Brainscape's Knowledge GenomeTM

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


See full index

Unit 6 > Exocrine, pancreas, gallbladder and liver pathology > Flashcards

Exocrine, pancreas, gallbladder and liver pathology Flashcards

1
Q

Pancreatic carcinoma - why is there obstructive jaundice with pale stools?

A

Carcinoma blocks the bile duct from emptying –> bilirubin backup and eventual leakage into the blood stream –> jaundice

Bilirubin is also what gives the stool its color so lack of bilirubin being secreted into duodenum will also result in pale stools

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

How does cirrhosis increase the risk of cholesterol stones?

A

Production of bile salts by hepatocytes

Cirrhosis –> decreased bile acid production –> decreased solubility of cholesterol

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

What diseases are associated with a deficiency of bilirubin canalicular transport protein?

What laboratory findings will you see?

A

Dubin-Johnson syndrome and Rotor syndrome

Both will result in increased serum conjugated bilirubin (transport protein responsible for transport of CB into the bile, w/o which will result in backup and leakage into the blood)

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

Bilirubin gallstones

A

Pigmented stones composed of bilirubin (what gives the stone its color)

Usually radiopaque

Risk factors

  • extravascular hemolysis (increased bilirubin in bile)
  • biliary tract infection (ie E coli, Ascaris lumbricoides, Clonorchis sinensis) – bacteria can de-conjugate bilirubin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Causes of viral hepatitis (3)

A

Mainly by hepatitis virus (1)

Can also be caused by EBV (2) and CMV (3)

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

Cirrhosis - what results from decreased detoxification?

A
  • mental status changes, asterixis, and eventual coma (due to increased serum ammonia) – metabolic, hence reversible
  • gynecomastia, spider angiomata, and palmar erythema due to hyperestrinism
    • ​liver plays an important role in removing estrogen from the blood
  • jaundice (remember liver hepatocytes conjugate bilirubin - cirrhosis –> damage to hepatocytes)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Wilson disease - what is the gene defect? Inheritance pattern?

A

Autosomal recessive defect in ATP7B gene (responsible for ATP-mediated hepatocyte copper transport)

  • can’t transport copper into bile and can’t incorporate into ceruloplasmin –> stored in tissues
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Acute hepatitis

A

Inflammation of liver parenchyma

  • inflammation involves lobules of liver and portal tracts and is characterized by apoptosis of hepatocytes
  • some cases may be asymptomatic with elevated liver enzymes
  • symptoms lasts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Most cholesterol gallstones are radiolucent, what would make it radiopaque?

A

Associated with calcium binding

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

Chronic pancreatitis

A

Fibrosis of pancreatic parenchyma – most often secondary to recurrent acute pancreatitis

  • Most commonly due to alcohol (adults) and cystic fibrosis (children) – however, many cases are idiopathic

Clinical features

  1. epigastric abdominal pain that radiates to the back
  2. pancreatic insufficiency – results in malabsorption w/ steatorrhea and fat-soluble vitamin deficiencies
  3. dystrophic calcification of pancreatic parenchyma on imaging – “chain of lakes” due to dilatation of pancreatic ducts
  4. secondary diabetes mellitus (due to destruction of islets in the body and tail)
  5. increased risk of pancreatic carcinoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Nonalcoholic fatty liver disease - how is it diagnosed?

A

Diagnosis of exclusion

ALT > AST

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

How does Crohn disease increase the risk of cholesterol stones?

A

Most common effected location is the terminal ileum –> decreased uptake of bile salts/acids –> decreased solubilization of cholesterol

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

How can alcohol cause chronic pancreatitis?

A

Many causes of acute pancreatitis are one-time events (ie trauma, scorpion stings, rupture, etc…)

Alcohol is one of the few causes that is chronic and won’t likely to be stopped. Recurrent bouts of acute pancreatitis –> fibrosis and chronic pancreatitis

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

Chronic pancreatitis - clinical features

A
  1. epigastric abdominal pain that radiates to the back
  2. pancreatic insufficiency – results in malabsorption w/ steatorrhea and fat-soluble vitamin deficiencies
  3. dystrophic calcification of pancreatic parenchyma on imaging – “chain of lakes” due to dilatation of pancreatic ducts
  4. secondary diabetes mellitus (due to destruction of islets in the body and tail)
  5. increased risk of pancreatic carcinoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Normal bilirubin metabolism

A
  1. RBCs when they are unhealthy or about to die are consumed by macrophages of the reticuloendothelial system (mainly located in the spleen)
  2. Protoporphyrin (from heme) is converted to unconjugated bilirubin (UCB)
  3. Albumin carries UCB to the liver
  4. Uridine glucuronyl transferase (UGT) in hepatocytes conjugates bilirubin
  5. Conjugated bilirubin (CB) is transferred to bile canaliculi to form bile, which is stored in the gallbladder
  6. Bile is release into the small bowel to aid in digestion
  7. Intestinal flora convert CB to urobilinogen, which is oxidized to stercobilin (makes stool brown) and urobilin (partially reabsorbed into blood and filtered by kidney, making urine yellow)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Gallbladder carcinoma

A

Adenocarcinoma arising from the glandular epithelium that lines the gallbladder wall

  • Gallstones are a major risk factor, especially when complicated by porcelain gallbladder*
  • Classically presents as cholecystitis in an elderly woman*
  • Poor prognosis*
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Complication(s) associated with chronic hepatitis

A

risk of progression to cirrhosis

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

Chronic cholecystitis - treatment

A

Cholecystectomy – especially if porcelain gallbladder is present

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

Reye syndrome

A

Fulminant (severe and sudden in onset) liver failure and encephalopathy in children with viral illness who take aspirin

  • likely related to mitochondrial damage to hepatocytes

Presents with:

  • hypoglycemia
  • elevated liver enzymes
  • nausea with vomiting
  • may progress to coma and death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Hepatocellular carcinoma

A

malignant tumor of hepatocytes

Risks:

  • Chronic hepatitis (HBV, HCV)
  • Cirrhosis (ie alcohol, nonalcoholic fatty liver disease, hemochromatosis, Wilson disease, A1AT deficiency)
  • Aflaxtoxins derived from Aspergillus (induce p53 mutations)

Increased risk for Budd-Chiari syndrome

  • liver infarction secondary to hepatic vein obstruction
  • presents with painful hepatomegaly and ascites
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Wilson disease - characteristic finding on physical exam

A

Kayser-Fleisher rings in cornea

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

Alcoholic hepatitis - when is it usually seen?

