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Year 3 > Week 15 - Liver failure, viral hepatitis, drug overdose > Flashcards

Week 15 - Liver failure, viral hepatitis, drug overdose Flashcards

1
Q

what will reverse the effect of opiate overdose, typically in the presence of CNS and respiratory depression

A

naloxone

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2
Q

what are the symptoms of benzodiazepine overdose

A

symptoms: agitation, euphoria, blurred vision, slurred speech, ataxia, slate-grey cyanosis

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3
Q

what can reverse the effect of benzodiazepine overdose

A

Flumazenil

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4
Q

what are the signs and symptoms of aspirin overdose

A

Tinnitus
Lethargy
Dizziness
Nausea / vomiting

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5
Q

what is usually the treatment of choice in beta-blocker overdose

A

glucagon

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6
Q

how is hypocalcaemia corrected

A

with calcium

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7
Q

what is the treatment for cocaine and amphetamine overdose

A

benzodiazepine e.g diazepam

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8
Q

what is the treatment for carbon monoxide poisoning

A

hyperbaric oxygen

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9
Q

what are the antidotes for anti-freeze poisoning

A

ethanol

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10
Q

what is the antidote for cyanide poisoning

A

dicobalt edetate

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11
Q

what is the antidote for lead poisoning

A

sodium calcium edetate

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12
Q

what is the antidote for organophosphate poisoning

A

atropine

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13
Q

what is the antidote for heparin overdose

A

protamine sulphate

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14
Q

what does fibrosis affect in the liver

A

affects the structure and blood flow, increasing the resistance of the vessels leading into the liver.

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15
Q

what is this increased resistance and pressure in the portal system called

A

portal hypertensionw

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16
Q

what are the four most common causes of liver cirrhosis

A

Alcohol-related liver disease
Non-alcoholic fatty liver disease (NAFLD)
Hepatitis B
Hepatitis C

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17
Q

what are the signs of liver cirrhosis on examination

A

Cachexia (wasting of the body and muscles)
Jaundice caused by raised bilirubin
Hepatomegaly (enlargement of the liver)
Small nodular liver as it becomes more cirrhotic
Splenomegaly due to portal hypertension
Spider naevi (telangiectasia with a central arteriole and small vessels radiating away)
Palmar erythema caused by elevated oestrogen levels
Gynaecomastia and testicular atrophy in males due to endocrine dysfunction
Bruising due to abnormal clotting
Excoriations (scratches on the skin due to itching)
Ascites (fluid in the peritoneal cavity)
Caput medusae (distended paraumbilical veins due to portal hypertension)
Leukonychia (white fingernails) associated with hypoalbuminaemia
Asterixis (“flapping tremor”) in decompensated liver disease

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18
Q

what does a non-invasive liver screen include

A

ultrasound liver (diagnose fatty liver)

hepatitis B and C serology

autoantibodies

immunoglobulins

caeruloplasmin (Wilson’s disease)

Alpha 1 antitrypsinogen

ferritin and transferrin

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19
Q

what are the autoantibodies relevant to liver disease

A

Antinuclear antibodies (ANA)
Smooth muscle antibodies (SMA)
Antimitochondrial antibodies (AMA)
Antibodies to liver kidney microsome type-1 (LKM-1)

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20
Q

what do the liver markers look like in decompensated cirrhosis

A

raised;
Bilirubin
Alanine transaminase (ALT)
Aspartate transferase (AST)
Alkaline phosphatase (ALP)

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21
Q

what will albumin look like in decompensated liver cirrhosis

A

low due to reduced synthetic function

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22
Q

what is a tumour marker for hepatocellular carcinoma

A

alpha-fetoprotein

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23
Q

what is the first-line investigation for assessing fibrosis in non-alcoholic fatty liver disease

A

enhanced liver fibrosis blood test

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24
Q

what may be seen in an ultrasound of liver cirrhosis

A

Nodularity of the surface of the liver
A “corkscrew” appearance to the hepatic arteries with increased flow as they compensate for reduced portal flow
Enlarged portal vein with reduced flow
Ascites
Splenomegaly

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25
Q

what is used as a screeing tool for hepatocellular carcinoma

A

Ultrasound is used as a screening tool for hepatocellular carcinoma (alongside alpha-fetoprotein).

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26
Q

what is the MELD score

A

NICE recommend using the MELD (Model for End-Stage Liver Disease) score every 6 months in patients with compensated cirrhosis. The formula considers the bilirubin, creatinine, INR and sodium and whether they require dialysis, giving an estimated 3-month mortality as a percentage.

