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ΩΩ 2a Bateman - Systems Based > Liver + Friends > Flashcards

Liver + Friends Flashcards

1
Q

WHAT IS LIVER CIRRHOSIS?

A

Cirrhosis is a condition that occurs as a response to liver damage

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2
Q

What is some causes of cirrhosis of the liver?

A

Alcoholic liver disease
Viral hepatitis - types B, C and delta

Metabolic:
Haemochromatosis - primary and secondary
Wilson’s disease
Alpha-1 anti-trypsin deficiency

Primary biliary cirrhosis; secondary biliary cirrhosis

Toxins/ drugs e.g. methrotrexate, amiodarone, bush tea

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3
Q

What are the symptoms of liver cirrhosis?

A

Symptoms:
Lethargy
Itch, especially in primary biliary cirrhosis
Fever
Weight loss
Swelling of abdomen and ankles.

Signs:
Jaundice
Finger clubbing
Leuconychia
Palmar erythema
Bruising
Spider naevi
Splenomegaly

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4
Q

What are some investigations for liver cirrhosis?

A

Investigations aimed at finding cause:

  • History of alcohol abuse
  • Mean cell volume, gamma GTP, serum ferritin, alpha-1 antitrypsin, ceruloplasmin
  • Viral titres and antibodies

Investigations aimed at determining severity:

  • Plasma biochemistry - clotting studies, bilirubin, AST, albumin, U+Es, glucose
  • Platelets
  • Ultrasound (for liver, spleen and ascites)
  • Liver biopsy
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5
Q

What is the treatment for liver cirrhosis?

A

There is no treatment that reverses liver cirrhosis.

There are treatments that may slow down the development of various types of liver cirrhosis, for example

  1. Alcohol abstinence for alcoholic hepatitis
  2. Venesection for haemochromatosis
  3. Steroids for autoimmune chronic active hepatitis
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6
Q

WHAT IS PORTAL HYPERTENSION?

A

The normal pressure in the venous portal system is 7-14 mm Hg.

In portal hypertension, levels may rise to 20-50 mm Hg.

In the UK, the most common cause is liver cirrhosis; worldwide, schistosomiasis is more likely.

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7
Q

What are the causes of portal hypertension?

https://www.youtube.com/watch?v=Cox6Z5pqMBo

A

Pre-hepatic
Portal vein thrombosis
Splenic vein thrombosis
Cancer compression

Hepatic
Pre-sinusoidal
Alcoholic hepatitis
Congenital hepatic fibrosis

Sinusoidal
Cirrhosis - Specific types include
Alcoholic
Viral

Post-sinusoidal
Budd-Chiari syndrome - hepatic vein thrombosis
Veno-occlusive disease
Constrictive pericarditis

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8
Q

What are the symptoms of portal hypertension?

A

Often symptomless

  1. Haematemesis or melaena - due to rupture of gastro - oesophageal varices
  2. Oedema - Peripheral or Ascites - with low plasma albumin
  3. Hepatic encephalopathy
  4. Porto-systemic shunts - e.g. caput Medusae
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9
Q

Where do varices most commly occur?

A

Gastro-oesophageal junciton

Ileocaecal junction

Rectum

Abdomen

ODG

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10
Q

What are the investivations for portal vein hypertension?

A

Low platelet
Low albumin
High bilirubin
Prolonged PT

USS abdo = nodular outline of the liver, fatty liver, reduced portal vein flow, splenomegaly ascites

Venogram - GOLD STANDARD

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11
Q

What is the management of portal hypertension?

A

Management of the bleeding

Prevention of recurrence of bleeding

Prophylaxis to prevent haemorrhage

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12
Q

How are varices formed from cirrhosis and portal hypertension?

A

Cirrhosis occurs which means less blow flow can get into liver

Pressure builds up in the veins and causes portal hypertension

Anastomosing vien take the path of lowest resistance

Flow towards the heart straight away rather than portal system

Smaller vein dilate causing varices

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13
Q

HOW DOES PORTAL HYPERTENSION CAUSE OESOPHAGAEL VARICES?

A

Oesophageal varices are varicosities of branches of the azygos vein

which anastomose with tributaries of the portal vein in the lower oesophagus, due to portal hypertension in conditions such as cirrhosis of the liver

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14
Q

What are the symptoms of oesophagael varices caused by cirhosis?

