Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

GI/Liver > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

why do people turn yellow with jaundice

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

how heavy is liver

A

1.5 kg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is glisson’s capsule

A

thin CT capsule deep to mesothelium around the entire liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

blood supply to liver (2) and route in liver

A
  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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

components of portal triad

A

branch of portal vein, branch of hepatic artery bile duct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what’s a portal lobule?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what’s the hepatic acini lobulation structure

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what kind of epithelium does bile duct have

A

simple cuboidal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

kupffer ceclls

A

fat, phagocytic cells lining hepatic sinusoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

ito cells

A

store vitamin A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

space of disse

A

between endothelium and hepatic parechymal cels - only see on EM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

gall bladder histology

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

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

A

alpha- glucagon
beta - insulin

alpha smaller darker and peripheral
beta larger lighter and central

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

centroacinar cells

A

cell between acinus and intercalated duct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

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

A

1- intercalated ducts (centroacinar cells at tips)

2- intralobular (cuboidal)

3- interlobular (low columnar)

4- main pancreatic (low columnar)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

is pancreas mostly endocrine or exocrine

A

exocrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

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

A

Calcium mediated:
CCK
ACh
GRP

cAMP mediated:
VIP
Secretin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

salivary versus pancreatic secretions - hypo hyper or iso osmotic

A

salivary is hypo, pancreatic is iso

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

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

A
  1. basolateral sodium bicarb co transporter
  2. basolateral sodium potassium ATPase
  3. apical CFTR chloride channel
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

phases of pancreatic secretion (4)

A
  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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

at what pH is secretin released

A

below 4.5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

bile salt independent flow regulators (3)

A
  1. increased in response to secretin
  2. opposed by somatostatin
  3. comprised of secretion of bicarb, absportion of Na and Cl
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

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

A
  1. IONIZED unconjugated/free
    bile acids
  2. conjugated bile acids (ionized or not)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

how does gut talk to the liver?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

when does glucuronidation happen

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

why is poop brown

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

why is pee yellow

A

urobilinogen gets oxidized to urobilin which is yellow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

how does bilirubin get into hepatocyte

A

via OATP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

how does bilirubin get into bile

A

conjugated to glucuronic acid via general transport MRP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

jaundice in infants

A

(UGT) UDP-glucuronyl transferase reduced in infants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

hemolytic jaundice - what kind of bilirubin do you see

A

lots of unconjugated bilirubin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

obstructive jaundice- what kind of bilirubin do you see

A

lots of conjugated bilirubin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

where does ammonia come from? (3)

A

50% from colon - bacterial ureases and AA metabolism

40% from kidneys - glutamine metabolism

red from RBC and muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

which is caudate and which is quadrate

A

quadrate = with gall bladder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

cystic artery comes off of what, and where is it

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

branches if iMA

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what does left crus of diaphragm do

A

nothing special

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what part of pancreas is intraperitoneal

A

tail next to spleen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what vessel is the neck of the pancreas laying over

A

SMA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what structures are posterior to the SMA

A

unctinate process of pancreas and duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

hepatic portal vein components

A

union of smv and splenic vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

inferior mesenteric vein dumps into where usually

A

splenic vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

in what part of the duodenum does bile enter into

A

2nd part

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

why do women get gallstones more than men

A

high estrogen states makes bile precipitate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

why do you get referred pain

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

extra GI manifestations of gallbladder obstruction

A
  • scleral icterus, jaundice and yellowing frenulum
  • abdominal tenderness (somatic localized or visceral diffuse pain)
  • mass (distended gall bladder, neoplasm)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

murphy’s sign

A

acute cholecystitis -

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

cullen’s sign and grey-turner

A

flank, peri-umbilical ecchymosis/ bleeding

- hemmorhhagic pancreatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

boas sign

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

rebound tenderness

A

peritoneal inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

lab data for gallbladder obstruction (3)

A

total and direct bilirubin (Extrahepatic obstrution)

gamma glutamyl transpepeitase (Extrahepatic)

amylase rises earlier in pancreatitis, lipase rises later

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

is normal gallbladder hypo or hyper echoic

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

acute cholecystitis on US (2)

A

obstruction causes contraction and thickening of the wall

increased bile density - super saturated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

fat stranding on CT - what does it indicate

A

haziness - indicates inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

HIDA scan

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

cystic duct obstruction

lab values

A

normal LFTs and normal pancreatic enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

when do you get gangrenous changes in gallbadder

A

if you let acute cholecystitis go on too long

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

what oxidation state of iron can cross through membranes

A

+2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

what oxidation state is stored as ferritin

A

+3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

which oxidation state of iron is more dangerous

A

+2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

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

A
  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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

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

A

makes 5ALA from glycine and succinyl co-a

get X-linked sideroblastic anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

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

A

takes 2 ALA and makes porphobilinogen

get ALA dehydratase deficient porphyria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

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

A

takes 4 porphobiliogen into hydroxymethylblaine

get acute intermittent porphyria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

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

A

takes hydroxymethylblaine and makes uroporphyrinogen 3

get congenital erythropoetic porphyria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