What mediates the damage?

A

Seen with binge drinking

Damage mediated by: acetaldehyde (metabolite of alcohol)

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

Most common metastatic sources of liver cancer?

A
  • colon
  • pancreas
  • lung
  • breast carcinomas
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Gallstones - possible complications (5)

A

Usually asymptomatic, but certain complications can arise:

  1. biliary colic
  2. acute and chronic cholecystitis
  3. ascending cholangitis
  4. gallstone ileus
  5. gallbladder cancer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Nonalcoholic fatty liver disease

A

Same classic 3 symptoms w/o exposure to alcohol

  • Fatty change
  • Hepatitis
  • Cirrhosis

Associated with obesity

Diagnosis of exclusion ALT > AST

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Hallmark of chronic cholecystitis

A

Rokitansky-Aschoff sinus (herniation of gallbladder mucosa into the muscular wall)

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

Cirrhosis - why is there hyperestrinism? (elevated estrogen)

What is a result of this?

A

Liver plays important role in removing estrogen. Increased levels results in

  • gynecomastia
  • spider angiomata
  • palmar erythema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Hemochromatosis

A

Excess body iron leading to deposition in tissues (hemosiderosis) and organ damage (hemochromatosis)

  • Tissue damage mediated by generation of free radicals (via the fenton reaction)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Chronic hepatitis

A

Characterized by symptoms that lasts > 6 months

Inflammation predominantly involves portal tract

risk of progression to cirrhosis

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

Hepatitis C - how is the infection confirmed?

A

HCV-RNA test confirms infection

Decreased RNA levels indicate recovery

RNA persistence despite treatment indicates chronic disease

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

Pancreatic carcinoma

A

Adenocarcinoma arising from pancreatic ducts

Most commonly seen in the elderly (average age is 70 years)

Major risk factors: smoking and chronic pancreatitis

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

What are the stones made of in cholelithiasis? (2)

A

Cholesterol or bilirubin stones

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

Nonalcoholic fatty liver disease - what is it associated with?

A

Associated with obesity

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

Gallstone ileus - cause

A

Due to cholecystitis with fistula formation between the gallbladder and small bowel (which would allow the passage of larger stones which can pass and then obstruct the small bowel)

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

Gallbladder carcinoma - risk factor(s)

A

Gallstones are a major risk factor, especially when complicated by porcelain gallbladder

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

Key marker of hepatitis B infection

A

Hep B surface antigen (first serologic marker to rise)

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

Bilirubin gallstones - risk factors

A
  • extravascular hemolysis (increased bilirubin in bile)
  • biliary tract infection (ie E coli, Ascaris lumbricoides, Clonorchis sinensis) – bacteria can de-conjugate bilirubin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Acute cholecystitis

A

Acute inflammation of the gallbladder wall

Impacted stone in the cystic duct results in dilatation with:

  • pressure ischemia
  • bacterial overgrowth (E coli)
  • inflammation

Presents with:

  • right upper quadrant pain often radiating to right scapula
  • fever with elevated WBCs
  • N&V
  • increased serum alkaline phosphatase (from duct damage)

Risk of rupture if untreated

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

Hepatocellular carcinoma - what is the prognosis? why?

A

Poor prognosis mainly because the tumors are often detected very late (symptoms are often masked by cirrhosis)

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

Hepatic adenoma

A

Benign tumor of hepatocytes

Associated with oral contraceptive use – regresses upon cessation of drug

Risk of rupture and intraperitoneal bleeding, especially during pregnancy

  • tumors are subcapsular and grow with exposure to estrogen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Jaundice in newborns – complications? treatments?

A

Complication: kernicterus (deposition of UCB in the basal ganglia)

Treatment: phototherapy – does not cause conjugation, but it does increase the solubility of UCB so it can be excreted into the water

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

Wilson disease - laboratory findings (Urinary copper, serum ceruloplasmin, copper)

A

Urinary copper – increased (can’t dump into bile so stays in blood stream)

Serum ceruloplasmin – decreased (defective transport –> can’t put into ceruloplasmin)

Copper – increased in tissues (especially liver hepatocytes)

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

Primary sclerosing cholangitis - clinical presentation

A

obstructive jaundice

cirrhosis is a late complication

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

Trousseau syndrome - what is it associated with?

A

pancreatic and lung cancer

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

Primary sclerosing cholangitis - etiology

A

unknown but associated with ulcerative colitis; p-ANCA is often positive

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

Hepatitis B (HBV) - mode of transmission

How is it most commonly obtained?

A

Parenteral transmission (via piercing of the skin or the mucosa)

  • childbirth
  • unprotected intercourse
  • IV drug abuse
  • needle stick
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Where is inflammation seen in chronic hepatitis?

A

Predominantly involves the portal tract
Figure: notice how there is inflammation in the portal tracts, but the hepatocytes (representing the liver lobules) is relatively clear

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

Gilbert syndrome - how does it present clinically?

A

Patients are usually normal, because UGT activity is still present, just decreased.

Jaundice occurs during stress (ie severe infection) otherwise, not clinically significant

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

Where is bile made? Where is it stored?

A

Made in liver. Stored in gallbladder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Wilson disease - presentation

A

Presents in childhood with

  1. Cirrhosis
  2. Neurologic manifestations (behavioral changes, dementia, chorea, and Parkinsonian symptoms due to deposition of copper in basal ganglia)
  3. Kayser-Fleisher rings in the cornea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Ascending cholangitis - most common organisms

A

enteric gram-negative bacteria

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

Primary biliary cirrhosis - what population does this disease classically affect?

A

Remember autoimmune – will classically affect women of childbearing age.

