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BCS Lectures > Michelle Ramsay > Flashcards

Michelle Ramsay Flashcards

1
Q

What is the immunological function of the liver (2)

A
  1. Secrete IgA into bile and upper GIT

2. Destruction of bacteria in blood via Kupffer and Nk cells

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2
Q

Which vitamins are stored in the liver (3)

A
  1. A
  2. D
  3. B12
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3
Q

Outline the metabolic functions of the liver

A

see Michelle Ramsay PBL notes for diagrams

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4
Q

Which acute phase proteins are synthesised by the liver? (5)

A 
C-reactive protein (CRP)
Caeruloplasmin
α1-antitrypsin
α1-acid glycoprotein
α2-macroglobulin
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5
Q

Which glyoprotein and lipoprotein transport proteins are synthesised by the liver? (5)

A
  1. Transcortin (corticosteroid-binding globulin)
  2. Thyroid-binding globulin
  3. Sex hormone-binding globulin (testosterone,
    oestradiol)
  4. Transferrin (Fe)
  5. Lipoproteins (lipids)
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6
Q

Which clotting factor is used to measure liver function?

A

Factor vii since it has the shortest 1/2 life (5 hours)

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7
Q

What are the different classsifications of cirrhosis (3)

A

Macroscopic:
• micronodular - uniform nodules <3 mm
• macronodular - nodular variation >3 mm
• mixed

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8
Q

What are the microscopic features of cirrhosis (3)

A
  1. Diffuse involvement of liver
  2. Fibrous septa
  3. Inflammation affecting border of nodules or within the nodules themselves

See picture in notes of cirrhosis

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9
Q

What are the vascular and architectural changes seen in cirrhosis (4)

A

• Activated myofibroblasts (derived from hepatic stellate cells) and portal or central vein
fibroblasts, proliferate and produce excess extracellular matrix (ECM) resulting in:

  1. fibrous portal tract expansion
  2. capillarization of the sinusoids, with loss of endothelial fenestrations
  3. congestion of the space of Disse with ECM
  4. central vein fibrosis
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10
Q

Explain the mechanisms by which alcohol causes liver damage and how it may alter the metabolism of other drugs. (PBL1+2)

A

in anki under IODs

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11
Q

Explain the mechanisms by which paracetamol causes liver damage. (PBL 2 + CPT session)

A

see michelle ramsay notes

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12
Q

Describe how to treat paracetamol overdose, and which clinical findings can be used to predict a patient with a poor prognosis who should be referred for liver transplantation. (PBL 2 + liver damage session)

A

see michelle ramsay notes

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13
Q

Explain the role of the liver in drug metabolism and the effect of liver disease. (CPT session)

A

see michelle ramsay notes

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14
Q

Which aspect of the liver do the hepatic veins arise form?

A

posterior aspect

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15
Q

What is the organisation o the structures at the porta hepatis

A

from anterior to posterior:

  1. Heptic ducts
  2. Hepatic artery
  3. Portal vein
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16
Q

Which ligaments attach the liver to the abdomen?

A
  1. Falicform

2. Left and right triangular ligaments

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17
Q

Where does the IVC lie in respect to the liver

A

lies in a deep groove on the posterior aspect

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18
Q

What is the hepatopancreatic ampulla surrounded by?

A

Sphincter of Oddi

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19
Q

What is the landmark location of the spleen

A

between 9, 10 and 11 ribs

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20
Q

What is the spleen covered by?

A

peritoneum

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21
Q

What are the three medial impression of the spleen

A
  1. Gastric
  2. Renal
  3. Colic
  • also has a hilum where the splenic artery enters and splenic vein exits
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22
Q

What are the embryological supplies to the abdomen

A

the foregut extends from the lower part of the oesophagus the
second part of the duodenum

the midgut extends to the splenic flexure of the transverse colon

the hindgut extends to the upper part of the anal canal

the liver, spleen and pancreas are supplied by the coeliac artery

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23
Q

What are the consequences of an obstruction in portal flow (4)

A
  • Shunts will open up between the portal and systemic circulation
  • Portal-left gastric wtih
    azygos veins in lower
    oesophagus:
    oesophageal varices
- Retroperitoneal veins
enlarged at junction of
mesenteric with
retroperitoneal veins and
also behind liver (‘bare area)
  • Portal-epigastric veins newly reopened
    in falciform ligament
    with paraumbilical veins (‘Caput
    Medusae’ around umbilicus)
  • Portal – splenic – inferior
    mesenteric – superior rectal
    with inferior rectal veins in
    lower rectum (haemorrhoids)
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24
Q

