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Medicine year 4 CDM > Block 5: PSC, NAFLD, Cirrhosis > Flashcards

Block 5: PSC, NAFLD, Cirrhosis Flashcards

1
Q

Diagnosis of NAFLD

A
  • Raised ALT and/or GGT and evidence of steatosis on imaging
  • Imaging evidence of steatosis
  • Raised ALT and/or GGT and evidence of insulin resistance / central obesity / metabolic risk factors
  • No history of excess alcohol (<14/21units/week), no known pre-existing liver disease, no hepatotoxic drugs, Negative blood screen for other liver disease (viral, autoimmune)
  • Liver biopsy if diagnostic uncertainty
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2
Q

Liver enzymes and NAFLD

A
  • Most common liver enzyme abnormality is raised GGT
  • ALT in the normal range in up to 80%
  • “Typical” abnormality is raised ALT and/or GGT
  • ALT typically falls with advanced fibrosis and advancing age (ALT > AST → ALT < AST)
  • We should not use liver enzymes to identify/diagnose patients with NAFLD as can be normal
  • Can have raised IgA and raised ferritin with normal transferrin saturation
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3
Q

Staging of NAFLD

A
  • Stage of liver fibrosis: fibrosis is the only indicator of prognosis
  • Steatosis vs NASH (steatosis + inflammation)
  • Liver biopsy is the gold standard for staging
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4
Q

Some tests for liver fibrosis

A
  • Blood tests: FIB-4 score (NAFLD), NAFLD fibrosis score, ELF score (NAFLD), Fibrotest, ProC3
  • Imaging: Transient elastography (probs that shoots a wave through the liver, detector measures elasticity. Stiffness corelates to fibrosis- non invasive), Acoustic force radiation imaging (ARFI), MR elastography
  • AST/ALT ratio >0.8 is suggestive of advanced fibrosis
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5
Q

Determining staging of NAFLD

A
  • Suspect NAFLD: calculate FIB-4 score
  • If FIB-4 score >1.3 in under 65 and more than 2 in over 65 then do Transient elastography (TE).
  • If TE <8kpa its low risk NAFLD
  • If TE >8kpa then consider liver biopsy
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6
Q

Types of NAFLD

A
  • F0-1 (low risk NAFLD): primary care, lifestyle advice, treat metabolic risk. Re-assess FIB-4/TE in 3 years
  • F2-3: Lifestyle advice, treat metabolic risk. NAFLD directed surgery. If non-diabetic vitamin E. If diabetic include GLP-1 or Pioglitazone or Empaglitazone. Clinical trial
  • F4: lifestyle advice, treat metabolic risk. NAFLD directed therapy. HCC + varices screen. Bone density assessment
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7
Q

Management of NAFLD

A
  • Weight loss >10%: VLCD, Orlistat, meal replacement
  • Healthy diet (Mediterranean diet is recommended)
  • Exercise: reduces steatosis and hepatic inflammation. Improves metabolic profile. Moderate intensity, high intensity and resistance exercise
  • Avoid/limit alcohol intake, Stop smoking
  • Control of diabetes, blood pressure and cholesterol
  • Refer patients withliver fibrosisto a liver specialist (indicated by scoring system)
  • Bariatric surgery: caution in cirrhosis. Improvement in steatosis, steatohepatitis and fibrosis
  • Specialist management may includevitamin E,pioglitazone,bariatric surgeryandliver transplantation
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8
Q

Practical tips for NAFLD

A
  • Explain that NAFLD is reversible with lifestyle change
  • Set achievable weight loss goals
  • Regular meal plan, reduce snacking, portion control
  • Count daily calories, use a pedometer/activity tracker
  • Sign post to exercise schemes, community gym, weight management programmes, walking groups
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9
Q

NAFLD: treatment for cardiovascular risk

A
  • T2DM: Metformin (reduce HCC risk), Pioglitazone and Liraglutide- slows fibrosis progression, Empagliflozin (reduce steatosis)
  • Hypertension: ARB’s, ACEi as anti-fibrotic
  • Dyslipidaemia: assess QRISK3, Statins are safe in NAFLD and hepatoxicity is rare
  • Look for sleep apnoea and treat
  • Smoking cessation
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10
Q