Average age is 40 years

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

Lipofuscin - what is it? where is it found? What is its function?

A

a brown pigment that is a by-product of the ‘wear-and-tear’ of peroxidized lipids that piles up in lysosomes

Typically found in neurons (because they live essentially throughout your whole life)

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

Role of anti-virus IgG in hepatitis infection

A

IgG is protective

Its presence indicates prior infection or immunization (immunization is ONLY available for hep A)

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

Hemochromatosis - what does it increase the risk of?

A

increased risk of hepatocellular carcinoma (due to damage to DNA from the free radicals)

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

Primary sclerosing cholangitis

A

Inflammation and fibrosis of intrahepatic and extrahepatic bile ducts

  • periductal fibrosis with an ‘onion-skin’ appearance
  • uninvolved regions are dilated resulting in a ‘beaded’ appearance on contrast imaging

presents with obstructive jaundice – cirrhosis is a late complication

increased risk for cholangiocarcinoma

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

HEV infection - major complication?

A

HEV commonly acquired from contaminated water or undercooked seafood

HEV infection in pregnant women is associated with fulminant hepatitis (liver failure with massive liver necrosis)

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

How does alcohol cause acute pancreatitis?

A

causes contraction of sphincter of Oddi at the ampulla where the pancreatic/bile ducts drain into the duodenum

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

Most common type of stones in cholelithiasis?

A

Cholesterol stones (yellow) – most common (90%) especially in the West

  • radiolucent (10% are radiopaque due to associated calcium)
  • risk factors
    • age (40s)
    • estrogen (female gender, obesity, multiple pregnancies, oral contraceptives)
    • clofibrate
    • Native American ethnicity
    • Crohn disease
    • cirrhosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Pancreatic carcinoma - what results if the cancer is in the body or tail?

A

secondary diabetes mellitus – due to destruction of islets

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

Wilson disease - complications

A

Increased risk of hepatocellular carcinoma – same concept as hemochromatosis (production of hydroxy radicals can cause damage to DNA)

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

Ceruloplasmin

A

The key molecule that carriers copper in the blood (just like how transferrin/ferritin is for iron)

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

If a stone is being passed and is lodged in the common bile duct, what are some complications that may result? (2)

A
  1. acute pancreatitis – backup of pancreatic enzymes, more prone to unwarranted activation
  2. obstructive jaundice – backup of bile results in bilirubin backflow into the blood –> jaundice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Primary sclerosing cholangitis - what disease is it associated with?

A

ulcerative colitis; pANCA is often positive

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

Primary sclerosing cholangitis - why is there a beaded appearance on contrast imaging?

A

Areas of inflammation and fibrosis creates the divets while uninvolved regions are dilated

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

hemochromatosis - liver biopsy

A

Accumulation of brown pigment in hepatocytes

Prussian blue stain distinguishes iron (blue) from lipofuscin

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

hemosiderosis

A

deposition of iron in tissues (without the organ damage)

characterized by repeated episodes of intra-alveolar bleeding that lead to abnormal accumulation of iron as hemosiderin in alveolar macrophages and subsequent development of pulmonary fibrosis and severe anemia.

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

Why is a fatty liver seen in alcoholics? Is it reversible?

A

Alcohol inhibits the oxidation of fatty acids (FAs) resulting in more FAs to be stored in the liver. However, if you remove the alcohol, the liver can continue to process the FAs hence why it is reversible.

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

3 main toxic effects of alcohol

A
  1. fatty liver
  2. alcoholic hepatitis (chemical injury by the alcohol)
  3. cirrhosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Hepatocellular carcinoma - serum marker

A

alpha-fetoprotein

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

Hemochromatosis - cause (primary vs secondary)

A

Primary - autosomal recessive defect in iron absorption

Secondary - chronic transfusions

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

Acute pancreatitis - cause

A

autodigestion of pancreatic parenchyma by pancreatic enzymes

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

Cirrhosis - why is there mental status changes?

A

Due to decreased detoxification of almost all drugs/toxic compounds (liver is responsible for detoxification)

  • primarily caused by the decreased detoxification of serum ammonia (results in increased levels in the blood)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Amylase and lipase markers in chronic hepatitis

A

They are an indicator of damage in acute pancreatitis but not useful serological markers in chronic pancreatitis. The pancreas has suffered a lot of damage level already –> doesn’t make enough of these enzymes to be useful

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Whipple procedure

A

en bloc (all together at the same time) removal of the head and neck of pancreas, proximal duodenum and gallbladder

Used for the treatment of pancreatic carcinoma

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

Acute pancreatitis - what is the first enzyme to be classically activated?

A

Trypsin

Activation of which will lead into the activation of other pancreatic enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Biliary colic

A

Waxing and waning right upper quadrant pain

Due to gallbladder contracting against a stone lodged in the cystic duct

  • If stone lodges in common bile duct, may result in acute pancreatitis or obstructive jaundice

Symptoms are relieve if stone passes

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

Most common causes of chronic pancreatitis (children vs adults)

A

Alcohol – adults

Cystic fibrosis – children

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

How does clofibrate increase the risk of cholesterol stones?

A

Fibrates are lipid lowering agents that:

  • increase Hmg-CoA reductase –> increases cholesterol synthesis
  • decrease conversion of cholesterol to bile acids –> decreased solubility + increased cholesterol in bile

Overall same effect as estrogen to increase cholesterol levels that will increase likelihood of precipitation

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

Pancreatic carcinoma - clinical features

A
  • Epigastric abdominal pain and weight loss
  • Obstructive jaundice with pale stools and palpable gallbladder – associated with tumors that arise in the head of the pancreas (most common location)
  • Secondary diabetes melltius – associated with tunmors that arise in the body or tail
  • pancreatitis
  • migratory thrombophlebitis (Trousseau syndrome) – presents as swelling, erythema, and tenderness in the extremities (seen in 10% of patients)
  • serum tumor marker is CA 19-9 (CA = cancer antigen)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Cholelithiasis

A

Gallstones – solid, round stones in the gallbladder

Due to precipitation of cholesterol (cholesterol stones) or bilirubin (bilirubin stones) in bile