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

A

takes uroporphyrinogen 3 and makes coproporphyrinogen 3

get porphyria cutanea tarda

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

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

A

takes coproporphyrinogen 3 and makes protoporphyringoen 9

get hereditary coproporphyria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

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

A

takes protoporphyrinogen 9 and makes protoporphyrin 9

get variegate porphyria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

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

A

adds iron to protoporphryin 9 and makes heme b

get erythropoetic protoporphyria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

which steps in heme biosynthesis happen in mitochondria

A

first and last 3:

enzymes:

  1. 5ALA synthase
  2. coproporphyrinogen oxidase
  3. protoporphyringen oxidase
  4. ferrocheletase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

what happens with water, sunlight and conjugated double bonds

A

make free radicals - peroxides etc.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

what kinds of porphyria are considered acute (3)

A
  1. acute intermittent
  2. variegate
  3. hereditary coproporphyria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

what are symptoms of acute porphyria (5)

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

inducible expression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

what kinds of porphyria are considered chronic (3)

A
  1. congenital erythropoeitic porphyria
  2. porphyria cutanea tarda
  3. veriegate porphyria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

chronic porphyria symptoms (4)

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

tx for acute porphyria

A

hemin - feedback inhibition of ALA synthase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

what oxygenation state likes to bind to cyanide

A

+3 - methemoglobin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

what helps RBCs off load more oxygen

A

rapaport luebering shunt - stabilizes deoxygenated state

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Glucose 6 phospate dehydrogenase deficiency

A

quinine generates free radicals - causes hemolytic anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

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

A

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

hemopexin - binds free heme or hemin to generate free radicals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

what oxygen state is the iron in hemin

A

+3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

structural difference between biliverdin and bilirubin

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

what’s the enzyme that’s deficient in neonates

A

glucuronosyl transferase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

why does phototherapy work for neonatal jaundice

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

van den bergh reaction equation

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

stellate cells - where are they, what do they do

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

what proteins does the liver make (2)

A

albumin and most clotting factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

when does jaundice become visible

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

halflife of bilirubin-dicluronide, vs bilirubin and biliprotein

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

how to measure direct and indirect

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

prehepatic - what kind of bilirubinemia do you get

A

increased all uncojugated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

hepatic- what kind of bilirubinemia do you get

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

post-hepatic - what kind of bilirubinemia do you get

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

cause of pre-hepaitc hyerbilirubinemia

A
  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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

parenchymal causes of hyperbilirubinemia (5)

A

high unconj:

  1. Gilberts
  2. Crigler-Najjar type 1

both:
3. Cirgler-Najjar type 2

more conj than unconj:

  1. cirrhosis
  2. hepatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

enzymes that indicate bile stasis (2)

A
  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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

decrease in albumin might mean acute or chronic liver problem

A

chronic - half life is 20 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

increased prothrombin time indicates what kind of liver problem

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

liver transaminase half-lives

A

cytosolic ALT is 48hours

cytosolic AST is 8 hours

mithochondrial AST is 10 days

lactate dehydrogenase - 4-6hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

acute, abrupt liver injury - which transaminase is higher

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

lower grade and sustained liver injury - which transaminase is higher

A

ALT is higher - longer half life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

alcohol-related liver injury - which transaminase is higher

A

AST is higher than ALT - alcohol inhibits ALT synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

injury versus function enzymes

A

bilirubin, albumin and PT are liver fucntion

AST and ALT and alk phos are mark of injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

congeintal anolomalies in gall bladder (6)

A
  1. sometimes under left lobe
  2. cysts and 3. diverticulae
  3. septate gallbladder, multpile gallbladders
  4. heterotopia - normal tissue in abnormal location- pancreatic tissue in wall of gallbladder
  5. hypoplasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

cholesterolosis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

composition difference between cholesterol and pigmented stones

A

cholesterol has more than 50% cholesterol component

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

different risk factors for choletsterol stones

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

risk factors for pigmented stones

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

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

A
  1. hemorrhage
  2. edema
  3. mucosal ulceration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

what do you see in histo for acute cholecystitis

A
  1. fibrin exudate
  2. neutrophils
  3. hemorrhage that can extend through wall and be necrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

chronic cholecystitis gross findings (1)

A

thickening of wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

chronic cholecystitis histo findings (5)

A
  1. Rokitansky-Aschoff sinuses (look like diverticuli)
  2. SM hypertrophy
  3. lymphocytic infiltrate
  4. granulomas +/-
  5. hyperplastic or metaplastic epithelium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

follicular cholecystits findings and associations (3)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

xanthogranulomatous cholecystitis findings (5)

A
  1. foamy macrophages
  2. cholesterol clefts
  3. extruded bile
  4. multinucleated giant cells and neutrophils
  5. thickening of wall with yellow-brown nodules
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

hyalinizing cholecystitis findings and associations (1)

A
  1. replacement of gallbladder wall by hyalinized fibrosis

2. associated with occult adenocarcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

gallbladder tumors (4)

A
  1. benign (adenomyoma)
  2. polyps (cholesterol non-neoplastic, adenoma papillary neoplasms)
  3. epithelial dysplasia (biliary intraepithelial neoplasia)
  4. malignant adenocarcinoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

where/when are adenocarcinomas usually found

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

What parts of the pancreas come from which embryological structures “buds”

