagonist - binds in ventral tegmental, prevents beta endorphins from stimulating them, decreases craving in these individuals

375

what is reward pathway (3)

dopa neurons in VENTRAL TEGMENTAL area, send processes to
acviate NUCLEUS ACCUMBENS which send processes to MEDIAL PREFRONTAL cortex (Reward cenral)

376

at what points in reward pathway does alcohol activate it

beta endorphis in ventral tegmental and dopamine in nucleus accumbens

377

what is neurochemical basis of replase

beta endorphins remain elevated in years, even in the absense of alcohol consumption - stimulate mu opioid receptors ventral tegmental area - lead to relapse

378

naltrexone adverse

1. hepatotoxic (contraindicated in liver failure or acute hepatitis) - disulfram also is, so don't give together

2. can cause severe withdrawal in opioid dependent individuals (give narcan challenge test - and give them disulfram, whic doesn't work on mu opioid receptor, or other anticraving)

379

anticraving drugs that you can give to opioid users (3)

1. acamprosate (anti-seizure drug) with increased effiacy in combo with disulfaram

2. topiramate (anti-seizure drug)

(don't treat the seizures from alcohol withdrawal with these, treat with long-active benzos)

3. SSRIs - anticraving esp in patients comorbid with major depression

380

moderate alcohol consumption and health

previous thought:

red wine has resveratrol antioxidant, decrease risk of MI

Lancet study (2018) proved that moderate alcohol consumption is NOT associated with benefit, in fact can decrease lifespan to up to 4 years

381

fomepizole mechanism

has high affinity for ADH - use in methanol and ethylene glycol poisoning (alternative to ethanol)

382

definition of chronic abdominal pain

2 or more months

383

functional abdominal pain - who gets it, what is it, characteristics

10-20% of children 4-6 and early teens

dysregulation of CNS and enteric nervous system

poorly localized, episodic, no red flags, may have other stressors
(biopsychosocial)

384

what 2 big things do you look at in CBC on kid with chronic abdominal pain

platelets
hematocrit

385

if you think small bowel is inflamed in chronic abdominal pain, what do you look for on CMP (1)

albumin

386

calprotectin

breakdown products in colon -- indicates inflammatory bowel disease

387

TEF presentation

(1/3,000 most common congenital atresia)
USUALLY also presents with cardiac abnormalities

presents in the first few hours of life:
presents with vomitting, distension (swallowing air), regurg into airways

388

duodenal atresia radigraphic finding

"double bubble"

389

symptoms of duodenal atresia (3)

vomit - may be bilious or non bilious depending on the site of atresia

gasless abdomen - NO distension

burping and vomitting gas from stomach and duodenum

390

hypertrophic pyloric stenosis - when does it present

3-6 weeks of life

391

etiology of hypertrophic stensois (4)

acquired - genetic and environemntal

- prematurity
- bottlefeeding
- maternal smoking
- macrolide antibiotics

392

hypertrophic stensosi symptoms/findings (3)

1. hypochloremic, hypokalemic contraction alkalosis
2. projectile non bilious vomiting
3. palpable "olive"

393

non-pathologic infantile GER - when does it present, what does it NOT present with (3)

at 3-6 months, resolves by 18-24 months


DOES NOT present with barret's or aspiration or poor growth

394

is a PPI acid blocker going to reduce vomitting in kids

no

395

eosinophilic esophagitis symptoms across ages

symptoms can vary with the age:

infants = feeding problems, gagging, poor growth

school-age = volmitting, abdominal pain

adolescents = dysphagia, food impaction (due to strictures)

396

who gets eosinophilic esophagitis

more men than women

atopic individuals - allergies, asthma, eczema, family history

397

tx for eosinophilic asophagitis (2)

1. diet changes (get rid of dairy etc.)
2. swallowed steroids (swallow flovent) - not great for kids, stunts growth
3

398

functional constipation symptoms (3)

1. withholding - cross legs
2. encopresis - poop leaking (more severe behavioral component)
3. enuresis - pressure pushing on bladder - bedweting

