Brainscape's Knowledge GenomeTM

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


See full index

Patho > Hepatobiliary Disease > Flashcards

Hepatobiliary Disease Flashcards

1
Q

Macrostrucure of Liver

A

Liver is the largest visceral organ in the body
- Right lobe is the largest
- 75 to 85% of blood supply is from the portal vein

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

Which lobe is the largest in liver?

A

Right lobe

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

The Liver Function

A
  • Metabolic
  • Storage
  • Excretory/Secretory
  • Protective
  • Circulatory
  • Coagulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Metabolic Functions

A
  • Carbohydrate Metabolism
    – Gluconeogenesis
    – Glycogenolysis and glycogenesis
  • Synthesis of fatty acid, lipoproteins, cholesterol
  • Ketogenesis (breakdown of fatty acids to keytones)
  • Protein Metabolism
  • Synthesis of plasma protein (albumin, globulin, fibrinogen)
  • Urea synthesis
  • Hormone Metabolism
  • Red blood cell production (in fetal liver during the first trimester of pregnancy)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Storage Function

A
  • Glycogen
  • Vitamins
    – A, D, E, K (Lipid Soluble)
    – B12 (water soluble)
  • Iron
  • Copper
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Excretory/Secretory Functions

A

Bile
- Water, Cholesterol, Bile pigments, Anions of the bile acids, Phospholipids (mainly lecithin), Bicarbonate and other ions

Insulin-like Growth Factor 1 (IGF-1)
Most blood protein
Cholesterol, fatty acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Protective Function

A
  • Purification, Transformation, and Clearance
    – Endogenous (hormones, ammonia)
    – Exogenous drugs and chemical
  • Kupffer cells (residential macrophages)
    – Bacteria and other foreign material from the portal blood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Circulatory Function

A

Antechamber of the heart
- Collecting portal blood from the GI tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Coagulation

A

Production of coagulation factors
- Fibrinogen I
- Prothrombin II
- Factors (V, VII, IX, X, XI)
- Protein C
- Protein S
- Antithrombin

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

Liver Enzymes—Indicators of Liver Function

A

Transaminases (from damaged/dead hepatocytes)
- Aspartate aminotransferase (AST or SGOT)
- Alanine aminotransferase (ALT or SGPT)

Cholestatic Enzymes (from injured biliary epithelial cells)
- Alkaline phosphotase (ALP)
- Gamma-glutamyl transferase (GGT)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Viral Hepatitis

Acute Liver Injury

A

HAV & HEV: direct disruption of hepatocytes
HBV and HCV: immuno attack of hepatocytes
- HCV: 75% asymptomatic

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

Direct disruption of hepatocytes

A

HAV & HEV

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

Immuno-attack of hepatocytes

A

HBV and HCV

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

Drug-induced Liver Injury (DILI)

Acute Liver Injury

A

High incidence
- 10% adverse drug reaction: DILI
- Hepatocellular (the most common type of primary liver cancer): tylenol
- Cholestatic (flow of bile from the liver is slowed or blocked) : methyl testosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Most common drugs for DILI

A
  1. Amoxicilin/Clavulanate
  2. Diclofenac
  3. Azathiopurin
  4. Infliximab
  5. Nitrofurantoin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Chronic Liver Injury

hepatitis, fibrosis, cirrhosis, HCC Etiology

A
  • Hepatitis
    – Viral
    – Alcohol
    – Drugs
    – Autoimmune
    – Obesity
  • Iron overload
  • Copper overload: Wilson’s disease (hepatolenticular degeneration)
  • Alpha1-antitrypsin deficiency
  • Autoimmunue
    – PSC-progressing sclerosing cholangitis
    – PBC-progressing biliary cholangitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

ASH and NASH

A

ASH: Alcoholic Steatohepatitis
NASH: Non-alcoholic steatohepatitis

Cause:
- Steatosis (Fatty liver disease)
- Inflammation
- Hepatocyte ballooning (cell swelling and enlargemen)

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

Specutrum of NADLD

A

Fatty Liver (fat accumulates in the liver) ==> NASH (Fat plus inflammation and scarring) ==> Cirrhosis (scar tissue replaces liver cells)

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

Alcoholic Hepatitis

A

Normal liver => Steatosis => Fibrosis => Cirrhosis => HCC

Risk Factors:
- Female
- Obesity
- Dietary Factors
- Polymorphisms
- Drinking
- Smoking

Comorbidity:
- Viral hepatitis
- Hemochromatosis
- HIV

20
Q

What happens in NASH + ASH

A

Macrovesicular steatosis + inflammation => Infiltration of both lymphocytes and Kupffer cells => Ballooned hepatocytes that also contain Mallory-Denk bodies => Perivenular/pericellular (chicken wire) fibrosis

21
Q

Epidemiology

A

Fatty liver diseases is the most common cause of abnormal liver enzyme tests
- Lean NASH (happens in the absence of overweight)

Liver steatosis affect 30-40% of population in developed countries
- Fibrosis, cirrhosis, hepatocellular carcinoma

Affect 2-3% of children (25-50% of obese children)

22
Q

N. American Incidence of NAFLD and NASH +/- Fibrosis

A

N. American prevalence of NASH + fibrosis – 2.1%
- US Census Estimated Population in July 2017 - 325,719,178
- Number of individuals in US with or will have NASH + fibrosis 7,078,411

NAFLD (by ultrasonography) – 25.2%
NASH among NAFLD patients – 21%
NASH patients who experience fibrosis (global) - 41%

