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MET 2 PBLS > PBL 2 - Hepatitis C + Cirrhosis > Flashcards

PBL 2 - Hepatitis C + Cirrhosis Flashcards

1
Q

Structure of Hepatitis C

A

Double stranded DNA virus

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2
Q

What is secreted by infected cells

A

HbeAg antigen

marker for active infection

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3
Q

What does Anti-HBc suggest

A

core antibody implies previous/current infection

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4
Q

Significance of Anti-HBs

A

Immunity

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5
Q

Symptoms of Hep C

A

Nausea
Fatigue
RUQ pain –> liver fibrosis/cirrhosis/hepatocellular carcinoma

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6
Q

How is hep C transmitted

A

o Sex, blood (transfusions), vertical (mother –> infant), injecting drugs,

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7
Q

Causes of cirrhosis

A

Viral - HepB, C
Alcohol
Autoimmune disesae
Wilson’s disease

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8
Q

Pathogenesis of cirrhosis

A

Alcohol or virus –> constant stress on liver –> inflammation and destruction of hepatocytes –> necrosis –> stellate cell activation producing TGF-beta –> increase collagen –> fibrosis –> macronodular or micronodular

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9
Q

Macronodular cirrhosis

A

Hepatitis B

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10
Q

Micronodular cirrhosis

A

Alcohol

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11
Q

Compensated cirrhosis

A

 Liver can still undergo its function, may be asymptomatic or have non-specific symptoms such as weight loss, fatigue, weakness

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12
Q

Decompensated cirrhosis

A

 Liver can’t function and do its normal jobs leading to a degree of liver failure(jaundice, pruritus, ascites, hepatic encephalopathy, easy bruising , leads to cancer

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13
Q

Diagnosis of cirrhosis

A

Fibroscan

Liver biopsy

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14
Q

What does fibroscan measure

A

measures how stiff the liver is, non-invasive, no sedation, no pain

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15
Q

Downsides of liver biopsy

A

invasive, sedation needed, requires hospitalisation

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16
Q

Why did the pt have high INR and low platelets

A

Coagulopathy
Clotting factors + platelets produced in liver
Poor blood flow to spleen due to fibrosis –> congestion of platelets in spleen –> retention

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17
Q

Why low albumin

A

Synthesised in liver
fibrosis/necrosis reduces synthesis –> equilibrium between oncotic pressure (maintained by albumin) and hydrostatic pressure –> ascites/oedema

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18
Q

High bilirubin why

A

o Breakdown of RBC removed and conjugated at liver with glucuronic level. Less conjugation –> less removed –> high level –>jaundice

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19
Q

ALT significance

A

more specific to liver cells

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20
Q

ALP significance

A

biliary duct/pagets/pregnancy/bone

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21
Q

yGT significance

A

induced by alcohol

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22
Q

AST significance

A

seen in heart/muscle/brain

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23
Q

AST:ALT ratio of 2:1

A

Alcoholic liver disease

24
Q

What causes reduces ALT

A

Reduced ALT production in alcoholic due to vit B6 deficienc

25
Q

Why high urea

A

o High GI bleeding due to oesophageal varices –> digested as a protein rich meal.
o Hepatorenal syndrome causing kidney failure –> reduces ability to produce urine hence a build-up of urea

26
Q

Why low blood glucose

A

Glucose homeostasis impaired due to reduced ability to undergo gluconeogenesis, store glycogen, undergo glycogenolysis

27
Q

Why low haemoglobin

A

o Alcohol –> macrocytic anaemia
o Loosing blood from varices –> haemolytic anaemia
o Alcohol –> direct effect damaging the bone marrow —> low platelet/haemoglobin count

28
Q

What causes ascites

A

1) albumin –> fluid shifts from intravascular compartment –>peritoneum
2) Less fluid in blood –> renal hypotension –> ADH/RAAS –> even more fluid retention
Non-osmotic secretion of ADH due to kidney impairment –> hyponatremia
3) Portal hypertension caused by scar tissue (fibrosis) blocks the flow of blood through liver (narrows sinusoids)–> raised capillary hydrostatic pressure
Hepatic portal vein (splenic + SMV) normal pressure 5-10, in hypertension above 14 mmHg.

29
Q

Oesophageal Varices

A

= Portal hypertension –> Blood diverted to area with least resistance –> directed away from portal system to systemic system
= At the point of anastomosis –> dilation of vessels –> when it happens at lower oesophagus it is called varices and they can bleed.

30
Q

How do you treat cirrhosis

A 
Diuretics
High Carb diet
Pabrinex
Terlipressin
Lactulose
Gastric Banding
Liver transplant
Anti virals
31
Q

Diuretics

A

o Clear fluid from interstitium – spironolactone + furosemide

32
Q

High carb diet

A

o To ensure not malnourished, raise BCAA –> prevent muscle wasting/brain problems

33
Q

Pabrinex

A

B1, B2, b6 –> Alcoholics have low thiamine, these B vits used in carbohydrate/lipid metabolism

34
Q

Terlipressin

A

Used as vasoactive drug in managing low BP

–> To counteract the dilation of splanchnic vessels

35
Q

Lactulose

A

Reduces absorption of ammonia from gut -> Helps with encephalopathy
Osmotic laxative –> reduces fluid intake from gut

36
Q

Gastric Banding

A

Reduces bleeding in the gut

37
Q

NtRTI (Nucleotide Reverse Transcriptase Inhibitor)

A

Tenofovir, entecavir

38
Q

Antivirals

A

Antivirals- PEGylated interferon alfa-2a

39
Q

Affect of alcohol on the liver

A

Alcohol becomes acetaldehyde

1) Oxidised by CYP, ROS is produced and damages proteins and DNA
2) Acetaldehyde –> acetate using NAD+, NADH:NAD ration is high –> increased synthesis of FA

40
Q

Progression of alcoholic disease on liver

A

1) Hepatic steatosis
2) Alcoholic hepatitis
3) Cirrhosis

41
Q

Hepatic steatosis

A
  • Increased levels of NADH increase f.a. production
  • Build up of fat in liver
  • Reversible
42
Q

Alcoholic hepatitis

A
  • ROS and cytokines generated
  • Inflammation leads to damage of hepatocytes
  • Neutrophil infiltration
  • Mallory bodies form (hyperpigmented)
  • Damaged intermediate filaments in cytoplasm
43
Q

Cirrhosis

A
  • Damaged hepatocytes are replaced by scar tissue forming regenerative nodules (micronodular)
  • Ultrasound can detect a fatty liver, and viral serology should be performed to look for hepA, B, C, EBV and CMV.
44
Q

Complications of cirrhosis

A 
Congestive splenomegaly 
Hepatorenal failure
Coagulopathy 
Hepatic encephalopathy 
Wernike-korsakoff syndrome
Hepatocellular carcinoma
Spontaneous bacterial periconditis
45
Q

Congestive splenomegaly

A

 Fluid backing up into the spleen due to portal hypertension

46
Q

Hepatorenal failure

A

NO released causing vasodilation in splanchnic circulation (supply intestines)
Effective circulatory volume of blood detected by JGA decreased –> Constriction of renal vessels –> renal hypoperfusion –> activation of RAAS –> further vasoconstriction of renal vessels –> reduced GFR (Hyperaldosteronism retaining water)

47
Q

Hepatic encephalopathy

A

• Due to decreased liver function→ metabolites which usually are supposed to be detoxified are unable to e.g. ammonia –> BBB
o Confusion, lethargic, asterixis, coma
o AAA –> imbalance in neurotransmitters

48
Q

Spontaneous bacterial periconditis

A

Weakened immune system, liver contains reticuloendothelial cells which clear bacteria + complement system proteins made by liver as well.

49
Q

A patient like Oliver is showing signs of protein malnutrition (like muscle
wasting). Would he be called “kwashiorkor-like” or “marastic”?

A

“kwashiorkor-like”

50
Q

As a prototypical transaminase, AST relies on which vitamin as cofactor to
transfer the amino group from aspartate (or glutamate) to the corresponding
ketoacid? This vitamin is also found in Pabrinex.

A

V B6

51
Q

What concentration of blood insulin would you expect in this patient? & Why? [1

A

Insulin levels low [1/2] due to low blood glucose [1/2]

52
Q

What would you anticipate to be the main muscle metabolic fuel for this patient?
[1 marks]

A

Fatty Acids

53
Q

Why measure the AST/ALT ratio?

A

This enables the differentiation of liver disease from other diseases and can also
suggest the potential cause of the liver disease

54
Q

Why is the patient at risk of infection?

A

Weakened immune system due to reduction in energy metabolism [1]. Build up of
fluid also increases risk (provides a perfect niche for bacterial growth) [1

55
Q

Which tissue is the main source of creatinine in the body? [1] What is the
rational behind testing this and how could the result change the treatment? [1
marks]

A

Byproduct of muscle metabolism [1]. Tested to check kidney function. If creatinine
is high this suggests kidney function is impaired so may change the prescription of
diuretics

56
Q

Lactulose is a very useful part of Oliver’s treatment for two reasons, what are
they?

A

i) It is an osmotic laxative (will help remove fluids via the gut) [1].
(ii) By acidifying the contents of the gut, lactulose reduces the absorption of
ammonia from the gut, thereby helping to prevent encephalopathy [1]

MET 2 PBLS (8 decks)

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