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ΩΩ 4 Bateman - Specialities + Endo + GI + Liver > 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
  1. Traditionally a liver biopsy was used. This procedure is however associated with adverse effects such as bleeding and pain
  2. Other techniques such as transient elastography and acoustic radiation force impulse imaging are increasingly used and were recommended by NICE in their 2016 guidelines
  3. for patients with NAFLD, NICE recommend using the enhanced liver fibrosis score to screen for patients who need further testing

Prothrombin time (PT) predicts liver failure

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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
  1. Pre-hepatic
    • Portal vein thrombosis
    • Splenic vein thrombosis
    • Cancer compression
  2. Hepatic
    • Alcoholic hepatitis
    • Congenital hepatic fibrosis
    • Cirrhosis - Specific types include
    • Alcoholic
    • Viral
  3. 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 investigations for portal vein hypertension?

A
  1. Venogram - GOLD STANDARD
  2. USS abdo = nodular outline of the liver, fatty liver, reduced portal vein flow, splenomegaly ascites
  3. Low platelet
  4. Low albumin
  5. High bilirubin
  6. Prolonged PT
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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
  1. Cirrhosis occurs which means less blow flow can get into liver
  2. Pressure builds up in the veins and causes portal hypertension
  3. Anastomosing vien take the path of lowest resistance
  4. Flow towards the heart straight away rather than portal system
  5. Smaller vein dilate causing varices
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13
Q

What is the prophylaxis for a variceal haemorrhage?

A
  1. Propranolol: reduced rebleeding and mortality compared to placebo
  2. Endoscopic variceal band ligation (EVL) is superior to endoscopic sclerotherapy
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14
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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15
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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16
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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17
Q

What is the management of ruptured 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. Sengstaken-Blakemore tube if uncotrlled variceal haemorrhage
  3. Transjugular intrahepatic portosystemic shunts (TIPS) if not controlled by band ligation
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18
Q

WHAT IS PRIMARY BILIARY CIRRHOSIS/CHOLANGITIS?

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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19
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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20
Q

What are the symptoms for primary biliary cirrhosis/cholangitis?

A

Mainly asymptomatic

Symptomatic
Fatigue
Pruritus

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21
Q

What are the investigations for primary biliary cirrhosis?

A
  1. Liver function tests
    • Serum alkaline phosphatase ALP RAISED x3 or x4
  2. Immunology
    • Anti-mitochondrial antibodies
  3. Liver biopsy
    • Confirms the diagnosis but not mandatory to make the diagnosis
  4. Imaging
    • MRI or endoscopic retrograde cholangiography – to exclude primary sclerosing cholangitis or other disorders that might lead to chronic cholestasis
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22
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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23
Q

What is the treatment of primary biliary cirrhosis?

A
  1. Symptomatic treatment
    • Pruritus - Cholestyramine
    • Fatigue doesn’t really respond to treatment
  2. Disease-modifying therapy
    • Ursodeoxycholic acid (UDCA) - slows progression
  3. Liver transplantation
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24
Q

WHAT IS ALCOHOLIC LIVER DISEASE?

A
  1. Liver manifestations of alcohol overconsumption, including
  2. Fatty liver
  3. Alcoholic hepatitis
  4. Fibrosis or cirrhosis
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25
Q

What are the risk factors for alcoholic liver disease?

A
  1. Drinking pattern
  2. Sex - Women
  3. Genetic
  4. Nutrition
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26
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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27
Q

What are the investigations for alcoholic liver disease?

A
  1. FBC
    • May reveal macrocytosis
  2. 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
  3. Liver biopsy
    • Reveals extent of liver damage and suggests prognosis
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28
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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29
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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30
Q

What is the cause of haemochromatosis?

A
  1. Autosomal recessive
  2. HFE gene
  3. Chromosome 6
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31
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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32
Q

What are the symptoms of haemochromatosis?

A

Often none until after 40 years

  1. Then non-specific e.g.
  2. Tiredness
  3. Arthralgia
  4. Weight loss

In chronic disease:

  1. Diabetes - ‘Bronze diabetes’ from iron deposition in pancreas
  2. Dilated cardiomyopathy
  3. Slate-grey skin pigmentation
  4. Erectile dysfunction
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33
Q

What are the investigations for haemochromatosis?

