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DT4- Exam 3 > HIGH YIELD LIVER/GALLBLADDER (PATHOMA) -- Leah > Flashcards

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
Q

Hepatitis:

  • fecal/ oral variants
  • ineffective type?
  • types spread by blood/ sex?
A
  • A/E = fecal oral (A trAvel, E sEEfood)
  • D= “D”ependent in HBV, otherwise ineffective
  • B/C= “B”LOOD AND “C”EX
26
Q

Two Hep strains that can cause CHRONIC hep?

A
  • B : 20% cases

- C: most all cases

27
Q

Hep strain that can cause fulminant hep in pregnant women?

A

-Hep E

28
Q

Ig that marks ACTIVE/NEW disease? Confers IMMUNITY?

A
  • IgM= new/ active

- IgG= protective

29
Q

Serologic markers for ACUTE HEP:

A
  • HBsAG
  • HBeAG
  • HBV DNA
  • HBcAB-IgM
30
Q

Serologic markers during “window” period?

A

-^^^IgM against HBcAG only.

31
Q

Serologic markers following immunization against hep?

A

-^^ IgG against HBsAG only.

32
Q

Serologic markers for resolved hep?

A

-^^ IgG against both HBs and HBc ag’s

33
Q

Serologic markers for CHRONIC hep?

What strains cause this?

A
  • HBsAG more than 6 months
  • +/- HBeAG/ HB DNA
  • IgG against HBcAG

-20% hep C, ~100% hep C

34
Q

Viruses that can cause hepatitis (3)

A
  • hepatits virus
  • EBV
  • CMV
35
Q

Histo of acute v chronic hep?

A
  • acute: inflammation of TRACTS + LOBULES and hepatocyte apoptosis
  • chronic: inflammation of ONLY PORTAL TRACTS + possible cirrhosis progression.
36
Q

Cirrhosis:
two histo features
cells that mediate?
cytokine that mediates?

A
  • bands of fibrosis + regenerative nodules

- Ito/stellate cells, stimulated by TGF-B

37
Q

Four general complications of cirrhosis

A
  • ascites
  • HSmegaly
  • shunts (i.e. varices)
  • hepatorenal syndrome (renal failure)
38
Q

Liver damaged causes decreased detox (NO MORE OF THE EFFING CYPS. I THINK I WANT CIRRHOSIS).

What is the result?

A
  • mental status change, asterixis –> ammonia induced coma
  • spider angiomatoma, gynecomastia (^^androgen –> estogen), palmar erythema

**asterixis = flapping tremor

39
Q

Two main results of decreased protein synthesis by the liver?

A
  • hypoalbuminemia –> edema

- coagulopathy

40
Q

1 cause liver disease in western world?

A

-Alcohol (AFLD) –> acetaldehyde mediated damage

But…. NON alcoholic fatty liver (obesity related) is quickly on the rise!

41
Q

How to diagnose NAFLD?

A
  • ALT higher than AST; AST higher with alcohol use

- diagnosis of exclusion

42
Q

Alcoholic fatty liver disease

  • 2 histo findings
  • cure?
A
  • mallory bodies
  • fat in hepatocytes

-resolves with abstinence UNLESS cirrhosis is reached (occurs in 10-20%)

43
Q

Primary Haemochromatosis

  • inheritance pattern
  • HLA linkage
  • effect on liver?
  • risk?
  • treatment?

**Also: what causes “secondary” type?

A

-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
Q

Haemochromatosis:
classic symptomatic triad?
labs?
two histo findings?

A
  • cirrhosis, DM, bronze skin
  • high ferritin, serum iron and %saturation
  • low TIBC
  • brown pigment in hepatocytes, prussian blue stain +
45
Q

Wilsons Disease

  • Whats the mutation?
  • Labs? (3)
  • Triad of symptoms
A
  • 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
Q

Wilsons Disease:

  • assc risk?
  • treatment?
A
  • ^^ HCC risk (just like haemachromatosis)

- treat with penicillamine chelation

47
Q

Primary “biliary cirrhosis” and “sclerosing cholangitis”:
in terms of location, whats the difference?
which causes ^^ risk of cholangiocarcinoma?

A
  • biliary cirrhosis= intrhepatic ducts only

- sclerosing cholangitis= intra + EXTRAhepatic ducts … so ^^ risk cholangiocarcinoma

48
Q

Primary biliary cirrhosis:

  • histo
  • assc Ab
  • population
A

-granulomatous inflammation
-antimitochondrial ab
~40 years of age, women

49
Q

Primary sclerosing cholangitis:

  • classic histo
  • classic CT
  • assc disease/ Ab
A
  • periductal fibrosis + onion skinning
  • beaded appearance on imaging
  • p-ANCA, ulcerative colitis
50
Q

Reyes:

cause + presentation

A
  • kids: viral illness + aspirin

- liver failure, encephalopathy, hypoglycemia, can be FATAL

51
Q

ONLY reason to kid aspirin to kids?

A

-Kawasaki Disease

52
Q

Hepatic Adenoma:
association?
malignant?

A
  • OCPs, regresses with cessation

- OMA= benign BUT risk rupture + bleeding esp with estrogen exposure

53
Q

Hepatocellular Carcinoma:
three possible causes?
marker?
prognosis?

A
  • cirrhosis, chronic hep B/C, aflatoxins (p53 mutations, think MOLDY PEANUTS!!)
  • marker AFP
  • poor prognosis
54
Q

What is Budd-Chiari?

A

-hepatic vein obstruction –> liver infarct –> hsmegaly + ascites

(can be caused by tumor compression i.e. hepatocellular carcinoma)

55
Q

From where are tumor mets most commonly

A
  • Cancer Sometimes Penetrates Benign Liver
  • Colon
  • Stomach
  • Pancreas
  • Breast
  • Lung
56
Q

How do you diagnose mets?

A

-HSmegaly, NODULAR FREE EDGE OF LIVER.

DT4- Exam 3 (14 decks)

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