What are the mechanisms of hepatic encephalopathy (6)

A
  1. Porto-systemic shunting
  2. Impaired NH3 metabolism to urea
  3. Impaired NH3 metabolism to glutamine
  4. Intrahepatic shunting
  5. Muscle breakdown, impaired NH3
    metabolism to glutamine
  6. Increased renal NH3 synthesis

also see michelle ramsay notes

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25
Q

Treatment of hepatic encephalopathy

A 
• Treat sepsis, dehydration and other predisposing
conditions
• Ammonia-lowering therapies:
– Lactulose
• shorter GIT transit time
• acidification of stool
• modification of gut flora
– Non-absorbable antibiotics
• rifaximin
• neomycin, vancomycin
• Dietary protein restriction not necessary (may worsen
encephalopathy)
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26
Q

What is the natural history of chronic liver disease

A

see michelle ramsay notes

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27
Q

What are the three types of liver failure (3)

A

– Acute: sudden, no pre-existing liver
disease

– Chronic: gradual, progression of CLD
(cirrhosis) causing decompensation

– Acute on chronic: acute deterioration
of previously well-compensated CLD

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28
Q

What is acute on chronic liver failure

A 
• Acute deterioration of liver function over
2-4 weeks in patients with previously
well-compensated CLD; high associated
mortality (>50% at 6 weeks)
• Responsible for 30% of decompensation
episodes in cirrhotic patients
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29
Q

What are the clinical manifestations of acute on chronic liver failure

A 
• Clinical manifestations:
– jaundice
– hepatic encephalopathy (HE)
– hepatorenal syndrome (HRS)
– rapidly evolving multiorgan failure

• Usually associated with a precipitating
event

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30
Q

What are examples of preciptating events in acute on chronic liver failure

A

• Direct:
– hepatotoxic drugs (NSAIDs, antibiotics)
– alcohol
– viral hepatitis (superinfection, reactivation)

• Indirect:
– sepsis
– variceal bleeding
– surgery
– sedative drugs
– electrolyte disturbances
– constipation
– high protein diet
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31
Q

How does acute (fulminant) liver failure manifest (5)

A

– jaundice
– coagulopathy (INR ≥1.5, PT >20 sec)
– encephalopathy (any degree)

• Onset of encephalopathy usually within 2 weeks
from the appearance of jaundice

• Can progress to multiorgan failure with a high
associated mortality

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32
Q

Classifcation of ALF

A

SEE MICHELLE RAMSAY NOTES

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33
Q

What is the most common cause of acute liver failure

A

viral hepatitis (A, B and E most common)

  • HCV very rare
  • HEV more severe
  • Prognosis worse in the elderly and those with CLD
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34
Q

Classifcation, clinial featues and prognosis of ALF

A

see michelle ramsay notes

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35
Q

What are the clinical features of ALF (3)

A 
• Progressive multiorgan failure
• Resembles septic shock (2o bacterial
infections, endotoxaemia)
• Severity of illness depends upon:
– adverse metabolic consequences of loss of
liver function
– systemic effects of circulating toxins
– rate and degree of liver regeneration
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36
Q

Why are ALF patients more prone to infection? (1) What are they most likely to be infected by? (3)

A

• ALF patients prone to infection - severe
complement deficiency, impaired neutrophil
and Kupffer cell function

• Bacteraemia and endotoxinaemia (20-80%),
predominantly Gm +ve (S. Aureus) and
Gm -ve bacteria (E. Coli)

• Fungaemia (30%), predominantly Candida
albicans, occurs late in the course of the
disease

• Antibiotic and antifungal prophylaxis (± gut
decontamination) usually given; predisposes
to development of multi-resistant strains

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37
Q

Tx of ALF in paracetamol toxicity

A

• N-acetylcysteine

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38
Q

Tx of ALF in mushroom poisoning

A

Silibilin + penicillin G

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39
Q

Tx of ALF in HBV

A

Nucleoside analogues

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40
Q

Tx of ALF in HSV

A

Aciclovir

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41
Q

Tx for ALF in pregnany

A

delivery

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42
Q

Does wilson disease induce ALF respond to chelation therapy

A

(Wilson’s disease-related ALF does NOT

respond to chelation therapy)

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43
Q

Describe tghe use of n acetylcysteine for Tx of ALF

A 
- Paracetamol induced ALF:
can prevent or reduce liver damage even
after large ODs if given within 24 h
– late administration (>24 h) recommended
but not proven

• Non-paracetamol ALF:
– well tolerated
– improves non-transplant survival if given
early in patients with low-grade HE

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44
Q

What are the two main determining factors oof ALF prognosis (2)

A
  1. Aetiology

2. Coma grade on admission

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45
Q

What is the only reliable treatment option for ALF?