A

Haematemesis

If the varices bleed slowly then the patient may present with melaena or anaemia

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15
Q

What are the investigations for oesophagael varices?

A

Endoscopy which permits identification of the site of bleeding as well as enabling treatment, e.g. endoscopic sclerotherapy.

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16
Q

What is the management of oesophagael variceal bleeding?

A
  • *Management of variceal bleeding**
    1. Terlipressin - to suspected variceal bleeding at presentation.
  • Stop treatment after definitive haemostasis has been achieved
    2. Prophylactic antibiotics
  • *Oesophageal varices**
    1. Band ligation
    2. Transjugular intrahepatic portosystemic shunts (TIPS) if not controlled by band ligation
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17
Q

WHAT IS PRIMARY BILIARY CIRRHOSIS?

https://www.youtube.com/watch?v=CQtHOMzLzwU&t=1s

A

Primary biliary cholangitis (previously known as primary bilary cirrhosis) cirrhosis is an autoimmune disease characterised by chronic, progressive, destruction of intrahepatic bile ducts, resulting in chronic cholestasis, portal inflammation, and fibrosis which will eventually lead to cirrhosis and liver failure

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18
Q

What is the cause of PBC?

A

Unknown environmental triggers

+ Genetic predisposition (IL12A)

Leading to loss of immune tolerance to self-mitochondrial proteins.

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19
Q

What are the symptoms for primary biliary cirrhosis?

A

Mainly asymptomatic

Symptomatic
Fatigue
Pruritus

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20
Q

What are the investigations for primary biliary cirrhosis?

A

Liver function tests
Serum alkaline phosphatase ALP RAISED x3 or x4

Immunology
Anti-mitochondrial antibodies

Liver biopsy
Confirms the diagnosis but not mandatory to make the diagnosis

Imaging
MRI or endoscopic retrograde cholangiography – to exclude primary sclerosing cholangitis or other disorders that might lead to chronic cholestasis

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21
Q

What is needed for the diagnosis of primary bilary cholangitis?

A

When 2 of the 3 are met:

  1. Biochemical evidence of cholestasis based mainly on alkaline phosphatase elevation of at least 1.5 times the upper limit of normal for more than 24 weeks
  2. Presence of AMA at titres of 1:40 or higher
  3. Compatible histologic evidence - nonsuppurative destructive cholangitis and destruction of interlobular bile ducts
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22
Q

What is the treatment of primary biliary cirrhosis?

A

Symptomatic treatment
Pruritus - Cholestyramine
Fatigue doesn’t really respond to treatment

**Disease-modifying therapy**
Ursodeoxycholic acid (UDCA) - slows progression

Liver transplantation

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23
Q

WHAT IS ALCOHOLIC LIVER DISEASE?

A

Liver manifestations of alcohol overconsumption, including

Fatty liver

Alcoholic hepatitis

Fibrosis or cirrhosis

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24
Q

What are the risk factors for alcoholic liver disease?

A

Drinking pattern

Sex - Women

Genetic

Nutrition

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25
Q

What are the symptoms of alcoholic liver disease?

A

Anorexia

Morning nausea with dry retching

Darrhoea

Vague right upper quadrant abdominal pain.

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26
Q

What are the investigations for alcoholic liver disease?

A

FBC
May reveal macrocytosis

LFTs:
Raised gamma GT indicates possible alcohol abuse
Abnormal ALT reflects hepatocellular damage
An AST:ALT ratio that is greater than 2 suggests alcoholic damage

Elevated serum IgA; anti-smooth muscle antibodies may be found

Liver biopsy
Reveals extent of liver damage and suggests prognosis

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27
Q

What is the treatment of alcoholic liver disease?

A
  1. Alcoholic Steatosis
    Reversible with abstinence
  2. Alcoholic Hepatitis
    Stop drinking
    Corticosteroids to suppress immune system
    Lorazapam for alcohol withdrawal/Delierium tremens
  3. Liver Cirrhosis
    Irreversible
    Treat complications
    Transplant
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28
Q

WHAT IS HAEMOCHROMATOSIS?

https://www.youtube.com/watch?v=T7ybRVFXRD0

A

Increased intestinal iron absorption

Iron deposition in joints, liver, heart, pancreas, pituitary, adrenals and skin.

