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OSD_GI > Pathoma_11_Liver GB Panc > Flashcards

Pathoma_11_Liver GB Panc Flashcards

1
Q

Acute hepatitis presents as

A

jaundice (mixed CB and UCB) with dark urine, fever, malaise, nausea, and elevated liver enzymes

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2
Q

Clinical features of acute pancreatitis?

A

epigastric abd pain that radiates to back nausea and vomiting
periumbilical and flank hemorrhage elevated serum lipase and amylase; lipase more specific for panc damage hypocalcemia

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3
Q

Clinical features of obstructive jaundice

A

Dark urine (bilirubinuria), pale stool
Pruritis bc of inc plasma bile acids Hypercholesterolemia w/xanthomas
Steatorrhea (no bile)

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4
Q

Complications of acute pancreatitis?

A

shock- due to peripancreatic hemorrhage and fluid secretion
Pancreatic pseudocyst
DIC and ARDS

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5
Q

Fibrosis in cirrhosis is mediated by

A

TGF-B from stellate cells

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6
Q

Finish alcohol related liver disease and NAFLD

A

…

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7
Q

Gallbladder ca is what type of cancer? What is a major risk factor? How does it present and in what population?

A

Adenocarcinoma Gallstones - especially porcelain GB Cholecystitis in an elderly women - not the normal demographic

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8
Q

HAV vs. HEV

A

Both are fecal-oral tx, cause only acute hepatitis IgM indicates active infection, IgG indicated immunity.
HAV - travelers - endemic to third world countries HEV - contaminated water or undercooked seafood

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9
Q

How can you distinguish a resolved HBV infection from an immunized individual?

A

Resolved - will have Abs to HBc and Hbs –> IgG Immunized - Ab only to Hbs

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10
Q

How can you tell infection/resolved infection with HCV?

A

HCV-RNA confirms infection
Dec RNA indicates recovery

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11
Q

How do we follow the degree of coagulopathy in liver disease?

A

Use PT

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12
Q

How do you get HDV?

A

Need preexisting infection with Hep B–> superinfection HDV + HBV-> co-infection, less severe

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13
Q

How would a gallstone be large enough to occlude the small bowel escape? (gallstone ileus)

A

Cholecystitis results in fistula btw gallbladder and small bowel

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14
Q

Inflammation in acute viral hepatitis occurs where?

A

lobules of the liver and portal tracts and is characterized by apoptosis of hepatocytes

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15
Q

Inflammation in chronic viral hepatitis is predominantly in the ____?
What can it progress to?

A

portal tract cirrhosis

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16
Q

Lab findings in hemochromatosis

A

Inc ferritin (more stored) Dec TIBC (more bound) Inc serum iron
Inc % saturation

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17
Q

Lipid lowering agents like Cholestyramine and Clofibrate can inc. risk for cholesterol stones. Explain how each works

A

Cholestyramine dec bile acid recycling …less bile acids => less bile solubility
Clofibrate increases LPL activity, increase cholesterol content of bile

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18
Q

Normal bilirubin metabolism
1. RES macrophages consume RBC, break heme into and
2. Protoporphyrin is converted into , which is carried on to the liver.
3. in hepatocytes conjugates bilirubin
4. CB is transferred to to form bile, which is stored in
5. Intestinal flora convert CB to , which makes stool brown and urine yellow.

A

Fe and protoporphyrin
UCB; albumin
UGT (uridine glucuronyl transferase)
bile canaliculi, gallbladder
Urobilinogen

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19
Q

A pancreatic abscess is usually caused by

A

E. coli

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20
Q

Pancreatic ca presents late.
What are the presenting symptoms, based on where the tumor is?

A

Tumors in the head of the pancreas will present with obstructive jaundice with pale stools and palpable gallbladder
Secondary DM arises with tumors in the body or tail. If an elderly person presents with new onset DM, think pancreatic ca.

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21
Q

A pancreatic pseudocyst is

A

formed by fibrous tissue surrounding liquefactive necrosis. No true lining
Presents as abdominal mass with persistently elevated amylase

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22
Q

Pathophysiology of hemochromatosis Mutation in __ gene

A

AR defect in iron transport from enterocytes to blood (normally they won’t pass along unless there is need for Fe)
HFE gene (C282Y) - cysteine replaced by tyrosine at aa 282

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23
Q

Presentation of wilson’s disease?

A

.

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24
Q

Presents vague RUQ pain, esp after eating?

A

Chronic cholecystitis

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25
Q

Primary biliary cirrhosis is autoimmune destruction of the bile ducts (intrahepatic).
What is the Ab?