Specific liver treatment in NAFLD

A
  • Vitamin E: for NASH with stage F3, assess ALT after 6 months
  • Pioglitazone: side effects are weight gain, increased bladder cancer risk, reduced bone density. Not widely used in non diabetic NASH
  • Liraglutide (GLP1 analogue): NASH with diabetes, causes weight loss
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11
Q

Monitoring for NAFLD

A
  • Every 3 years
  • FIB-4 or NFS is effective for those with a low score to begin with
  • For those with an increased FIB4/NFS (but low fibroscan): follow up with the fibroscan is needed
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12
Q

Cirrhosis: pathophysiology

A

Due to chronic inflammation and damage to liver cells. Functional liver cells are replaced with scar tissue (fibrosis). Nodules of scar tissue form within the liver, separated by fibrous tissue.

Normal liver → Steatosis → Steatohepatitis → Fibrosis/cirrhosis

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13
Q

Causes of cirrhosis

A
  • Alcohol-related liver disease
  • Non-alcoholic fatty liver disease (NAFLD)
  • Hepatitis B
  • Hepatitis C
  • Rare: autoimmune hepatitis, Primary biliary cirrhosis, Haemochromatosis, Wilsons disease, Alpha-1 antitrypsin deficiency, cystic fibrosis, Drugs (amiodarone, methotrexate and sodium valproate)
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14
Q

Assessing severity of cirrhosis

A
  • Childs-Pugh score
  • MELD score: bilirubin, INR and creatinine. For end stage liver disease
  • UKELD score: sodium, bilirubin, creatinine, INR: have to get a minimum score to be considered for liver transplantation in the UK
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15
Q

Stages of cirrhosis

A
  • Stage 1: compensated with no varices or ascites
  • Stage 2: compensated with varices but no ascites
  • Stage 3: variceal bleeding without any other complication
  • Stage 4: Non-bleeding decompensation i.e. ascites, HE, jaundice
  • Stage 5: any second decompensating event
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16
Q

Decompensated cirrhosis

A
  • Deterioration in liver function
  • Manifests as jaundice, increasing ascites, hepatic encephalopathy, renal impairement/hypovolaemia, signs of sepsis
  • May be precipitated by: GI bleeding, infection/sepsis, alcoholic excess, Drugs (opiates, NSAID’s), development of HCC, portal vein thrombosus, dehydration, constipation
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17
Q

Ascites

A
  • Commonest complication of cirrhosis
  • Abdo distension/shifting dullness
  • Radiological detection (US) before clinical
  • Can be treated with diuretics but eventually is resistant
  • Cirrhosis causes increased intrahepatic vascular resistance and portal blood flow, causing portal hypertension. There is renal sodium retention causing overload of lymphatics and ascites
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18
Q

Ascites

A
  • Commonest complication of cirrhosis
  • Abdo distension/shifting dullness
  • Radiological detection (US) before clinical
  • Can be treated with diuretics but eventually is resistant
  • Cirrhosis causes increased intrahepatic vascular resistance and portal blood flow, causing portal hypertension. There is renal sodium retention causing overload of lymphatics and ascites
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19
Q

Ascitic fluid analysis

A
  • Diagnostic paracentesis: required at onset of new ascites and in all hospitalised patients
  • SAAG: Albumin (serum) - Albumin (ascites)
  • If >11g/l ascites is usually due to portal hypertension
  • Ascites is most commonly but not exclusively caused by cirrhosis
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20
Q

Spontaneous bacterial peritonitis

A
  • Infection of the ascitic fluid in the absence of a secondary cause, diagnose by fluid analysis
  • Most common organism: E.coli and Klebsiella pneumoniae
  • Usually asymptomatic: fevers, abdo pain, renal impairement
  • Polymorphonuclear cells >250/mm in ascitic fluid or Neutrophil 0.25 x10^9 on automated testing
  • Treat with antibiotics according to sensitivities (co-amoxiclav or ciprofloxacin)
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21
Q

