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PBLs > Week 13 - Liver > Flashcards

Week 13 - Liver Flashcards

1
Q

what is used to assess the scale of symptoms of alcohol wihdrawal?

A

CIWA score

0-9 for minimal withdrawal
10-19 moderate
>20 severe

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2
Q

what drug treatment should be offered in acute alcohol withdrawal?

A

consider benzodiazepine or carbamazepine

prophalactic thiamine to prevent wernickes encephalopathy

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3
Q

what is wernickes encephalopathy?

A

a life-threatening illness caused by thiamine deficiency, which primarily affects the peripheral and central nervous systems

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4
Q

what triad of symptoms is seen in wernickes encephalopathy?

A

ophthalmoplegia, ataxia and confusion

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5
Q

What is the treatment of wernickes encephalopathy?

A

parenteral thiamine

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6
Q

when should prophylactic thiamine be given for wernickes encephalopothy?

A
  • if they are malnourished or at risk of malnourishment; or
    * if they have decompensated liver disease; or
    * if they are in acute withdrawal; or
    * before and during a planned medically assisted alcohol withdrawal.
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7
Q

what is the CAGE questionnaire?

A

screens for excessive drinking and alcoholism

cut down drinking?
have people Annoyed you by critisizing your drinking?
felt Guilty about drinking?
Eye-opener - drink first thing in the morning?

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8
Q

what is AUDIT-C?

A

3-item alcohol screen that can help identify persons who are hazardous drinkers or have active alcohol use disorders.

how often did you have a drink containnig alcohol in the past year?
how many drinks a day?
how often did you have more than 6 drinks in one go?

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9
Q

what is hepetitis?

A

inflammation of the liver
leads to large areas of necrosis and liver failure

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10
Q

how does hepatitis occur?

A

1) Viruses enter the blood stream and spread to the liver.
2) They infect the hepatocytes and multiply.
3) They change the antigen structure on the virus site.
4) The body begins to use self-mediated immune response attempting to damage the hepatocytes.
5) In Hep B and C, they can continue this process over and over for years increasing the risk of cirrhosis
Liver cirrhosis is the result of chronic inflammation and damage to liver cells. The functional liver cells are replaced with scar tissue (fibrosis). Nodules of scar tissue form within the liver.

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11
Q

what are some causes of hepatitis?

A
  • Alcoholic hepatitis
    • Non alcoholic fatty liver disease
    • Viral hepatitis - most common cause
    • Autoimmune hepatitis
      Drug induced hepatitis (e.g. paracetamol overdose)
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12
Q

what is the presentation of hepatitis?

A

Hepatitis may be asymptomatic or could present with non-specific symptoms:
* Abdominal pain
* Fatigue
* Pruritis (itching)
* Muscle and joint aches
* Nausea and vomiting
* > 5 Spider naevi
* Jaundice
Fever (viral hepatitis)

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13
Q

what is seen on LFTs in hepatitis?

A

raised transaminases (AST/ALT)
refered to as a hepatic picture

Transaminases are liver enzymes that are released into the blood as a result of inflammation of the liver cells. Bilirubin can also rise as a result of inflammation of the liver cells. High bilirubin causes jaundice.

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14
Q

what is the most common hepatitis worldwide?

A

hep A
rare in UK

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15
Q

how is hepatitis A spread?

A

faecal oral route
usually contaminated water or food

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16
Q

how does hepatitis present?

A

N+V
anorexia
jaundice

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17
Q

what can hepatitis A cause and what signs are seen in this?

A

cholestasis (slowing of bile flow through the biliary system) with dark urine and pale stools and moderate hepatomegaly

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18
Q

what is the management of hepatitis A?

A

resolves without treatment in around 1-3 months
basic analgesia

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19
Q

what type of virus is hepatitis B?

A

DNA virus

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20
Q

how is hepatitis B transmitted?

A

direct contact with blood or bodily fluids
e.g. sex, needles, toothrush, minor cuts

can also be passed from mother to child

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20
Q

what do HBsAG (surface antigens) suggest?

A

active infection

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20
Q

what do HBeAg (E antigen) suggest?

A

marker of viral replication and implies high infectivity

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21
Q

what do HBcAb (core antibodies) suggest?