A

Liver transplantation

46
Q

Indications for liver transplantation

A

see notes

47
Q

Contraindications for liver transplantation (4)

A

Contraindications: severe multi-organ failure and
comorbidity, alcohol and substance abuse, social and
psychiatric problems

48
Q

What is the survival following liver transplantation

A

• Emergency OLT outcomes worse than those of elective OLT; high early
post-op mortality due to sepsis and multiorgan failure
• Surgical outcomes show progressive improvement; currently 1-year
survival ca. 80%
• Outcome affected by: age of recipient, severity of pre-transplant illness
and the quality of the donor liver

49
Q

What are the liver support systems in ALF (2)

A

• Principle: extracorporeal devices to replace
liver function, either to stabilise the patient
as a bridge to OLT or until spontaneous
liver regeneration occurs
• 2 types:
– biological with live hepatocytes
– non-biological blood detoxification using
adsorption and dialysis techniques
• Systems experimental - no conclusive
evidence of clinical benefit

50
Q

Indications for nutrition support in hospital and the community (NICE, 2006) (5)

A

Nutritional support should be considered in people who are malnourished, defined by any of the following:

  1. BMI < 18.5 kg/m2
  2. Unintentional weight loss > 10% within the last 3-6 months
  3. BMI < 20 kg/m2 and unintentional weight loss > 5% within the last 3-6 months
  4. Have eaten little of nothing for more than 5 days and/or are likely to eat little or nothing for the next 5 days or longer
  5. Have a poor absorptive capacity, and/or have high nutrient losses and/or have increased nutritional needs from causes such as catabolism
51
Q

WHich anthropometric measurements are most commonly used? (4)

A

Most commonly used:
Body weight

Height

Adiposity (waist, BMI, skinfold)

Muscle mass (MAMC, grip strength)

Estimates of body water, body composition

52
Q

Use of albumin to evaluate nutrition

A

Serum proteins – indicate visceral protein status and hence clinical outcome

Serum albumin:
Normal range: 3.5 to 5.5 g/dL or 35-55 g/l
Long half-life (14-20 days)
Not a very sensitive indicator to short-term changes in protein status

Affected by age, infection, zinc depletion and dehydration

Low levels correlate poorly with nutritional status

But albumin concentration <35 g/l, indicates body’s impaired ability to cope with major illness and can be used in nutritional ax.

53
Q

Use of prealbumin (transthyretin) to evaluate nutritional status

A

Prealbumin (transthyretin):

Normal range: 19-38 mg/dl or 190-380 mg/l

Sensitive index of early response to nutritional support

Short half life <2 days

Also affected by hydration and acute changes in liver and renal function, but less than albumin

Concentration may be depressed in inflammatory states independently of nutritional status

Consider C-reactive protein concentration

54
Q

Use of nitrogen in nutritional evaluation

A

Measurement of nitrogen excretion over a period of time will reflect nitrogen balance and changes in total body protein mass

Urinary urea nitrogen is measured using 24-hour urine collection
24-hour nitrogen intake is calculated as: 24-hour protein intake/6.25

Nitrogen output is calculated taking into account renal losses, skin & faecal losses

Positive nitrogen balance = patient excretes less nitrogen than they consumed, thus incorporating nitrogen into newly formed protein (i.e. muscle).

N balance (g/day) = Protein intake/6.25* – UUN** + faecal losses + obligatory losses (faecal and obligatory losses= 2-4 g/day)

  • conversion coefficient might be different for specialized enteral or parenteral formulations

** urinary urea nitrogen

55
Q

What is the mini nutritional assessment used for?

A

Mini Nutritional Assessment for screening people over 65 years for malnutrition

Available also as a mobile application

56
Q

Wht is total energy expenditure

Hoe does this differ in stressed indivduals

A

In healthy individuals:
TEE = BMR + DIT + PAL
BMR = most dominant part of TEE (45-70%)
= metabolic activity for life e.g. respiration, heat etc.
DIT = energy expended in nutrient digestion/absorption/transport
PAL = physical activity level

In stressed individuals:

TEE = BMR + DIT + PAL + stress factor

e.g. recent surgery/
inflammation/trauma/burns

57
Q

Revise the different types of drug interactions from last year

A 
Augmented
Bizarre
Chronic
Dose related
End of reaction
58
Q

What is the function of phase 2 metabolism

A

Phase 1 metabolism

Catabolic

Oxidation, reduction or hydrolysis

Metabolism may

Activate a pro-drug

Inactivate a drug

Create a toxic metabolite

59
Q

What is phase 2 metabolism

A

Phase 2 metabolism

Anabolic

Produces inactive or readily excretable metabolite by
conjugating with another substance

60
Q

which type of drug reaction is a paracetamol overdose

A

Type A “Augmented” toxicity

Predictable, dose-related

Will affect everyone if they receive enough of the
drug

61
Q

Why is NAPQI toxic

A

NAPQI

Highly reactive

Oxidizes key enzymes causing cell death

Also can bind renal cells to cause renal failure

62
Q

What does N acetyl cysteine do

A

replenishes glutathione - cysteine is an aa - glutathione made of aa’s

63
Q

When is the optimal time of Nacetylcysteine admin

A

8 hours

64
Q

What do you give <1 hour since overdose

A

activated charcoal - prevents absorption of paracetamol into blood stream

65
Q

What are other examples of type a drug reactions

A
  1. Carbon tetrachloride (dry-cleaner) –
    apoptosis/necrosis
  2. Alcohol – hepatitis
66
Q

Chlorpromazine is a…?

A

D2 antagonist

67
Q

Slide 16 in the liver drug Dr Soulla lectures

A

CHOLESTATIC HEPATITIS

  • bizarre reaction
  • GGT raised
  • Pale stools and dark urine = obstruction - increase CB = blockage makes the buildup of CB to enter blood stream = dark urine
  • Due to the fact that amine group have a positive charge and bile acids form a negative charge = precipitate and form salts and block bile ducts = bizarre because you can’t predict which patients will experience this
  • can occur in low doses since they are bizarre
  • usually occurs within four weeks of starting Tx
  • May be accompanied by fever and eosinophilia as immune system is activated to get rid of the precipitates
68
Q

Patient 3 of lecture

A

ACUTE HEPATOCELLULAR NECROSIS

  • Allergic to halothane - first exposure to antibodies
  • Immune mediated usually classified under bizarre
69
Q

What are the difference in Patient 4’s tests

A

these are functional tests whereas the other tests were structural

70
Q

What blooop pressure hormones is excreted by the liver - what are the clinical imlications

A

aldosterone = cannot be excreted = retention of water

71
Q

mechanism of palmar erythema

A

low albumin usually binds estrogen - low albumin = high estrogen which is a vasodilation = palmar erythema

72
Q

Why does the MEOS pathway lead to liver damage

A

produces reactive oxygen species

73
Q

how does acetate create fatty acids from alcohol

A

through the production of mannolyl co A

74
Q

Which drugs may cause chronic drug reactions (3)

A

Methotrexate - fibrosis

Amiodarone - fibrosis and cirrhosis

Methyldopa (not commonly used but used in gestational HTN), isoniazid - chronic hepatitis

75
Q

Which type of drug reaction did patient 5 have

A

delayed type

May occur even if drug has been stopped

Synthetic androgens, oral contraceptive pill
(OCP)

Benign liver tumours, hepatocellular
carcinoma - risk of either problem very low

Cholestasis more common with OCP

76
Q

Are end of treatment reactions common with the liver

A

uncommon

Other examples include

Alcohol – seizures (depresses CNS - therefore sudden cessation may cause it to go hyperexcitable state)

Beta blockers – angina (oxygen demand goes up after you remove them)

Steroids – psoriasis recurrence

77
Q

Patient 6

A

Rifaminpicin is an inducer and isonizid produces toxic metabolites

to prevent what happened to patient you should be monitoring the patient

78
Q

Drugs to avoid in liver failure (5)

A

Opiates (increase risk of hepatic encephalopathy)

Diuretics (increase risk of hepatic encephalopathy) - decreased blood volume increases concentration of toxins that cause the ecephalopathy

Oral hypoglycemics (loss of glucose homeostasis)

Warfarin (effects enhanced)

79
Q

How do sinsusoids appear and what are they made of

A

Composed mainly of collagen type III and this

may be demonsrated with a reticulin stain.