Arises due to:

  1. supersaturation of cholesterol or bilirubin
  2. decreased phospholipids (ie lecithin) or bileacids, both of which increase the solubility of cholesterol
  3. stasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Solubility: conjugated vs unconjugated bilirubin

A

Conjugation makes bilirubin soluble in water

Unconjugated bilirubin is much more prone to precipitation

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

Primary biliary cirrhosis - clinical presentation

A

Presents with features of obstructive jaundice (due to the knockout of the bile ducts –> backup of bile/bilirubin into the blood)

84
Q

Annular pancreas

A

developmental malformation in which the pancreas forms a ring around the duodenum

risk of duodenal obstruction

85
Q

Pancreatic carcinoma - major risk factors

A

Smoking

Chronic pancreatitis

86
Q

Acute cholecystitis - clinical presentation

A

Remember infection is typically due to a bug so you will get typicaly symptoms associated with an infection.

  • right upper quadrant pain often radiating to right scapula
  • fever with elevated WBCs
  • N&V
  • increased serum alkaline phosphatase (from duct damage)
87
Q

Wilson disease - mechanism of damage

A

Copper and iron both catalyze the fenton reaction generating hydroxy radicals.

If copper cannot be dumped into the bile and then out of our bodies, it accumulates within tissues inducing free radical damage

88
Q

Hepatic adenoma - cause?

A

Associated with oral contraceptive use – regresses upon cessation of drug

89
Q

Acute pancreatitis - clinical features

A
  • epigastric abdominal pain that radiates to the back
  • nausea and vomiting
  • periumbilical and flank hemorrhage (necrosis spreads into the periumbilical soft tissue and retroperitoneum)
  • elevated serum lipase and amylase – lipase more specific for pancreatic damage
  • hypocalcemia (calcium is consumed during saponification in fat necrosis)
90
Q

How long do symptoms in acute hepatitis last?

A
91
Q

If an elderly woman presents with cholecystitis, what is at the top of your differential?

A

Carcinoma – cholecystitis classically affects 40-50 year olds… not elderly

92
Q

Alcoholic hepatitis - characteristic findings on histology

A
  • Swelling of hepatocytes with formation of Mallory bodies (damage cytokeratin filaments)
  • necrosis
  • acute inflammation
93
Q

How does viral hepatitis cause jaundice?

What other clinical findings would be present?

A

Via inflammation that disrupts hepatocytes and small bile ductules

  • disruption/death of hepatocytes –> inability to conjugate –> increased serum UCB
  • disruption/death of small bile ductules –> inability to excrete the CB –> increased serum CB

There will also be dark urine due to increased urine bilirubin (increased CB can be filtered by the kidney and excreted resulting in a pigmentation of the urine)

Urine urobilinogen is normal if not decreased (damage to the ductules will result in decreased released of bile into the gut –> less formation of urobilinogen)

94
Q

Acute pancreatitis - pancreatic abscess

A

Often due to E. coli

presents with abdominal pain, high fever and persistently elevated amylase

95
Q

Primary sclerosing cholangitis - appearance on histology?

A

periductal fibrosis with an ‘onion-skin’ appearance

uninvolved regions are dilated resulting in a ‘beaded’ appearance on contrast imaging

96
Q

What gallstones are normally radiolucent? Radiopaque?

A

Cholesterol – radiolucent unless associated with calcium

Bilirubin – radiopaque

97
Q

Why is hypercalcemia a risk factor for acute pancreatitis?

A

calcium is an enzyme activator

increased calcium –> increased chance of premature/random activation of pancreatic enzymes before they are secreted into the duodenum

98
Q

Hepatitis viral infections - which ones can result in chronic hepatitis?

A

Hep A and Hep E – no risk for chronic hepatitis

Hep B – 20% of chronic

Hep C – chronic disease occurs in most cases

99
Q

What is the molecular cause of jaundice?

A

Increased serum bilirubin, usually > 2.5mg/dL

100
Q

Primary biliary cirrhosis

A

Autoimmune granulomatous destruction of intrahepatic bile ducts

  • classically arises in women (average age is 40 years)
  • associated with other autoimmune diseases

Etiology is unknown; antimitochondrial antibody present

101
Q

Where are bile acids reabsorbed?

A

Ileum

102
Q

Primary biliary cirrhosis - cause?

A

unknown. However, there is an anti-mitochondrial antibody present

103
Q

Cirrhosis - what is the fibrosis mediated by?

A

Fibrosis mediated by TGF-β from stellate cells which lie beneath the endothelial cells that line the sinusoids

104
Q

Which hepatitis is immunization available for?

A

ONLY available for hepatitis A

105
Q

pancreatic carcinoma - prognosis

A

very poor; 1-year survival is

106
Q

How does rupture of a posterior duodenal ulcer increase risk for acute pancreatitis?

A

Head of pancreas sits posterior to the duodenum.

107
Q

Gallstone ileus

A
  • Gallstone enters and obstructs the small bowel
  • Due to cholecystitis with fistula formation between the gallbladder and small bowel (which would allow the passage of larger stones which can pass and then obstruct the small bowel)
108
Q

Generally, never give a child with a viral illness aspirin. However, there is one disease that may mimic a viral illness but requires the use of aspirin. What is that disease?

A

Kawasaki Syndrome – vasculitis that preferentially involves the coronary arteries, but presents with symptoms that mimic a viral illness such as N&V, fever, pain in abdomen or joints, etc…)

109
Q

How does ineffective erythropoiesis cause jaundice?

What are some laboratory findings?