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27
Q

what is the child pugh score

A

The Child-Pugh scores uses 5 factors to assess the severity of cirrhosis and the prognosis. Each factor is considered and scored 1, 2 or 3. The minimum overall score is 5 (scoring 1 for each factor), and the maximum is 15 (scoring 3 for each factor).

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28
Q

what is the pneumonic for the child pugh score

A

You can remember the features with the “ABCDE” mnemonic:

A – Albumin
B – Bilirubin
C – Clotting (INR)
D – Dilation (ascites)
E – Encephalopathy

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29
Q

what are the four principles of management in liver cirrhosis

A

Treating the underlying cause
Monitoring for complications
Managing complications
Liver transplant

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30
Q

what are the monitoring systems in place for liver cirrhosis

A

MELD score every 6 months
Ultrasound and alpha-fetoprotein every 6 months for hepatocellular carcinoma
Endoscopy every 3 years for oesophageal varices

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31
Q

what are the four key features of decompensated liver disease

A

The four key features can be remembered with the “AHOY” mnemonic:

A – Ascites
H – Hepatic encephalopathy
O – Oesophageal varices bleeding
Y – Yellow (jaundice)

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32
Q

what is the 5 year survival rate once cirrhosis has developed

A

50%

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33
Q

what are the several important complications of cirrhosis

A

Malnutrition and muscle wasting
Portal hypertension, oesophageal varices and bleeding varices
Ascites and spontaneous bacterial peritonitis
Hepatorenal syndrome
Hepatic encephalopathy
Hepatocellular carcinoma

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34
Q

what does the back pressure of blood in portal hypertension result in

A

splenomegaly

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35
Q

Back pressure in the portal system causes swollen and tortuous vessels at sites where collaterals form between the portal and systemic venous systems. These collaterals can occur at several locations, notably the:

A

Distal oesophagus (oesophageal varices)
Anterior abdominal wall (caput medusae)

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36
Q

what is the prophylaxis of bleeding in stable oesophageal varcies:

A

Non-selective beta blockers (e.g., propranolol) first-line

Variceal band ligation (if beta blockers are contraindicated)

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37
Q

what is TIPS

A

Transjugular intrahepatic portosystemic shunt (TIPS) is a technique where an interventional radiologist inserts a wire under x-ray guidance into the jugular vein, down the vena cava and into the liver via the hepatic vein. A connection is made through the liver between the hepatic vein and portal vein, and a stent is inserted. This allows blood to flow directly from the portal vein to the hepatic vein, relieving the pressure in the portal system.

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38
Q

what are the two main indictors for TIPS

A

bleeding oesophageal varices

refractory acities

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39
Q

what does ascites refer to

A

fluid in the peritoneal cavity

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40
Q

describe and explain the method behind ascites

A

The increased pressure in the portal system causes fluid to leak out of the capillaries in the liver and other abdominal organs into the peritoneal cavity. The drop in circulating volume caused by fluid loss into the peritoneal cavity causes reduced blood pressure in the kidneys.

41
Q

what happens when the kidneys sense this lower pressure

A

The kidneys sense this lower pressure and release renin, which leads to increased aldosterone secretion via the renin-angiotensin-aldosterone system. Increased aldosterone causes the reabsorption of fluid and sodium in the kidneys, leading to fluid and sodium retention. Cirrhosis causes transudative (low protein content) ascites.

42
Q

what are the management options for ascites

A

Low sodium diet
Aldosterone antagonists (e.g., spironolactone)
Paracentesis (ascitic tap or ascitic drain)
Prophylactic antibiotics (ciprofloxacin or norfloxacin) when there is <15 g/litre of protein in the ascitic fluid
Transjugular intrahepatic portosystemic shunt (TIPS) is considered in refractory ascites
Liver transplantation is considered in refractory ascites

43
Q

what is a complication that arises in 10-20% of patients with ascites

A

spontaneous bacterial peritonitis

44
Q

what are the presenting features of spontaneous bacterial peritonitis

A

Fever
Abdominal pain
Deranged bloods (raised WBC, CRP, creatinine or metabolic acidosis)
Ileus (reduced movement in the intestines)
Hypotension

45
Q

what are the most common organisms of spontaneous bacterial peritonitis

A

Escherichia coli
Klebsiella pneumoniae

46
Q

what is the management for spontaneous bacterial peritonitis

A

Taking a sample of ascitic fluid for culture before giving antibiotics
Intravenous broad-spectrum antibiotics according to local policies (e.g., piperacillin with tazobactam)

47
Q

what is hepatorenal syndrome

A

involves impaired kidney function caused by changes in the blood flow to the kidneys related to liver cirrhosis and portal hypertension

48
Q

what is one toxin worth remembering that is associated with hepatic encephalopathy

A

ammonia produced by intestinal bacteria when they break down proteins

49
Q

what are the two reasons that ammonia builds up in the blood of patients with cirrhosis

A

Firstly, the liver cells’ functional impairment prevents them from metabolising the ammonia into harmless waste products.

Secondly, collateral vessels between the portal and systemic circulation mean that the ammonia bypasses the liver and enters the systemic system directly.

50
Q

how does hepatic encephaolpathy present

A

Acutely, hepatic encephalopathy presents with reduced consciousness and confusion. It can present more chronically with changes to personality, memory and mood.

51
Q

what is the management of hepatic encephalopathy

A

Lactulose (aiming for 2-3 soft stools daily)

Antibiotics (e.g., rifaximin) to reduce the number of intestinal bacteria producing ammonia

Nutritional support (nasogastric feeding may be required)

52
Q

what are the three ways that lactulose works to reduce ammonia

A

Speeds up transit time and reduces constipation (the laxative effect clearing the ammonia before it is absorbed)

Promotes bacterial uptake of ammonia to be used for protein synthesis

Changes the pH of the contents of the intestine to become more acidic, killing ammonia-producing bacteria

53
Q

what is the usual choice of antibiotic and why

A

Rifaximin is the usual choice of antibiotic as it is poorly absorbed and stays in the gastrointestinal tract. Neomycin and metronidazole are alternatives.

54
Q

what is Wilson’s disease

A

an autosomal recessive genetic condition resulting in the excessive accumulation of copper in the body tissues, particularly in the liver

55
Q

what is Wilson’s disease caused by

A

mutations in the Wilson disease protein gene on chromosome 13 (also called the ATP7B copper-binding protein). This copper-transporting protein is important in helping remove excess copper from the body via the liver. Copper is excreted in the bile.

56
Q

in who does Wilson’s disease typically present

A

in teenagers or young adults

57
Q

what does the copper deposition to in the liver and in the CNS

A

Copper deposition in the liver leads to chronic hepatitis, eventually leading to cirrhosis. Copper deposition in the central nervous system can lead to neurological and psychiatric problems.

58
Q

what are the neurological symptoms invovled

A

Neurological symptoms can include tremor, dysarthria (speech difficulties) and dystonia (abnormal muscle tone). Copper deposition in the basal ganglia causes Parkinsonism (tremor, bradykinesia and rigidity).

59
Q

what are the psychiatric symptoms seen in Wilson’s

A

Psychiatric symptoms can include abnormal behaviour, depression, cognitive impairment and psychosis.

60
Q

what is seen in the cornea in Wilson’s disease

A

Kayser-Fleischer rings (deposition of copper in Descemet’s membrane)

these are green brown circles surrounding the iris of the eye. they can usually be seen by the naked eye but proper assessment is made using slit lamp examination

61
Q

what kind of anaemia may also be a feature of Wilson’s disease

A

haemolytic anaemia

62
Q

what is the initial screening test for suspected Wilson’s disease

A

serum caeruloplasmin

63
Q

what is caeruloplas,in

A

A low serum caeruloplasmin is suggestive of Wilson’s disease. Caeruloplasmin is the protein that carries copper in the blood. It can be falsely normal or elevated in cancer or inflammatory conditions.

64
Q

what kind of urine copper assay will show high copper

A

A 24-hour urine copper assay will show high urinary copper.

65
Q

what is the management of Wilson’s disease

A

Treatment is with copper chelation using either:

Penicillamine
Trientine

66
Q

what other treatments are available for Wilson’s disease

A

Zinc salts (inhibit copper absorption in the gastrointestinal tract)
Liver transplantation

67
Q

what are the two main organs affected by alpha-1 antitrypsin deficiency

A

Chronic obstructive pulmonary disease and bronchiectasis in the lungs (typically after 30 years old)

Dysfunction, fibrosis and cirrhosis of the liver (depending on the specific genotype)

68
Q

what is the gene that codes for alpha-1 antitrypsin

A

SERPINA1 gene and is found on chromosome 14. the gene has many potential variations, each with different effects on the quantity and funcitonality of alpha-1 antitrypsin

69
Q

how is alpha-1 antitrypsin deficiency inherited

A

in an autosomal co-dominant pattern

70
Q

what is alpha-1 antitrypsin

A

a protease inhibitor

71
Q

where is alpha-1 antitrypsin produced

A

in the liver

72
Q

what is diagnosis of alpha-1 antitrypsin deficiency based on

A

low serum alpha-1 antitrypsin

genetic tesitng

73
Q

what will liver biopsy show in alpha-1 antitrypsin deficiency

A

Liver biopsy shows periodic acid-Schiff positive staining globules in hepatocytes, resistant to diastase treatment. These represent a buildup of the mutant proteins.

74
Q

what is the management in alpha-1 antitrypsin deficiency

A

Stop smoking
Symptomatic management (e.g., standard treatment of COPD)
Organ transplant for end-stage liver or lung disease
Monitoring for complications (e.g., hepatocellular carcinoma)
Screening of family members

75
Q

what are the viral RNA hepatitis

A

hep A,C,D,E

76
Q

what is the viral DNA hepatitis

A

hep B

77
Q

which hepatitis are faecal-oral route of transmission

A

Hep A and Hep E

78
Q

what is the transmission pattern of hep B and hep D

A

Hep B - blood/bodily fluids

Hep D -always with hep B

79
Q

what is the transmission route of Hepatitis C

A

blood

80
Q

for which viral hepatitis’ is there a vaccine

A

Hep A and B

81
Q

for which viral hepatitis’ is there treatment

A

Hep B - antivirals
Hep C - direct acting antivirals
Hep D - pegylated interferon alpha

82
Q

what kind of diseases are all viral hepatitis

A

are all notifiable disease

83
Q

what is the presentation of viral hepatitis

A

Abdominal pain
Fatigue
Flu-like illness
Pruritus (itching)
Muscle and joint aches
Nausea and vomiting
Jaundice

84
Q

what is the hepatitic picture on liver function testd

A

A “hepatitic picture” on liver function tests refers to high transaminases (AST and ALT) with proportionally less of a rise in ALP. Transaminases are liver enzymes released into the blood due to inflammation of the liver cells.

Bilirubin can also rise as a result of inflammation of the liver cells. High bilirubin causes jaundice.

85
Q

what does hep A cause

A

cholestasis with pruitius, significant jaundice, dark urine and pale stools

86
Q

what is diagnosis of hep A based on

A

IgM antibodies to hep A

it usually resolves withut treatment

87
Q

what are the key viral markers to remember with hep B

A

Surface antigen (HBsAg) – active infection

E antigen (HBeAg) – a marker of viral replication and implies high infectivity

Core antibodies (HBcAb) – implies past or current infection

Surface antibody (HBsAb) – implies vaccination or past or current infection

Hepatitis B virus DNA (HBV DNA) – a direct count of the viral load

88
Q

what does the screening for hep B involve

A

Screening for hepatitis B involves testing for HBcAb (for previous infection) and HBsAg (for active infection). When these are positive, further testing is performed for HBeAg and viral load (HBV DNA).

89
Q

what does IgM imply

A

an active infection

90
Q

what does IgG imply

A

a past infection

91
Q

which antibody correlates with infectivity

A

HBeAg correlates with infectivity. Where the HBeAg is present, it implies the patient is in the acute phase of infection, where the virus is actively replicating. When the HBeAg is high, they are highly infectious to others. When the HBeAg is negative, but the HBeAb is positive, this implies they have been through a phase where the virus was replicating but has now stopped replicating and are less infectious.

92
Q

what is the management of hep B

A

A low threshold for screening patients at risk of hepatitis B
Screen for other viral infections (e.g., HIV, hepatitis A, C and D)
Referral to gastroenterology, hepatology or infectious diseases for specialist management
Avoid alcohol
Education about reducing transmission
Contact tracing and informing potential at-risk contacts
Testing for complications (e.g., 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 liver failure (fulminant hepatitis)

93
Q

what are the complications of hep C

A

Liver cirrhosis and associated complications of cirrhosis
Hepatocellular carcinoma

94
Q

what is the testing done for hep C

A

Hepatitis C antibody is the screening test

Hepatitis C RNA testing is used to confirm the diagnosis of hepatitis C, calculate the viral load and identify the genotype

95
Q

what is HBsAB

A

HBsAb demonstrates an immune response to HBsAg. The HBsAg is given in the vaccine, so having a positive HBsAb may indicate they have been vaccinated and created an immune response. The HBsAb may also be present in response to an infection. The other viral markers are necessary to distinguish between the presence of HBsAb due to previous vaccination and infection.

96
Q

what is HBcAb

A

HBcAb can help distinguish acute, chronic and past infections. We can measure IgM and IgG versions of the HBcAb. IgM implies an active infection and will give a high titre with an acute infection and a low titre with a chronic infection. IgG indicates a past infection where the HBsAg is negative.

97
Q

what does the vaccination for hep B involve

A

Vaccination is available and involves injecting the hepatitis B surface antigen (HBsAg). Vaccinated patients are tested for HBsAb to confirm their response to the vaccine. The vaccine requires 3 doses at different intervals. Vaccination for hepatitis B is included as part of the UK routine vaccination schedule (as part of the 6-in-1 vaccine).

98
Q
A

Year 3 (63 decks)

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