A

implies past infection

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22
Q

what do HBsAb (surface antibodies) suggest?

A

implies vaccination or past or current infection

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23
Q

what do HBV DNA show?

A

hepatitis B virus DNA
direct count of viral load

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24
Q

what is tested for to confirm response to hep B vaccine?

A

HBsAb

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25
Q

what is the management for hep B

A
  • Have a low threshold for screening patients that are at risk of hepatitis B.
    • Screen for other blood born viruses (hepatitis A and B and HIV) and other sexually transmitted diseases
    • Refer to gastroenterology, hepatology or infectious diseases for specialist management
    • Notify Public Health (it is a notifiable disease)
    • Stop smoking and alcohol
    • Education about reducing transmission and informing potential at risk contacts
    • Testing for complications: FibroScan for cirrhosis and ultrasound for hepatocellular carcinoma
    • Antiviral medication can be used to slow the progression of the disease and reduce infectivity
      Liver transplantation for end-stage liver disease
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26
Q

what is shown on a hepatitis screen for vaccinated people?

A

HBsAb positive
HBsAg and HBcAb negative

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27
Q

what is shown on a hepatitis screen for people who have previously been infected?

A

HBsAb and HBcAb positive
HBsAG negative

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28
Q

what is shown on a hepatitis screen for someone with an acute infection?

A

HBsAg positive
HBcAb IgM positive
HBsAb negative

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29
Q

what is shown on a hepatitis screen for someone with a chronic infection?

A

HBsAg positive
HBcAb IgG positive
HBsAb negative

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30
Q

how do you distinguish between an acute and chronic hep b infection of a hep screen?

A

acute = IgM HBcAb
chronic = IgG HBcAb

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31
Q

what type of virus is hepatitis C?

A

RNA virus

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32
Q

how is hepatitis C spread?

A

blood and bodily fluid

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33
Q

what are some complications of hepatitis C?

A

liver cirrhosis
hepatocellular carcinoma

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34
Q

what is the management of hepatitis C?

A
  • Have a low threshold for screening patients that are at risk of hepatitis C
    • Screen for other blood born viruses (hepatitis A and B and HIV) and other sexually transmitted diseases
    • Refer to gastroenterology, hepatology or infectious diseases for specialist management
    • Notify Public Health (it is a notifiable disease)
    • Stop smoking and alcohol
    • Education about reducing transmission and informing potential at risk contacts
    • Testing for complications: FibroScan for cirrhosis and ultrasound for hepatocellular carcinoma
    • Antiviral treatment with direct acting antivirals (DAAs) is tailored to the specific viral genotype. They successfully cure the infection in over 90% of patients. They are typically taken for 8 to 12 weeks
      Liver transplantation for end-stage liver disease
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35
Q

what type of virus is hepatits D?

A

RNA virus

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36
Q

what is hepatitis D infection associated with?

A

hepatitis B infection
It can only survive in patients who also have a hepatitis B infection.
It attaches itself to the HBsAg to survive and cannot survive without this protein

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37
Q

which hepatitis cases need to be notified to public health?

A

A
D
E

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38
Q

what type of virus is hepatitis E?

A

RNA virus

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39
Q

how is hepatitis E transmitted?

A

faecal oral route
injestion of contaminated food or water

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40
Q

what are the 2 types of autoimmune hepatitis and when are they seen?

A

Type 1 typically affects women in their late forties or fifties. It presents around or after the menopause with fatigue and features of liver disease on examination. It takes a less acute course than type 2.

In type 2, patients in their teenage or early twenties present with acute hepatitis with high transaminases and jaundice.

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41
Q

what is seen in LFTs in autoimmune hepatitis?

A

raised transmaniases
raised IgG levels

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42
Q

what autoantibodies are seen in type 1 and type 2 autoimmune hepatitis?

A

Type 1 Autoantibodies:
* Anti-nuclear antibodies (ANA)
* Anti-smooth muscle antibodies (anti-actin)
* Anti-soluble liver antigen (anti-SLA/LP)

Type 2 Autoantibodies:
* Anti-liver kidney microsomes-1 (anti-LKM1)
Anti-liver cytosol antigen type 1 (anti-LC1)

43
Q

how do you diagnose autoimmune hepatitits?