A

Same reasons as extravascular hemolysis. The BM creates ineffective RBCs that are lysed either intravascularly (in the vessels) or extravascularly (in the spleen)

  • High levels of hemolysis overwhelms the conjugating ability of the liver.
  • Results in:
    • Increased UCB
    • Dark urine (despite having increased UCB, the liver is working at maximum efficiency for conjugating meaning there will be increased CB being filtered resulting in a darker urine)
    • increased risk for pigmented bilirubin gallstones (increased UCB results in increased risk for stone formation – pigmented because it bilirubin)
110
Q

Primary biliary cirrhosis - complication(s)

A

cirrhosis is a late complication

acutely, it causes obstructive jaundice

111
Q

Rotor syndrome

A

Dubin-Johnson syndrome without the liver discoloration

Deficiency of bilirubin canalicular transport protein –> increased serum conjugated bilirubin

112
Q

Porcelain gallbladder

A

Shrunken, hard gallbladder due to chronic inflammation, fibrosis and dystrophic calcification – makes it very easily visible on xray

A late complication of chronic cholecystitis

Also an indicator for increased risk for carcinoma

113
Q

Cirrhosis - what does portal HTN result in?

A
  1. ascites (fluid in the peritoneal cavity)
  2. congestive splenomegaly/hypersplenism (consumption of RBCs by an enlarged spleen)
  3. portosystemic shunts (esophageal varices, hemorrhoids, and caput medusae)
    • all caused by obstruction
  4. hepatorenal syndrome == rapidly developing renal failure secondary to cirrhosis
114
Q

How do you distinguish between metastatic and primary liver tumors?

A

Metastatic – multiple nodules

Primary – most often a single nodule

115
Q

Chronic cholecystitis - clinical presentation

A

RUQ pain especially after eating

Porcelain gallbladder is a late complication

116
Q

hemochromatosis - laboratory findings (ferritin, TIBC, serum iron, % saturation)

A

Ferritin – increased

TIBC – decreased

serum iron – increased

% saturation – increased

117
Q

What is the origin of pancreatic carcinoma?

A

They arise from the ducts NOT the acinar cells

118
Q

Trousseau syndrome

A

Episodes of vessel inflammation due to blood clot which are recurrent or appearing in different locations over time (thrombophlebitis migrans or migratory thrombophlebitis)

  • Location of the clot is tender and can be felt as a nodule under the skin
  • Presents as: swelling, erythema, and tenderness in extremities

Particularly associated with pancreatic and lung cancer

119
Q

What hepatitis infection(s) is(are) associated with only acute hepatitis with no risk for chronic state?

A

Hep A (HAV)

Hep E (HEV)

120
Q
A

Cirrhosis: end-stage liver damage characterized by disruption of the normal hepatic parenchyma by bands of fibrosis and regenerative nodules of hepatocytes

  • Fibrosis mediated by TGF-β from stellate cells which lie beneath the endothelial cells that line the sinusoids
121
Q

Annular pancreas - major concern/complication

A

duodenal obstruction (remember it wraps around the duodenum – contraction of pancreas can cause obstruction)

122
Q

How does trauma cause acute pancreatitis? What trauma is most common?

What population is this mostly associated with?

A

Most common trauma is automobile accidents with children.

Seat belt in children is over the abdomen. Compression of abdominal structures can cause premature release of enzymes resulting in possible premature activation

123
Q

What happens to conjugated bilirubin? How is it excreted out of our bodies?

A

First is transfered to bile canaliculi to form bile which is stored in gallbladder

When bile is released into the duodenum, intestinal flora convert CB to urobilinogen, which is oxidized to stercobilin (makes stool brown) and urobilin (partially reabsorbed into blood and filtered by kidney, making urine yellow)

124
Q

What factors results in cholelithiasis? (3)

A
  1. supersaturation of cholesterol or bilirubin
  2. decreased phospholipids (ie lecithin) or bileacids, both of which increase the solubility of cholesterol
  3. stasis
125
Q

Acute vs chronic hepatitis

A

Acute:

  • Inflammation of lobules of liver AND portal tracts w/ apoptosis of hepatocytes
  • symptoms

Chronic

  • Inflammation predominantly of portal tract
126
Q

Dubin-Johnson syndrome

A

Deficiency of bilirubin canalicular transport protein (normally responsible for transport of CB into the bile; if it doesn’t work, CB will backup and leak into the blood)

Autosomal recessive

Presents with:

  • increased conjugated bilirubin
  • liver is dark (can’t empty via bile duct –> leakage of bile into to bloodstream and liver –> pigmentation of liver due to excess bilirubin)
  • otherwise NOT clinically significant
127
Q

Acute hepatitis - clinical presentation

A
  • jaundice (mixed CB and UCB)
  • dark urine (due to CB)
  • fever
  • malaise
  • nausea
  • elevated liver enzymes (ALT > AST)
    • remember AST > ALT is highly associated with alcohol induced liver damage (alcohol is a direct mitochondrial toxin)
128
Q

What gives urine its yellowish color?

A

urobilin (a breakdown product of urobilinogen)

129
Q

CB vs UCB

What is more soluble in water?

If urine has a color, what it is due to?

A

UCB is NOT water soluble. It will stay in the blood until it can be conjugated causing jaundice in the meanwhile.

CB is water soluble. It is what gives urine its color. After it is conjugated, it can finally be filtered by the renal system and secreted which gives urine its color

130
Q

Acute pancreatitis - complications

A
  1. shock – due to peripancreatic hemorrhage and fluid sequestration (from tissue damage)
  2. pancreatic pseudocyst – formed by fibrous tissue surrounding liquefactive necrosis and pancreatic enzymes
    • presents as an abdominal mass w/ persistent elevated serum amylase
    • rupture is associated w/ release of enzymes into the abdominal cavity and hemorrhage
  3. pancreatic abscess – often due to E. coli – presents with abdominal pain, high fever and persistently elevated amylase
  4. DIC – pancreatic enzymes in blood can activate coagulation factors
  5. ARDS – enzymes chewing up the alveolar-capillary interface
131
Q

Jaundice by acute hepatits – what is it due to?

A

Mixed CB and UCB

  • remember that acute hepatitis causes damage to both the bile ductules and the hepatocytes
    • dmg to ductules –> increased CB
    • dmg to hepatocytes –> increased UCB
132
Q

Clinical causes of jaundice?

