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PBL SEM 4 > CASE 5 > Flashcards

CASE 5 Flashcards

1
Q

Hep A — what type of virus, incubation period, transmission methods

A
  • RNA virus from picornavirus family
  • 30 days (4-6 weeks)
  • faecal oral transmission — associated with poor sanitation
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2
Q

which hepatitis is always acute?

A

hepatitis A

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3
Q

complications of Hep A

A

prolonged cholestasis, liver failure —> RARE but more likely in older adults and those with pre-existing liver disease

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4
Q

what antibodies are seen in acute Hep A infection?

A

HAV IgM then IgG

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5
Q

what hepatitis is endemic in developing world?

A

Hep A

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6
Q

Hep B — virus type, incubation period, transmission methods

A
  • DNA virus with multiple genotypes
  • from Hepadmaviridae family
  • 75 days (6 weeks to 6 months)
  • contact with infected blood, sexual, and mother to baby transmission - later is most important route globally - high risk of chronicity
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7
Q

what is the outcome of Hep B infection linked to?

A

maturity of immune system and effectiveness of response (linked to age)

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8
Q

which 2 viral hepatitis infections have the greatest risk of progressing to liver cancer?

A

B and C

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9
Q

what in blood shows a chronic infection of hep B?

A

surface Ag > 6 months

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10
Q

Hep C — virus type, incubation period, transmission methods

A
  • RNA flavivirus
  • 6 major subtypes
  • 2 weeks - 6 months
  • contact with infected blood (most important), sexual transmission, mother to baby — in UK : acute infections mainly in IVDU, HCV often acquired in childhood associated with poor sterilisation practices
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11
Q

acute infection in Hep C?

A

often asymptomatic

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12
Q

HCV:

__% develop chronic infection irrespective of age, immune status. __% will develop chronic liver disease, __-__% will develop cirrhosis, __-__% will die of cirrhosis or liver cancer

A

75% develop chronic infection irrespective of age, immune status. 60% will develop chronic liver disease, 5-20% will develop cirrhosis, 1-5% will die of cirrhosis or liver cancer

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13
Q

what are the different classes of direct acting antivirals used for Hep C?

A

protease inhibitors, NS5A inhibitors, NS5B inhibitors

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14
Q

Hep D — virus type, transmission methods

A
  • defective RNA virus — cannot replicate by itself — uses surface antigen of HBV as its viral envelope
  • contact with infected blood, sexual, and mother to baby transmission
  • superinfection vs simultaneous
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15
Q

describe hepatitis delta

A
  • cannot replicate by itself — needs HBV
  • severe hepatitis
  • 70% progress to cirrhosis
  • lifetime risk of hepatocellular carinoma doubled
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16
Q

how is HDV diagnosed?

A

Hep D IgM, IgG, HDV RNA

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17
Q

how is HDV treated?

A

clearance of HBV sAg —> eradication of delta. pegylated interferon for > 48 weeks. has a poor success rate

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18
Q

how is HDV prevented?

A

Hep B vaccination

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19
Q

Hep E — virus type, incubation period, transmission methods

A
  • RNA virus (Herpevirus family)
  • average incubation period of 40 days
  • oral-faecal transmission. HEV contamination of blood supply in many countries
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20
Q

describe the different HEV genotypes

A
  • genotype 1,2 — large, water borne outbreaks
  • genotype 3,4 — zoonotic, sporadic cases — associated with undercooked pork, wild boar, deer
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21
Q

in who can hepatitis E become chronic?

A

immunosuppressed

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22
Q

there is a higher morality for Hep E in who?

A

cirrhotic, pregnant women

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23
Q

Hep E is linked to a range of acute neurological syndromes. give an example

A

transverse myelitis

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24
Q

what is the most common cause of acute viral hepatitis in the UK?

A

Hep E

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25
Q

how is HEV diagnosed?

A

HEV IgM (Hep E IgG, HEV RNA blood, stool). chronic Hep E - check for hep E RNA in blood

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26
Q

which viral hepatitises have a vaccine?

A

A, B, E (only in China)

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27
Q

what are less common causes of VIRAL hepatitis?

A
  1. cytomegalovirus (congenital and perinatal infection)
  2. Epstein-Barr virus (adolescence)

rarer:
3. Herpes simplex (congenital and perinatal infection)
4. yellow fever

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28
Q

splenomegaly is an uncommon finding in clinical examination in viral hepatitis. what does it suggest?

A

either underlying pre-existing liver disease or perhaps infection with a different virus, such as Epstein Barr or cytomegalovirus

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29
Q

what else causes hepatitis?

A

• alcohol - hepatitis, fatty change, cirrhosis
• drugs - prescribed and misused
• autoimmune disease — each have a characteristic set of antibodies and target within the liver

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30
Q

what autoimmune diseases can cause hepatitis?

A
  • primary sclerosis cholangitis
  • primary biliary cirrhosis
  • autoimmune hepatitis
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31
Q

HDV vs HBV virus type

A

HDV = RNA virus
HBV = DNA virus

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32
Q

which hepatitis cannot become chronic?

A

A and E

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33
Q

what can hep B, C and D develop into?

A

chronic infection - can develop into cirrhosis and hepatocellualr carincoma

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34
Q

how does hepatitis B replicate?

A
  1. HBV binds to the NTCP bile receptor on hepatocytes. this allows the virus to enter the cell
  2. the HBV DNA is partially double stranded
  3. the viral DNA enters the host cell nucleus and sues the host cell’s DNA to complete its DNA from partially double-stranded to a ‘covalently closed circular DNA’ = cccDNA
  4. the viral DNA is now transcribed into viral RNA
  5. this is then translated to produce viral antigens and other viral proteins
  6. the viral RNA undergoes reverse transcription in the viral nucleocapsid to form its partially double stranded DNA once again
  7. this is now packaged within the viral antigens
  8. this is then exocytosed and infects other cells
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35
Q

hepatitis viruses are non-cytopathic - what does this mean?

A

hepatitis viruses don’t cause damage themselves to the hepatocytes — it is the immune response to the virus that gives rise to the damage — hepatocyte damage is immune mediated

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36
Q

what happens when eg. Hep B enters a hepatocyte?

A
  • hep B enters hepatocyte, then the hepatocyte will express certain antigens recognised by cytotoxic T cells, which will then destroy the hepatocyte
  • antigen recognition by cytotoxic T cells : apoptosis
  • chemokines drive recruitment of Ag-nonspecific cells
  • mild inflammation ranging to massive necrosis if liver
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37
Q

what are symptoms of hepatitis?

A
  • non-specific and include fatigue, lethargy, itching
  • may also lead to some specific symptoms, for example : jaundice, right upper quadrant pain
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38
Q

what will be elevated in a hepatitis infection?

A

AST and ALT

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39
Q

what does it suggest if AST > ALT?

A

alcoholic hepatitis

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40
Q

what does it suggest if ALT > AST?

A

other causes than alcoholic hepatitis. mainly viral

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41
Q

what is the course of viral hepatitis?

A
  1. acute infection = this can be resolved by the body and the symptoms aren’t severe. an acute infection can develop into a chronic infection
  2. chronic infection = symptoms are more severe than an acute infection and can develop into cirrhosis/hepatocellular carcinoma
  3. fulminant infection
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42
Q

what does chronic viral hepatitis cause?

A

chronic liver inflammation, and subsequent healing with fibrosis, which, over time can progress to cirrhosis

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43
Q

what enzymes are released into the bloodstream from breakdown of hepatocytes, and are indicative of liver inflammation and injury?

A

ALT and AST

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44
Q

what is indicative of damage to the bile canaliculi and along with bilirubin is elevated in cholestasis?

A

alkaline phosphatase

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45
Q

what tests are best to show how liver is functioning?

A

PT and INR — liver cells synthesise clotting factors (measured by PT, INR) and other proteins such as albumin, and hence these tests are the best indicator of how the liver is functioning.

liver also synthesises proteins, so again we can access how liver is functioning by measuring serum albumin

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46
Q

what are high levels of ALT, AST, ALP, bilirubin>

A

ALT > 35 U/L
AST > 40 U/L
ALP > 150 U/L
Bilirubin > 21 umol/L

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47
Q

what are the commonest symptoms of acute hepatitis?

A

= prodrome of nausea, fatigue, malaise, fever
- become jaundiced when fever settles, dark urine, pale stools
- RUQ tenderness, hepatomegaly

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48
Q

what are dark urine and pale stools in acute hepatitis due to?

A

cholestasis

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49
Q

why is there pain in hepatomegaly?

A

pain felt because there are only pain receptors in the capsule of the liver. there are none in the actual substance. therefore if liver is enlarged, the patient may experience pain

50
Q

elevation of what is seen in acute hepatitis?

A

• elevated ALT/AST - can be >1000 U/L
• bilirubin, ALP less marked

51
Q

the sequelae of ongoing inflammation in chronic hepatitis leads to what?

A

liver fibrosis

52
Q

the progression of fibrosis to cirrhosis in chronic hepatitis (20-30 years) is accelerated by what co factors?

A

alcohol, HIV, diabetes, steatohepatitis

53
Q

chronic hepatitis is asymptomatic until what?

A

liver decompensation (so little functioning liver left so patient develops complications such as ascites or jaundice)

54
Q

____is found in high concentrations within hepatocytes and enters the blood following hepatocellular injury. It is, therefore, a useful marker of hepatocellular injury.

____ is particularly concentrated in theliver,bile duct andbone tissues. ___ is often raised in liver pathology due to increased synthesis in response to cholestasis. As a result, ___ is a useful indirect marker of cholestasis.

A

ALTis found in high concentrations within hepatocytes and enters the blood following hepatocellular injury. It is, therefore, a useful marker of hepatocellular injury.

ALP is particularly concentrated in theliver,bile duct andbone tissues. ALP is often raised in liver pathology due to increased synthesis in response to cholestasis. As a result, ALP is a useful indirect marker of cholestasis.

55
Q
  1. a greater than 10-fold increase in ALT and a less than 3-fold increase in ALP suggests what?
  2. what does a less than 10-fold increase in ALT and a more than 3-fold increase in ALP suggest?
A
  1. predominately hepatocellular injury
  2. cholestasis
56
Q

what can a raised GGT be suggestive of?

A

biliary epithelial damage and bile flow obstruction. it can also be raised in response to alcohol and drugs

57
Q

a markedly raised ALP with a raised GGT is highly suggestive of what?

A

cholestasis

58
Q

ALT > AST is associated with ______________
AST > ALT is associated with ______ and ____________________

A

ALT > AST is associated with chronic liver disease
AST > ALT is associated with cirrhosis and acute alcoholic hepatitis

59
Q

what are investigations to assess synthetic liver function?

A

• serum bilirubin
• serum albumin
• prothrombin time
• serum blood glucose

60
Q

what are common causes of acute hepatocellular injury?

A

• poisoning (paracetamol overdose)
• infection (hepatitis A and B)
• liver ischaemia

61
Q

what are common and some less common causes of chronic hepatocellular injury?

A

common causes of chronic hepatocellular injury:

• alcoholic fatty liver disease
• non-alcoholic fatty liver disease
• chronic infection (hepatitis B or C)
• primary biliary cirrhosis

less common causes:

• alpha-1 antitrypsin deficiency
• Wilson’s disease
• haemachromatosis

62
Q

what is cholestasis?

A

decrease in bile flow due to impaired secretion by hepatocytes or to obstruction of bile flow throguh intra or extra hepatic bile ducts

63
Q

describe Wilson’s disease + symptoms

A

in wilson’s disease, the liver doesn’t adequately process the mineral copper. if left untreated and allowed to build up, copper can damage the brain. this is a rare genetic disorder. symptoms of toxic copper levels include:
• asterixis
• muscle stiffness
• personality changes

= a less common cause of chronic hepatocellular injury

64
Q

anything causing inflammatory damage in the liver can lead to what?

A

cirrhosis

65
Q

when does cirrhosis happen?

A

when parenchymal cells (functional cells) are destroyed and replaced with fibrous tissue that eventually contracts around the blood vessels — thereby greatly impeding the flow of portal blood through the liver

cirrhosis = disease of all of the liver with parenchymal nodules and surrounding fibrosis

66
Q

what are some causes of cirrhosis?

A

> alcoholism
ingestion of positions such as carbon tetrachlordie
viral disease such as infectious hepatitis — esp HBV and HCV
obstruction of bile ducts
infectious processes in the bile ducts
autoimmune diseases (“lupoid” : antinuclear and anti-smooth muscle antibodies. “primary biliary cirrhosis” : anti-mitochondrial antibodies)
metabolic diseases (iron (excess Fe - lots of transfusions, haemachromatosis (inherited), copper, glycogen storage disease, lipid disorders, a-1 antitrypsin deficiency)

67
Q

what are the 2 cirrhosis types and what are they typically caused by?

A

1) micronodular - typically alcohol
2) macronodular - typically viral

68
Q

what are some effects of cirrhosis?

A
  1. liver failure
  2. portal hypertension
  3. hepatocellular carcinoma
69
Q

signs of liver failure

A
  • protein synthesis : low albumin - peripheral oedema, ascites
  • coagulation factors : bleeding
  • jaundice
  • encephalopathy : confusion — if liver doesn’t process toxic substances, they bypass hepatocellular nodules and enter systemic bloodstream. asterixis = hepatic flap = sign of encephalopathy
70
Q

what are signs of portal hypertension?

A

• ascites
• varices — increased pressure in portal vein, blood bypasses liver — lower oesophageal/periumbilcial/perinanal veins
• splenomegaly

71
Q

raised levels of what suggest hepatocellualr carcinoma (but are not sufficient alone for diagnosis)?

A

raised serum alpha-fetoprotein levels

72
Q

what is chronic liver disease

A

= progressive destruction of the liver parenchyma over a period greater than 6 months leading to fibrosis and cirrhosis

73
Q

presentations of chronic liver disease

A
  • fatigue
  • encephalopathy
  • hands — Dupuytren’s contracture, palmar erythema, leuconychia (white nails)
  • asterixis
  • face — jaundiced sclera, fetor hepaticus (bad smelling breath characteristic of someone with severe parenchymal liver disease, said to resemble smell of rotten eggs and garlic)
  • chest — spider naevi, gynaecomastia
  • abdomen — hepatomegaly, splenomegaly (due to portal hypertension), ascites, caput medusa (swollen and distended superficial epigastric veins)
  • polyneuropathy
74
Q

normal average plasma conc of bilirubin in mg/dl

A

0.5 mg/dl

75
Q
A
76
Q

pegylated interferon is contraindicated in what?

A

hyperbilirubinaemia

77
Q

glycogenolysis:

makes ____ available in ____ state. promoted by _____

A
  • glucose
  • fasting
  • glucagon
78
Q

ketogenesis:

use of ______ to produce emergency fuel (________). promoted by surplus of _______ in starvation or T1D. suppressed by ______.

A
  • acetyl-coa
  • ketone bodies
  • mobilised fatty acids
  • insulin
79
Q

surplus ammonia arrives in the liver as _____, _____ or _____. it is de- or transamination. N is eventually disposed as urea

A

glutamate, glutamine or alanine

80
Q

what does amino acid metabolism produce?

A

precursors for gluconeogenesis

81
Q

what does hepatic glucose production (HGP) consist of?

A

glycogenolysis and gluconeogenesis

82
Q

____ blood glucose normally suppresses HGP via _____. failure to regulate HGP is the main reason for _____ in t2d mellitus.

A
  • high
  • insulin
  • hyperglycaemia
83
Q

what converts glucose-6-phosphate to glucsoe?

A

glucose-6-phosphatase

84
Q

what process makes acetyl-coa from fatty acids?

A

B-oxidation

85
Q

GLUT2 vs GLUT4 location

A

glut2- liver
glut4 - adipose tissue

86
Q

what can facilitate both glucose entry into liver cells and exit?

A

GLUT2

87
Q

what traps glucsoe in the cell?

A

phosphorylation — because the ionic phosphate cannot cross the membrane spontaneously

88
Q

hexokinase I-III vs glucokinase

A

hexokinase I-III — relatively slow but are fully active at very low concs of glucose. in most tissues

glucokinase = hexokinase IV = has a much higher capacity to trap glucose in liver, but only worlds when glucose concs are high eg. after a meal

89
Q

what is the most critical regulated step in glycolysis?

A

F-6-P phosphorylated to F-1.6-BP — commits the molecule for further degradation — want to avoid in fasting state

90
Q

what is the only oxidative step in glycolysis?

A

GA-3P is converted to 1,3-BPG

NADH + H+ generated in this oxidative step can be regenerated under anaerobic conditions by reducing pyruvate to lactate, the liver can re-oxidise lactate to pyruvate

91
Q

net generation of ___ ATP per glucsoe in glycolysis

A

2

92
Q

warburg effect

A

2 vs 28 ATP; excessive glucsoe consumption of tumours. aerobic glycolysis is inefficient but fast

tumours gain energy entirely by glycolysis

93
Q

glucagon triggers the production of ____ in cells, which in turn activates ____. ____ phopshorylates glycogen synthase directly and glycogen phosphorylase via ________ ________. glycogen synthase becomes ______ and glycogen phosphorylase becomes _______. as a result, glucagon promotes _______ and inhibits _________./

A
  • cAMP
  • protein kinase A (PKA)
  • PKA
  • phosphorylase kinase
  • inactive
  • active
  • glycogenolysis
  • glycogenesis
94
Q

lactate for gluconeogenesis: lactate from skeletal muscle is re-oxidised to ______. this liver-muscle cycle is called ____ cycle.

A
  • pyruvate
  • Cori
95
Q

where do glycerol and amino acids come from for gluconeogenesis?

A
  • glycerol is released by the hydrolysis of fat (TAGs) in adipocytes
  • amino acids from tissue protein are metabolised to a-keto acids like oxaloacetate and a-ketoglutarate via transamination
96
Q

gluconeogenesis:

________ is the main regulator of gluconeogenesis. it acts by repressing ________, this increasing the availability of ____ for gluconeogenesis. it also increases the expression of _________.

finally, ____ represses the formation of ______, whcih is a repressor of _______ in gluconeogenesis (while it is an activator of ______ in glycolysis)

A
  • glucagon
  • pyruvate kinase
  • PEP = phosphoenolypyruvate
  • PEP carboxykinase
  • glucagon
  • F-2,6-BP
  • fructose-1,6-bisphosphatase
  • PFK-1
97
Q

what do pyruvate kinase and PEP carboxykinase do?

A

pyruvate kinase — converts phosphoenolpyruvate to pyruvate in glycolysis.

PEPCK — converts oxaloacetate to PEP in gluconeogenesis

98
Q

what enzyme is the point of no return in glycolysis and what represses it?

A

pyruvate kinase (PEP to pyruvate) — repressed by glucagon therefore PEP can still be recycled easily into glucsoe

99
Q

what is the most important, rate-limiting step in glycolysis? what catalyses it?

A

fructose-6-P to fructose-1,6-BP

catalysed by PFK-1 = phosphofructokinase-1

100
Q

PFK-1 is allosterically activated by ____ and repressed by ____ and _____

PFK-1 is activated by _______ whose biosynthesis is in turn regulated by insulin and glucagon

A
  • AMP (signal for serious energy depletion in cell)
  • ATP + citrate (reflect well-fed cell state)
  • fructose-2,6-BP
101
Q

fructose-2,6-P promotes glycolysis by activating ____

A

PFK1

102
Q

where do all TCA cycle reactions happen?

A

mitochondria

103
Q

the TCA cycle provides for full oxidation of acetyl-CoA to how many CO2?

A

2

104
Q

TCA Cycle: oxidation of NADH and FADH2 in the mitochondria generates ___ ATP per molecule of glucose and __ GTP

A
  • 28
  • 2
105
Q

what is the rate limiting step in fatty acid synthesis? enzyme? what is it activated by? what is it inactivated by?

A

acetyl CoA —> malonyl CoA

  • catalysed by acetyl-CoA carboxylase (ACC)_
  • activated by citrate
  • inactivated directly by fatty acyl-CoA and by phosphorylation by AMPK
106
Q

via regulation of ACC phosphorylation, _____ indirectly activates and _____ + ______ inactivate ACC

A
  • inuslin
  • glucagon and AMP
107
Q

describe the hormonal state favouring synthesis vs degradation of fatty acids

A

synthesis: high inuslin/glucagon ration

degradation: low insulin/glucagon ratio

108
Q

major tissue site: synthesis vs degradation of FAs

A

synthesis - primarily liver
degradation - muscle, liver

109
Q

sub cellular localisation: synthesis vs degradation of FAs

A

synthesis - cytosol
degradation - primarily mitochondria

110
Q

what is the product of FA degradation?

A

acetyl-CoA

111
Q

what in adipocytes is repressed by insulin?

A

hormone sensitive lipase

112
Q

what is the name of an enzyme in muscle tissue that can regenerate acetoacetyl CoA by adding CoA?

A

thiaphorase

113
Q
A
114
Q

ALT vs AST

A

ALT is quite a specific marker for liver damage, but AST is more sensitive because there is so much more AST in the liver than ALT

ALT is fully reversible and doesn’t strongly favour one direction
AST - flux is mostly in the direction of the transamination of oxaloacetate to aspartate — feeds into the urea cycle as well

AST : ALT ratio is diagnostic for different types of liver damage.
high ratio over 2 - liver damage caused by alcoholic liver injury

115
Q

in amino acid metabolism, excess ammonia is converted to glutamine and shuffled to the liver. in the liver, 2 molecules NH3 can be released from glutamine by _______ and then ________

NH3 can also be transferred to _________ by _________

A

glutaminase and then glutamate dehydrogenase

oxaloacetate by aspartate transaminase (AST)

116
Q

high levels of glucose-6-phosphate promote NADPH production in what pathway?

A

the pentose phosphate pathway

117
Q

although the liver normally reduces glucose rather than consume it, after a meal, the low-affinity ______ takes up glucose from the blood

A

GLUT2 transporter

118
Q

surplus carbs from a meal are converted to ________ and then manly channelled into _________

A
  • acetyl-CoA
  • fatty acid synthesis
119
Q

ACC is activated by ___________ and by ________

A

dephosphorylation (low glucagon levels) and by citrate

ACC is for fatty acid SYNTHESIS

120
Q

glucagon triggers a reduction in the conc of _______ by shifting ____ towards phosphatase activity. this reduction means that _________ is favoured over _________: the key enzyme ________ is no longer inhibited by _________

A
  • fructose-2,6-bisphosphate
  • PFK-2
  • gluconeogenesis
  • glycolysis
  • fructose-1,6-bisphosphate
  • F-2,6-BP
121
Q

abundant acetyl-CoA activates _________ (for gluconeogenesis) and inhibits the degradation of _______ (inhibition of PDH)

A
  • pyruvate carboxylase
  • pyruvate
122
Q

ACC inhibition lowers ________, which in turn activates _______

A
  • malonyl-CoA
  • B-oxidation

PBL SEM 4 (50 decks)

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