A

liver biopsy

44
Q

what is the management of autoimmune hepatitis?

A

high dose steroids (prednisolone) that are tapered over time as other immunosuppressants, particularly azathioprine, are introduced.

Immunosuppressant treatment is usoually successful in inducing remission however it is usually required life long.

Liver transplant may be required in end stage liver disease, however the autoimmune hepatitis can recoccur in transplanted liver

45
Q

what LFTs are seen in hepatitis A?

A

ALT>AST

46
Q

how is EBV transmitted?

A

saliva and bodily fluids

47
Q

which people are more likely to develop liver symptoms from EBV?

A

immunocompromised

48
Q

how does EBV induce liver injury?

A

T lymphocyte- driven immune response against EBV-infected B cells causing inflammation and damage to hepatocytes

49
Q

what symptoms are seen in EBV infection?

A
  • Sore throat and throat inflammation (swelling)
    • Fatigue
    • Fever
    • Swollen lymph nodes
    • Rashes
      Enlarged spleen and liver
50
Q

what is cytomegalovirus and what complications does it cause?

A

causes inflammation of the liver

51
Q

what symptoms are seen in cytomegalovirus hepatitis infection?

A
  • Fever
    • Pain in URQ
      Jaundice anamia
52
Q

what are the common symptoms of drug induced liver injury?

A

jaundice, then weakness, abdominal pain, dark stools or urine, nausea and pruitis.

53
Q

what is portal hypertension caused by?

A

Obstruction of the portal vein or its branches by a tumour, thrombus, cirrhosis, ligation during surgery or vascular diseases such as Budd-Chiari syndrome

54
Q

what is portal hypertension?

A

elevated blood pressure in the portal vein resulting in reduced flow of detoxified blood into the IVC and SVS

55
Q

what is hepatic encephalopathy?

A

build up of ammonia in blood
confusion

56
Q

what are the 3 connections between the portal system and the systemic system?

A

inferior protion of oesophagus
superior portion of anal canal
round ligament of the liver

57
Q

what happens at the 3 portosystemic shunts in portal hypertension?

A

oesophageal varices
haemorrhoids
caput medusa = abdominal veins dilate

58
Q

what happens to the blood in portal hypertension?

A
  • Blood is backed up into the spleen causing hypersplenism , trapping RBC and WBC = anaemia, leukopenia and thrombocytopenia
59
Q

how does portal hypertension cause vasodilation and what effect does this have?

A

endothelial cells lining blood vessels, release more NO, causing arteries to dilate, decreased BP = release of aldosterone, kidneys then retain h2o and sodium,

Plasma volume expands so fluid eventually gets pushed across tissues and into open spaces à peritoneal cavity = ASCITES

Within the liver endothelial dysfunction of the liver sinusoidal cells decrease production of NO which then favours vasoconstriction (increasing the hepatic resistance and micro circulation)

60
Q

what symptoms are seen in portal hypertension?

A

ascites
bleeding
caput medusa
decreased liver function
enlarged spleen

61
Q

what are some risk factors of abnormal liver function?

A
  1. Obesity
  2. An undiagnosed hepatitis infection
  3. Alcohol misuse
  4. Poor diet and low activity levels
  5. Type 2 diabetes
  6. High cholesterol
  7. Middle age onwards
  8. Smoking
    High blood pressure
62
Q

what investigations should be done in someone with abnormal liver funciton?

A

ultrasound
hep b and c serology
autoantibodies
Immunoglobulins
caeruloplasmic
alpha 1 anti-trypsin levels
ferritin and tranferrin saturation

63
Q

what are some complications of chronic alcohol use?

A
  • Neurological: ischaemic stroke, encephalopathy, seizures, peripheral neuropathy
    • Cardiovascular: increased rate of myocardial infarction and stroke, hypertension, dilated cardiomyopathy
    • Hepatology: alcoholic liver disease, liver cirrhosis, liver fibrosis, pancreatitis
    • Oncology: increased risk of head and neck cancer, oesophageal cancer, liver cancer, breast cancer, colorectal cancer
    • Psychiatric: alcoholic hallucinosis, delirium tremens, Wernicke-Korsakoff syndrome
64
Q

what management is given to someone with stable varices?