A

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

congenital pancreatic disorders (4)

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

acute pancreatitis gross/histo findings (4)

A
  1. interstitial edema
  2. hemorrhage
  3. necrosis (and fat necrosis)
  4. pancreatic pseudocysts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

chronic pancreatitis findings gross and histo (3)

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

causes of chronic pancreatitis (6)

A
  1. genetic (CFTR)
  2. toxic (calc, lipid, alcohol, smoking, hydrocarbons, drugs -thiazides)
  3. obstruction
  4. autoimmune
  5. infectious
  6. other (radiation, post-transplant)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

pseudocyst composition

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

pancreatic tumors (4)

A

most are malignant and solid:

  1. ductal adenocarcinoma
  2. neuroendocrine tumors
  3. anaplastic carcinoma
  4. acinar cell carcionma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

panIN

A

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

pancreatic neuroendocrine tumor types and grading

A

“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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

anaplastic carcinoma characteritsics (4)

A

undifferentiated, large eosinophilic cells
rare
poor porgnosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

acinar cell carcinoma characteristics (3)

A
  1. metastatic at presentation
  2. syndrome of lipase hypersecretion - polyarthralgias, fat necrosis, peripheral eosinophilia
  3. sheet of acinar cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

serous cystadenoma characteristics (4)

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

solid pseudopapillary neoplasm - characteristics (4)

A
  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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

mucinous cystic neoplasm (4)

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

intraductal papillary mucinous neoplasm findings (4)

A
  1. more in men
  2. mucinous materal and epithelium
  3. are associated with pancreatic duct
  4. KRAS and/or GNAS mutations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

what do mets to the pancreas look like

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

are cholesterol stones seen on xray?

A

no - low calcium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

what kind of bilirubin is in pigmented stone

A

unconjugated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

do you see pigmented stones on xray?

A

yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

which kind of stones are infectious

A

brown pigmented stones (E. coli)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

what kind of stones are seen in hemolysis and sickle cell

A

black pigmented stones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

why does rapid weight loss result in gall stones

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

charcot’s triad

A

RUQ pain, fever, jaundice

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

reynolds pentad

A

charcot’s triad plus sepsis and mental status changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

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

A

15mm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

when do you intervene in sphincter of oddi dysfunction

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

causes of acute pancreatitis (6)

A
  1. stones
  2. alcohol
  3. trauma
  4. post-op
  5. meds (steroids, estrogens, HIV meds, antibiotics)
  6. high triglycerides (over 1000) and calcium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

what can kill you with acute pancreatitis (2)

A

ARDS

splenic artery rupture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

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

A
  1. ab pain
  2. CT findings
  3. abnormal lab work (increased lipase and amylase)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

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

A

have to burn through 90% of exocrine function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

fecal elastase indication

A

if low, then it indicates poor exocrine pancreas function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

how likely are people with chronic pancreatitis to get cancer

A

4x more likely

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

primary biliary cholangitis associations/patient demographic

A
  1. 30-65 age
  2. female predominance
  3. associated with thyroid and autoimmne
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

primary biliary cholangitis physical exam and symptoms (8)

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

what do you do when someone has elevated alk phos

A

elevated ggtp and 5nt - indicate liver

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

primary biliary cholangitis lab findings (5)

A
  1. elevated alk phos
  2. AMA pos (95%)
  3. ANA pos (70%)
  4. elevated IgM
  5. elevated cholesterol and lipids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

histo findings for primary biliary cholangitis (3)

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

treatment for primary biliary cholangitis (2)

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

primary sclerosing cholangitis associations/patient demographics (4)

A
  1. mean age 41
  2. 70% male
  3. 80% have UC
  4. maybe bacterial infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

what size ducts are affecting in primary sclerosing cholangitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
164
Q

symptoms of primary sclerosing cholangitis (5)

A
  1. RUQ pain
  2. fatigue
  3. pruritis
  4. fevers, chills, night sweats
  5. jaundice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
165
Q

lab findings in primary sclerosing cholangitis (3)

A
  1. elevated alk phos
  2. high IgG4 (steroid responsive) and IgM levels
  3. P-ANCA positive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
166
Q

imaging findings for primary sclerosing cholangitis (3)

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
167
Q

histo findings for pirmary sclerosing cholangitis

A

fibrous obliteration of small bile ducts - onion skinning pattern

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
168
Q

treatment for primary sclerosing cholangitis

A

ursodeoxycholic acid - possible, not shown

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
169
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
170
Q

direct toxic pattern - timing of enzymes

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
171
Q

alcohol related pattern - timing of enzymes

A

flat - inhibit the synthesis of enzymes to some extent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
172
Q

acute viral heptatis histology findings

A

red swollen liver

  1. infiltrate in portal tract and in parenchyma
  2. necrosis
  3. drop out and apoptotic bodies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
173
Q

unpredictable drug reaction liver injury

A

parenchymal hepatitis that looks a lot like viral hepatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
174
Q

predictable drug reaction liver injury

A

see necrosis in zone 3 - looks like ischemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
175
Q

alcohol hepatitis injury pattern

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
176
Q

ascending cholangitis on histology (5)