A
  1. FIRST LINE - Transferrin saturation - Is the proportion of the iron transport protein transferrin that is saturated with iron
    • Increased
  2. Serum ferritin
    • Increased
  3. Total iron bind capacity
    • Reduced
  4. HFE genotyping
  5. Liver biopsy
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34
Q

What is the treatment for haemochromatosis?

How is this monitored?

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

Ferritin and transferrin saturation

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35
Q

WHAT IS ALPHA-1 ANTITRYPSIN DEFICIENCY?

A

Genetic condition when alpha-1 antitryspin is absent

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36
Q

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

A

Austosomal recessive / co-dominant

Chromosome 14

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37
Q

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

A
  1. Misfolded alpha-1 antitrypsin builds up in hepatocytes
  2. Leading to cirrhosis
  3. Results in inability to export alpha1-antitrypsin from liver
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38
Q

What are the symptoms of alpha-1 antitrypsin?

A
  1. Jaundice
  2. Cirrhosis
  3. Inability to make coagulation factors
  4. Buildup of toxins
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39
Q

What are the investigations for alpha-antitrypsin deficiency?

A
  1. Serum alpha1-antitrypsin (1AT) levels lower
  2. Liver biopsy
    • Periodic acid Schi (PAS) +ve
    • Diastaise resistant
  3. Liver ultrasound
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40
Q

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

A
  1. Danazol therapy - increases alpha-1-antitrypsin levels
  2. Liver transplant
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41
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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42
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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43
Q

What is the pathology of Wilson’s disease?

A
  1. In the liver, copper is incorporated into caeruloplasmin.
  2. Copper incorporation into caeruloplasmin in hepatocytes and its excretion into bile are impaired.
  3. Therefore, copper accumulates in liver, and later in other organs.
  4. ROS made and damage liver
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44
Q

What are the symptoms of Wilson’s disease?

A
  1. Kayser–Fleischer (KF) rings
    • Copper in iris
  2. Neurological signs - parkinsonian tremor, dysarthria
    • Due to copper in CNS
  3. Liver failure
  4. Hepatosplenogmegaly
  5. Blue nails
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45
Q

What are the investigations for Wilson’s disease?

A
  1. Urine Copper + Free Copper
    • HIGH
  2. Total serum copper + serum caeruloplasmin
    • LOW
    • Molecular genetic testing can confirm the diagnosis
  3. Slit lamp examination for Kayser-Fleischer rings
  4. Liver biopsy
    • Increase Hepatic copper
  5. MRI
    • Degeneration of brain
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46
Q

What is the management of Wilson’s disease?

A
  1. Penicillamine
    • Bind copper, easier to excrete
  2. Zinc
    • Decrease copper reabsorption
  3. Liver transplantation
    • If severe
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47
Q

WHAT IS ASCITES?

A

Abnormal accumulation of fluid in the abdominal (peritoneal) cavity

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48
Q

What are the causes of ascites?

A
  1. Liver cirrhosis
  2. Intra-abdominal malignancy
  3. Nephrotic syndrome
  4. Constrictive pericarditis
  5. Meig’s syndrome
  6. Budd-Chiari syndrome
  7. Tuberculous peritonitis
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49
Q

What are the symptoms of ascties?

A
  1. Rapid weight gain
  2. Abdominal swelling
  3. Sacral oedema
  4. Ankle swelling
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50
Q

What are the differential diagnosis of ascites?

A

5 F’s

Fat

Feaces

Flatus

Fetus

Fliipin big tumour

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51
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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52
Q

What is the managent of ascites?

A

Tense ascites

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

Non-tense ascites

  1. Treat cause
  2. Limit dietary sodium intake if sodium <125 mmol/L
  3. Diuretics - Spironolactone
  4. Therapeutic paracentesis
  5. Surgical shunts
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53
Q

WHAT IS APPENDICITIS?

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

A

Inflammation of the appendix

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54
Q

Where is the appendix?

A

Connected to the cecum

Also known as veriform appendix (worm shaped)

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55
Q

What are the causes of appendicits?

A

Obstruction

  1. Feacalith
  2. Undigested seeds
  3. Pinworm infection
  4. Lymphoid follicle growth
  5. Collection of lymphocytes become maximum size in adolesence
  6. Viral infection caues follicle growth
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56
Q

What bacteria become trapped in appendicitis and what happens as a result?