A
  1. Extravascular hemolysis or ineffective erythropoeisis
  2. Physiologic jaundice of the newborn
  3. Gilbert syndrome
  4. Crigler-Najjar syndrome
  5. Dubin-Johnson syndrome
  6. Biliary tract obstruction (obstructive jaundice)
  7. Viral hepatitis
133
Q

Breakdown products of urobilinogen

A

Oxidation into:

  • stercobilin (makes stool brown)
  • urobilin (makes urine yellow, partially reabsorbed)
134
Q

Cirrhosis - what happens to protein synthesis?

What is a result of this?

A

Liver makes albumin and a lot of other proteins. Cirrhosis –> damage to liver –> decreased protein synthesis

Results in:

  • hypoalbuminemia with edema
  • coagulopathy due to decreased synthesis of clotting factors –> increased PT and PTT
    • degree of deficiency is followed by PT
    • liver makes majority of coagulation factors and responsible for vitamin K epoxide reductase activity
135
Q

Ascending cholangitis - what prevents this from normally happening? What would make some more prone to it?

A

Increased incidence with choledocholithiasis (presence of 1 or more gallstones in the common bile duct)

  • Normally, bile secretions will wash away any bacteria trying to climb up the ducts. If there is an obstruction, the ascending infection is much more feasible because the flow is blocked
136
Q

Ascending cholangitis - clinical presentation

A
  • Sepsis – high fever and chills (remember it is still an infection by bacteria)
  • jaundice (blockade of bile duct –> bile backup into blood)
  • abdominal pain
137
Q

How does estrogen increase the risk of cholesterol stones?

A

Estrogen:

  • increases the activity of Hmg-CoA reductase –> increased synthesis of cholesterol
  • increase lipoprotein receptors on hepatocytes –> increased cholesterol uptake

Increased cholesterol in liver (where bile synthesis occurs) –> increased cholesterol in bile –> stored in gallbladder (where stones can form)

138
Q

Hemochromatosis - treatment

A

Phlebotomy – drain blood (essentially just drains iron)

139
Q

Hepatic adenoma - complications?

A

Risk of rupture and intraperitoneal bleeding, especially during pregnancy

  • tumors are subcapsular (right underneath the capsule so it can easily bleed out into the peritoneum) and grow with exposure to estrogen
140
Q

Chronic cholecystitis - what finding is classically associated with an increased risk for carcinoma?

A

Porcelain gallbladder on imaging

141
Q

Ascending cholangitis

A
  • Bacterial infection of the bile ducts
  • Usually due to an ascending infection with enteric gram-negative bacteria
  • Presents as sepsis (high fever and chills), jaundice and abdominal pain
  • Increased incidence with choledocholithiasis (stone in common bile duct)
142
Q

hepatorenal syndrome

A

rapidly developing renal failure secondary to cirrhosis

143
Q

What helps to keep cholesterol solubilized (2)? (removal of which will likely result in cholesterol stones)

A

phospholipids (ie lecithin)

bile acids

144
Q

How does jaundice in newborns occur?

A

Newborn liver has transiently low UGT (uridine glucuronyl transferase) activity –> insufficient conjugating capability –> Increased UCB –> jaundice

145
Q

Why does biliary tract infection result in gallstones? What type of stones will most likely result?

A

bilirubin gallstones will result from infection – due to ability of certain bacteria to de-conjugate bilirubin

  • Deconjugated bilirubin is much less soluble (esp in water) and will have much higher chance of precipitating out
146
Q

Pancreatic carcinoma - most common age group

A

elderly (average age is 70)

147
Q

Association of Budd-Chiari syndrome with hepatocellular carcinoma?

A

Increased risk for Budd-Chiari syndrome

  • liver infarction secondary to hepatic vein obstruction
  • presents with painful hepatomegaly and ascites
148
Q

Reye syndrome - what is the likely cause of the disease?

A

Unknown mechanism but it is thought to be related to mitochondrial damage of hepatocytes

149
Q

Hepatitis E (HEV) - mode of transmission

How is it most commonly obtained?

A

fecal-oral transmission

Commonly acquired from contaminated water or undercooked seafood

150
Q

Acute pancreatitis - what enzymes would you expect to find in blood?

A

Elevated lipase and amylase

lipase is more specific for pancreas. Amylase can be from any of the salivary glands

151
Q

Chronic cholecystitis

A
  • Chronic inflammation of the gallbladder
  • Due to chemical irritation from longstanding cholelithiasis w/ or w/o superimposed bouts of acute cholecystitis
  • Characterized by herniation of gallbladder of mucosa into the muscular wall (Rokitansky-Aschoff sinus)
  • Presents as vague RUQ pain, especially after eating
  • Porcelain gallbladder – late complication
152
Q

Acute pancreatitis - most common causes

A

Most common:

  • alcohol – causes contraction of sphincter of Oddi at the ampulla where the pancreatic/bile ducts drain into the duodenum
  • gallstones – obstruction

Other causes:

  • trauma – automobile accidents where compression of the abdominal cavity (esp in children) –> premature release and activation of enzymes
  • hypercalcemia
  • hyperlipidemia
  • drugs
  • scorpion stings
  • mumps
  • rupture of a posterior duodenal ulcer (head of pancreas sit slightly posterior to the duodenum)
153
Q

What does iron look like on biopsy? How do you distinguish it out?

A

Looks like lipofuscin (a brown pigment that is a by-product of the ‘wear-and-tear’ of peroxidized lipids that piles up in lysosomes)

Prussian blue can be used to distinguish iron (blue) from lipofuscin (does not stain)

154
Q

Alcoholic hepatitis: what happens to AST and ALT? Which one is higher?

A

Both increase due to damage to liver

AST > ALT

  • AST is located in the mitochondria. Alcohol is a mitochondrial poison –> preferentially increases AST over ALT, but both will increased due to damage to hepatocytes
155
Q

Biliary atresia

A

Failure to form OR early destruction of extrahepatic biliary tree

Leads to biliary obstruction within the first 2 months of life

presents with jaundice and progresses to cirrhosis (due to back pressure into liver which over time will cause damage to liver cells)

156
Q

Biliary atresia - clinical presentation

A

Jaundice – leakage of bile (containing conjugated bilirubin) into blood

cirrhosis – backup/pressure into liver over time causing damage to liver cells

157
Q

Hepatocellular carcinoma - risk factors?

