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Pathology And Medicine > Liver Diseases 1 > Flashcards

Liver Diseases 1 Flashcards

1
Q

Trachea

A
  • Cartilage plates & smooth muscle
  • Respiratory epithelium
  • Submucosal glands
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2
Q

Bronchi

A
  • Cartilage foci & smooth muscle
  • Respiratory epithelium
  • Submucosal glands
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3
Q

Bronchioles

A
  • No cartilage, thinner muscular layer
  • Simple ciliated epithelium
  • Clara cells
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4
Q

the main function of the liver

A

→ synthesis and metabolism of carbohydrate, lipids, protein and drugs

→ metabolism and excretion of bilirubin and bile acids

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5
Q

major primary liver diseases

A

→ viral hepatitis

→ alcohol liver diseases

→ non-alcoholic fatty liver diseases

→ nonalcoholic fatty liver disease

→ hepatocellular carcinoma

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6
Q

major causes of liver disease
(west and east)

A

→ in the west = alcohol and hepatitis C virus

→ elsewhere = hepatitis B virus, but the incidence is decreasing (vaccination)

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7
Q

two facts about the liver

A
  • dual supply of blood vessels
  • vulnerability to a wide variety of insults → metabolic, toxic, microbial, circulatory and neoplastic
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8
Q

What is another name for jaundice?

A

icterus

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9
Q

What are the symptoms of jaundice?

A

yellow sclerae and skin

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10
Q

Serum bilirubin in jaundice patients

A

> 10 micromole

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11
Q

What is pre-jundice?

A

haemolytic jaudice

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12
Q

What is non-haemolytic jaundice?

A

congenital hyperbilirubinaemias

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13
Q

What are the three types of jaundice?

A
  • haemolytic jaudice - pre-hepatic
  • congenital hyperbilirubinaemias - non-haemolytic
  • cholestatic jaundice
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14
Q

Haemolytic Jaundice (Pre-Hepatic)

A

increased breakdown of RBC

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15
Q

Investigation of Haemolytic Jaundice

A
  • haemolysis
  • increase serum unconjugated bilirubin
  • normal alkaline phosphatase (ALP) and transferase
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16
Q

Congenital Hyperbilirubinaemias

A
  • most common - Gilbert’s syndome
  • decreased UDP-glucuronyl transferase activity
  • decreased conjugation of bilirubin with glucuronic acid
  • unconjugared bilirubin increases and other tests are normal
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17
Q

What are the two types of chlostatisis?

A

intrahepatic cholestatsis

extrahepatic cholestasis

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18
Q

intrahepatic cholestatsis

A
  • abnormal bile excretion
  • bile channel obstruction
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19
Q

extrahepatic cholestasis

A

bile flow obstruction - distal to the bile canaliculi

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20
Q

How do you investigate cholestatic jaundice?

A
  • serum liver biochemistry - jaudice (conjugated bilirubin)
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21
Q

Hepatitis Pathology

A

liver cell necrosis and inflammatory infiltration

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22
Q

Hepatitis Presentation

A
  • enlarged and tender liver (+/)
  • jaundice (+/-)
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23
Q

Hepatitis Investigation

A

serum transferase increases etc.

24
Q

Hepatitis types

A

acute and chronic

25
Q

Causes of acute hepatitis

A
  • viruses = hepatitis viruses
  • non-viral infections - toxoplasma gondii etc.
  • alcohol
  • drugs - anti-TB (isoniazid)
  • others - pregnancy etc
26
Q

Clinical Features of acute hepatitis

A
  • usually (viral) self-limiting, return to normal structure and function
  • occasionally profession into massive liver necrosis and even death
27
Q

Investigation of acute hepatitis

A
  • increased serum ALT (best indicator of acute hepatic injury)
  • prothrombin time and bilirubin (reflect disease severity)
28
Q

Chronic Hepatitis

A

a sustained inflammatory disease

29
Q

Causes of chronic hepatitis

A
  • viral
  • chemical
  • autoimmune
30
Q

How long does chronic hepatitis last?

A

more than 6 months

31
Q

What is Hepatitis A?

A

acute viral hepatitis

32
Q

How is acute viral hepatitis spread?

A

faecal-oral

33
Q

how does acute viral hepatitis damage the liver?

A

cytopathic and immunity-mediated by t cells

34
Q

acute viral hepatitis virus

A

HAV

35
Q

Clinical Features of Hepatitis A

A

relatively short incubation period, non-specific symptoms - flu-like

36
Q

Hepatitis A signs

A
  • jaundice +/-
  • hepatomegaly - moderate
  • spleen palpable
37
Q

lab testing of Hepatitis A

A

serum transferase increases

38
Q

Hepatitis A characteristics

A

Acute, self-limiting; no chronic stage - fulminant hepatitis, rare

39
Q

Hepatitis A management

A
  • no specific treatment
  • Prophylaxis - immunisation
40
Q

active Hepatitis A vaccine

A

inactive strain

41
Q

inactive Hepatitis A vaccine

A

immunoglobulin

42
Q

Hepatitis B Epidemiology

A

worldwide, prevalent in parts of Africa, middle and far east

43
Q

Hepatitis B virus

A

HBV, DNA virus

44
Q

HBV Protein

A

core - protein of core particle

pre-core - pre-core/core cleaves to HBeAg

surface - envelope protein; HBsAg; basis of current vaccine

45
Q

Spread of Hepatitis B

A
  • parenteral
  • close personal contact
  • vertical
46
Q

Hepatitis B - Mechanism of Liver Damage

A

immunity-mediated by t-cells

47
Q

Clinical Features of Hepatitis B

A
  • long incubation period
  • chronic carriers - HBsAg >6mo ; HBeAg or viral DNA - highly infectious, risk of chronic hepatitis and cirrhosis
  • chronic hepatitis - 3-5% acute hep B, serum liver biochemistry abnormal; liver biopsy/histology: mild inflammatory changes to cirrhosis
48
Q

Hepatitis B Treatment

A
  • antiviral agents with indications eg serum HBsAg, HBV DNA
  • Prophylaxis → avoid high-risk factors, immunisation: active (vaccine) and passive
49
Q

Hepatitis C viruses

A

HCV; non-A, non-B

50
Q

Hepatitis C spread

A

blood or blood products, other routes eg. vertical but rare

51
Q

Hepatitis C mechanisms of liver damage

A

immunity mediate by t-cells

52
Q

Hepatitis C Special Clinical Features

A
  • short incubation
  • 60-90% becoming carriers
  • high risk of developing → chronic, active hepatitis cirrhosis, hepatocellular carcinoma
53
Q

Hepatitis C Diagnosis

A

by exclusion

54
Q

Management of Hepatitis C

A
  • interferon used in acute cases to prevent chronic diseases
  • needle-stick injuries must be followed and treated early
55
Q

Prophylaxis

A

HCV is a RNA virus; a rapid change in envelope proteins hence vaccine is difficult

Pathology And Medicine (15 decks)

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