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T2 GI > MOD (biliary stuff) > Flashcards

MOD (biliary stuff) Flashcards

1
Q 
What is a choledochalcele/cyst? 
Pop?
Etiology?
Sx? CT?
Assoc?
Classification?
A

Dilation of the biliary tract (chole=bile tract/duct)

  • asian females
  • etio: congen weakness of bile duct wall or obstruction, or reovirus, bile ducts fibrous (from chronic inflam)
  • sx: abd pain, jaundice, palpable mass (usu incidental), dilated bile ducts on CT
  • assoc: incr risk for biliary cancers except type III
  • Todani classification of cysts
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2
Q

Type V choledochal cyst name?
pop?
assoc?
tx?

A

Type V Caroli’s disease

  • usu kids
  • assoc with stones, recurrent bacterial cholangitis from liver dilation, renal insuff, PCKD
  • tx: ursodeoxycholic acid to reduce stones, or liver transplant
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3
Q 
Cholangitis
causes?
clinical triad/pentad sx?
dx?
tx?
A

Irritation of gb tract due to BILE STASIS

  • causes: stasis from obstruction due to stones, strictures, maligs etc. bacterial: enterococci (gram neg), maybe e coli or kleb and immunosuppr
  • clinical triad: fever/pain/jaundice (charcot’s), pentad adds confusion and hypotension (from sepsis)
  • dx: elev WBC and liver enzymes (ast/alt/alk phos/bili)
  • tx: cipro (antiobios that can penetrate biliary), or drainage (percutaneous and ERCP endoscope)
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4
Q 
Choledocholothiasis 
What are the stones made of?
Etiology?
sx?
dx?
assoc?
A

bile duct stones made of cholesterol or Ca, supersaturated bile forms cholest crystals that accum

  • etio: EDP glucoronyltransferase converts unconj bili to conj which pigments stones, can get backed up
  • sx females, any kind of biliary pain, RUQ gnawing spasm or cresc-decresc, murphy’s sign when patient stops inhaling when hand is on liver, maybe jaundice/itching
  • dx: US first, can show non calc stones CT skips, more
  • assoc risk of cholangitis etc from inflam/scarring/obstr etc, can give antibios to reduce risk, stone removal, cholecystectomy
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5
Q

Gall bladder cancer?
Risk factors/assoc
Cx/sx
Usual types?

A
  • Very rare, cancer of gb itself
  • increase risk with chronic inflam, incr risk with abnormal jxn, gb polyps
  • porcelain gb from chronic inflam
  • usu adenocarcinoma
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6
Q

Cholangiocarcinoma
Increase risk of?
Px?
Dx?

A

Cancer of gb TRACT

  • incr risk with primary sclerosing cholangitis, chronic liver dis/hep/alc/cirr, cysts, parasites (foreign)
  • dx, usual, bloodwork: hyperbilirubinemia, maybe other stuff
  • px: not good
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7
Q

Cholestasis?

A

Impairment of bile through liver

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8
Q

What is bile made of / what is elev in cholestasis

A

Bile made of water, bile acids and bilirubin

-so bilirubin is elevated in pts with cholestasis

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9
Q

Bilirubin pathway steps?

A

RBCs make bili and also make heme which is conv to biliverden which is conv to bili.

  • Bili binds albumin and goes to liver to get CONJ!
  • conj bili goes thru bile ducts to gb, and after meal gets released to duod from pancr as bile to emulsify fats from food
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10
Q

Direct vs indirect biilirubin?

what pathology might high indirect bili level indicate?

A

DIRECT=CONJ!
indirect=unconj

indirect may mean bili can’t get conj, thus issue with RBC (sickle cell anemia, hemolysis, resorbing, liver disease where liver cant conj), but nmost liver disease is DIRECT

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11
Q

Main causes of elevated bilirubin

A 
Extra production of it from liver
Reduced hep uptake
Impaired conj
Decreased hep excretion
Impaired bile flow
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12
Q

Cholestasis cells involved/histo features?

A

Hepatocytes swollen with bile and enlarged/obstructed cannaliculus, kupffer cells (macros) enter, apop and “feathery degen” in cholestsasis, inflam bile ducts

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13
Q

1 drug induced caused of liver injury (which can lead to cholestasis)?