A

Anti-mitochondrial Ab

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26
Q

Primary sclerosing cholangiitis is associated with this disease and this serum marker

A

UC
p-ANCA

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27
Q

Symptoms of acute viral hepatitis last how long? Symptoms of chronic viral hepatitis last how long?

A

< 6 months
> 6 months

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28
Q

This pathology presents with “onion skin” appearance and “beading” of the bile ducts

A

Primary sclerosing cholangiitis - periductal fibrosis

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29
Q

Triad in hemochromatosis, other findings

A

Cirrhosis
Bronze skin
2ndary DM
Arrhythmias Gonadal dysfunction (from iron deposition)

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30
Q

Viral hepatitis is usually due to which 3 viruses?

A

Hepatitis virus, EBV, CMV

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31
Q

What are 4 syndromes/conditions that will increase the levels of UCB in blood? Explain each.

A

Extravascular hemolysis or ineffective erythropoeisis
- high UCB overwhelms conjugating ability of liver
Physiologic jaundice of newborn - UGT activity is low
Gilbert syndrome - autosomal recessive, mild dec of
UGT activity
Crigler-Najjar syndrome - congenital absence of UGT

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32
Q

What are organisms that can cause bilirubin stones?

A

Ascaris lumbricoides (roundworm) Clonorchis sinensis (Chinese liver fluke) - inc risk for stones, cholangitis, and cholangiocarcinoma

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33
Q

What are Rokitansky- Aschoff sinuses and where do you see them?

A

Herniation of gallbladder mucosa down into muscular wall - Chronic cholecystitis

34
Q

What are some (9) risk factors for cholesterol stones?

A

Fat Female Forties
Fertile (multiple pregnancies or oral contraceptives) Clofibrate
Cholestyramine
Native American heritage
Crohn’s
Cirrhosis

35
Q

What are some causes of acute pancreatitis?

A

Alcohol (constricts sphincter of Oddi) Gallstones
Trauma (seatbelt on a child in accident) HyperCalciumia
Hyperlipidemia
Drugs
Scorpion sting
Mumps
Rupture of posterior duodenal ulcer (head of panc is posterior to duodenum)

36
Q

What are some clinical signs of cirrhosis/liver failure?

A

Asterixis, mental status changes, coma due to inc serum ammonia causing encephalopathy
Gynecomastia, spider angioma, palmar erythema due to hyperestroginism (liver is normally responsible for inactivating estrins and synthesizing estrogen binding protein)

37
Q

What are the common causes of chronic pancreatitis, by age group?

A

Alcohol (adults) CF (children)

38
Q

What are the copper rings in Wilson’s disease called?
Where are they?

A

Kaiser-Fleisher; cornea

39
Q

What are the levels of urine bilirubin/urobilinogen in viral hepatitis?

A

Inc urine bilirubin (dark urine) Urobilinogen is normal or decreased because less
bilirubin is entering duodenum
- leaking into blood)

40
Q

What are the Mallory bodies in alcoholic hepatitis?

A

damaged intermediate filaments within hepatocytes

41
Q

What are the serum markers for obstructive jaundice?

A

Inc CB (has been conjugated but can’t escape biliary tract)
Dec urine urobilinogen (CB isn’t reaching intestinal flora to be converted)
Inc alk. phos

42
Q

What can chronic pancreatitis look like on imaging? What is the “chain of lakes” pattern?

A

Dystrophic calcification Dilation of pancreatic ducts

43
Q

What cancers commonly metastasize to liver?

A

Colon Pancreas Breast Lung
*see multiple nodules on free edge of liver

44
Q

What causes jaundice?

A

inc serum bilirubin

45
Q

What causes RUQ pain radiating to R scapula?
What are the other signs/symptoms?

A

Acute cholecystitis inc WBC count, nausea, vomiting, and inc serum phosphatase

46
Q

What happens to CB/UCB
in viral hepatitis?

A

Both increase because inflammation is disrupting both the hepatocytes and bile ductules
Destruction of hepatocytes will inc. UCB Destruction of bile ductules will inc CB

47
Q

What is a bacterial infection of bile ducts?
What causes the infection?
How does it present?

A

ascending Cholangitis ascending infection with enteric gram neg bacteria sepsis, jaundice, and abdominal pain

48
Q

What is a hepatic adenoma? What causes it to grow?

A

Benign tumor, related to oral contraceptive use, subcapsular Grows with exposure to estrogen - risk of rupture esp. during pregnancy

49
Q

What is a late complication of chronic cholecystitis?