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29
Q

What is the cause of haemochromatosis?

A

Autosomal recessive

HFE gene

Chromosome 6

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30
Q

What does the excess iron cause to happen in haemochromatosis?

A

Produces ROS (reactive oxygen species) which damage the cells they are in

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31
Q

What are the symptoms of haemochromatosis?

A

Often none until after 40 years
Then non-specific e.g.
Tiredness
Arthralgia
Weight loss

In chronic disease:
Diabetes - ‘Bronze diabetes’ from iron deposition in pancreas

Dilated cardiomyopathy

Slate-grey skin pigmentation

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32
Q

What are the investigations for haemochromatosis?

A

Transferrin saturation - is the proportion of the iron transport protein transferrin that is saturated with iron
Increased

Serum ferritin
Increased

HFE genotyping

Liver biopsy

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33
Q

What is the treatment for haemochromatosis?

A
  1. Venesect (removing blood)
  2. Iron chelation therapy
    Deferoxamine OR defarasirox
    Binds iron and excretes in urine
  3. Low iron diet
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34
Q

WHAT IS ALPHA-1 ANTITRYPSIN DEFICIENCY?

A

Genetic condition when alpha-1 antitryspin is absent

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35
Q

What is the genetics of alpha-1(4)-antitrypsin?

A

Austosomal recessive / co-dominant

Chromosome 14

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36
Q

What is the pathology of alpha-1-antitrypsin deficiency?

A

Misfolded alpha-1 antitrypsin builds up in hepatocytes

Leading to cirrhosis

Results in inability to export alpha1-antitrypsin from liver

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37
Q

What are the symptoms of alpha-1 antitrypsin?

A

Jaundice

Cirrhosis

Inability to make coagulation factors

Buildup of toxins

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38
Q

What are the investigations for alpha-antitrypsin deficiency?

A

Serum alpha1-antitrypsin (1AT) levels lower

Liver biopsy
Periodic acid Schi (PAS) +ve

Diastaise resistant

Liver ultrasound

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39
Q

What is the treatment for anti-1-antitrypsin deficiency?

A

Danazol therapy - increases alpha-1-antitrypsin levels

Liver transplant

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40
Q

WHAT IS WILSON’S DISEASE?

https://www.youtube.com/watch?v=Cr8R_bnKAtk

A

Too much copper (Cu) in liver and CNS

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41
Q

What type of gene disease is Wilson’s disease?

A

Autosomal recessive

Chromosome 13

Codes for a copper transporting ATPase

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42
Q

What is the pathology of Wilson’s disease?

A

In the liver, copper is incorporated into caeruloplasmin.

Copper incorporation into caeruloplasmin in hepatocytes
and its excretion into bile are impaired.

Therefore, copper accumulates in liver, and later in other organs.

ROS made and damage liver

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43
Q

What are the symptoms of Wilson’s disease?

A

Kayser–Fleischer (KF) rings
Copper in iris

Neurological signs - parkinsonian tremor, dysarthria
Due to copper in CNS

Liver failure

Hepatosplenogmegaly

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44
Q

What are the investigations for Wilson’s disease?

A

Urine Copper + Free Copper
HIGH

Total serum copper + serum caeruloplasmin
LOW

Molecular genetic testing can confirm the diagnosis.

Liver biopsy
Increase Hepatic copper

MRI
Degeneration of brain

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45
Q

What is the management of Wilson’s disease?

A

Penicillamine
Bind copper, easier to excrete

Zinc
Decrease copper reabsorption

Liver transplantation
If severe

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46
Q

WHAT IS ASCITES?

A

Abnormal accumulation of fluid in the abdominal (peritoneal) cavity

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47
Q

What are the causes of ascites?

A

Liver cirrhosis

Intra-abdominal malignancy

Nephrotic syndrome

Constrictive pericarditis

Meig’s syndrome

Budd-Chiari syndrome

Tuberculous peritonitis

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48
Q

What are the symptoms of ascties?

A

Rapid weight gain

Abdominal swelling

Sacral oedema

Ankle swelling

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49
Q

What are the differential diagnosis of ascites?

