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Hepato Biliary System > Liver > Flashcards

Liver Flashcards

1
Q

Mention the lobes of the liver and what ligament separates them from one another

A

Right including caudate and quadrate) and left lobe separated by falciform ligament

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2
Q

Name fissures of the liver.Most hepatic vessels enter and leave the liver through which fissure?

A

Left and right sagittal fissures, porta hepatis fissure. Porta hepatis fissure

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3
Q

Portal triad is made up of

A

Hepatic artery proper, portal vein and bile duct

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4
Q

Describe blood supply and drainage of the liver

A

Blood supply
Hepatocytes- Portal vein
Bile ducts- Hepatic artery proper

Drainage
In hepatic lobule;From periphery to central through sinusoid , blood drains in central vein- collecting vein- right/intermediate/left hepatic vein- inferior venacava

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5
Q

Which one is not specific to liver damage btn AST and ALT. And which conditions may lead to it’s increase?

A

Aspartate aminotransferase
Hemolysis, rhabdomyolysis, myocardial infarction

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6
Q

Above or below which figure should the ratio of AST/ALT be in order to determine that disease may be not only from the liver ?

A

AST/ALT>/= to 5

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7
Q

AST/ALT ratio > 2 suggests what kinds of liver disease?

A

Alcohol related liver disease

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8
Q

Tests that involve hepatocellular injury are ?

A

AST and ALT

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9
Q

Tests to indicate bile duct injury or obstruction include

A

GGT- gamma glutamyl transferase, ALP- Alkaline phosphatase, Bilirubin

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10
Q

Which one is a more appropriate test to confirm liver( biliary) injury between GGT and ALP test

A

GGT

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11
Q

Alkaline phosphatase levels can also be affected by?

A

Pregnancy, bone disease such as paget’s disease, kidney injury

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12
Q

Differential diagnosis for low levels of albumin include?
Symptoms of hypoalbunemia

A

Nephrotic syndromes, Gastric related issues( malabsorption)
Symptoms; edema, ascites

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13
Q

Clotting factors dependant on vitamin K include?

A

II, VII,IX,X, protein C and S

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14
Q

How is PT/INR used to test for hepatobiliary function?

A

Increased PT/INR indicates that there is a problem in the production of coagulation proteins 2,7,9,10,C&S

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15
Q

How do you determine if increased PT/INR is due to vit K deficiency or liver failure?

A

Administer IV vit K, if problem is due to Vit K deficiency then PT/INR should be normal after IV vit K but if problem is due to liver failure, then there will be no change in PT/INR, it will remain high

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16
Q

What are the symptoms associated with elevated PT/INR

A

Coagulopathies; high risk of bleeding

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17
Q

How does the liver influence the production of platelets

A

It produces thrombopoietin which stimulates the bone marrow to produce platelets

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18
Q

How to distinguish between thrombocyotpenia caused by liver failure from one caused by DIC

A

Test for factor VIII which is not produced in the liver, if it is low then thrombocytopenia is likely due to DIC, but is it is normal then thrombocytopenia is likely due to liver failure

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19
Q

Name the tests used to determine helatobiliary function

A

Albumin levels, PT/INR, Platelet count

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20
Q

In case of hepatocellular injury which LFTs are to be elevated?
What is the approach in distinguishing between Viral hepatitis and autoimmune hepatitis?

A

AST,ALT and sometimes Direct bilirubin
For viral hepatitis check for HAV,HBV,HCB,HDV,HEV
For autoimmune hepatitis check for ANA,ASMA,IgG titre

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21
Q

What can be tested for in drug induced hepatitis?

A

APAP (acetaminophen) overdose
Alcohol overdose

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22
Q

How to approach Hepatocellular injury due to vascular damage?

A
  1. Test for RHF by Echo
  2. Test for Budd-Chiari syndrome ( obstruction of hepatic veins) by US( doppler flow)
  3. Test for Shock affecting the hepatic artery by checking hypotension etc
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23
Q

What is used to confirm autoimmune hepatitis?

A

A biopsy

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24
Q

In case of Non alcoholic fatty liver disease/ non alcoholic steatohepatitis, what is criteria is used to confirm

A
  1. Negative evaluation of viral, autoimmune, drug toxicity and vascular related hepatitis
  2. AST> ALT
  3. Elevated LDL, TG, BMI, Glucose
  4. Biopsy
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25
Q

In case of hereditary hepatitis what should we check for?

