Liver Pathology Flashcards

(17 cards)

1
Q

Portal triad

A

Portal vein
Hepatic artery
Bile duct

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2
Q

What are the 3 zones

A

Zone 1: Periportal
Zone 2: Mid zonal
Zone 3. Centrilobular (closet to terminal hepatic vein)

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3
Q

Patterns of liver disease

A

Cirrhosis ( end stage from chronic persistent damage to liver)

Portal hypertension (COmplication of cirrhosis etc)

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4
Q

Common Liver diseases

A

– Infectious disorders of the liver
– Drug and toxin induced liver injury
– Metabolic liver disease
– Haemochromatosis

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5
Q

Cirrhosis liver anatomy findings (3)

A
  1. Bridging fibrous septae (link portal tracts)
  2. Parenchymal nodules (proliferating hepatocytes encircled by fibrosis) micronodules (<3mm), macronodules (up to several centimetres)
    - caused by fibrosis I bridging fibrosis (scarring between portal triads
  3. Disruption of entire architecture
    – Vascular architecture reorganised with shunts; PV & HA blood bypasses functional liver cells
    – Progressive fibrosis (due to response of proliferation of hepatocytes - causes nodules AND loss of synthetic a detoxification functions of liver)
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6
Q

Portal Hypertension
- what is it
-Types
-consquences

A

elevated pressures within portal venous system

Types:
1. Prehepatic (obstructive thrombosis, often underlying thrombotic disorder)

  1. Posthepatic (severe R sided heart failure)
  2. Intrahepatic (cirrhosis)
  • Consequences
    – Ascites accumulation of fluid within abdomen
    – Portosystemic shunts blood doesn’t go through liver. bypasses developing where systemic and portal circulation share capillary beds
    – Congestive splenomegaly ↑ pressures a congestion
    – Hepatic encephalopathy -> build up of toxic metabolites causes brain dysfunction consequence of blood bypassing liver. lose filtering stepa control of toxins
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7
Q

Symptoms/Signs of Portal hypertensio in setting of cirrhosis

A
  • Heaptic encephalopathy (due to loss of normal detoxification functions of the liver)
  • Ascites (portal hypertension can push fluid out of the reins into the
    abdomen due to loss of oncotic pressure caused by low protein level due to loss of synthetic function & excess pressure in the veins 12 factors)
  • Malnurtrition
    -Skin spider angiomata
    -Esophageal varices (veins become dilated, varices can rupture I bleed due to portal hypertension, causes nematemesis (vomiting blood)
    -Portal Vein (↑ pressure a dilation , may get reverse flow)
    -Splenic Vein
    -Splenomegaly (↑ pressure causes spleen to be enlarged (palpable
    due to portal hypertension)
    -Periumblicial caput medusae
    -Hemorrhoids (due to portal hypertension ↑ flow through the hemorrhoidal veins)
    -Testicualr atrophy
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8
Q

Infectious disorders

A
  • Hepatitis A, B, C, D and E viruses

Cytomegalovirus

Epstein Barr Virus

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9
Q

Hep A
- Benign?
-Incubation period
-Cause of Chronic hep?
-Transmission/cause of infection
-symtpoms
-liver test results

A

Benign self-limited disease

Incubation period 2-6 weeks

Does not cause chronic hepatitis

  • Substandard hygiene and sanitation
  • Person to person, faecal-oral transmission
  • Asymptomatic or mild febrile illness +/- jaundice

↑ in enzymes within the hepatocytes (ALTIAST)
↑ bilirubin

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10
Q

Hep B
- causes acute or chronic hep?
-Incubation period
-Transmission/cause of infection
-liver test results

A

Acute hepatitis with resolution OR if cant clear virus then Chronic hepatitis may lead to cirrhosis/cancers. Immune response to viral antigens expressed on infected hepatocytes leads to liver cell damage

  • 4-26 weeks incubation
  • Blood and body fluid borne

Increased bilirubin, ALT and AST

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11
Q

Flowchart of Hep B outcomes

A

Lecture Slide

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12
Q

Hep C
-transmission
-acute or chronic?

A

Infected blood / blood products eg blood transfusions, needle sharing

Acute infection usually undetected so Chronic disease occurs in majority

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13
Q

Drug and Toxin-Induced Liver Injury
CLASSIFICATION
ACTION
PATTERN OF INJURY
MOST COMMON DRUG/TOXIN CAUSING ACUTE LIVER FAILURE AND CHRONIC LIVER DISEASE

A

1.predictable hepatotoxins
- act in dose-dependent manner
- occur in most individuals

  1. unpredictable / idiosyncratic hepatotoxins

ACTION:
-directly cell toxic
-hepatic conversion to an active toxin

Pattern of injury
cholestasis, hepatocellular necrosis, fatty liver disease
fibrosis, granulomas, vascular lesions, neoplasms

Most common drug/toxin
acute liver failure - paracetamol in excessive dose

chronic liver disease - alcohol

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14
Q

Alcoholic Liver disease
-how does it chnage the liver
-causes what other complications

A

– changes in lipid metabolism
– decreased export of lipoproteins
– cell injury caused by reactive oxygen species (ROS) and cytokines

  1. hepatic steatosis (fatty change AKA fatty liver)
    - ↑ lipid within hepatocytes,
    causes liver dysfunction
  2. alcoholic hepatitis
  3. cirrhosis (& hepatocellular carcinoma)

** aditional notes for understanding:
- When processing alcohol, your body converts NAD+ to NADH. NAD+ stimulates less fatty acid oxidation and NADH stimulates the production of fatty acids. Causing more fat production in the liver. Therefore as more NAD goes to NADH- there is more fatty acids being made creating the FATTY LIVER seen wiht alcohol consumption

Cirrhosis is caused because as the liver processes alcohol to make acetaldehyde it generates ROS. ROS destroy heptocyte proteins and DNA. Further, acetaldehyde binds to macromolecules (acetaldehyde adducts) which the IS recognise as foreign ctreating an immune attack against hepatocytes leading to liver cell destruction aka cirrhosis

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15
Q

Alcoholic liver disease flowchart

A

Lecture Slide

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16
Q

Non-alcoholic fatty liver disease (NAFLD)
- assosicated with

A

Associated with metabolic syndrome, obesity, type 2 diabetes,
dyslipidaemia, hypertension

Non-alcoholic fatty liver disease (NAFLD) develops when too much fat accumulates in the liver, often due to a combination of factors like obesity, insulin resistance, and high blood sugar. This excess fat can lead to inflammation and damage to the liver,

17
Q

Haemochromatosis
- what is it
-cause

A
  • Excessive accumulation of body iron that gets Deposited in liver and pancreas

Results from genetic defect causing excessive iron absorption
* Genetics: autosomal recessive
Cys282Tyr mutation in HFE gene, homozygous
* Transfusion transmitted iron overload