A

○ Propranolol – reduces portal hypertension (non-selective beta blocker)
○ Elastic band ligation of varices
○ Injection of sclerosant
TIPS – procedure where stent is placed between hepatic and portal vein.

65
Q

what management is given in bleeding oesophageal varices?

A

○ Resuscitation
→ Vasopressin analogues (terlipressin) – vasoconstriction, slow bleeding
→ Correct coagulopathy with vitamin K and fresh frozen plasma
→ Broad spectrum antibiotics
→ Intubation and ICU if life threateningly unwell, bleeding rapidly
○ Urgent endoscopy
→ Injection of sclerosant into varices – cause inflammatory obliteration of vessel
→ Elastic band ligation
→ Sengstaken-Blakemore tube – inflatable tube inserted into oesophagus to tamponade bleeding varices – used when endoscopy fails

66
Q

what management is given in hepatic encephalopathy?

A

Laxatives (lactulose) – promote excretion of ammonia from gut before it is absorbed. Aim: 2-3 soft motions daily. May require enemas initially

Antibiotics (rifaximin) – reduces number of intestinal bacteria producing ammonia, poorly absorbed = stay in GI tract decreasing ammonia production

Nutritional support – nasogastric feeding if required

67
Q

what is hepatorenal syndrome?

A

portal hypertention leads to hypotension of kidneys .: activate RAAS .: renal vasoconstriction .: kidney function deteriorates

68
Q

what is alpha-1 antitrypsin defeciency?

A

usually alpha-1 antitrypsin provides protection by inhibiting the neutrophil elastase enzyme
in A1AT deficiency this is not happening

69
Q

what chromosome is A1AT deficiency coded for on and what type of defect is in the gene?

A

chromosome 14
autosomal recessive

70
Q

what 2 organs does alpha-1 antitrypsin deficiency affect?

A

liver
lungs

71
Q

how does alpha-1 antitrypsin deficiency affect the liver?

A

normally alpha-1 antitrypsin is produced in the liver
in alpha-1 antitrypsin deficiency a mutent protein is created
this causes liver damage and cirrhosis
can overtime lead to hepatocellular carcinoma

72
Q

how does alpha-1 antitrypsin deficiency affect the lungs?

A

absent inhibition of neutrophil elastase causes lung damage leading to COPD
causes attack of connective tissue in lungs

73
Q

list the pulmonary and hepatic features of Alpha -1-antitrypsin deficiency?

A

Pulmonary clinical features
Dyspnoea
Cough
Wheeze
Ankle swelling (right-sided heart failure from chronic lung disease)

Hepatic clinical features
Jaundice
Bruising
Spider naevi
Palmar erythema
Hepatomegaly
Ascites
Leuconychia
Confusion
Asterixis: flapping tremor (suggests encephalopathy)
Cachexia

74
Q

how is Alpha -1-antitrypsin deficiency diagnosed?

A

low serum Alpha -1-antitrypsin (<0.8g/L)

liver biopsy shows cirrhosis and acid-Schiff-positive staining globules (this stain highlights the mutant alpha-1-antitrypsin proteins) in hepatocytes

genetic testing

CT thorax shows bronchiectasis and emphysema

75
Q

what is the management of Alpha -1-antitrypsin deficiency?

A
  • Stop smoking (smoking dramatically accelerates emphysema)
    • Decrease alcohol intake
    • Nutritional support
    • Pulmonary rehab (if needed)
    • Seasonal vaccination (to prevent respiratory infections)
    • Symptomatic management
    • NICE recommend against the use of replacement alpha-1-antitrypsin, however the research and debate is ongoing regarding the possible benefits
    • Organ transplant for end-stage liver or lung disease
      Monitoring for complications (e.g. hepatocellular carcinoma)
76
Q

what is hereditary haemochromotosis?

A

iron storage disorder that results in excessive total body iron and deposition of iron in tissues.

77
Q

where is mutation for hereditary haemochromotosis found and what type is it?

A

chromosome 6
autosomal recessive

78
Q

when does hereditary haemochromotosis usually present?