A
  1. Hemachromatosis- Iron studies, HFE gene mutation+ve
  2. Wilson’s disease- copper levels in the blood
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26
Q

When hepatocellular injury is confirmed, what are the most likely causes ? Least likely causes?

A
  1. Viral, autoimmune, drug induced, vascular related hepatitis
  2. Hereditary, non alcoholic fatty liver disease
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27
Q

Formula for R- value?
Wy is R-value significant?

A

(ALT/upper limit of ALT)/(ALP/upper limit of ALP)
It helps to determine whether LFTs are indicative of hepatocellular or biliary injury ( R>/= 5 : hepatocellular, R= 2-5: mixed, R < 2 biliary)

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28
Q
  1. Cholesystitis?
  2. Cholangitis?
  3. Cholelithiasis?
  4. Choledocholithiasis?
A
  1. Inflammation of the gallbladder
  2. Inflammation of the biliary tree
  3. Formation of gallstones
  4. Presence of gallstones in the common bile duct
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29
Q
  1. What are some of Extrahepatic duct obstruction leading to biliary injury?
  2. How are they diagnosed?
A

1.
Tumors of the head of the pancrease, Tumors of bile ducts ( Cholangiocarcinoma),Choledocholithiasis ,Primary sclerosing cholangitis ( order ANA,ASMA, P-ANCA)

  1. US- ductal dilation near the area of obstruction, then ERCP, MRCP or CT of abdomen to further confirm
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30
Q

Biliary injury caused by intrahepatic obstruction maybe due to?
Which tests?

A
  1. Primary biliary cholangitis- Anti mitochondrial antibody test
  2. Drug induced
  3. Estrogen increase: oral contraceptives or pregnancy
  4. Sepsis
  5. Infiltrative disease ( rare); malignancies, granulomas, amyloidosis, liver flukes - biopsy
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31
Q

Prehepatic jaundice, what are the most likely causes for it? What indicates it?

A

Hemolysis, inhibition of transport of indirect bilirubin into the hepatocytes, problems with UGT enzyme

Elevation in Indirect bilirubin

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32
Q

How is hemolysis determined?

A

Tests including elevated Lactate dehydrogenase , increased reticulocytes, elevated indirect bilirubin, decreased Hgb and hematocrit , decreased Haptoglobin and to confirm schistocytes in Peripheral blood smear

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33
Q

Inhibition of transporter for indirect bilirubin can be due to

A

Drugs such as rifampin and probenecid ( chech medication history)

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34
Q

Decreased in UGT activity may be due to?

A

Genetic disorders
1. Gilbert’s syndrome
2. Crigler najjar syndrome

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35
Q

How to determine prehepatic jaundice?

A

Elevated Total bilirubin, elevated indirect bilirubin

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36
Q

What indicates Intrahepatic/ post hepatic jaundice in LFTs

A

Increased Total bilirubin and super elevated direct bilirubin

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37
Q

What is an indication of intrahepatic jaundice?

A

Elevated direct bilirubin

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38
Q

What are the causes of intrahepatic jaundice?

A
  1. Transporter malfunctions: Rotor syndrome ( genetic testing ), dubin johnson’s syndrome ( genetic testing, biopsy- black pigment on liver)
  2. Hepatocellular injury: Virus, autoimmune, liver vascular related, drugs related, metabolic, genetic- hemachromatosis:Fe, wilson’s disease:cu deposits
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39
Q

What are indications of posthepatic jaundice?

A

Elevated direct bilirubin

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40
Q

Posthepatic jaundice causes?

A
  1. Extrahepatic obstruction: choledocolithiasis, pancreatic tumor, cholangicarcinoma,
  2. Intrahepatic cholestasis: Primary biliary cholangitis, drug induced, pregnancy, sepsis
  3. Infiltrative diseases: malignancy, granuloma, amyloidosis,
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41
Q

Does Hepatitis A virus cause an acute or chronic infection?

A

Acute infection

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42
Q

Mention the route of transmission of HAV

A

Fecal-Oral route

43
Q

Does HAV have envelope?

A

No, it has only caspid

44
Q

What kind of genetic material is in HAV?

A

a positive sense Single stranded RNA

45
Q

Does HBV cause acute, chronic or both kind of infection?