A
  1. hepatocytes with feathery degeneration (xanthomatous degeneration)
  2. bile infarcts/plugs
  3. bile lakes
  4. ductular proliferation
  5. neutrophils
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
177
Q

causes of chronic hepatitis (3)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
178
Q

causes of metabolic chronic liver injury (3)

A

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

179
Q

causes of vascular chronic liver injury

A
  1. venous outflow obstruction (Budd-Chiari)

2. CHF and ischemic necrosis

180
Q

examples of chronic cholestatic syndromes (3)

A
  1. partial extrahepatic obstruction
  2. primary biliary cirrhosis
  3. primary sclerosing cholangitis
181
Q

clinical definition of chronic hepatitis (2)

A

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

182
Q

histology of chronic viral hepatitis

A

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

183
Q

top 3 causes of liver disease

A
  1. hep B and C
  2. alcohol
  3. non-alcoholic (getting greater)
184
Q

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

A

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
Q

fibrous stages in chronic hepatitis

A
  1. enlarged portain tract
    2-3. bridges of fibrosis - portal to portal tract
  2. cirrhosis encircling fibrosis around regenerative nodules of hepatocytes
186
Q

clues to distinguish chronic hepatitis causes (3)

A

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

autoimmune - PLASMA CELLS

drug tox - EOSINOPHILS

187
Q

who gets autoimmune hepatitis

A

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

188
Q

diagnosis of autoimmune heptatitis - tests (3)

A

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

189
Q

tx for autoimmune hepatitis

A

steroid

190
Q

what do you see with chronic ischemic fibrosis

A

chronic centrilobular fibrosis (zone 3)

191
Q

risk factors for chronic liver ischemic/vascular congestion/necrosis

A

Budd Chiari:

  1. young woman - oral contraceptives or pregnancy, and other hypercoaguable states
  2. hepatocellular carcinoma
  3. right heart failure- cor pulmonale
192
Q

gross characteristic of chronic vascular congestion/necrosis/ischemia

A

NUTMEG LIVER - congestion and dilation in sinusoids

193
Q

treatment for budd-chiari (3)

A
  1. antithormbotics if quick enough
  2. management of ascites
  3. TIPS stent to relieve pressure
194
Q

alpha-antitrypsin deficiency also causes

A

emphysema

195
Q

genes involved in hereditary hemochromatosis

A

C282Y

H63D gene

196
Q

extrahepatic manifestations of hereditary hemochromatosis (4)

A
  1. cardiomyopathy
  2. skin and pancreas - bronze diabetes
  3. degenerative arthritis (does not resolve with tx)
  4. low libido (pituitary - hypogonadism)
197
Q

histo - hereditary hemochromatois

A

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

198
Q

gene related to wilson’s

A

ATP7B

199
Q

when do you start to see copper in extrahepatic tissue

A

when liver is overwhelmed - probably already cirrhotic

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

200
Q

what’s the best diagnostic test for wilsons

A

24hr urine copper excretion test is good

liver biopsy is gold standard

201
Q

copper accumulation in histo

A

Rhodanine stain - red granules

202
Q

alpha-antitrypsin deficiency gene

A

protease inhibitor PiZZ

203
Q

histo finding for alpha antitrypsin

A

PAS diastase resistant red granules

204
Q

difference between steatohepatitis and fatty liver disease

A

steatohepatitis has inflammatory component - worse- cause chronic damage

205
Q

nonalcoholic steatohepatitis findings (lab)

A

ALT>AST (opposite for alcohol)

20% lead on to cirrhosis

206
Q

treatment for nonalcoholic steatohepatitis

A

vitamin E

weight loss and diabetic control

207
Q

steatohepatitis gross presentation

A

“micronodular” cirrhosis (nodules less than 0.5cm

208
Q

difference between forms of steatohepatitis on histo

A

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

209
Q

flroid duct associated iwth what

A

PBC

210
Q

onion skin fibrosis of ducts associated with

A

PSC

211
Q

how to make diagnosis of PSC

A

imaging

212
Q

what about hepatocytes and sinusoids changes in cancer

A

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
Q

chronic cholestasis extrahepatic manifestations

A

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

214
Q

hepcidin role

A

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
Q

lab values/test for hemochromatosis (2)

A
  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
Q

goal of phlebotomy in hemochromatosis

A

get ferritin less than 50

217
Q

what should people with hemochromatosis NOT do (3)

A
  1. take iron supplements
  2. drink alcohol
  3. get cirrhotic - higher chance of cancer
218
Q

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

A

Wilson’s

219
Q

why does Wilson’s lead to hemolysis

A

copper damages RVC cell membrane

220
Q

what lab values/tests do you look for in wilsons

A

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

urine 24hour commer excretion

221
Q

tx for wilson’s (3)

A

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

oral zinc - decreases copper stores, and dietary modification

222
Q

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

A

alpha 1 antitrypsin deficiency

223
Q

dx for alpha 1 antirtyprsin (2)