A

after 40yo
later in females due to menstruation regularly eliminating iron from body

79
Q

what is the presentation of hereditary haemochromotosis?

A

○ Chronic tiredness
○ Joint pain
○ Pigmentation (bronze / slate-grey discolouration)
○ Hair loss
○ Erectile dysfunction
○ Amenorrhoea
Cognitive symptoms (memory and mood disturbance)

80
Q

what is the main diagnostic mechanism in hereditary haemochromotosis?

A

serum ferritin level
can do transferrin saturation to check if high iron is from iron overload or inflammation

high ferritin and high transferrin = hereditary haemochromotosis

81
Q

what tests are used in diagnosing herediatry haemachromotosis?

A

serum ferritin
genetic testing
liver biopsy with perls stain - establishes iron conc in parenchymal cells
CT abdomen - increased attenuation in liver

82
Q

what are some complications of hereditary haemochromotosis?

A
  • Type 1 Diabetes (iron affects the functioning of the pancreas)
    • Liver Cirrhosis
    • Iron deposits in the pituitary and gonads lead to endocrine and sexual problems (hypogonadism, impotence, amenorrhea, infertility)
    • Cardiomyopathy (iron deposits in the heart)
    • Hepatocellular Carcinoma
    • Hypothyroidism (iron deposits in the thyroid)
      Chrondocalcinosis / pseudogout (calcium deposits in joints) causing arthritis
83
Q

what is the management of hereditary haemachromotosis?

A
  • Venesection = a weekly protocol of removing blood to decrease total iron
    • Iron chelation therapy
    • Monitoring serum ferritin
    • Avoid alcohol
    • Genetic counselling
      Monitoring and treatment of complications
84
Q

what are the risk factors for primary hepatocellular carcinoma?

A

○ Cirrhosis = up to 1/3 of patients with cirrhosis will develop HCC
○ Hepatitis B/C/D virus
○ Aflatoxin B1 - produced by certain moulds
○ Betel nut chewing
○ Alcohol
○ Smoking
○ Non-alcoholic fatty liver disease
○ Genetic susceptibility
§ E.g. Tp53 mutation (tp53 is usually a tumour suppressor gene)

85
Q

what is the presentation of primary hepatocellular carcinoma?

A
  • Asymptomatic
    • Fever
    • Anorexia
    • Night sweats
    • Weight loss
      Fatigue
86
Q

what are the 2 ways of diagnosing primary hepatocellular carcinoma?

A

○ Imaging: specific criteria for HCC can be used in patients with cirrhosis.
§ Nodules are >1cm with typical vascular features
○ Histology: required in patients without cirrhosis. May be needed in equivocal cases with cirrhosis.

87
Q

what staging system helps guide treatment in primary hepatocellular carcinoma?

A

barcelona clinic liver cancer staging system

	○ 0 (very early): Performance status 0, Child-Pugh A, single tumour < 2cm
	○ A (early): Performance status 0, Child-Pugh A-B, single tumour or up to 3 nodules ≤ 3 cm
	○ B (intermediate): Performance status 0, Child-Pugh A-B, multinodular tumours
	○ C (advanced): Performance status 1-2, Child-Pugh A-B, tumour with portal invasion or extrahepatic spread D (terminal): Performance status >2, Child-Pugh C (decompensated liver disease)
88
Q

what is the management of primary hepatocellular carcinoma?

A
  • Locoregional therapies: liver resection, percutaneous ablation, transarterial therapies
    • Liver transplantation
    • Systemic therapy: multikinase inhibitors (e.g. Sorafenib), others.
    • Other therapies: radiotherapy, brachytherapy, immunotherapy
      Best supportive care
89
Q

what is alt and when is it raised?

A

enzyme that catalyses a reaction between an amino acid and a keto-acid

liver damage

90
Q

what is ast and when is it raised?

A

type of enzymes have a similar function to ALT enzymes. These enzymes are found in the liver, RBC’s, cardiac and skeletal muscle, kidney and brain tissue

damage to any of these areas can result in an increased level on test result.

91
Q

what is alp and when is it deranged?

A

enzymes work best in an alkaline environment are involved in hydrolysis reactions

found in bile duct and bone

raised = damage to one of these areas

physiologically raised with high bone turnover e.g. pregnancy and adolescence

bile duct blockage and liver disease

92
Q

what is GGT and when is it raised?