Treatment options in cirrhosis

A
  • Liver transplant
  • Sinusoidal portal hypertension: TIPS (transjugular intrahepatic porto-systemic shunt)
  • Renal sodium retention: diuretics, Na restrict
  • Ascites: Paracentesis
22
Q

Examination findings cirrhosis 1

A
  • Cachexia(wasting of the body and muscles)
  • Jaundicecaused byraised bilirubin
  • Hepatomegaly(enlargement of the liver)
  • Small nodular liveras it becomes more cirrhotic
  • Splenomegalydue toportal hypertension
  • Spider naevi(telangiectasia with a central arteriole and small vessels radiating away)
  • Palmar erythemacaused by elevated oestrogen levels
23
Q

Examination findings cirrhosis 2

A
  • Gynaecomastiaandtesticular atrophyin males due to endocrine dysfunction
  • Bruisingdue to abnormal clotting
  • Excoriations(scratches on the skin due to itching)
  • Ascites(fluid in the peritoneal cavity)
  • Caput medusae(distended paraumbilical veins due toportal hypertension)
  • Leukonychia(white fingernails) associated withhypoalbuminaemia
  • Asterixis(“flapping tremor”) indecompensated liver disease
24
Q

Non-invasive liver screen

A
  • Ultrasound liver(used to diagnose fatty liver)
  • Hepatitis BandCserology
  • Autoantibodies(autoimmune hepatitis,primary biliary cirrhosisandprimary sclerosing cholangitis): ANA, SMA, AMA, LKM-1
  • Immunoglobulins(autoimmune hepatitisandprimary biliary cirrhosis)
  • Caeruloplasmin(Wilsons disease)
  • Alpha-1 antitrypsin levels(alpha-1 antitrypsin deficiency)
  • Ferritinandtransferrin saturation(hereditary haemochromatosis)
25
Q

Cirrhosis: blood results

A
  • Raised bilirubin, ALT, AST, ALP
  • Low albumindue to reducedsynthetic functionof the liver
  • Increased prothrombin timedue to reducedsynthetic functionof the liver (reduced production of clotting factors)
  • Thrombocytopenia(low platelets) is a common finding and indicates more advanced disease
  • Hyponatraemia(low sodium) occurs with fluid retention insevere liver disease
  • Urea and creatininebecome deranged inhepatorenal syndrome
  • Alpha-fetoproteinis a tumour marker forhepatocellular carcinoma
  • Enhanced liver fibrosis (ELF) blood test: 10.51 or above is advanced fibrosis
26
Q

Ultrasound with cirrhosis

A
  • Nodularityof the surface of the liver
  • A “corkscrew” appearance to the hepatic arteries with increased flow as they compensate for reduced portal flow
  • Enlarged portal veinwith reduced flow
  • Ascites
  • Splenomegaly
  • Fatty areas have increased echogenicity
27
Q

Cirrhosis: Transient elastography (Fibro scan) when is it used

A

Assess stiffness of liver using high frequency sound waves. Can show degree of fibrosis to test for liver cirrhosis. Is used in patients at risk of cirrhosis:

  • Alcohol-related liver disease
  • Heavy alcohol drinkers (men drinking more than 50 units or women drinking more than 35 units per week)
  • Non-alcoholic fatty liver disease and advanced liver fibrosis (score 10.51 or more on the ELF blood test)
  • Hepatitis C
  • Chronic hepatitis B
28
Q

Other investigations for cirrhosis

A
  • Endoscopycan be used to assess for and treatoesophageal variceswhenportal hypertensionis suspected.
  • CT and MRIcan be used to look for hepatocellular carcinoma, hepatosplenomegaly, abnormal blood vessel changes and ascites.
  • Liver biopsycan be used to confirm the diagnosis of cirrhosis.
29
Q