80
Q

How does ballooning degeneration apper on histology

A

See slide 24

Damage
from toxic or immunologic insult cause
hepatocytes to take a swollen
appearance, pycnotic centered nucleus.
These are sick hepatocytes undergoing
apoptosis, and the process of ballooning
is irreversible
81
Q

How does foamy degeneration appear o histology

A

Biliary deposits cause a foamy, swollen
appearance of the hepatocytes

see slide 24

82
Q

When do you see alcoholic steatosis

A

Appear in conditions such as alcoholic
liver disease and acute fatty liver of
pregnancy

83
Q

What are councilman bodies

A

Formation of Councilman Bodies-
Eosonophilic globule with often fragmented
nucleus. It represents a hepatocyte that is
undergoing apoptosis

see slide 26

84
Q

What is the most common area of necrosis in the lboule

A

The most common is necrosis of the hepatocytes around the terminal hepatic
vein- centrilobular necrosis.

Midzonal and periportal necrosis is rare.

85
Q

What is the risk of hepatotoxicity following paracetamol posioning

A

• Risk of severe liver damage and death is
determined by the extent of delay beyond 8 h until
Rx with the antidote N-acetylcysteine (NAC)
commences

NAC Rx within 8 h will prevent all serious hepatic
injury
• Do not treat all patients with NAC as it has frequent
side-effects, is moderately expensive and requires
hospitalisation

86
Q

When are low phosphate levls seen

A

early in paracetemol poisoning

low phosphate feature of APAP overdose with or without
hepatotoxicity; reflects severity of overdose

87
Q

What is the glucose oxidation rate?

A

(4-7mg/kgbwt/min/day)

88
Q

What is the aim of estimating accurate carbohydrate requirements?

A

Avoid excess CO2 production

89
Q

What percentage of total energy do carbohydrates contribute

A

45-65%

90
Q

How to estimate fluid requirements

A

30 - 35mls/kgbwt/day *

Consider:

Fever = increased reqs (by 2-2.5 ml increase per 1°C increase above 37°C)

Xs losses due to wound exudate, diarrhoea etc = increased reqs.

Obesity – review total volume

Consider all sources of fluid to prevent over-prescription
e.g. feeds, intravenous feeds and medication.

Estimate fluid requirements by assessing losses:

Fluid input = Urinary losses + 500-750 ml (to allow for insensible
fluid losses)

91
Q

What are the NICE guidelines for suggested total intake

A

25-35 kcal/kg/day total energy (including that derived
from protein)

0.8-1.5 g protein (0.13-0.24 g nitrogen)/kg/day

30-35 ml fluid/kg (with allowance for extra losses e.g. from
drains and fistulae and extra input from e.g. intravenous
drugs)

92
Q

What are the indications for gastrostomy feeding

A

Unsafe swallow

CVA

Parkinson’s disease

Motor neurone disease

Chronic inability to meet
oral requirements

Anorexia

dementia

Oesophageal stricture

Pre-head and neck
surgery/DXT

93
Q

What are the complications of gastonomy feeding

A

Refeeding syndrome

Aspiration

Diarrhoea

Tube blockage

Feed contamination

Infected stoma site

Tube displacement

94
Q

What is refeeding syndrome

A
  • Complication that occurs when a malnourished person begins receiving nutrition again
  • During periods of starvation:
    1. Secretion of insulin is decreased in response to reduced intake of carbohydrates
    2. Fat and protein stores are catabolised for energy
    3. Results in intracellular loss of electrolytes - especially phosphate however serum levels remain normal due to compensatory mechanisms
    4. When carbohydrates are given again, energy source switches to carbohydrates and insulin is released which results in cellular uptake of phosphate resulting in severe depletion of serum phosphate (within four days of starting to feed again)
    5. phsophate needed for phosphorylation reactions and lack of it leads to refeeding syndrome which is:
Rhabdomyolysis
Leukocyte dysfunction
Resp failure
Cardiac failure
Hypotension 
Arrythmias 
Seizures
Coma
Sudden death

also see michelle ramsay notes for each electrolyte sequelae

95
Q

What does low magnesium as a result of refeeding syndrome lead to

A

Decreased PTH secretion leading to hypocalcemia

96
Q

When/how to give nutritional support - what so you need to consider

A

see michelle ramsay notes

97
Q

Which conditions make a person more at risk of refeeding syndrome?

A

Very little or no food for >5 days (Esp BMI<20)

Unintentional weight loss >5% within the last 3-6
months

98
Q

Who is at HIGH RISK of refeeding syndrome

A

With any of the following:

BMI<16

Unintentional weight loss >15% in last 3-6 months

Very Little or no nutrition for >10 days

Low levels of potassium, phosphate or magnesium
prior to feeding

__________________

  1. With two or more of the following:

BMI<18.5

Unintentional weight loss >10% in last 3-5 months

Very little or no nutrition for >5 days

History of alcohol abuse or drugs –insulin,
chemotherapy, antacids, diuretics

99
Q

What nutrtion should you give to someone at risk of refeeding syndrome

A

Nutrition support should be cautiously introduced

It should be started at no more than 50% of the
estimated target energy and protein needs

Built-up to meet full needs over the first 24-48
hours according to metabolic and gastrointestinal
tolerance.

Full requirements of fluid, electrolytes, vitamins
and minerals should be provided from the outset
of feeding.

100
Q

Nutrtion support for people at HIGH RISK of refeeding syndrome

A

Starting nutrition support at a maximum of 10 kcal/kg/day,
increasing levels slowly to meet or exceed full needs by 4-7
days.

Using only 5 kcal/kg/day in extreme cases (e.g. BMI < 14
kg/m2) and monitoring cardiac rhythm continually.

Restoring circulatory volume and monitoring fluid balance and
overall clinical status closely.

Providing immediately before and during the first 10 days of
feeding: oral thiamin 200-300 mg daily, Vitamin B co strong
1-2 tablets 3 times a day, and a balanced multivitamin/trace
element supplement once daily.

Providing oral, enteral or intravenous supplements of
potassium (2-4 mmol/kg/day), phosphate (0.3-0.6
mmol/kg/day) and magnesium (0.2 mmol/kg/day IV, 0.4
mmol/kg/day oral) unless pre-feeding plasma levels are high.
Pre-feeding correction of low plasma levels is unnecessary.

101
Q

Indications for parenteral nutrtion

A 
Parenteral nutrition (PN): administration of nutrients by the intravenous
route via a dedicated central or peripheral placed line.

Used where there is:

a. failure of gut function (e.g. with obstruction, ileus, dysmotility, fistulae,
surgical resection or severe malabsorption) to a degree that definitely
prevents adequate gastrointestinal absorption of nutrients

and

B. the consequent intestinal failure has either persisted for several days (e.g.
>5 days) or is likely to persist for many days (e.g. 5 days or longer) before
significant improvement.

It may also be needed in patients with reasonable gut function who
cannot eat when ETF is impossible or impractical for reasons of tube

Intestinal obstruction

Intestinal perforation

Short bowel

Anatomical

Functional

High output small bowel fistula

(prolonged ileus)

Multi-organ failure where requirements cannot be
met by the enteral route

Intractable vomiting

Chronic malabsorption

102
Q

What is a NON INDICATION for parenteral nutrition

A

Post major (GI) surgery

Acute pancreatitis

Absence of bowel sounds

103
Q

Problems with parenteral nutrition?

A

infection

thrombosis

electrolyte disturbances

hepatic dysfunction

Hyperglycaemia

104
Q

What are the five main responses to hgepatic injury

A

Degeneration and Intracellular Accumulation

Necrosis and Apoptosis

Inflammation

Regeneration

Fibrosis

105
Q

Which is more common micro or macrovesicular steatosis

A

Macro

106
Q

In which conditions are fatty livers seen

A
  1. Alcoholic liver disease

2. Acute fatty liver of pregnancy

107
Q

What is the term for Injury to the liver which associate with an influx of acute or chronic inflammatory
cells

A

hepatitis

108
Q

Main difference in appearance between acute and chronic viral hepatitis

A

Acute viral hepatitis:
inflammation is scattered
throughout lobule as well as
portal tract.

Chronic viral hepatitis:
inflammation is mainly in portal
tracts, with focal interface
hepatitis

see slide 31

109
Q

What is the basis of hepatocellular regeneration

A

Liver has the ability to regenerate. Hepatocellular proliferation is
signified by mitoses, thickening of the hepatocyte chords and some
disorganization of the liver parenchyma

110
Q

What is cholestasis

A

condition

characterized systemic retention of bilirubin and other solutes eliminated in bile.

111
Q

How do regenerative nodules appear on histology

A

see slide 38 of histology lecture

112
Q

how doe smassive hepatic necrosis appear on histology

A

a wide spectrum of morphological changes in the parenchyma,
from areas of extensive hepatocyte loss and parenchymal
collapse to areas of hepatocytic regeneration with the
appearance of regenerating nodules.

BCS Lectures (8 decks)

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