23
Q

Molecular Mechanism of NASH

A

Two-hit (multi-hit) theory
- First Hit: fat accumulation in the liver
– Obesity, Long term fasting
- Additional/parallel hit: injury leading to inflammation
– Drugs, Pathogenes, Leaky Guts (LPS), Genetic abnormalities (PTEN, FXR or..), Oxidative stress

24
Q

ASH Pathophysiology

A
  • Hepatic fat storage
  • Inflammation: Increased hepatic uptake of gut-derived endotoxins triggering Kupffer cell activation and release of proinflammatory factors
  • Oxidation: Induction of cytochrome P4502E1 producing toxic acetaldehyde and reactive oxygen species
  • ER stress: ethanol-mediated endoplasmic reticulum stree, protein mis-folding
25
Q

Why is inflammation Important in ASH

A

Because it increased hepatic uptake of gut-derived endotoxins
- This end up triggering Kupffer cell activation
- Which will cause the release of proinflammatory factors

26
Q

What Cytochrome do oxidation induce

A

P4502E1
- Produce toxic acetaldehyde and reactive oxygen species

27
Q

Mechanism of ALD-Inflammation

A
  • Activation of innate immunity
  • Increase pro-inflammatory cytokine production in all cells in the liver
  • Increase adaptive immunity
28
Q

Liver Fibrosis

A
  • Presitent HSC activation
  • Fibrosis potentially irreversible
  • Low hepatic blood flow
  • Numerous sequelae
  • No therapeutic agents
  • Requires liver transplantation
29
Q

Cirrhosis induced by NASH

A

“burnt out” NASH
Some features of NASH will no longer exist
- Steatosis
- Ballooned hepatocytes,
- Lobular inflammationt

The characteristic perivenular/ pericellular fibrosis may still be present

25% of patient never develop cirrhosis

30
Q

Liver Cysts

A

Cysts: closed sac filled with liquid or other tissue

Types:
- Simple Cyst
- Hydatid Cyst: Due to parasite (Echinococcus granulosus)
- Choledochal Cyst: Congenital, Dilation of bile duct
– Common in east Asia

31
Q

Primary Biliary Cholangitis (PBC)

Cholangiopathies Intrahepatic Bile Duct

A

T-cell mediated apoptotic destruction of biliary epithelial cells
- Middle Aged Women

4 Stages:
- Florid duct lesion
- Ductular proliferation
- Fibrotic septa
- Cirrhosis

32
Q

Primary Sclerosing Cholangitis (PSC)

A

Inflammation, progressive fibrosis and destruction of bile duct
- 10-30 yrs old male
- Duct affected: all ducts
- Associated with IBD

Histology
- Onion skin fibrosis
- Inflammatory infiltrate is typically mild and limited to biliary epitherlum and portal tracts

33
Q

T-cell mediated apoptotic destruction of biliary epithelial cells

Bile Duct

A

Primary Biliary Cholangitis (PBC)

34
Q

Duct affected: all ducts

Bile Duct

A

Primary Sclerosing Cholangitis (PSC)

35
Q

Common in 10-30 yrs old males

Bile Ducts

A

Primary Sclerosing Cholangitis (PSC)

36
Q

Middle aged females are affected

Bile Duct

A

PBC

37
Q

Onion skin fibrosis

Bile Duct

A

PSC

38
Q

Congenital Gall Bladder Pathology

A

Most sever case: Biliary atresia
- Biliary tree fail to develop
– Toxins involved (isoflavonid) biliatresone from plants: Dysphania genus, tight junction disruption

39
Q

extrahepatic biliary atresia

A

Inflammation with stricture of hepatic or common bile ducts.
- Leads to marked cholestasis
- intrahepatic bile duct proliferation
- fibrosis
- cirrhosis

This liver was rock hard. The dark green color comes from formalin acting on bile pigments in the liver from marked cholestasis, turning bilRUBIN to bilIVERDIN

40
Q

Diseases of Gall Bladder

A

Cholelithiasis (gallstone)
Carcinoma of the bile duct
Carcinoma of the gall bladder
Biliary obstruction

41
Q

Gallstone Disease: Cholelithiasis

A

Cholesterol stones form if there is an imbalance between the ration of Cholesterol and Bile Salt
- Normally bile salt enclose the hydrophobic cholesterol => this mean gallstone result from EXCESS cholesterol or DEFICIT of bile salt

42
Q

Risk Factors for Gallstone Disease

A
  • Female
  • Forties
  • Fat
  • Fertile
  • FXR mutation
43
Q

Liver tumors

Benign tumors

A
  • Liver cell adenoma
  • Angioma
  • Bile Duct hamartoma
  • Focal nodular hyperplasia
44
Q

Liver Tumors

Malignant

A

Primary:
- Liver cell carcinoma (hepatocellular carcinoma-HCC)
- Cholangiocarcinoma (adenocarcinoma of bile ducts)
- Angiosarcoma (malignant neoplasm of vascular endothelium)
- Hepatoblastoma (primary liver tumor in childhood)

Secondary: Metastases from
- GI
- Lung
- Breat cancer

45
Q

Molecular Mechanisms of Hepatocellular Carcinoma

A

Heterogenic

Screen Shot

46
Q

HCC Types

A

Well Differentiated
- Tumor cell resemble hepatocytes
- Form trabeculae, cords and nests
- May contain bile pigment in cytoplasm

Poorly Differentiated
- Malignant epithelial cells are discohensive
- Plemorphic anaplastic and giant

47
Q

Cholangiocarcinoma

A

Malignant Tumors in the Bile Duct

Patho (17 decks)

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