A
  • Chronic hepatitis (HBV, HCV)
  • Cirrhosis (ie alcohol, nonalcoholic fatty liver disease, hemochromatosis, Wilson disease, A1AT deficiency)
  • Aflaxtoxins derived from Aspergillus (induce p53 mutations)
158
Q

What type of necrosis is associated with acute pancreatitis?

A

Liquefactive hemorrhagic necrosis (lot of blood vessels in the pancreas)

Fat necrosis of peripancreatic fat

159
Q

Alcoholic hepatitis - clinical presentation

A
  • Painful hepatomegaly
  • elevated liver enzymes (AST>ALT)
    • AST is located in the mitochondria. Alcohol is a mitochondrial poison –> preferentially increases AST over ALT, but both will increased due to damage to hepatocytes
  • May result in death
160
Q

What is the association between cystic fibrosis and pancreatitis?

A

Thick secretions from pancreas –> slower motility (more travel time) –> increased chance of premature activation

161
Q

What cells are responsible for extravascular hemolysis? What are the breakdown products?

A

splenic macrophages in the reticuloendothelial system.

hemolysis of RBCs results in heme, iron and globin

  • Globin –> broken down into amino acids
  • Iron –> recycled
  • Heme –> broken down into unconjugated bilirubin
162
Q

viral hepatitis - what happens to the levels of urine urobilinogen?

A

The gut bacteria is responsible for forming urobilinogen.

Urine urobilinogen levels should be normal, if not less.

  • If hepatocytes are damaged, then there is less CB to release into the gut.
  • If the bile ductules are damaged then can’t put the CB into the gut
  • Either way, likely will result in less urobilinogen (and thus less in the urine) if not normal
163
Q

How does extravascular hemolysis cause jaundice?

What are some laboratory findings?

A

High levels of hemolysis overwhelms the conjugating ability of the liver.

Results in:

  • Increased UCB
  • Dark urine (despite having increased UCB, the liver is working at maximum efficiency for conjugating meaning there will be increased CB being filtered resulting in a darker urine)
  • increased risk for pigmented bilirubin gallstones (increased UCB results in increased risk for stone formation – pigmented because it bilirubin)
164
Q

what enzyme is responsible for bilirubin conjugation?

where does this occur?

A

Uridine glucuronyl transferase (UGT)

Occurs in the liver

165
Q

What is the marker that indicates an active hepatitis infection?

A

Anti-virus IgM

166
Q

If dark urine is due to bilirubin, what type of bilirubin is it associated with? Why?

A

Conjugated bilirubin. CB in the blood is filtered by the renal system resulting in pigmentation in the urine

UCB is not water soluble and will NOT be dumped into the urine.

167
Q

Pancreatic carcinoma - treatment

A

Whipple procedure – en bloc (all together at the same time) removal of the head and neck of pancreas, proximal duodenum and gallbladder

168
Q

Acute pancreatitis

A
  • Inflammation and hemorrhage of the pancreas
  • Due to autodigestion of pancreatic parenchyma by pancreatic enzymes
  • Results in liquefactive hemorrhagic necrosis of the pancreas and fat necorsis of the peripancreatic fat
169
Q

Wilson disease - treatment

A

D-penicillamine (chelates copper)

170
Q

What age group does cholecystitis classically affect?

A

40-50 year olds

171
Q

What is a long-term complication of alcohol-induced liver damage?

A

Cirrhosis - occurs in 10-20% of alcoholics

172
Q

Primary hemochromatosis

A

Most commonly due to mtuations in the HFE gene (C282Y mutation – cysteine is replaced by tyrosine)

  • puts the intestinal iron absorption into overdrive
173
Q

Metastatic liver tumors – what is the physical exam finding?

A

Hepatomegaly with a nodular free edge of the liver

174
Q

Earliest sign of jaundice

A

Scleral icterus (yellow discoloration of the sclera)

175
Q

Why are iron and copper associated with hepatocellular carcinoma?

A

Both induce the fenton reaction. If there is too much iron (hemochromatosis) or copper (Wilson disease) then there will be an increase in generation of hydroxy radicals which can cause damage to DNA

176
Q

thrombophlebitis

A

vessel inflammation due to a blood clot

177
Q

Where is inflammation in acute hepatitis?

A
  • involves lobules and liver AND portal tracts
  • characterized by apoptosis of hepatocytes
  • Figure: inflammation pretty much everywhere, both in the tracts and within the lobules in the liver (surroundings the hepatocytes)
178
Q

Hepatitis C (HCV) - mode of transmission

How is it most commonly obtained?

A

Parenteral transmission (via piercing of the skin or the mucosa)

  • IV drug abuse
  • unprotected intercourse

Risk of transfusion is almost nonexistent due to the screening for the blood supply

179
Q

Acute pancreatitis - how does hypocalcemia occur?

A

Fat necrosis –> release of free fatty acids –> saponification (fat binding to calcium)

180
Q

Pancreatic carcinoma - serum tumor marker

A

CA 19-9 (CA = cancer antigen)

181
Q

pancreatic pseudocyst

A
  • pseudocyst because it lacks an epithelial lining (remember it surrounds pancreatic enzymes, very likely that the enzymes just ate up the cells and left behind the fibrotic material)
  • formed by fibrous tissue surrounding liquefactive necrosis and pancreatic enzymes
  • presents as an abdominal mass w/ persistent elevated serum amylase
  • rupture is associated w/ release of enzymes into the abdominal cavity and hemorrhage
182
Q

What kind of coagulopathy do you expect with cirrhosis? Why?