A

E.Coli
Bacteriodes fragilis

Immune cells calls WBC

Pus builds up in appendix

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57
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

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58
Q

What are the signs of peritonitis from appendicitis?

A
  1. Flushed
  2. Fever
  3. Tachycardia
  4. Rebound tenderness
  5. Abdominal guarding
  6. Tenderness over McBurney’s point
  7. Right iliac fossa
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59
Q

What are the investigations for appendicitis?

A

Inclusion

  1. Full blood count - leukocytosis is generally present
  2. Urea and electrolytes - assessment of dehydration

Exclusion

  1. Pregnancy test
  2. Serum amylase - if pancreatitis suspected
  3. Abdominal radiology - helpful to distinguish:
  4. Volvulus
  5. Intussusception
  6. Renal stones (90%)
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60
Q

What is the treatment for appendicitis?

A
  1. Laproscopic Appendectomy
  2. Antibiotics prior to surgery
    • Cefuroxime and metronidazole IV
  3. Drain abscess
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61
Q

WHAT IS PANREATITIS?

A

Pancreatitis is an inflammatory disorder of the pancreas.

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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
  1. Abdominal pain
    • Acute onset of a persistent, severe, epigastric pain often radiating to the back)
  2. Serum lipase activity (or amylase activity)
    • x3 greater than the upper limit of normal
  3. 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
  1. Alcohol
  2. Cystic fibrosis
  3. Hypercalcaemia
  4. 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
  1. Fair
  2. Fat
  3. Fertile
  4. 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
  1. Ultrasound
  2. Oral Cholecystogram
  3. 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
  1. Biliary colic is felt in the right upper quadrant but epigastric and left abdominal pain are common, and some patients experience praecordial pain
  2. 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.
  3. 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?

A
  1. Ultrasound
80
Q

What is the treatment for biliary colic?

A

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

  1. First line treatment is a NSAID
  2. 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

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 Yes No

Obstructive jaundice. Maybe Yes

Cholangitis No Yes

Pancreatitis No Yes

83
Q

WHAT IS CHOLECYSTITIS?

A

Cholecystitis is inflammation of the gallbladder.

84
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.

85
Q

What is the pathology of cholecystitis?

A
  1. Stone stuck in cystic duct
  2. Causes stretching out of gall bladder
  3. Irritates nerves around the gall bladder (pain)
  4. Bile stays in gall bladder causing release of mucus and inflammatory mediators
  5. Results in inflammation and pressure increase
  6. Bacteria start to build up
  7. Pressure builds up and bacteria go through wall causing peritonitis (rebound tenderness)
  8. Immune system starts response with neutrophils
86
Q

What are the symptoms of cholecystitis?

A
  1. Right midepigastric pain at first
    • Then RUQ pain (referred to the right shoulder)
  2. Vomiting
  3. Fever
  4. Local peritonism, or a GB mass.
87
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.

88
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

89
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
90
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
91
Q

What is the treatment for cholecystitis?

A
  1. Acute
    • Analgesia - NSAIDs and opiates
    • Anti-emetics
    • IV fluids
    • Antibiotics- IV Co-amoxiclav
    • Laparoscopic cholecystectomy
  2. Chronic
    • Laparoscopic cholecystectomy
92
Q

What is a complication of cholecystectomy?

A

Bile-acid malabsorption

93
Q

What are the investigations for bile-acid malabsorption?

A
  1. The test of choice is SeHCAT
  2. Nuclear medicine test using a gamma-emitting selenium molecule in selenium homocholic acid taurine or tauroselcholic acid (SeHCAT)
  3. Scans are done 7 days apart to assess the retention/loss of radiolabelled 75SeHCAT
94
Q

What is the treatment for bile-acid malabsorption?

A
  1. Bile acid sequestrants e.g. cholestyramine
95
Q

WHAT IS ASCENDING CHOLANGITIS?

A

Acute cholangitis is acute inflammation and infection of the biliary tract

96
Q

What happens in ascending cholangitis?

A
  1. 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
97
Q

What are the common bugs for ascending cholangitis?

A

E. coli

Klebsiella

Enterococcus (group D strep)

98
Q

What are the symptoms for ascending cholangitis?

A

Charcot’s Triad

Fever, RUQ pain, Jaundice

Reynold’s Pentad

Hypotension + confusion

99
Q

What tests can you do for ascending cholangitis?