MELD

A

MELD (Model for end stage liver disease) score: used every 6 months in compensated cirrhosis. Considers bilirubin, creatinine, INR and sodium and whether they require dialysis. Gives an estimates 3 month mortality as a percentage

30
Q

Child Pugh score

A

Assesses the severity of cirrhosis and the prognosis

  • Each factor is scored 1,2 or 3
  • Overall score is 5-15
  • Features (A,B,C,D,E): Albumin, Bilirubin, Clotting (INR), Dilation (ascites), Encephalopathy
31
Q

Monitoring for cirrhosis complications include

A
  • MELD scoreevery 6 months
  • Ultrasound and alpha-fetoprotein every 6 months forhepatocellular carcinoma
  • Endoscopyevery 3 years foroesophageal varices
32
Q

Cirrhosis: treatment for underlying cause

A
  • Stop drinking alcohol
  • Lifestyle changes for non-alcohol fatty liver disease
  • Antiviral drugs for hepatitis C
  • Immunosuppressants for autoimmune hepatitis
33
Q

When to consider liver transplantation

A

When there are features of decompensated liver disease (AHOY):

  • A–Ascites
  • H–Hepatic encephalopathy
  • O–Oesophageal varices bleeding
  • Y–Yellow (jaundice)
34
Q

Cirrhosis: main complications

A
  • Malnutrition and muscle wasting: poor intake and malabsorption. Causes worse prognosis
  • Portal hypertension,oesophageal varicesandbleeding varices
  • Ascites and spontaneous bacterial peritonitis
  • Hepatorenal syndrome: blood supply to the kidney is reduced causing functional renal failure. An acute type which tends to be secondary to a precipitant and responds to albumin and Terlispressin. Or there is a more chronic form which is diuretic resistant, retractable ascites which has a poor prognosis
  • Hepatic encephalopathy
  • Hepatocellular carcinoma
34
Q

Management of 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 inrefractory ascites
  • Liver transplantationis considered inrefractory ascites
35
Q

Varices management: bleeding

A
  • Immediate senior help
  • Consider blood transfusion(activate the major haemorrhage protocol)
  • Treat anycoagulopathy(e.g., withfresh frozen plasma)
  • Vasopressin analogues(e.g.,terlipressin or somatostatin) cause vasoconstriction and slow bleeding: IV infusion
  • Prophylactic broad-spectrum antibiotics
35
Q

Varices management: surgical

A
  • Urgent endoscopy with variceal band ligation: bands are kept on 2 weeks repeated till eradicated
  • Consider intubation andintensive care
  • Sengstaken-Blakemore tube(an inflatable tube inserted into the oesophagus to tamponade the bleeding varices)
  • TIPS: main indications is bleeding oesophageal varices (majority) and refractory ascites. Used if endoscopy is ineffective. Can only be done in specialist liver units with radiology support. Risk of re-bleeding
35
Q

Pathophysiology of portal hypertension

A

The portal vein comes from the superior mesenteric and splenic veinsand delivers blood to the liver.Liver cirrhosisincreases the resistance to blood flow and increased back pressure on theportal system. This is calledportal hypertension. The back pressure of blood results insplenomegaly. Causes swollen and tortuous vessels at sites where collaterals form between the portal and systemic venous systems (oesophageal varices)

35
Q

Where varices are

A
  • Distal oesophagus: oesophageal varices
  • Anterior abdominal wall: caput medusae
  • Veins in the lower third of the oesophagus
  • Prophylaxis: beta blockers (propranolol) or variceal band litigation if beta blockers contraindicated
  • No issues with varices till they spontaneously bleed can be life threatening
35
Q

Hepatic encephalopathy

A
  • Spectrum of neuropsychiatric abnormalities in patients with liver failure
  • Porto-systemic shunting and increased gut toxins in blood
  • Ammonia is often elevated: liver cells impairement means they cant metabolise ammonia. Secondly collateral vessels means ammonia enters the systemic system directly. Diagnosed clinically
  • In Chronic liver disease cerebral oedema is uncommon
  • Acute: reduced consciousness and confusion
  • Chronic: changes to personality, memory and mood
36
Q