A

5 F’s

Fat

Feaces

Flatus

Fetus

Fliipin big tumour

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50
Q

What are the investigations for ascites?

A

Ultrasound

Diagnostic paracentesis - in which 30 to 50 ml of fluid is withdrawn. This will enable identification of:
Protein content: albumin and total protein
Malignant cells
Bacteria
White blood cells
Glucose

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51
Q

What is the managent of ascites?

A

Tense ascites
Therapeutic paracentesis of 4-6 litres
Plasma volume expansion with albumin is used by many at the same time as therapeutic paracentesis

Non-tense ascites
Treat cause
Limit dietary sodium intake
Diuretics - Spironolactone
Therapeutic paracentesis
Surgical shunts

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52
Q

WHAT IS APPENDICITIS?

https://www.youtube.com/watch?v=r9amif1DQMc

A

Inflammation of the appendix

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53
Q

Where is the appendix?

A

Connected to the cecum

Also known as veriform appendix (worm shaped)

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54
Q

What are the causes of appendicits?

A

Obstruction
From

Feacalith

Undigested seeds

Pinworm infection

Lymphoid follicle growth
Collection of lymphocytes become maximum size in adolesence

Viral infection caues follicle growth

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55
Q

What bacteria become trapped and what happens as a result?

A

E.Coli
Bacteriodes fragilis

Immune cells calls WBC

Pus builds up in appendix

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56
Q

What are the symptoms of appendicits?

A

Abdo pain

  1. Left upper quadrant to start - colicky if obstructive in nature
  2. After 2-3 days the pain shifts to the right iliac fossa and is intense and continuous

Patient wishes to lie still, often with legs drawn up

Nausea and vomiting after the onset of pain

loss of appetite - often precedes the pain by a few hours - a reasonably sensitive symptom

57
Q

What are the signs of peritonitis from appendicitis?

A

Flushed

Fever

Tachycardia

Rebound tenderness

Abdominal guarding

Tenderness over McBurney’s point
Right iliac fossa

58
Q

What are the investigations for appendicitis?

A

Inclusion
Full blood count - leukocytosis is generally present

Urea and electrolytes - assessment of dehydration

Exclusion
Pregnancy test

Serum amylase - if pancreatitis suspected

Abdominal radiology - helpful to distinguish:
Volvulus
Intussusception
Renal stones (90%)

59
Q

What is the treatment for appendicitis?

A

Appendectomy

Antibiotics
Cefuroxime and metronidazole IV

Drain abscess

60
Q

WHAT IS PANREATITIS?

A

Pancreatitis is an inflammatory disorder of the pancreas.

61
Q

What is acute pancreatitis?

62
Q

What is the cause of acute pancreatitis?

A

Idiopathioc

Gallstone
Ethanol
Trauma

  • *S**teroids
  • *M**umps/Malignancy
  • *A**utoimmune
  • *S**corpion Sting
  • *H**yperglyceamia
  • *E**RCP
  • *D**rugs (Azathioprine)
63
Q

What are the clinical features of acute pancreatitis?

A

Symptoms

  1. Upper abdominal pain - upper left quadrant, periumbilical region, and/or epigastrum
  2. May radiate to back
  3. Nausea and vomiting
  4. Shoulder tip pain referral
  5. Indigestion, abdominal fullness

Signs

  1. Jaundice
  2. Gray-Turner’s sign - ecchymosis of the flank and Cullen sign - ecchymoses in the periumbilical region
64
Q

What is need for the diagnosis of acute pancreatitis?

A

Abdominal pain
Acute onset of a persistent, severe, epigastric pain often radiating to the back)

Serum lipase activity (or amylase activity)
x3 greater than the upper limit of normal

Contrast-enhanced computed tomography (CECT)
Characteristic findings of acute pancreatitis on

65
Q

What is the management of acute pancreatitis?

A

Fluid management
Hartmann’s solution
2.5-4 litres in 24 hours

Analgesia

Nutritional support

Surgery if necessary
ERCP
Cholecystectomy

66
Q

What is chronic pancreatitis?

A

Chronic pancreatitis is characterised by irreversible glandular destruction and permanent loss of endocrine and exocrine function. It may follow episodes of acute pancreatitis or may occur without an identifiable attack.

67
Q

What is the cause of chronic pancreatitis?