399

peak age for IBD presentation

15-30

400

which IBD is more common in kids

crohn's colitis

401

2 unique complications in kids with IBD

growth failure
pubertal delay

402

when do you want to do a bone scan

with crohn's

403

contrast for X rays (2)

iodine (vascular, oral, enema, cath)

barium (per oral, enema)

404

contrast for ultrasound

microbubbles

405

contrast for MRI

gadolinium

406

contrast for nuclear medicine

technicium 99m (radioactive isotopes)

407

ratio of radiation between a CT scan of abdomen to a chest xray

500:1

408

"string sign" on barium study - what does it indicate

indicates crohns

409

MR enterography - what do you see for crohn's

areas of hyperemia around a portion of intestine - shows active inflammation

410

air fluid levels in small bowel - what might that indicate

small bowel obstruction - small bowel loops have to also be dilated

411

what's the measurement for dilated appendix in appendicitis

more than 6mm, also see thick wall

412

radiographic alternatives to colonoscopy (2)

1. contrast barium enema
2. CT colonography (better for smaller polyps)

413

what radiolgraphic options are there to detect acute cholecystitis

1. US to see edema
2. 00mTc-IDA scan

414

when do you image acute pancreatitis

only if it's severe and has complications (hypotensive, drops pO2 etc.)

415

greater spanchnic nerve - what are its origins, and where synapse

from T5-T9
pierces crux of diaphragm and synapses in the celiac ganglia and plexus

416

lesser spanchnic nerve - what are its origins, where does it synapse

from T10-T11
synapses in SMA ganglia

417

least splanchnic nerve - what are its origins, and where does it synapse

from T12
symapses on renal plexus and aorticorenal ganglion

418

lumbar splanchinic nerves from what origins and where does it synapse

from L1-L2,
synapse in inferior mesenteric ganglion and superior hypogastric plexus

419

is thoracic and lumbar splanchnic sympathetic or parasymptatheic

sympathetic

420

what are the origins of the parasympathetic innervation to abdominal cavity (2)

vagus -- supplies foregut and midgut

sacral parasymathetics (From S2,3,4) -- supplies hindgut and pelvic organs (including descending, sigmoid, rectum and anus)

421

is pelvic splangchic sympathetic or parasymp?

parasympathetic

422

lymph draining from stomach gall bladder spleen

celica nodes

423

lymph draiing from midgut

SMA ndes

424

lymph draining from hindgut

iMA nodes

425

after celiac nodes, where does lymph drain to

cisterna chylii and thoracic duct

426

at what spine segment is rectosigmoidal junction

S3

427

how many transverse rectal folds are tehre

3

428

what is the muscle that keeps the anorectal flexure at 90 degrees

the puborectalis portion of the levator ani

429

what does superior rectal artery com from

IMA

430

what does middle rectal artery come from?

internal rectal artery

431

what does inferior rectal artery come from

internal pudendal artery

432

what is venous drainage of superior rectal vein

to inverior mesenteric to PORTAL system

433

what is venous drainage of middle rectal vein

to interla iliac vein to CAVAL system

434

what is venous drainage of inferior rectal vein

to internal pudendal vein to CAVAL system

435

superior half of rectum drains into what nodes

inferior mesenteric nodes

436

inferior half of rectum drains into what nodes

internal iliac nodes

437

what are anal columns made by

bulging of veins

438

what do anal valves and sinuses do

secrete mucus

439

below pectinate line nodal drainage

superfical inguinal nodes

440

internal hemorrhoids are dilations of what veins

superior rectal veins which drain to portal system

441

external hemorrhoids are dilations of what veins

inferior rectal veins which drain to caval system and are innervated somatically

442

portal hypertension can cause what heorrhoids

internal (portal system)

443

wha are the selective shunts

distal spleno-renal
meso-caval

444

what does TIPS connect

inflow of portal vein and outflow of hepatic vein WITHIN liver