A
  1. USS abdomen
  2. Endoscopic retrograde cholangiopancretography - ERCP
  3. Blood tests
    • FBC
    • Urea and electrolytes
100
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 - ULTRASOUND
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

101
Q

What are the treatment options for ascending cholangitis?

A
  1. ERCP (Endoscopic Retrograde Cholangio-Pancreatography)
    • Remove stone
  2. Surgery
  3. Antibiotics for bacterial cholangitis
    • Cephalosporin + Metronidazole
102
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.

103
Q

What is this cause of hepatic enchephalopathy?

A

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

Due to:

  1. Acute liver failure
  2. Hepatic cirrhosis
  3. Portosystemic shunt operations
104
Q

What are the symptoms of hepatic enchephalopathy?

A
  1. Psychomotor slowing - is the first neuropsychological feature seen in HE patients.
  2. Subtle cognitive impairment and difficulties in concentration
  3. Trivial lack of awareness
  4. Euphoria or anxiety
  5. Reversal of the sleep-wake cycle – early sign in some patients
  6. Agitation and aggression can progress to acute confusion leading to progressive stupor and coma.
  7. Asterixis ( “liver flap”)
105
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

106
Q

What is the management for hepatic enchephalopathy?

A

First step in management

  1. 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. Rifaximin - Decreases intestinal production and absorption of ammonia
107
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

108
Q

What is PSC associated with?

A
  1. Complication of cholangiocarcinoma
  2. Correlation with ulcerative colitis
109
Q

What happens in PSC?

A

Autoimmune destruction of cells lining bile duct

110
Q

What autoanitbody is PSC associated with?

111
Q

How does PSC present?

A

Leads to strictures (areas of narrowing) ± gallstones

  1. Itching
  2. Pain ± rigors
  3. Jaundice
112
Q

What are the tests for PSC?

A
  1. MRCP - FIRST LINE
  2. ERCP
  3. Blood:
    • Increased Alk phos, increased gammaGT, and mildly increased AST & ALT.
  4. Late disease
    • Increased bilirubin, decreased albumin, increased prothrombin time.
  5. Immunoglobulins
    • pANCA and IgM
    • TSH & cholesterol increased or same
  6. Ultrasound
    • Excludes extrahepatic cholestasis.
113
Q

What is the treatment for PSC?

A
  1. Colestyramine for pruritus
  2. Vitamin ADEK supplementation since they are fat soluble
114
Q

WHAT IS NON-ALCOHOLIC FATTY LIVER DISEASE?

A

Results from fat deposition in the liver not from alcohol

115
Q

What are the risk factors for non-alcoholic liver?

A
  1. Obesity
  2. SUDDEN WEIGHT LOSS
  3. Hypertension
  4. Diabetes
  5. Hypertriglyceridemia
  6. Hyperlipidaemia
116
Q

How does non-fatty liver disease cause damage?

A

Production of ROS

117
Q

What are the symptoms of non-alcoholic liver?

A

Usually asymptomatic

Hepatomegaly

118
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)
119
Q

How can you treat non-alcoholic liver?

A
  1. Still no effective drug treatments
  2. Wt loss works- the more the better
120
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.

121
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
122
Q

What are the clinical features of acute liver failure?

A
  1. Jaundice
  2. Coagulopathy: raised prothrombin time
  3. Hypoalbuminaemia
  4. Hepatic encephalopathy
  5. Renal failure is common (‘hepatorenal syndrome’)
123
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

124
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

125
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.

126
Q

What are the two types of hepatorenal syndrome?

A
  1. 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,
  2. Type 2
    • Which renal failure progression did not meet the criteria for type I
127
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

128
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

129
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.

130
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

131
Q

What are the clinical features of liver cancer?

A
  1. General - malaise, fatigue
  2. Gastrointestinal - anorexia, jaundice, constipation, ill-defined upper abdominal pain, abdominal fullness, bleeding oesophageal varices
  3. Hepatomegaly - liver is often irregular or nodular, and may be tender
  4. Ascites
  5. Dyspnoea - a late finding; may indicate diaphragmatic involvement or compression, or pulmonary metastases
132
Q

What are the investigations for liver cancer?

A
  1. Biochemical
    • Raised alkaline phosphatase
    • Serum transaminases
  2. Haematologic
    • Raised whtie cell count
    • Raised platelet count
  3. Serology
    • Alpha-feto protein
133
Q

What is the treatment for liver cancer?