A

Alcohol

Cystic fibrosis

Hypercalcaemia

Idiopathic

68
Q

What are the symptoms of chronic pancreatitis?

A

Abdominal pain
Mainly epigastric and upper abdominal; may radiate to the back

anorexia and weight loss
Due to malabsorption and / or small meals

Features of exocrine insufficiency
Steatorrhoea
Hypocalcaemia

Features of endocrine insufficiency
Impaired glucose tolerance

69
Q

What are the investigations for chronic pancreatitis?

A

Endoscopic retrograde cholangiopancreatography (ERCP)

  1. Gold standard - reveals duct dilatation and distortion of main pancreatic duct and side branches

Blood tests

  1. Albumin and clotting studies - cirrhosis or malabsorption
  2. Low calcium or serum vitamin B12 - malabsorption
  3. Elevated alkaline phosphatase ALP - biliary tract obstruction if gamma GT is raised, or rarely, osteomalacia

Imaging

  1. Abdo X-ray - calcification
  2. Ultrasound - gallstones
70
Q

What is the treatment of chronic pancreatitis?

A

Underlying cause treated

Conservative management

Dietitian assessment

Stop drinking alcohol

71
Q

WHAT ARE GALLSTONES MADE UP OF?

A

70% cholesterol, 30% pigment(mainly bilirubin) +/- calcium.

Pigment stones:
Small.
Causes: haemolysis.

Cholesterol stones:
Large.
Causes: gender, age, obesity

Mixed stones: Faceted (calcium salts, pigment, and cholesterol).

72
Q

WHAT ARE GALLSTONES?

A

Gallstones are calculi formed in the gallbladder or bile duct

73
Q

What are the risk factors for gallstones?

A

Fair

Fat

Fertile

Female of forty

74
Q

What are the symptoms of gallstones?

A

Asymptomatic
Approximately 50-70% of patients with gallstones are asymptomatic at the time of diagnosis (1)

Usually patients becomes symptomatic after many years, once stones reach a certain size (>8mm) (1)

Can lead to:
Biliary Colic
Acute Cholecystits

75
Q

What are the investigations for gallstones?

A

Ultrasound

Oral Cholecystogram

ERCP

76
Q

What is the management for gallstones?

A

Non surgical
Analgesia, adequate hydration and antibiotics
Diclofenac and an opioid (morphine or pethidine) used in combination or separately are effective

Surgical
Cholecystectomy

77
Q

WHAT IS BILIARY COLIC?

A

Biliary colic is the term applied to the system complex occuring when there is sudden and complete obstruction of the cystic duct by gall stone

78
Q

What are the symptoms of biliary colic?

A

Biliary colic is felt in the right upper quadrant but epigastric and left abdominal pain are common, and some patients experience praecordial pain

The pain is severe and steady. It usually begins abruptly and subsides gradually, lasting from a few minutes to several hours and often occurring postprandially.

There may be nausea and often a bout of vomiting signifies the end of an attack.

79
Q

What are the investigations for biliary colic?

80
Q

What is the treatment for biliary colic?

A

Many cases of biliary colic can safely be managed at home.

First line treatment is a NSAID

Opioids

81
Q

What is spider naevus? Why is it important?

A

Swollen blood vessels below the skin. Extensive could indicate liver disease.

82
Q

What are some risk factors for gallstones?

A

Female

Fat

Forty

Fertile.

83
Q

Compare gallstones for the gallbladder and bile duct locations?

Biliary pain.

Cholecystitis.

Obstructive jaundice.

Cholangitis.

Pancreatitis.

A

Gallbladder Bile Duct

Biliary pain. Yes Yes

Cholecystitis (inflammation of gall bladder). Yes No

Obstructive jaundice. Maybe Yes

Cholangitis (infection of bile duct). No Yes

Pancreatitis. No Yes

84
Q

WHAT IS CHOLECYSTITIS?

A

Cholecystitis is inflammation of the gallbladder.

85
Q

What happens when somebody eats some food containing a lot of fat?

A

The small intestine secretes CCK which travels in the blood to cause the gallbladder to contract and release bile.

86
Q

What is the pathology of cholecystitis?