A

porcelain gallbladder-> inc risk for ca

50
Q

What is a late complication of chronic pancreatitis?

A

Secondary DM

51
Q

What is a risk for a newborn with inc UCB levels?

A

Kernicterus - UCB is fat soluble and can deposit in basal ganglia -> neurological deficits and death
Tx with phototherapy

52
Q

What is a toxin associated with HCC?

A

Afloxotins from Aspergillus
(p53 mutations)

53
Q

What is a Whipple procedure?

A

Removal of head and neck of pancreas, proximal duodenum, and gallbladder Tx: pancreatic carcinoma

54
Q

What is an annular pancreas? Risk?

A

The head of pancreas forms a ring around the duodenum
duodenal obstruction

55
Q

What is biliary atresia?

A

Failure to form or early destruction of extrahepatic biliary tree. Biliary obstruction and jaundice in first 3mo of life. Progresses to cirrhosis

56
Q

What is biliary colic?

A

Waxing and waning RUQ pain caused by the gallbladder contracting against a stone in the cystic duct

57
Q

What is Budd Chiari syndrome?

A

liver infarction secondary to hepatic vein obstruction
presents with painful hepatomegaly and ascites
**hepatocellular carcinoma gives an increased risk for Budd Chiari syndrome

58
Q

What is damaged in Reye’s syndrome? What disease looks like a viral illness but the required treatment is aspirin?

A

Mitochondria of hepatocytes Kawasaki disease

59
Q

What is Dubin-Johnson syndrome?

A

Autosomal recessive deficiency of bilirubin canalicular transport - can conjugate but not into bile (inc CB). Not clinically significant
Dark liver

60
Q

What is Rotor syndrome?

A

SImilar to Dubin-Johnson but lacks liver discoloration

61
Q

What is the ALT/AST ratio in viral hepatitis?
In alcohol-related liver disease?
In NAFLD?

A

ALT>AST ALTAST

62
Q

What is the difference clinically between Gilbert and Crigler-Najjar syndromes?

A

Gilbert is usually asymptomatic unless stressed
(infection) (mild deficit of UGT)
Crigler usually has fatal kernicterus (total absence of UGT)

63
Q

What is the first serological marker to rise in Hep B infection?

A

HBsAG key marker of acute infection

64
Q

What is the metabolite of alcohol that directly damages the hepatocytes?

A

Acetaldehyde - damages mitochondria

65
Q

What is the serum tumor marker for HCC?

A

alpha-fetoprotein

66
Q

What is the serum tumor marker for pancreatic ca?

A

CA 19-9

67
Q

What is the special risk with HEV?

A

Causes fulminant hepatitis in pregnant women (liver failure with massive liver necrosis)

68
Q

What is the treatment for
Wilson’s disease?

A

D-penicillamine

69
Q

What is Trosseau sign?

A

Migratory widespread thrombi (swelling, erythema, tenderness in extremities); indicative of pancreatic carcinoma

70
Q

What normally binds copper in serum?

A

ceruloplasmin

71
Q

What serological marker for Hep B indicates the person can infect others?

A

HBeAG (need envelope)

72
Q

What serum marker is increased in acute cholecystitis?

A

Serum alk. phos

73
Q

What stain can you use to distinguish iron deposition in the liver from normal lipofuscin pigment -
>hemochromatosis

A

Prussian blue

74
Q

What substances increase solubility of cholesterol and bilirubin in bile?

A

Lecithin (phospholipids), bile acids

75
Q

What types of necrosis do you see in acute pancreatitis?

A

Liquefactive and fat necrosis (peripancreatic fat)

76
Q

Which pancreatic enzyme must be activated first to activate all the others?

A

Trypsin

77
Q

Why are amylase and lipase levels not useful in diagnosis of chronic pancreatitis, unlike acute?

A

Most of the pancreas has been destroyed in chronic, so there are less enzymes produced

78
Q

Why can hypercalcemia lead to acute pancreatitis? Why do you see hypocalcemia in
active acute pancreatitis?

A

Causes activation of enzymes The Ca is being used up in saponification in fat necrosis

79
Q

Why can pancreatitis cause DIC and ARDS?

A

pancreatic enzymes in blood will activate coag factors
(secondary to vascular damage?)
In the lung, will chew on the alveolar/capillary factors

80
Q

Why does estrogen increase risk for formation of cholesterol stones?

A

Increases HMG CoA reductase activity and increases LP receptors on hepatocytes

OSD_GI (13 decks)

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