A

blood test for levels and function of antitrypsin protein

liver biopsy

224
Q

tx for alpha 1 antirtyprsin (1)

A

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

225
Q

what BMI is morbid obesity

A

over 40

226
Q

swollen smooth liver can be seen with (2)

A

edema

fat

227
Q

what test is less useful in people with morbid obesity

A

NAFLD fibrosis score calculator

228
Q

where does collagen get laid down in fatty liver

A

perisinusoidal - in SPACE OF DISSE

229
Q

where is scar in steatohepatitis and cirrhosis

A

steato = centrilobular

cirrhosis - encircling hepatocytes

230
Q

drinks/week risk factors for alcoholic liver disease

A

14/week for women

21/week for males

231
Q

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

A
  1. fasting glucose >100
  2. obesity
  3. triglycerids >150
  4. BP over 130/85
  5. HDL <40 in men and 50 in women
232
Q

pathogenesis of non alcoholic fatty liver disease and steatohepatitis

A

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
Q

pioglitazone recommendation and adverse

A

recommeneded for NASH, but everyone gains weight on it

234
Q

vitamin E adverse

A

in men is linked to prostate cancer

235
Q

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

A

Autoimmune hepatitis

236
Q

what immune cell is predominant in the infiltrate in autoimmune hepatitis

A

T cells (also plamsa cells)

237
Q

type 1 autoimmune hepatitis demographics and antibodies

A

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

238
Q

type 2 AIH demographics and antibodies

A

anti LKM1 and/or anti LC1 or LKM3

mostly children
other immune diseases
progresssion to cirrhosis is common

239
Q

which Ig levels are abnormal in AIH?

A

IgG is high

240
Q

histo of AIH (2)

A

interface hepatitis (zone1 and triad)

plasma cells, lymphocytes

241
Q

tx for AIH (3)

A

corticosteroids
azathioprine
6MP

242
Q

phase 1 and 2 reaction enzymes and “zones” for drug metabolism

A

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

phase 2 glutathione (in zone1 - O2 rich areas)

243
Q

R value

A

ratio of ALT/Alk phos:

greater than 5 = hepato
less than 2 = cholestasis

244
Q

high INR means what

A

can’t clot quickly enough

245
Q

what kind of pathology does amox/calv cause

A

intrahepatic cholestasis

246
Q

are NSAIDS predicatable or unpredictable

A

unpredictable

247
Q

hepatic encephalopathy causes (4)

A

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

causes:

  • infection
  • upper GI bleed
  • constipations
  • electrolyte abnormalities
248
Q

west-haven criteria/staging

A

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
Q

how to dx hepatic encephalopathy

A

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

diagnosis of exclusion and clinical, eps with known cirrhosis

250
Q

tx for hepatic encephalopathy (2)

A
  1. lactulose - facilitates ammonia to ammonium, less absorbed
  2. rifaximin - reduce bacterial production of ammonia

AVOID BENZOS

251
Q

3 main mechanisms of ascites

A
  1. portal htn
  2. low albumin
  3. peritoneal diseases - TB, cancer
252
Q

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

A

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
Q

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

A

spontaneous bacterial peritonitis - do culture for PMN count>250

254
Q

what causes spontaneous bacterial peritonitis

A

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

255
Q

tx for spontaneous bacterial peritonitis

A

life-long antibiotics

256
Q

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

A

10% - risk for variceal hemorrhage

257
Q

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

A

red wale - vein very close to the surface,

white nipple - fibrin clot on varices (in esophagus) makes you very worried about hemorrhages

258
Q

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

A

non selective beta blockers (propranolol, nadolol)

banding if BB not tolerated

259
Q

what is acute management of variceal hemmorage (4)

A
  1. volume, coag and hemodynamic stability recussitation
  2. intubate
  3. octreotide
  4. antibiotics
260
Q

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

A
  1. tamponade iwth balloon

2. TIPS (in portal system) shunt surgery

261
Q

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

A

chronic heptatitis (hep B with or without cirrhosis)

can indicate hepatocellular carcinoma when it’s over 250

262
Q

how do you dx hepatocellular carcinoma

A

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
Q

tx for HCC

A

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
Q

surveillance for HCC

A

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

265
Q

hepatorenal syndrome type 1

A

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

266
Q

hepatorenal syndrome type 2

A

less rapid - may be manged in outpatient

267
Q

tx for hepatorenal syndrome

A

IV albumin, octreotide, midodrine

only as bridge to liver transplant (necessary)

268
Q

how do dx hepatorenal syndrome (3)

A
  1. cirrhosis WITH ascites
  2. serum creat >1.5
  3. no response to volume expansion with albumin
269
Q

non-specific stigmata of chronic liver disease 94)

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

increase in female estrogenic hormones and nitric oxide

270
Q

portal hypertension cause classifications

A

prehepatic (portal vein thrombosis)

hepatic (cirrhosis, shistosoma)

posthepatic (budd-chiare, CHF)