Hepatic encephalopathy: management and causes

A
  • Main cause: infection, GI bleeding, electrolyte disturbance, constipation, sedative drugs
  • Management: Lactulose (2-3 stools a day), antibiotics (rifaximin- to reduce intestinal bacteria. For persistent HE or >1 admission with HE), nutritional support i.e. Ng feeding, Phosphate enemas
37
Q

Hepatic encephalopathy grades

A
  • Grade 1: mild confusion, euphoria, anxiety or depression, reversed sleep rhythm, slurred speech
  • Grade 2: drowsiness, lethargy, gross deficits in the ability to perform mental tasks, relatively moderate confusion
  • Grade 3: somnolent but arousable, severe confusion, inability to perform mental tasks
  • Grade 4: Coma with (IVa) or without (IVb) response to painful stimuli
38
Q

Liver cancer

A
  • Hepatocellular carcinoma: accounts for majority of primary liver cancer. On the rise
  • Cirrhosis is the biggest risk factors for HCC, multiple causes including viral hepatitis, chronic alcohol use, NAFLD
  • Most frequent causes of HCC: HCV, HBV and alcohol

Progression: normal liver cells → inflamed/fibrotic → cirrhotic → Intraepithelial neoplasia → dysplastic nodules → nodules of HCC

39
Q

Surveillance in patients at high risk of HCC

A
  • Cirrhotic patients: Child-pugh stage A and B
  • Cirrhotic patients: Child-pugh stage C waiting liver transplant
  • Non-cirrhotic HBV patients at intermediate or high risk of HCC
  • Non-cirrhotic F3 patients based on an individual risk assessment
  • Screened every 6 months with US
40
Q

Management of HCC

A
  • early disease: surgical resection
  • liver transplantation
  • radiofrequency ablation
  • transarterial chemoembolisation
  • sorafenib: a multikinase inhibitor
41
Q

Indications for liver transplant

A
  • Chronic liver failure: UKELD >49, cirrhosis with decompensating event (give up alcohol first, treat viral hepatitis)
  • Hepatocellular carcinoma: multiple up to 5 tumours ≤3cm, or single up to 5cm or 7cm if stable
  • Acute liver failure
42
Q

Investigations for Hepatocellular carcinoma

A
  • Alpha-fetoprotein(tumour marker forhepatocellular carcinoma)
  • Liver ultrasoundis the first-line imaging investigation
  • CTandMRI scansare used for further assessment and staging of the cancer
  • Biopsyis used for histology
43
Q

Decompensated liver disease: signs on examination

A
  • Spider naevi
  • Jaundice and scleral icterus
  • Digital clubbing
  • Ascites and caput medusa
  • Flapping tremor
44
Q

Blood results: decompensated liver disease

A
  • Macrocytic anaemia: high MCV low haemoglobin. Due to chronic alcohol use, B12 deficiency and upper GI bleed
  • Thrombocytopaenia: increased platelet destruction die to hypersplenism reduced production and maturation of platelets due to myelosuppression and reduced thrombopoietin levels, and haemodilution due to fluid retention.
  • Deranged LFT’s
  • Raised urea and low creatinine: renal function is affected in liver disease, low creatinine can be due to malnutrition
  • Mildly elevated CRP
  • Elevated PT: reduction in production of clotting factors
45
Q

Blood tests for decompensated liver disease

A
  • HIV serology
  • Hepatitis serology
  • Autoantibody screen (AMA, ANA, anti SMA, p-ANCA)
  • AST
  • Iron studies (ferritin, transferrin saturation)
  • Serum caeruloplasmin
  • B12 and folate
  • Tumour markers (AFP, Ca19-9)
  • Serum immunoglobulins
  • Alpha 1 antitrypsin levels
  • Ammonia
  • Alkaline phosphatase isoenzymes

Medicine year 4 CDM (41 decks)

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