A

ANTIOBIOS! esp Amox/Clavulanic acid! (augmentin)

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14
Q

Which other drugs can cause cholestasis

A

antidepresseants, steroids, antiinflam, other

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15
Q

Hereditary defects in bilirubin metabolism (unconj and conj) causing hyperbili?

A

CONJ: dubin johnson, rotor’s
Unconj: crigler-najjar I and II, and Gilbert’s

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16
Q

Crigler-Najjar?
Types
Gene

A

UNCONJ
INtrahepatic cholestasis
Type I fatal, absent UGT1A (AR)
Type II mild, low UGT1A (AD), rec later, tx with transplant

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17
Q

Gilbert’s
causes
type

A

UNCONJ

benign, dereased UGT1A1 (AR), common, doesn’t cause limitations, aggr by stress/fast

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18
Q

Dubin-Johnson?
gene/deficiency
type
signs

A

CONJ
mutated MRP2 (AR)
pigmented granules in hepatocytes

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19
Q

Rotors

sx, type

A

Rare, hepatocyte lvl impairment
NO pigments
no lims

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20
Q

What does UGTA1 do?

A

Conjugates bili! (enz)

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21
Q

Which is more common b/n gilberts and CN II

A

Gilberts!

22
Q

Familial Intrahepatic Cholestasis (PFIC)
genetics
def
results

A

Congen disease in duct, inv abnormal bile salt secretion, causes cholestasis, fibrosis, duct prolif
AR ATP8B1

23
Q

PFIC-1 sx? diff w PFIC-3?

A

itching, jaundice/cirr usual, severe portal HTN, normal gamma-glutamyl transferase (GGT, which would be ABNORMAL in PFIC-3)

24
Q

Primary biliary cholangitis? results

A

Primary biliary cholangitis/cirrhosis
Autoimmune dis that targets small bile ducts, dmg, bile made by liver has nowhere to go, cause inflam and fibrosis then cirrhosis

25
Q

Primary sclerosing cholangitis?

A

Automimmune disease that targets large ducts

26
Q

Secondary biliary cirrhosis

A

caused from other stuff to do w bile duct etc

27
Q

In PBC (primary biliary cholangitis) why might sx include

  • fatigue and incr alk phosphate
  • sicca
  • hypothyroidism
  • splenomegaly and low platelet ct
  • xanthelasma around eyes
  • incr cholest
  • conj bili elev and increased echogen of liver
A
  • fatigue is main complaint, alk phosphate disprop elev compared to ALT/AST
  • hypothy from multiple autimm
  • xanthe are cholest deposits aroudn eyes
  • liver stiffness from res to flow causing portal HTN, so blood backs up from liver into splenic vein causing enlarged spleen which cant make platelets well
  • elev cholest due to impariment of bile flow so elev lipids
  • conj and echogen of liver suggests liver dis which can occur in primary biliary cholangitis
28
Q 
Primary biliary cholangitis
Pop
Etio
What is positive and elevated on dx tests?
assoc
A
  • pop: middle aged women!
  • autoimmune
  • (+) for AMA (anti mito ab’s in blood), elev alk phos, and liver biopsy showing PBC
29
Q

PBC histo (early vs late) and tx?

A
  • histo: JIGSAW pattern of fibrosis, bile duct lesions/prolifs with lympos surrounding ducts, florid duct lesion, cholestasis with copper deposits, granulomatous destruction, portal fibrosis/cirr
  • early: florid duct lesion and duct prolif, late: scarring and cirrhosis
  • Ursodeoxycholic acid (bile salt), others (know?)
30
Q

Elevated direct bilirubin likely means

A

liver issue!

31
Q

D bili means

A

direct bili!

32
Q 
Primary sclerosing cholangitis 
sx
asocs
dx
complications
pop
A
  • pop: men
  • Assocs: ulcerative colitis, E coli (can get cholangitis after procedure)
    sx: itching, GI, jaundice, ulcerative colitis, beading (important) /strictures of hepatic ducts
  • dx: made by cholangiogram, NOT liver biopsy, ahs beading, should get colonoscopy
  • incr risk of cirrhosis/cholangiocarc
33
Q

PSC histo

A

-histo: less inflam than PBC, fibrosis and scarring, segmental dilation of duct, onion skinning layers of fibrosis surr bile duct, still has jigsaw pattern

34
Q 
PSC/PBC main diffs?
pop
assocs
histo/angiogram
tests
A

PBC has stronger ass with sicca and thyroid issues, and is more common in women, has granulomas and is AMA POSITIVE

PSC is more assoc with IBD and is more common in men, has fibrosis, and lesioned extrahep ducts

35
Q

Histopath of secondary sclerosing cholangitis?

A

neutrophils indicate obstructive not chronic, bile duct prolif, bile stasis

36
Q

Most common congen anomaly of pancr?

A

Pancreatic rest (pancr tissue in upper GI tract), asymp

37
Q

Other congen anomalies of pancreas:
Pancreas divisum?
Annular pancreas?

A
  • pancreas divisum: pancreatic buds never fuse, major and minor pancr glands (minor drains), usu asymp, common
  • annular pancr: pancr fusing leaves trail of pancr tissue aroudn duod which can cause obstr/narrowing and thus pancreatitis
38
Q

Acute vs chronic pancreatitis

A
  • acute: reversible inflam without fibrosis,

- chronic: persistent inflam causing fibrotic change

39
Q

Most common causes of pancreatitis?

-classification sys?

A 
ALCOHOL
and GALLSTONES (acute)
-TIGARO classification sys
40
Q

Less common causes of pancreatitis

A

Hyperlipidemia
Autoimm (Primary biliary cirrhosis, sjogrens, IBD; so would show auto-ab’s like ANA and elev IgG etc, mild sx, dx with biopsy and steroids)
Ampullary cancer–esp in older pt who’s never had episode of pancreatitis
Drugs (esp azathioprine, estros, dideoxy, pentamidine prote inhibs, valproic acid–know?)

41
Q

Cells/pathophys of pancreas

A

Acinar cells produce exocrine enzymes of pancr, which are flushed out by bicarb (from ductal cells) into duod
-then trypsinogen from pancr juice gets converted to trypsin on duod

42
Q

Why might A1AT def cause pancreatitis?

A

A1AT protects pancr if trypsin activates there before getting to duod

43
Q

Why might cystic fibrosis cause pancreatitis?

A

if transport of ions thru duct channels is dysfxnl, would result in sticky fluid to try and prevent pancr dmg to trap enzymes, causes inflam ***huh?

44
Q

Complications of pancreatitis

A

Enlarged pancr can block other organs

  • duod obstruction (nausea/vom)
  • bile duct obstr (stasis, hyperbili)
  • splenic vein thrombosis (inflam that obstructs splenic v and causes gastric varocele bleeding)
  • pseudoaneurysm– inflam around arteries can cause this due to weakening of walls
  • splenic rupture- tail of pancr next to spleen
  • infected pancr necrosis due to inflam fluid stasis
  • pancreatic ascites of inflam fluids
  • retroperitoneal hemorrhage
45
Q

Clinical symptoms of pancreatitis?

A
  • Severe epigastric pain that usu goes thru the back
  • Nausea/vom decreased bowel sounds
  • Cullen sign (dark see around belly button) and Gray-Turner’s sign (discoloration of flanks) indicates retroperitoneal bleeding
46
Q

What things (4) should we check in bloodwork of patients with pancreatitis

A
  • CBC (hemo, WBC, platelets)
  • amylase/lipase levels 3x normal value
  • trypsinogen lvls but not v sensitive
  • exocrine fxn test (low bicarb levels), esp FECAL ELASTASE LEVEL
47
Q

Imaging of pancreatitis

A 
US is first to detect gallstones
-COLON CUT OFF is specific for pancr
-calcifications of pancreas
-fluid collection
-pancreatic enlargement
etc
48
Q

Tx for pancreatitis

A

Resting pancreas

  • antacid doesnt work bc feedback loops not functioning (only work for steat)
  • ERCP to detect and drain fluid, relieve strictures
  • whipple procedure–removes head of pancr and nerves inv in inflam to reduce pain
  • pancreatectomy and islet cell transplant to reduce risk for pancr cancer in chronic pancreatitis
49
Q

Congenital and Inflammatory pancreatic cysts

A

congen–rare, small, epith lining

  • assoc with ADPKD and VHL cause cysts all over body
  • inflam due to irritation/trauma, no epith lining, can mature into cyst w/fluid with amylase (want to drain if gives pt early satiety or pain after eating)
50
Q

Most common type of pancreatic cancer

  • pop
  • sx
  • px
A

Adenocarcinoma!

elderly, bad px, painless jaundice/weight loss, other pancr cancers have better px

T2 GI (6 decks)

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