271
Q

what’s a dangerous hepatic wedge pressure

A

over 12 - usually means cirrhosis

272
Q

“compensatory” hypothesis for ascites

A

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

273
Q

“overflow” hypothesis for ascietes

A

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

274
Q

what drugs do you stop if patient has ascites

A

NSAIDS and renal-toxic drugs like aminoglycodie antibiotics

275
Q

tx for ascites (3)

A

diuretics: spironolactone and furosemide (watch for hypovolemic shock)

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

with concurrent albumin infusion

276
Q

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

A

hepatic encephalopathy , breath caused by mercaptor

277
Q

child’s pugh score

A

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
Q

meld score critea

A

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
Q

liver neoplasms - benign (2) and malignant

A

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
Q

what viruses ONLY cause acute hepatitis (7)

A 
1- hep A
2- hep E
3- EBV
4- CMV
5- HSV
6- VZV
7- yellow fever
281
Q

what viruses cause BOTH acute and chronic hepatitis (3)

A

hep B
hep C
hep D

282
Q

average incubation for acute hep A

A

30 days - infectious 1-2 weeks before symptoms present

283
Q

labs for symptomatic acute hep A and E (2)

A

ALT>AST, over 1,000

elevated total bilirubin

284
Q

types of hep E

A

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
Q

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

A

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

286
Q

why is there a high mortality rate with hep E?

A

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

14-30% mortality rate in preg women

287
Q

chronic hep E - what patients

A

transplant, chemo, HIV infected - rapid development of cirrhosis

288
Q

definition of chronic viral hepatitis (timing)

A

hepatitis lasting longer than 3 months

289
Q

hep B - when do infections occur

A

perinatal or early childhood

290
Q

which of the hepatitis viruses are DNA

A

hep B

291
Q

what antigens are specific for Hep B (3)

A
  1. hep B surface antigen
  2. hep B core antigen
  3. hep B e antigen - marker of viral replication and infectivity
292
Q

horizontal transmission of HBV (3)

A
  1. needle sticks
  2. sex
  3. dialysis and transfusion
293
Q

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

A

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

294
Q

chronic hep B symptoms (4)

A

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
Q

HBV tx

A

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

296
Q

hep D - who gets it

A

needs hep B for replication cycle

297
Q

what causes symptoms of hep D

A

direct cytopathicity of virus - not from immune response like others

298
Q

different classes of clinical preserntations of hep D (2)

A

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
Q

hep C viral characteristics (5)

A
  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
Q

what percentage of people with acute hepC progress to chronic

A

80-85%

301
Q

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

A

alcohol
HIV
male sex
older age

302
Q

extra-hepatic manifestations of hep C (6)

A
  1. cryoglobulinemia and assctd vasculitis
  2. sjogren’s
  3. lymphoproliferative disorders
  4. porphyria cutanea tarda
  5. neuropathy
  6. membranoproliferative glomeruloneprhtitis
303
Q

fibroscan implication and use

A

for staging of liver disease

shear wave - faster it is the more scar you have

304
Q

ribaviron mechanism of action

A

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

used for HCV

305
Q

ribavirin adverse effect

A

hemolytic anemia

306
Q

pegylated interferon mechanism of action

A

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
Q

pegylated intereron adverse effects

A

induces horrible flu-like symptoms

308
Q

simeprevir mechanism of action

A

HCV protease inhibitor

used to treat HCV1

309
Q

simeprevir adverse effects (3)

A

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

(can have reactivation of HBV if co-infected)

310
Q

sofosbuvir mechanism of action

A

RNA-dependent NS5B RNA polymerase inhibitor

has activity against all HCV genotypes and those resistant to PIs

311
Q

sofosbuvir adverse effects (2)

A
  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
Q

ledipasvir mechanism of action

A

inhibits NS5A protein which normally assembles the replisome

in combo with sofosbuvir = harvoni –> more effective

approved for HCV 1

313
Q

ledpasvir adverse effects

A

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
Q

benefits of most recent HCV txs (3)

A

approved for all genotypes of HCV

Zepatier can be used with renal impairment

cheaper

315
Q

dx for acute hep A

A

IgM antibodies in first 3 months

316
Q

what kind of bilirubin gets into urine to make it dark

A

conjugated

317
Q

what’s the cause of bruising in acute liver disease

A

decreased clotting factors

318
Q

cause of small liver in acute case

A

hepatocyte drop out

319
Q

how long does it take for albumin to get affected

A

20 days

320
Q

viral has higher AST or ALT?

A

ALT (symptomatic 2-4 weeks post infection)

321
Q

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

A

none - inflammation is througout

322
Q

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

A

zone 1 around portal tract

323
Q

zonaity for balloon cells and mallory bodies

A

zone 3

324
Q

what does pos AMA tell you

A

primary biliary sclerosis

325
Q

what characteristic histo do you see for primary biliary sclerosis

A

florid duct lesion:

granulomatous infiltrate around intrahepatic bile ducts

326
Q

what liver lab test is high for primary biliary sclerosis

A

alk phos

327
Q

really really high alpha fetal protein indicates what

A

cancer

328
Q

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

A

past infection:

  1. HepB surface antibody
  2. HepB core antibody

vaccination
1. just HepB surface antibody

329
Q

what lab values do you need for chronic hep B

A

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
Q

what lab distinguishes chronic from acute hep B

A

acute has IgM and chronic has IgG

331
Q

what weight/age is suspicious of poor growth

A

<5% on MORE THAN ONE occasion

332
Q

what is hind milk and what is special about it

A

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

333
Q

how regularly should the baby feed

A

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

334
Q

pyogenic liver abscess demographic and causes

A

middle-aged

  • from biliary tree (cholangitis, stone)
  • portal vein (diverticulitis, appendicitis, etc.)
  • hepatic artery (endocarditis)
  • penetrating trauma
335
Q

deductive vs inductive vs abductiv reasoning

A

deductive (general hypothesis –> specific conclusion)

inductive (specific observations –> general conclusions)

abductive (incomplete observations –> likely explanation)

336
Q

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

A

increased diastolic

337
Q

thromboelastograph (TEG) purpose

A

Tells about time, rate, quality of clotting

338
Q

ATP and NADH and alcohol

A

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
Q

how is ethanol produced in yeast

A

pyruvate –> acetaldehyde –> ethanol + co2 + NAD+

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

340
Q

ehtanol metabolism in liver

A

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

341
Q

MEOS system

A

electron transport system cyp2E1

alcohol –> acetaldehyde

produces FREE RADICALS

342
Q

what percentage of alcohol goes through MEOS vs alcohol dehydrogenase system

A

20% through MEOS
80% through alcohol dehdyrogenase

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

343
Q

what enzyme changes causes asian flush syndrome

A

increased ADH1 activity along with decreased ALDH2

344
Q

which aldehyde dehydrogenase isoform localizes to mitochondria

A

ALDH2

345
Q

which ADH has to do with retinol

A

ADH7

346
Q

Which ADH has to do with alcohol metabolism

A

ADH1 dimers - alpha beta and gamma

347
Q

which ADH isoforms has the highest/lowerst affinity for substrate

A

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
Q

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

A

acetaldehyde is toxin and will build up if you consume alcohol

349
Q

ecxess exposure to acetaldehyde can cause (3)

A

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

too much acetaldehyde causes FREE RADICALS

350
Q

where is cyp2E1 found

A

inducible microsomal membrane based mini electron transport chain (MEOS)

converts alcohol to acetaldehyde and radicals

351
Q

schiff bases and acetaldehyde

A

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

352
Q

VLDL in excess ehtanol systems

A

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
Q

gluconeogenesis, NADH and ethanol

A

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

354
Q

at what BAC does acetaldehyde dehydrogenase work and stop working

A

when BAC is less than 0.1% ADH works

above than, MEOS kicks in

355
Q

disulfram mechanism

A

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

356
Q

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

A

metronidazole and some cephalosporins

hypoglycemics (sulfonylureas)

357
Q

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

A

tricyclic antidepressnants
h1 antihistamines
OPIOIDS
BENZOs

358
Q

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

A

acetaminophen

give n-acetylcysteine

359
Q

how many grams of ethanol is in a typical drink

A

15g

360
Q

BAC calculation for one drink

A

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

361
Q

how long does ADH metabolize asingle drink

A

1.5 - 2 hours

362
Q

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

A

0.5% (BAC of greater than 500)

363
Q

ethanol CNS effects (3)

A

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
Q

benzos and ethanol CNS effects

A

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

365
Q

two kinds of tolerance

A
  1. MEOS enzyme induction

2. functional tolerance

366
Q

3 ways that functional tolerance happens

A

reduction of CNS sensitivity to ethanol due to

  • down reg of GABAa
  • upreg of NMDA receptors
  • up reg of voltage gated cA2+ channels
367
Q

malabsorption of what vitamin causes unique syndrome in chronic alcoholics?

A

thiamine (B1)

368
Q

Wernicke - Korakoff syndrome

A

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

presents with ataxia, confusion, memory loss, paralysis

369
Q

where do lesions occur in wernicke-korsakoff

A

mammary bodies - repsonsible for spacial memory

370
Q

teratogenic effects of alcohol

A

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

371
Q

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

A

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

372
Q

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

A

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

give tapered DIAZEPAM or other long acting BENZOs

373
Q

how does disulfram work

A

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

374
Q

Naltrexone mechanism

A

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
Q

what is reward pathway (3)

A

dopa neurons in VENTRAL TEGMENTAL area, send processes to

acviate NUCLEUS ACCUMBENS which send processes to MEDIAL PREFRONTAL cortex (Reward cenral)

376
Q

at what points in reward pathway does alcohol activate it

A

beta endorphis in ventral tegmental and dopamine in nucleus accumbens

377
Q

what is neurochemical basis of replase

A

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

378
Q

naltrexone adverse

A
  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
Q

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

A
  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)

  1. SSRIs - anticraving esp in patients comorbid with major depression
380
Q

moderate alcohol consumption and health

A

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
Q

fomepizole mechanism

A

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

382
Q

definition of chronic abdominal pain

A

2 or more months

383
Q

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

A

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
Q

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

A

platelets

hematocrit

385
Q

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

A

albumin

386
Q

calprotectin

A

breakdown products in colon – indicates inflammatory bowel disease

387
Q

TEF presentation

A

(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
Q

duodenal atresia radigraphic finding

A

“double bubble”