A
  1. Resection
  2. Ablation
  3. Transplantation
134
Q

WHAT IS THE CAUSE OF PANCREATIC CARCINOMA?

135
Q

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

A
  1. Smoking
  2. Alcohol
  3. Increased BMI
  4. Diabetes
  5. Chronic pancreatitis
136
Q

What type of cancers are pancreatic carcinoma?

A

Adenocarcinomas

137
Q

What are the clinical features of pancreatic cancer?

A

Abdominal pain

Jaundice

Unexplained weight loss

138
Q

What are the investigations for pancreatic cancer?

A
  1. Ultrasound has a sensitivity of around 60-90%
  2. High-resolution CT scanning is the investigation of choice if the diagnosis is suspected
  3. Imaging may demonstrate the ‘double duct’ sign - the presence of simultaneous dilatation of the common bile and pancreatic ducts
  4. Can see an enlarged gall bladder TOO
139
Q

What is the treatment for pancreatic cancer?

A
  1. Less than 20% are suitable for surgery at diagnosis
  2. A Whipple’s resection (pancreaticoduodenectomy) is performed for resectable lesions in the head of pancreas
    • Side-effects of a Whipple’s include dumping syndrome and peptic ulcer disease
  3. Adjuvant chemotherapy is usually given following surgery
  4. ERCP with stenting is often used for palliation
140
Q

What are the causes of painless jaundice?

A
  1. Pancreatic cancer
  2. Liver cirhhosis e.g. alcoholic
  3. Haemochromatosis
141
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

142
Q

WHAT IS BUDD-CHIARI SYNDROME?

A

Budd-Chiari syndrome, or hepatic vein thrombosis, is usually seen in the context of underlying haematological disease or another procoagulant condition

143
Q

What are the causes of Budd-Chiari syndrome?

A
  1. polycythaemia rubra vera
  2. thrombophilia: activated protein C resistance, antithrombin III deficiency, protein C & S deficiencies
  3. pregnancy
  4. combined oral contraceptive pill: accounts for around 20% of cases
144
Q

What are the features of Budd-Chiari syndrome?

A
  1. abdominal pain: sudden onset, severe
  2. ascites → abdominal distension
  3. tender hepatomegaly
145
Q

What are the investigations for Budd-Chiari syndrome?

A
  1. Ultrasound with Doppler flow studies is very sensitive and should be the initial radiological investigation
146
Q

WHAT IS AUTOIMMUNE HEPATITIS?

A
  1. Autoimmune hepatitis is condition of unknown aetiology which is most commonly seen in young females.
  2. Recognised associations include other autoimmune disorders, hypergammaglobulinaemia and HLA B8, DR3.
  3. Three types of autoimmune hepatitis have been characterised according to the types of circulating antibodies present
147
Q

What are the features of autoimmune hepatitis?

A
  1. May present with signs of chronic liver disease
  2. Acute hepatitis: fever, jaundice etc (only 25% present in this way)
  3. Amenorrhoea (common)
148
Q

What are the investigations for autoimmune hepatitis?

A
  1. ANA/SMA(anti smooth muscle antibodies)/LKM1 antibodies, raised IgG levels
  2. Liver biopsy: inflammation extending beyond limiting plate ‘piecemeal necrosis’, bridging necrosis
149
Q

What are the management options for autoimmune hepatitis?

A
  1. Steroids, other immunosuppressants e.g. azathioprine
  2. Liver transplantation
150
Q

WHAT IS SPONTANEOUS BACTERIAL PERITONITIS?

A

Spontaneous bacterial peritonitis (SBP) is a form of peritonitis usually seen in patients with ascites secondary to liver cirrhosis.

151
Q

What are the features of spontaneous bacterial peritonitis?

A
  1. ascites
  2. abdominal pain
  3. fever
152
Q

What is needed for diagnosis of spontaneous bacterial peritonitis?

A
  1. paracentesis: neutrophil count > 250 cells/ul
  2. the most common organism found on ascitic fluid culture is E. coli
153
Q

What is the used for the management of spontaneous bacterial peritonitis?

A
  1. intravenous cefotaxime is usually given

ΩΩ 4 Bateman - Specialities + Endo + GI + Liver (6 decks)

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