A
  • Commonly raised in increased alcohol intake

obstruction of bile duct

  • GGT is often used to confirm that ALP readings are due to liver damage and not another cause.
  • If ↑ALP but normal GGT – likely bone – consider checking calcium
    If ↑ALP and ↑GGT – likely liver cause
93
Q

what if patient is jaundice but alt and alp levels are normal?

A

isolated rise in bilirubin is likely pre-hepatic cause

e.g. gilberts syndrome
haemolysis

94
Q

what are some common causes of acute hepatocellular injury and what lfts would be seen?

A
  • Poisoning (paracetamol overdose)
  • Infection (Hepatitis A and B)
    Liver ischaemia

high alt
high bilirubin
slightly raised alp/ggt

95
Q

what are some common causes of chronic hepatocellular injuries and what would lfts show?

A
  • Alcoholic fatty liver disease
  • Non-alcoholic fatty liver disease
  • Chronic infection (Hepatitis B or C)
    Primary biliary cirrhosis

slighlt raised alt/alp/ggt/bilirubin

96
Q

what lfts are seen in cholestasis?

A

raised alp/ggt/bilirubin
slightly raised alt

97
Q

what is gluconeogenesis?

A
  • → synthesis of glucose from non-carbohydrate substrates
    Occurs after around 8 hours of fasting when liver glycogen stores start to deplete
98
Q

what is glycogenesis?

A

Liver maintains steady blood glucose levels by converting excess glucose into glycogen

99
Q

what is glycogenolysis?

A

When there is demand for glucose, glycogen is converted back into glucose

occurs within liver cytosol and cytosol of skeletal muscle

100
Q

what binds to fatty acids to make them blood soluble?

A

albumin

101
Q

what are the forms of bilirubin?

A
  • Unconjugated → insoluble in water. Can only travel in bloodstream bound to albumin. Cannot be directly excreted.
    • Conjugated → water soluble. Can travel through bloodstream without requiring proteins.
102
Q

how is conjugated bilirubin excreted?

A

into duodenum in bile

103
Q

what is primary sclerosising cholangitis?

A

condition where the intrahepatic or extrahepatic ducts become strictured and fibrotic

obstruction to the flow of bile out of the liver and into the intestines

104
Q

what is cholangitis?

A

inflammation of the bile ducts

105
Q

what is primary sclerosising cholangitis associated with?

A

ulcerative cholitits

106
Q

what is the stepwise progression of alcoholic liver disease?

A
  1. Alcohol related fatty liver
    Drinking leads to a build-up of fat in the liver. If drinking stops this process reverses in around 2 weeks.
    The hepatocytes have to divert resources away from metabolising fats to metabolising alcohol. As a result, fat metabolism is altered resulting in fat deposits inside the cells. There are more fats released into the blood stream (fatty acids) and within the hepatocytes, there is increased synthesis of triglycerides and fatty acids.
  2. Alcoholic hepatitis
    Drinking alcohol over a long period causes inflammation in the liver sites. Binge drinking is associated with the same effect. Mild alcoholic hepatitis is usually reversible with permanent abstinence.
    The hepatocytes, there is increased synthesis of triglycerides and fatty acids.
    Acetaldehyde is a product of alcohol metabolism. It binds to liver cell proteins, and causes hepatocytes injury, leading to inflammation. This inflammation can be a causatory factor in cirrhosis. It is likely that this produces Mallory’s sign.

Alcohol stimulates collagen synthesis by fibroblasts as well as fibroblast proliferation.

  1. Cirrhosis
    This is where the liver is made up of scar tissue rather than healthy liver tissue. This is irreversible. Stopping drinking can prevent further damage. Continued drinking has a very poor prognosis.
    Ultimately, the fibrosing process will end up linking hepatic veins to portal veins, and in these places, cell regeneration occurs, and nodules form – this is the start of the process of cirrhosis
107
Q

what are some causes of hepatocellular jaundice?

A

hepatitis
medication
acute liver injiry
chronic liver injury
haemochromatosis
infection
alcoholic hepatitis
exposure to toxic materials

PBLs (19 decks)

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