A

Both acute and chronic infections

46
Q

HBV route of transmission?

A

Sex, blood, perinatal

47
Q

Does HBV have an envelope?

A

Yes, a lipid bilayer

48
Q

What kind of genetic material is present in HBV?

A

partially Double stranded DNA

49
Q

Does HCV cause acute, chronic or both?

A

Both

50
Q

HCV mode of transmission?

A

Sex, blood, perinatal

51
Q

HCV structure?

A

Have envelope

52
Q

HCV genetic material

A

Positive sense Single stranded RNA

53
Q

HDV cause chronic or acute?

A

Chronic infection

54
Q

HDV mode of transmission?

A

Sex, blood, perinatal

55
Q

Which virus does HDV need in order to infect the body?

A

It needs HBV, either as co-infection or superinfection

56
Q

HDV structure?

A

Has envelope

57
Q

HDV genetic material?

A

Negative sense Circular single stranded RNA

58
Q

What kind of infection does HEV cause?

A

Acute

59
Q

Mode of transmission of HEV?

A

Fecal oral

60
Q

HEV structure?

A

No envelope

61
Q

HEV genetic material?

A

Positive sense single stranded RNA

62
Q

The hepatitis viruses enter the hepatocytes through which process?

A

Endocytosis

63
Q

Process of replication of hepatitis A,C,D,E viruses?

A

Enter the hepatocytes by endocytosis- shed off their envelopes and capsids, RNA then goes to be directly translated by ribosomes to be translated to produce other proteins such capsomeres, RNA dependent RNA polymerase etc, then RdRNA polymerase transcribes viral RNA to form more positive sense RNA using intermediate negative sense viral RNA, then assembling of proteins in Golgi apparatus, then new virus is formed and lysis

64
Q

How does hepatitis B virus replicate?

A

It enters the hepatocytes by endocytosis , then sheds it’s envelope and capsid in the cytoplasm of the host cell, then injects it’s DNA in nucleus of host cell where it is converted from partial circular DNA to covalently closed circular DNA by host cell DNA repair and synthesis enzymes , then uses host cell RNA polymerase to make mRNA and Pre-genomic RNA, then the mRNA gets translated to produce proteins, the pgRNA is acted upon by enzyme reverse transcriptase to form partial DsDNA, then assembling of DNA and proteins to form new virus, then lysis leading to cell death.

65
Q

How does the hepatitis virus cause cell death?

A
  1. Lysis
  2. Immune response by cytotoxic T cells, they release perforins and granzymes which induce apoptosis
66
Q

Once the liver is infected which products are produced and what do they do?

A
  1. IL-1,IL-6,TNF-alpha: they go to the brain via the bloodstream, they stimulate PGE2, PGF2 and these alter the thermostat of hypothalamus resulting to fever and malaise. INF-gamma is produced which attract macrophages which attract Cytotoxic t cells
  2. Bilirubin ( CB and UCB) and bile salts: goes to the sclera and cause jaindice( icterus ), goes to the thick skin ( palms and soles)- jaundice, excreted by kidneys causing dark urine
  3. Hepatotoxins: they travel through the blood stream to the Chemoreceptor trigger zone ( CTZ) in the brain stem which detects the toxins and activate the vomiting center which activates nerves that supply the GI tract causing reverse peristalisis leading to nausea and vomiting. This leads to dehydration, loss of electrolytes and overtime weight loss. It also leads to diarrhea
  4. Decreased production of bile: this leads to decreased bilirubin in the gut therefore decreased stercobilin causing acholic stool ( clay colored)
67
Q

Prodromal phase of hepatitis infection involve which symptoms and signs?

A
  1. Fever
  2. Malaise
  3. Vomiting
  4. Diarrhea
  5. Weight loss
  6. Electrolytes imbalance
68
Q

In icteric phase of hepatitis which symptoms and signs are involved?

A
  1. Jaundice ( eyes and palms, soles)
  2. Dark urine
  3. Clay colored stool
  4. RUQ abdominal pain caused by hepatomegaly
69
Q

Which liver tests are to be checked in hepatitis?

A
  1. Elevation in ALT, AST
  2. Elevation in GGT, ALP
  3. Decrease in PT ( extrinsic pathway clotting factors I,II, VII, V, X)and PTT ( intrinsic and common pathway clotting factors I, II, V, VIII, IX, X,XI,XII)
  4. Increased bilirubin
  5. Increased lymphocyes
70
Q

In cases of HBV and HCV, what can be seen?