A
  1. Decreased coagulability due to decreased synthesis of clotting factors –> increased PT and PTT
    • degree of deficiency is followed by PT (just like how warfarin is used – blocks epoxide reductase)
  2. liver is responsible for vitamin K epoxide reductase activity
183
Q

Wilson disease

A

Autosomal recessive defect (ATP7B gene) in ATP-mediated hepatocyte copper transport

  • Results in lack of copper transport into bile and lack of copper incorporation into ceruloplasmin
  • Copper builds up in hepatocytes, leaks into serum, and deposits within tissues
    • Copper-mediated production of hydroxy free radicals –> tissue damage
184
Q

Kernicterus

A

deposit of UCB in the basal ganglia resulting in neurological deficits and death

Increased risk when there is elevated in UCB in neonates or fetus

185
Q

If a patient with hepatocellular carinoma presents with painful hepatomegaly and ascites, what would you expect?

A

Likely liver infarction secondary to hepatic vein obstruction (Budd-Chiari syndrome)

186
Q

What organ does mumps virus classically affect? What other organs does it hit?

A

Mainly infects the parotid

Also classically hits:

  • testicles (orchitis)
  • pancreas (pancreatitis)
  • meninges (meningitis)
187
Q

When there is fat necrosis in acute pancreatitis, what comes to mind? (Severity of disease? Complications?)

A
  • Since the fat is surrounding the pancreas, when there is fat necrosis, it is a sign of how bad the damage has gotten that it is now destroying the fat that surrounds the pancreas.
  • Additionally, the release of fatty acids in fat necrosis results in saponification (binding to calcium) which can induce a hypocalcemia.
188
Q

Acute cholecystitis - Why is there an increase in serum alkaline phosphatase levels?

What other cancer(s) would you think of when you see an elevated alkaline phosphatase?

A

The surface epithelium of gallbladder and biliary tract contain alkaline phosphatase

This is also characteristically seen in bone cancer

189
Q

If a patient recovers from a bout of acute pancreatitis but has persistently elevated serum amylase, what do you think of? (2)

How would you distinguish them apart?

A

Possible pancreatic pseudocyst or pancreatic abscess

Can be distinguish by other symptoms. Pseudocyst will have relatively nothing else besides an abdominal mass while pancreatic abscess (often due to E. coli ) will have high fever and abdominal pain

190
Q

Hallmark of cirrhosis

A

broad bands of fibrosis that separates nodules of liver parenchyma

  • these nodules are regenerative attempts to heal itself, but is impeded by the fibrosis present
191
Q

Cholestyramine – what is it used for? Mechanism?

What is its association with cholelithiasis?

A

Bile acid sequestrant –> prevents recycling of bile acids by the ileum

Decreases bile acids in the body. Bile acids normally help to solubilize cholesterol so that stones do not form

192
Q

What 2 syndromes are associated with decreased UGT (uridine glucuronyl transferase) activity?

A

Gilbert syndrome – mildly low UGT activity

Crigler-Najjar syndrome – absence of UGT

193
Q

What is the common principle in causes of acute pancreatitis?

A

Obstruction –> stops the flow of enzymes out of the pancreas. Enzymes are secreted only when needed (ie upon eating). The longer the enzymes sit in the ducts, the more likely they can be randomly activated.

Activation of trypsin will start a chain reaction that activates all the other digestive enzymes.

194
Q

Crigler-Najjar syndrome

A

Absence of UGT

Results in kernicterus and is usually fatal

195
Q

Metastatic cancers in the liver

A

More common than primary liver tumors

Most common sources include:

  • colon
  • pancreas
  • lung
  • breast carcinomas

Results in multiple nodules in the liver

196
Q

A patient presents with obstructive jaundice. Biopsy of the liver shows autoimmune granulomatous destruction of the intrahepatic bile ducts. Labs show the presence of an antimitochondrial antibody. What is at the top of the Dx?

A

Primary biliary cirrhosis

197
Q

Hepatitis D (HDV) - mode of transmission

How is it most commonly obtained?

A

Dependent on HBV for infection

  • superinfection = hep D superimposed on a hep B infection (hep B then hep D)
  • coinfection = hep D + hep B together
198
Q

Biliary tract infections – what bugs are most commonly seen to cause stone formation?

A
  1. E coli
  2. Ascaris lumbricoides
    • common roundworm that infects 25% of the world’s population
    • especially affects areas with poor sanitation (fecal-oral transmission)
  3. Clonorchis sinensis
    • endemic in China, Korea, and Vietnam (Chinese liver fluke)
    • infects biliary tract, increasing risk for gallstones, cholangitis and cholangiocarcinoma
199
Q

Gilbert syndrome

A

Mildly low UGT activity

autosomal recessive

200
Q

What compound gives stool its color?

A

Stercobilin – breakdown product (via oxidation) of urobilinogen

201
Q

Pancreatic carcinoma - most common location

A

head of pancreas

202
Q

Cirrhosis - clinical features

A
  1. Portal HTN leads to
    • ascites (fluid in the peritoneal cavity)
    • congestive splenomegaly/hypersplenism (consumption of RBCs by an enlarged spleen)
    • portosystemic shunts (esophageal varices, hemorrhoids, and caput medusae)
    • hepatorenal syndrome (rapidly developing renal failure secondary to cirrhosis)
  2. Decreased detoxification results in
    • mental status changes, asterixis, and eventual coma (due to increased serum ammonia) – metabolic, hence reversible
    • gynecomastia, spider angiomata, and palmar erythema due to hyperestrinism
    • jaundice (remember liver hepatocytes conjugate bilirubin - cirrhosis –> damage to hepatocytes)
  3. Decreased protein synthesis leads to
    • hypoalbuminemia with edema
    • coagulopathy due to decreased synthesis of clotting factors; degree of deficiency is followed by PT
203
Q

Reye syndrome - clinical presentation

A
  • hypoglycemia
  • elevated liver enzymes
  • nausea with vomiting
  • may progress to coma and death
204
Q

Hepatitis A (HAV) - mode of transmission

How is it most commonly obtained?

A

fecal-oral transmission

Commonly acquired by travelers

205
Q

hemochromatosis - clinical presentation

A

Classic triad – all due to iron deposits resulting in damage due from radical formation

  1. cirrhosis (iron deposits in the liver)
  2. secondary diabetes mellitus (iron deposits in the islets)
  3. bronze skin (iron deposits in the skin)

Unit 6 (10 decks)

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