389
Q

symptoms of duodenal atresia (3)

A

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
Q

hypertrophic pyloric stenosis - when does it present

A

3-6 weeks of life

391
Q

etiology of hypertrophic stensois (4)

A

acquired - genetic and environemntal

  • prematurity
  • bottlefeeding
  • maternal smoking
  • macrolide antibiotics
392
Q

hypertrophic stensosi symptoms/findings (3)

A
  1. hypochloremic, hypokalemic contraction alkalosis
  2. projectile non bilious vomiting
  3. palpable “olive”
393
Q

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

A

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

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

394
Q

is a PPI acid blocker going to reduce vomitting in kids

A

no

395
Q

eosinophilic esophagitis symptoms across ages

A

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
Q

who gets eosinophilic esophagitis

A

more men than women

atopic individuals - allergies, asthma, eczema, family history

397
Q

tx for eosinophilic asophagitis (2)

A
  1. diet changes (get rid of dairy etc.)
  2. swallowed steroids (swallow flovent) - not great for kids, stunts growth
    3
398
Q

functional constipation symptoms (3)

A
  1. withholding - cross legs
  2. encopresis - poop leaking (more severe behavioral component)
  3. enuresis - pressure pushing on bladder - bedweting
399
Q

peak age for IBD presentation

A

15-30

400
Q

which IBD is more common in kids

A

crohn’s colitis

401
Q

2 unique complications in kids with IBD

A

growth failure

pubertal delay

402
Q

when do you want to do a bone scan

A

with crohn’s

403
Q

contrast for X rays (2)

A

iodine (vascular, oral, enema, cath)

barium (per oral, enema)

404
Q

contrast for ultrasound

A

microbubbles

405
Q

contrast for MRI

A

gadolinium

406
Q

contrast for nuclear medicine

A

technicium 99m (radioactive isotopes)

407
Q

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

A

500:1

408
Q

“string sign” on barium study - what does it indicate

A

indicates crohns

409
Q

MR enterography - what do you see for crohn’s

A

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

410
Q

air fluid levels in small bowel - what might that indicate

A

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

411
Q

what’s the measurement for dilated appendix in appendicitis

A

more than 6mm, also see thick wall

412
Q

radiographic alternatives to colonoscopy (2)

A
  1. contrast barium enema

2. CT colonography (better for smaller polyps)

413
Q

what radiolgraphic options are there to detect acute cholecystitis

A
  1. US to see edema

2. 00mTc-IDA scan

414
Q

when do you image acute pancreatitis

A

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

415
Q

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

A

from T5-T9

pierces crux of diaphragm and synapses in the celiac ganglia and plexus

416
Q

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

A

from T10-T11

synapses in SMA ganglia

417
Q

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

A

from T12

symapses on renal plexus and aorticorenal ganglion

418
Q

lumbar splanchinic nerves from what origins and where does it synapse

A

from L1-L2,

synapse in inferior mesenteric ganglion and superior hypogastric plexus

419
Q

is thoracic and lumbar splanchnic sympathetic or parasymptatheic

A

sympathetic

420
Q

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

A

vagus – supplies foregut and midgut

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

421
Q

is pelvic splangchic sympathetic or parasymp?

A

parasympathetic

422
Q

lymph draining from stomach gall bladder spleen

A

celica nodes

423
Q

lymph draiing from midgut

A

SMA ndes

424
Q

lymph draining from hindgut

A

iMA nodes

425
Q

after celiac nodes, where does lymph drain to

A

cisterna chylii and thoracic duct

426
Q

at what spine segment is rectosigmoidal junction

A

S3

427
Q

how many transverse rectal folds are tehre

A

3

428
Q

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

A

the puborectalis portion of the levator ani

429
Q

what does superior rectal artery com from

A

IMA

430
Q

what does middle rectal artery come from?

A

internal rectal artery

431
Q

what does inferior rectal artery come from

A

internal pudendal artery

432
Q

what is venous drainage of superior rectal vein

A

to inverior mesenteric to PORTAL system

433
Q

what is venous drainage of middle rectal vein

A

to interla iliac vein to CAVAL system

434
Q

what is venous drainage of inferior rectal vein

A

to internal pudendal vein to CAVAL system

435
Q

superior half of rectum drains into what nodes

A

inferior mesenteric nodes

436
Q

inferior half of rectum drains into what nodes

A

internal iliac nodes

437
Q

what are anal columns made by

A

bulging of veins

438
Q

what do anal valves and sinuses do

A

secrete mucus

439
Q

below pectinate line nodal drainage

A

superfical inguinal nodes

440
Q

internal hemorrhoids are dilations of what veins

A

superior rectal veins which drain to portal system

441
Q

external hemorrhoids are dilations of what veins

A

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

442
Q

portal hypertension can cause what heorrhoids

A

internal (portal system)

443
Q

wha are the selective shunts

A

distal spleno-renal

meso-caval

444
Q

what does TIPS connect

A

inflow of portal vein and outflow of hepatic vein WITHIN liver

GI/Liver (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions