HIGH YIELD LIVER/GALLBLADDER (PATHOMA) -- Leah Flashcards

1
Q

Biliary Atresia:

  • age group
  • cause
  • presentation
A
  • babies
  • failure to form/ destruction of EXTRAhepatic biliary tree
  • jaundice (conjugated bilirubin) –> cirrhosis
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2
Q

Cholelithiasis is the big word for _____.

  • three causes
  • most common type?
A
  • gallstones
    1. supersaturation (cholesterol or bile)
    2. decreased bile or phospholipids
    3. stasis

**Most common type = cholesterol (90%); bile less common.

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3
Q

Cholesterol stones:

  • color
  • xray appearance
  • major risks
A

-yellow
-radiolucent
-FAT FERTILE FEMALE FORTY
(ALSO– clofibrate)

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4
Q

What does radioLUCENT mean? OPAQUE?

A

(Sorry, dumb card guys, I know. But I mess these up.)

  • Lucent= too “L”ight to be seen
  • Opaque= seen on xray
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5
Q

Bile stones:

  • color
  • xray appearance
  • 2 risk factors
A
  • pigmented (dark)
  • radiopaque
  • (clonorchiasis, ascaris lumbricoides)
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6
Q

Gallstones:

  • most common presentation
  • possible complications
A
  • usually ASYMPTOMATIC!!!!

- until they cause….. biliary colic, cholecystitis, ascending cholangitis, gallstone ileus, gallbladder cancer

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7
Q

Biliary colic:

what is it?

A

-waxing/ waning RUQ pain caused by gallbladder contracting against a stone in the cystic duct

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8
Q

Common bile duct obstruction may lead to?

A

-acute pancreatitis/ obstructive jaundice

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9
Q

What is unexplained jaundice in and older person until proven otherwise?

A

-PANCREATIC CANCER BECAUSE THIS CAN BLOCK COMMON BILE DUCT.

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10
Q

Acute cholecystitis:

  • cause?
  • how is it different from biliary colic?
  • risk?
A
  • stone in cystic duct –> dilation/ pressure ischemia/ bacterial overgrowth of the gallbladder
  • more constant RUQ pain, also see that “pericolic –however you say it– fluid” on U/S (not mentioned in pathoma) ++ fever, N/V, ^^WBC also seen (patient is SICK, not just in pain)
  • risk gallbladder rupture
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11
Q

Chronic cholecystitis:

  • classic histo findings
  • classic xray finding + risk
  • gross appearance
  • cause
A
  • herniation of mucosa into muscular wall (Rokitansky Aschoff sinuses)
  • porcelain gallbladder –> risk carcinoma (take it out!!)
  • shrunken/ fibrotic gallbladder
  • chemical irritation 2ndary to long standing cholelithiasis
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12
Q

Ascending cholangitis:

  • cause
  • presentation
  • risk
A
  • bacterial (#1 gram neg) infection of bile ducts
  • SEPSIS + abdominal pain +jaundice
  • more common with choledocholithiasis
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13
Q

Cause of gallstone ileus

A

-fistula between gallbladder and small bowel –> stone gets stuck in intestine –> obstruction

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14
Q

Gallbladder carcinoma

  • type
  • major risk factor
  • presenation
A
  • adenocarcinoma
  • stones major risk
  • cholecystitis in ELDERLY (DOESNT FIT THE FAT, FERTILE, FORTY, FEMALE) criteria
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15
Q

Jaundice

  • bilirubin level when icterus (yellow eyes) begins
  • most dangerous type?
A
  • 2.5 mg/dl

- kernicterus (DEPOSITS IN BABY’S BASAL GANGLIA.)

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16
Q

Describe steps of leading up to the synthesis of conjugated bilirubin in a healthy person (4)

A
  1. reticuloendothelial macs break down RBCs
  2. Heme –> protoporphyrin –> unconjugated bili
  3. unconjugated bili to liver via albumin
  4. unconjugated –> conjugated via uridine glucuronyl transferase (UGT)
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17
Q

How is conjugated bilirubin removed from the body?

A

Intestinal Flora:
conjugated bili –> stercobilin + urobilin
(sterco goes to stool, uro to urine)

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18
Q

What can overwhelm the bilirubin conjugating ability of the liver?
Two assc findings?

A
  • hemolysis/ ineffective erythropoiesis
  • jaundice
  • dark urine
  • pigminted gallstones
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19
Q

What causes physiologic jaundice of the newborn?

Treatment?

A
  • ineffective UGT enzyme

- phototherapy makes UCB water soluble

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20
Q

Gilbert Syndrome & Crigler- Najjar:

  • enzyme effected?
  • difference in presenation?
  • type of jaundice?
A
  • both effect UGT; low in gilbert but ABSENT in CN
  • Gilbert- benign; transient stress induced jaundice
  • CN: kernicterus + fatal
  • both cause ^^UNconjugated bili UCB
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21
Q

Dubin Johnson & Rotor Syndromes

  • defect
  • type of jaundice
  • difference in clinical presentation?
A
  • deficient bile canalicular transport protein (AR)
  • causes ^^ CB
  • DUBIN causes a DARK liver; Rotor does not.

(I think of Dubin Johnson as a black man….)

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22
Q

Obstructive Jaundice:

  • type?
  • two other lab findings?
  • stool? urine?
  • other symptoms?
A
  • Conjugated
  • ^^ urine urobilinogen + alk phos
  • pale stool, dark urine
  • pruritis, xanthomas, fat malabsorption
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23
Q

Possible causes of obstructive jaundice:

A
  • stones
  • cancers (pancreatic v cholangiocarcinoma)
  • parasites/ liver fluke
24
Q

Viral hep:

  • type of ^^ bili?
  • why?
  • urine findings?
A
  • conjugated + unconjugated
  • inflammation disrupts BOTH hepatocytes + bile ductules
  • dark urine but low –> normal urobilinogen
25
Hepatitis: - fecal/ oral variants - ineffective type? - types spread by blood/ sex?
- A/E = fecal oral (A trAvel, E sEEfood) - D= "D"ependent in HBV, otherwise ineffective - B/C= "B"LOOD AND "C"EX
26
Two Hep strains that can cause CHRONIC hep?
- B : 20% cases | - C: most all cases
27
Hep strain that can cause fulminant hep in pregnant women?
-Hep E
28
Ig that marks ACTIVE/NEW disease? Confers IMMUNITY?
- IgM= new/ active | - IgG= protective
29
Serologic markers for ACUTE HEP:
- HBsAG - HBeAG - HBV DNA - HBcAB-IgM
30
Serologic markers during "window" period?
-^^^IgM against HBcAG only.
31
Serologic markers following immunization against hep?
-^^ IgG against HBsAG only.
32
Serologic markers for resolved hep?
-^^ IgG against both HBs and HBc ag's
33
Serologic markers for CHRONIC hep? | What strains cause this?
- HBsAG more than 6 months - +/- HBeAG/ HB DNA - IgG against HBcAG -20% hep C, ~100% hep C
34
Viruses that can cause hepatitis (3)
- hepatits virus - EBV - CMV
35
Histo of acute v chronic hep?
- acute: inflammation of TRACTS + LOBULES and hepatocyte apoptosis - chronic: inflammation of ONLY PORTAL TRACTS + possible cirrhosis progression.
36
Cirrhosis: two histo features cells that mediate? cytokine that mediates?
- bands of fibrosis + regenerative nodules | - Ito/stellate cells, stimulated by TGF-B
37
Four general complications of cirrhosis
- ascites - HSmegaly - shunts (i.e. varices) - hepatorenal syndrome (renal failure)
38
Liver damaged causes decreased detox (NO MORE OF THE EFFING CYPS. I THINK I WANT CIRRHOSIS). What is the result?
- mental status change, asterixis --> ammonia induced coma - spider angiomatoma, gynecomastia (^^androgen --> estogen), palmar erythema **asterixis = flapping tremor
39
Two main results of decreased protein synthesis by the liver?
- hypoalbuminemia --> edema | - coagulopathy
40
#1 cause liver disease in western world?
-Alcohol (AFLD) --> acetaldehyde mediated damage But.... NON alcoholic fatty liver (obesity related) is quickly on the rise!
41
How to diagnose NAFLD?
- ALT higher than AST; AST higher with alcohol use | - diagnosis of exclusion
42
Alcoholic fatty liver disease - 2 histo findings - cure?
- mallory bodies - fat in hepatocytes -resolves with abstinence UNLESS cirrhosis is reached (occurs in 10-20%)
43
Primary Haemochromatosis - inheritance pattern - HLA linkage - effect on liver? - risk? - treatment? **Also: what causes "secondary" type?
-AR defect in iron absorption (HFE gene mutation --> ^hepcidin --> ^ iron) -^^ iron due to transfusions in secondary type - H(A3)machromatosis= HLA-A3 linkage (MHC1) - damage by free radicals - HCC risk ^^ - treat with phlebotomy
44
Haemochromatosis: classic symptomatic triad? labs? two histo findings?
- cirrhosis, DM, bronze skin - high ferritin, serum iron and %saturation - low TIBC - brown pigment in hepatocytes, prussian blue stain +
45
Wilsons Disease - Whats the mutation? - Labs? (3) - Triad of symptoms
- AR mutation in ATP mediated Cu transport --> copper incorporated in ceruloplasmin - urinary copper, low ceruloplasmin, copper in liver - kid with neuro maifestations, cirrhosis, & kayser fleisher rings
46
Wilsons Disease: - assc risk? - treatment?
- ^^ HCC risk (just like haemachromatosis) | - treat with penicillamine chelation
47
Primary "biliary cirrhosis" and "sclerosing cholangitis": in terms of location, whats the difference? which causes ^^ risk of cholangiocarcinoma?
- biliary cirrhosis= intrhepatic ducts only | - sclerosing cholangitis= intra + EXTRAhepatic ducts ... so ^^ risk cholangiocarcinoma
48
Primary biliary cirrhosis: - histo - assc Ab - population
-granulomatous inflammation -antimitochondrial ab ~40 years of age, women
49
Primary sclerosing cholangitis: - classic histo - classic CT - assc disease/ Ab
- periductal fibrosis + onion skinning - beaded appearance on imaging - p-ANCA, ulcerative colitis
50
Reyes: | cause + presentation
- kids: viral illness + aspirin | - liver failure, encephalopathy, hypoglycemia, can be FATAL
51
ONLY reason to kid aspirin to kids?
-Kawasaki Disease
52
Hepatic Adenoma: association? malignant?
- OCPs, regresses with cessation | - OMA= benign BUT risk rupture + bleeding esp with estrogen exposure
53
Hepatocellular Carcinoma: three possible causes? marker? prognosis?
- cirrhosis, chronic hep B/C, aflatoxins (p53 mutations, think MOLDY PEANUTS!!) - marker AFP - poor prognosis
54
What is Budd-Chiari?
-hepatic vein obstruction --> liver infarct --> hsmegaly + ascites (can be caused by tumor compression i.e. hepatocellular carcinoma)
55
From where are tumor mets most commonly
- Cancer Sometimes Penetrates Benign Liver - Colon - Stomach - Pancreas - Breast - Lung
56
How do you diagnose mets?
-HSmegaly, NODULAR FREE EDGE OF LIVER.