A

Stone stuck in cystic duct

Causes stretching out of gall bladder

Irritates nerves around the gall bladder (pain)

Bile stays in gall bladder causing release of mucus and inflammatory mediators

Results in inflammation and pressure increase

Bacteria start to build up

Pressure builds up and bacteria go through wall causing peritonitis (rebound tenderness)

Immune system starts response with neutrophils

87
Q

What are the symptoms of cholecystitis?

A

Right midepigastric pain at first

Then RUQ pain (referred to the right shoulder)

Vomiting

Fever

Local peritonism, or a GB mass.

88
Q

What is Murphy’s sign?

A

Lay 2 fingers over the RUQ; ask patient to breathe in. This causes pain & arrest of inspiration as an inflamed GB impinges on your fingers. It is only +ve if the same test in the LUQ does not cause pain.

89
Q

What are the investigations for cholecystitis?

A

1st line - Ultrasound

2nd line - Radio-isotpic scanning - HIDA scanning

MRCP

FBC - usually a leukocytosis

Liver function test - to detect any obstructive jaundice

90
Q

What is needed for the radiological diagnosis of cholecystitis?

A
  1. Thickening of the gallbladder wall (5 mm or greater)
  2. Pericholecystic fluid
  3. Ultrasonographic Murphy’s sign
    - Pain which occurs when the probe is pushed against the gallbladder
    - Is superior to ordinary Murphy’s sign
91
Q

How do you diagnose cholecystitis?

A
  1. Local signs of inflammation
    Murphy’s sign,RUQ mass/pain/tenderness
  2. Systemic signs of inflammation
    Fever, elevated CRP, elevated WBC count
  3. Imaging findings:
    Ultrasound
92
Q

What is the treatment for cholecystitis?

A

Acute
Analgesia - NSAIDs and opiates
Anti-emetics
IV fluids
Antibiotics- IV Co-amoxiclav

Laparoscopic cholecystectomy

Chronic

Laparoscopic cholecystectomy

93
Q

WHAT IS ASCENDING CHOLANGITIS?

A

Acute cholangitis is acute inflammation and infection of the biliary tract

94
Q

What happens in ascending cholangitis?

A

The flow of bile prevents intestinal bacteria from migrating up the biliary tree and this process can be stopped due to several factors:

Choledocholithiasis - gallstone

Benign biliary stricture

congenital factors

inflammatory factors (oriental cholangitis, etc.)

Malignant occlusion - bile duct tumor, gallbladder tumor, ampullary tumor, pancreatic tumor

95
Q

What are the common bugs for ascending cholangitis?

A

E. coli

Klebsiella

Enterococcus (group D strep)

96
Q

What are the symptoms for ascending cholangitis?

A

Charcot’s Triad

Fever, RUQ pain, Jaundice

Reynold’s Pentad

Hypotension + confusion

97
Q

What tests can you do for ascending cholangitis?

A

USS abdomen

Endoscopic retrograde cholangiopancretography - ERCP

Blood tests
FBC
Urea and electrolytes

98
Q

How is ascending cholangitis diagnosed?

A

A. Systemic inflammation
A-1. Fever and/or shaking chills
A-2. Laboratory data: evidence of inflammatory response

B. Cholestasis
B-1. Jaundice
B-2. Laboratory data: abnormal liver function tests

C. Imaging
C-1. Biliary dilatation
C-2. Evidence of the etiology on imaging (stricture, stone, stent etc.)

Suspected diagnosis: one item in A + one item in either B or C

Definite diagnosis: one item in A, one item in B and one item in C

99
Q

What are the treatment options for ascending cholangitis?

A

ERCP (Endoscopic Retrograde Cholangio-Pancreatography)
Remove stone

Surgery

Antibiotics for bacterial cholangitis
Cephalosporin + Metronidazole

100
Q

WHAT IS HEPATIC ENCHEPHALOPATHY?

A

Hepatic encephalopathy (HE) is a metabolic disorder of the central nervous system and neuromuscular system that occurs in decompensated cirrhosis.

101
Q

What is this cause of hepatic enchephalopathy?

A

Liver’s failure to remove toxic metabolites from the portal blood
Ammonia, amino acids, short chain fatty acids and amines

Due to:

Acute liver failure

Hepatic cirrhosis

Portosystemic shunt operations

102
Q

What are the symptoms of hepatic enchephalopathy?

A

Psychomotor slowing - is the first neuropsychological feature seen in HE patients.

Subtle cognitive impairment and difficulties in concentration

Trivial lack of awareness

Euphoria or anxiety

Reversal of the sleep-wake cycle – early sign in some patients

Agitation and aggression can progress to acute confusion leading to progressive stupor and coma.

Asterixis ( “liver flap”)

103
Q

What are the investigations for hepatic enchephalopathy?

A

Psychometric tests
Used for diagnosis of covert hepatic encephalopathy
Considered in patients with known or suspected liver cirrhosis

EEG
May show findings e.g- triphasic waves
It is nonspecific and may be influenced by accompanying metabolic disturbances, such as hyponatremia as well as drugs

CT or MRI
Should be carried out in all suspected HE patients to rule out other conditions such as intracranial haemorrhage or space occupying lesions

104
Q

What is the management for hepatic enchephalopathy?

A

First step in management
Address underlying precipitants of encephalopathy - such as hypoglycaemia, hypoxia, haemorrhage, sepsis, drug toxicity, or electrolyte disturbance, should be corrected.

  • *Laxatives and antibiotics**
    1. Lactulose- Reduces pH and excretion of ammonia as well as the utilisation of ammonia in the metabolism of gut bacteria
    2. Refaximin - Decreases intestinal production and absorption of ammonia
105
Q

WHAT IS PRIMARY SCLEROSIS CHOLANGITIS?

https://www.youtube.com/watch?v=ycDfF0EJssY

A

Fibrosing of intra-hepatic and extra-hepatic duct

No continous

Onion skin fibrosis

106
Q

What is PSC associated with?

A
  1. Complication of cholangiocarcinoma
  2. Correlation with ulcerative colitis
107
Q

What happens in PSC?

A

Autoimmune destruction of cells lining bile duct

108
Q

What autoanitbody is PSC associated with?

109
Q

How does PSC present?

A

Leads to strictures (areas of narrowing) ± gallstones

  1. Itching
  2. Pain ± rigors
  3. Jaundice
110
Q

What are the tests for PSC?

A

Blood: increased Alk phos, increased gammaGT, and mildly increased AST & ALT.

Late disease
Increased bilirubin, decreased albumin, increased prothrombin time.

Immunoglobulins
pANCA and IgM

TSH & cholesterol increased or same

Ultrasound
Excludes extrahepatic cholestasis.

111
Q

What is the treatment for PSC?

A
  1. Colestyramine for pruritus
  2. Vitamin ADEK supplementation since they are fat soluble
112
Q

WHAT IS NON-ALCOHOLIC FATTY LIVER DISEASE?

A

Results from fat deposition in the liver not from alcohol

113
Q

What are the risk factors for non-alcoholic liver?

A

Obesity

Hypertension

Diabetes

Hypertriglyceridemia

Hyperlipidaemia

114
Q

How does non-fatty liver disease cause damage?

A

Production of ROS

115
Q

What are the symptoms of non-alcoholic liver?

A

Usually asymptomatic

Hepatomegaly

116
Q

What investigations can you do for non-alcoholic liver?

A
  1. LFTs
  2. ALT > AST
  3. GGT often normal
  4. Fat, sometimes with inflammation, fibrosis (NASH)
117
Q

How can you treat non-alcoholic liver?

A

Still no effective drug treatments

Wt loss works- the more the better

118
Q

WHAT IS ACUTE LIVER FAILURE?

A

Acute hepatic failure occurs when there is a massive loss of hepatocytes.

It is defined as severe hepatic dysfunction occuring within 6 months of the onset of symptoms of liver disease, with a clinical manifestation of hepatic encephalopathy or coagulopathy.

119
Q

What are some causes of acute liver failure?

A
  1. Paracetamol poisoning
  2. Viral hepatitis
  3. Drug reactions
    Halothane
    Isoniazid
    Methyldopa
    Phenytoin
  4. Alcohol
120
Q

What are the clinical features of acute liver failure?

A

The patient is jaundiced.

Other primary features of hepatic failure can be divided into:

CNS complications

renal failure

sepsis

coagulopathy

cardiovascular complications

metabolic complications

121
Q

What are some investigations for acute liver failure?

A

Blood tests:
Coagulation studies, glucose, and potassium as soon as possible
Full blood count, group and save, bilirubin, albumin, AST, amylase
Hepatitis serology, paracetamol levels, serum copper and
Caeruloplasmin, plus 24 hour copper where appropriate

Radiology:
Chest radiograph
Ultrasound scan of liver and pancreas

122
Q

What is the treatment for acute liver failure?

A

Intensive care situation nursing - transfer to specialist centre to ensure optimal treatment

Monitor hourly the blood glucose, urine output, vital signs

Monitor twice daily the potassium, full blood count, creatinine, albumin, coagulation

Do not administer IV saline - there is a secondary hyperaldosteronism in hepatic failure which causes retention of sodium

123
Q

WHAT IS HEPATORENAL SYNDROME?

A

Purely ‘‘functional” type of renal failure that often occurs in patients with cirrhosis in the setting of marked abnormalities in arterial circulation, as well as overactivity of the endogenous vasoactive systems.

124
Q

What are the two types of hepatorenal syndrome?

A

Type 1
Defined as rapid reduction of renal function by doubling of initial serum creatinine to a concentration of at least 2.5 mg/dL or a 50% reduction in less than two weeks in the initial 24 hour creatinine clearance to below 20 mL/min, or,

Type 2
Which renal failure progression did not meet the criteria for type I

125
Q

Why is hepatorenal syndrome different from an AKI?

A

In contrast to other causes of acute kidney injury (AKI), hepatorenal syndrome results from functional changes in the renal circulation and is potentially reversible with liver transplantation or vasoconstrictor drugs

126
Q

What is the management of hepatorenal syndrome?

A

Avoidance of hypotension, nephrotoxic drugs, excessive diuretic therapy or paracentesis

Promptly treatment of sepsis

Maintenance of diuresis before and after any surgery

127
Q

WHAT IS THE MOST COMMON CANCER OF THE LIVER?

A

The most usual form of liver cancer is the result of secondaries; however of those cancers arising primarily in the liver, hepatoma accounts for over 90%.

The distribution of hepatocellular carcinoma is linked to that of hepatitis B virus.

128
Q

What are the causes of liver cancer?

A

In 80% of cases there is some existing liver cirrhosis

Other causes of primary liver cancer include:
Chronic HBV or HCV carriage
Cirrhosis of any cause but especially alpha-1 antitrypsin deficiency, haemochromatosis, primary biliary cirrhosis

129
Q

What are the clinical features of liver cancer?

A

General - malaise, fatigue

Gastrointestinal - anorexia, jaundice, constipation, ill-defined upper abdominal pain, abdominal fullness, bleeding oesophageal varices

Hepatomegaly - liver is often irregular or nodular, and may be tender

Ascites

Dyspnoea - a late finding; may indicate diaphragmatic involvement or compression, or pulmonary metastases

130
Q

What are the investigations for liver cancer?

A

Biochemical
Raised alkaline phosphatase
Serum transaminases

Haematologic
Raised whtie cell count
Raised platelet count

Serology
Alpha-feto protein

131
Q

What is the treatment for liver cancer?

A

Resection

Ablation

Transplantation

132
Q

WHAT IS THE CAUSE OF PANCREATIC CARCINOMA?

133
Q

What are the risk factors for the development of pancreatic carcinoma?

A

Smoking

Alcohol

Increased BMI

Diabetes

Chronic pancreatitis

134
Q

What type of cancers are pancreatic carcinoma?

A

Adenocarcinomas

135
Q

What are the clinical features of pancreatic cancer?

A

Abdominal pain

Jaundice

Unexplained weight loss

136
Q

What are the investigations for pancreatic cancer?

A

FBC

Tumour markers

Imaging
Abdo ultrasound

ERCP

Diagnosis - CT

137
Q

What is the treatment for pancreatic cancer?

A

Pancreaticoduodenectomy

138
Q

HOW ARE DIFFERENT HEPATITS TRANSMITTED?

A

Faeco-oral route cause a self-limiting disease:

Hepatitis A virus

Hepatitis E virus

Hepatitis viruses which are transmitted parenterally more commonly cause chronic complications:

Hepatitis B virus

Hepatitis C virus

Hepatitis D virus

GB viruses

ΩΩ 2a Bateman - Systems Based (11 decks)

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