A
  1. Immune complexes ( antibody- antigen complexes) may be deposited in other organs of the body causing inflammation, i.e; Myocarditis, pericarditis, arthritis , vasculitis ( polyarteritis nodosa- PAN), glomerulonephritis.
  2. Immune complexes may also attach to RBCs- hemolytic anemia, Platelets- Thrombocytopenia, Neutrophils- Neutropenia
71
Q

In convalescent phase what happens

A

Resolving of all symptoms

72
Q

Why is there a risk of cirrhosis and Hepatocellular carcinoma in HBV and HCV Infections?

A

Because they are chronic infections:
Cirrhosis happens when there is increased cell death which then leads to increased rate of fibrosis
HCC can happen when there is increased cell death leading to increased mitosis there increased rate of mutations leading to HCC

73
Q

In serology of HBV can we interpret the following results?
1. HBVsAg +
2. HBVeAg +
3. HBVcAg usually not measured
4. HBV DNA +

  1. Anti HBs +
  2. Anti HBe +
  3. Anti HBc +
A
  1. Presence of infection
  2. Replication and highly infectious
  3. Replication and highly infectious

5.Cured or vaccinated
6. Decreased replication and infectivity
7. If IgM= Acute infection, IgG= Chronic infection

74
Q

In Window period of HBV infection, what are the serum markers results?

A
  1. HBsAg -, anti-HBs -
  2. HBeAg -, anti-HBe -
  3. Anti-HBc -/+
  4. HBV DNA + ( most accurate test for this period)
75
Q

In Acute phase of Hepatitis B, what are the serum marker results?

A
  1. HBsAg+, anti-HBs-
  2. HBeAg+, anti-HBe -
  3. Anti-HBc Igm+
  4. HBV DNA+
76
Q

What is the difference between serology results in recover and immunized patients of HBV?

A

In recovery:
1. HBsAg -, Anti-HBs +
2. HBeAg -, Anti-HBe N/A
3. HBV DNA -
4. Anti- HBc IgG+

In immunized

  1. HBsAg -, Anti-HBs +
  2. HBeAg-, N/A
  3. HBV DNA -
  4. Anti-HBc -
77
Q

What are serology results for Chronic (replicative) vs chronic ( non replicative) HBV?

A

Chronic replicative
1. HBsAg+, anti-HBs -
2. HBeAg+, anti-HBe-
3. Anti-HBc IgG+
4. HBV DNA +

Chronic non replicative
1. HBsAg+, Anti-HBs -
2. HBeAg-, Anti-HBe +
3. Anti- HBc IgG+
4. HBV DNA -

78
Q

What is the approach and interpretation of HCV serology?

A

First, test for HCV antibody ( IgG), if +ve then do PCR test for HCV RNA, if -ve the patient is cured, if +ve check how long more or less than 6 months.

Second check for degree of fibrosis
1. APRI score formula:( AST/upper limit of AST)/ platelet count * 100. If greater than 1.5 then cirrhosis very high
2. Liver biopsy
3. Fibrosure test

79
Q

Approach and interpretation of HDV serology

A

First confirm HBV +ve
In Acute :
HDV RNA +ve,
HDV Ag +/-, Anti- HDVAg IgM +

In Chronic
HDV RNA +ve
HDV Ag -ve, Anti-HDVAg IgG +

80
Q

Approach and interpretation of HAV serology?

A

It only causes acute infections
Therefore :
1. HAV RNA +, Antibody IgM
2. If previously exposed or immunized: HAV RNA -ve, Antibody IgG

81
Q

Approach and interpretation of HEV serology?

A

It only cause acute infections
1. HEV RNA +ve, Antibody IgM
2. Post exposure: HEV RNA -ve, Antibody IgG ( 2-3 yrs) +/-

82
Q

In which conditions is HEV extremely dangerous?

A

In Pregnancy, it causes fulminant hepatitis

83
Q

Hepatocytes undergoing apoptosis are known as?

A

Councilman bodies

84
Q

Anti-hepatitis drugs are divided into two groups namely based on their mechanism of action, namely?

A
  1. Nucleoside/ nucleotide analogs
  2. Interferons
85
Q

Mention the nucleoside analogs

A
  1. Ribavirin- HCV
  2. Entecavir -HBV
  3. Lamivudine -HBV
86
Q

Mention the nucleotide analogues

A
  1. Adefovir - HBV
  2. Tenofovir - HBV
  3. Sofobuvir - HCV
87
Q

Ribavirin side effects?

A

Hemolytic anemia, hyperuricemia, itching, rashes, birthdefects in pregnancy, insomnia

Increases efficacy of interferons

88
Q

Lamivudine side effects?

A

Aneroxia , prone to HBV resistance

89
Q

Adefovir side effects

A

Damage kidneys

90
Q

Types of interferons?

A

Type 1: alpha and beta
Type 2: gamma

91
Q

HCV has the highest rate of ?

A

Chronicity

92
Q

Chronic hepatitis C usually progress to ?

A

Cirrhosis

93
Q

HCV induced cirrhosis may result to?

A

Hepatocellular carcinoma

94
Q

Alcohol related liver disease stages?

A
  1. Alcohol associated hepatic steatosis
  2. Alcoholic hepatitis
  3. Alcohol associated cirrhosis
95
Q

Risk factors for alcohol related liver disease

A
  1. Quantity of alcohol consumed
  2. Sex- women more susceptible
  3. Genetic and metabolic traits
  4. Obesity
  5. Concomitant viral hepatitis
  6. Hemochromatosis
96
Q

When alcohol enters the body what happens? ( pathophysiology)

A

Alcohol goes to the liver
In the liver: There are three ways that alcohol is metabolized,
1st using Alcohol dehydrogenase ( ADH)
2nd using Cytochrome P450 2E1
3rd Catalase enzymes in peroxisomes
to convert alcohol to acetaldehyde

There will be a oxidation of NAD+ to NADH
Also there will be production of Reactive oxygen species
As well as metabolites of Alcohol such as acetaldehyde

All these contribute to disrupted metabolism of fat in the liver cells, destruction of proteins and DNA by ROS as well as inflammation and immune response by neutrophils leading to ARLD

97
Q

The effect of alcohol in the gut?

A

Alcohol changes gut permeability allowing the gut to absorb endotoxins produced by bacteria in the gut, at this point the liver can not detoxify the endotoxins therefore kuppfer cells release free radicals increasing oxidate damage

98
Q

What are the results of inflammation in the liver?

A

Once the liver is inflammed due to immune response, it leads to cell necrosis and apoptosis thus loss of hepatocytes. This triggers regeneration processes which lead to fibrosis of the liver. Fibrosis leads to decreased perfusion of liver due to narrowing of sinusoids, and as it happens to terminal hepatic venules, it leads to portal hypertension. Extensive fibrosis which is often also a result of stellate cells proliferation causing excess deposition of collagen 1 and extracellular matrix, this causes liver nodules and eventually cirrhosis

99
Q

What exactly is seen in Hepatic steatosis?

A

Fat vesicles accumulate in hepatocytes displacing the nucleus, the liver enlarges.
This stage is usually asymptomatic and potentially reversible.

100
Q

What exactly is seen in alcoholic hepatitis ( Steatohepatitis)

A

Here there is a combination of steatosis, inflammation and necrosis
Under the microscope, there will be ballooning degeneration, granular cytoplasm, mallory bodies, narrowing of sinusoids and necrotic hepatocytes

Symptoms include jaundice, fever, nausea, vomiting, abdominal pain

101
Q

What exactly is seen in Alcohol associated cirrhosis

A

Here there is extensive fibrosis
Under the microscope we can see micronodular cirrhosis, these are small nodules formed as a result of attempted regeneration of liver cells. Over time fibrosis forms large bands separating liver tissue into large nodules ( macronodular cirrhosis) . As a result the liver shrinks.

102
Q

What are complicated that may arise due to Alcohol associated cirrhosis?

A
  1. Portal hypertension often with esophageal varices
  2. Ascites
  3. Hepatic encephalopathy
  4. Coagulopathy
103
Q

Diagnosis of ARLD

A
  1. Confirmed history of alcohol consumption
  2. Alcohol biomarkers- urine ehthyl sulfate, urine ethyl glucoronide etc
  3. Liver function tests and CBC
  4. Liver biopsy

Hepato Biliary System (2 decks)

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