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Hepatology > Liver Disease > Flashcards

Liver Disease Flashcards

1
Q

Alcoholic Liver Disease stages / stepwise progression

A
  1. Alcohol related fatty liver

Drinking leads to a build-up of fat in the liver. If drinking stops this process reverses in around 2 weeks.

  1. Alcoholic hepatitis

Drinking alcohol over a long period causes inflammation in the liver sites. Binge drinking is associated with the same effect. Mild alcoholic hepatitis is usually reversible with permanent abstinence.

  1. Cirrhosis

This is where the liver is made up of scar tissue rather than healthy liver tissue. This is irreversible. Stopping drinking can prevent further damage. Continued drinking has a very poor prognosis.

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2
Q

recommended alcohol consumption

A

do not regularly drink more than 14 units per week for women and men

spread over 3 days or more, no more than 45 units per day

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3
Q

CAGE questions

A

The CAGE question can be used to quickly screen for harmful alcohol use:

C – CUT DOWN? Ever thought you should?
A – ANNOYED? Do you get annoyed at others commenting on your drinking?
G – GUILTY? Ever feel guilty about drinking?
E – EYE OPENER? Ever drink in the morning to help your hangover/nerves?

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4
Q

complications of alcohol

A 
Alcoholic Liver Disease
Cirrhosis and the complications of cirrhosis including hepatocellular carcinoma
Alcohol Dependence and Withdrawal
Wernicke-Korsakoff Syndrome (WKS)
Pancreatitis
Alcoholic Cardiomyopathy
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5
Q

signs of liver disease

A 
Jaundice
Hepatomegaly
Spider Naevi
Palmar Erythema
Gynaecomastia
Bruising – due to abnormal clotting
Ascites
Caput Medusae – engorged superficial epigastric veins
Asterixis – “flapping tremor” in decompensated liver disease
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6
Q

investigations for alcoholic liver disease

A

bloods

FBC – raised MCV
LFTs – elevated ALT and AST (transaminases) and particularly raised gamma-GT. ALP will be elevated later in the disease. Low albumin due to reduced “synthetic function” of the liver. Elevated bilirubin in cirrhosis.
Clotting – elevated prothrombin time due to reduced “synthetic function” of the liver
U+Es may be deranged in hepatorenal syndrome.

Ultrasound

An ultrasound of the liver may show fatty changes early on described as “increased echogenicity”. It can also demonstrate changes related to cirrhosis if present.

“FibroScan” can be used to check the elasticity of the liver by sending high frequency sound waves into the liver. It helps assess the degree of cirrhosis.

Endoscopy

Endoscopy can be used to assess for and treat oesophageal varices when portal hypertension is suspected.

CT and MRI scans

CT and MRI can be used to look for fatty infiltration of the liver, hepatocellular carcinoma, hepatosplenomegaly, abnormal blood vessel changes and ascites.

Liver Biopsy

Liver biopsy can be used to confirm the diagnosis of alcohol related hepatitis or cirrhosis. NICE recommend considering a liver biopsy in patients where steroid treatment is being considered.

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7
Q

general management of ALD

A

Stop drinking alcohol permanently
Consider a detoxication regime
Nutritional support with vitamins (particularly thiamine) and a high protein diet
Steroids improve short term outcomes (over 1 month) in severe alcoholic hepatitis but infection and GI bleeding need to be treated first and do not improve outcomes over the long term
Treat complications of cirrhosis (portal hypertension, varices, ascites and hepatic encephalopathy)
Referral for liver transplant in severe disease however they must abstain from alcohol for 3 months prior to referral

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8
Q

alcohol withdrawal symptom

A

6-12 hours: tremor, sweating, headache, craving and anxiety
12-24 hours: hallucinations
24-48 hours: seizures
24-72 hours: “delerium tremens”

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9
Q

delirium tremens

A

medical emergency of alcohol withdrawal

alcohol stimulates GABA receptors (relax) and inhibits glutamate receptors /NMDA (inhibitory effect on the electrical affect of brain)

chronic alcohol- GABA up regulated, glutamate down regulated

remove alcohol- GABA under functions, glutamate over functions

extreme excitability of the brain = excess adrenergic activity.

Acute confusion
Severe agitation
Delusions and hallucinations
Tremor
Tachycardia
Hypertension
Hyperthermia
Ataxia (difficulties with coordinated movements)
Arrhythmias
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10
Q

managing alcohol withdrawl

A

CIWA-Ar= tool*

Benzodiazepines= chlordiazepoxide (librium)
(diazepam less common alternative)
10-40mg every 1-4 hours continued for 5-7 days

IV high dose B vitamins (pabrinex) followed by a regular lower dose of thiamine

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11
Q

WKS- Wernicke Korsakoff Syndrome

A

Alcohol excess leads to thiamine (vitamin B1) deficiency. Thiamine is poorly absorbed in the presence of alcohol and alcoholics tend to have poor diets and rely on the alcohol for their calories. Wernicke’s encephalopathy comes before Korsakoffs syndrome. These result from thiamine deficiency.

werkicker’s:

  • confusion
  • oculomotor disturbances
  • ataxia

korsakoff:

  • memory impairment (retrograde, anterograde)
  • behavioural changes
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12
Q

wernicker’s encephalopathy

A

medical emergency
high mortality rate
often irriversible
full time institutional care

prevention- thiamine and abstain from alcohol

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13
Q

what is liver cirrhosis

A

chronic inflammation and damage to liver cells. replaced with scar tissues (fibrosis) and nodules of scar tissues in the liver.

this effects the blood flow through the liver which causes increased resistance in the vessels (portal hypertension)

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14
Q

most common causes of liver cirrhosis

A

Alcoholic liver disease
Non Alcoholic Fatty Liver Disease
Hepatitis B
Hepatitis C

(rarer)
Autoimmune hepatitis
Primary biliary cirrhosis
Haemochromatosis
Wilsons Disease
Alpha-1 antitrypsin deficiency
Cystic fibrosis
Drugs (e.g. amiodarone, methotrexate, sodium valproate)
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15
Q

signs of cirrhosis

A

Jaundice – caused by raised bilirubin
Hepatomegaly – however the liver can shrink as it becomes more cirrhotic
Splenomegaly – due to portal hypertension
Spider Naevi – these are telangiectasia with a central arteriole and small vessels radiating away
Palmar Erythema – caused by hyperdynamic cirulation
Gynaecomastia and testicular atrophy in males due to endocrine dysfunction
Bruising – due to abnormal clotting
Ascites
Caput Medusae – distended paraumbilical veins due to portal hypertension
Asterixis – “flapping tremor” in decompensated liver disease

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16
Q

liver cirrhosis investigations

A

bloods:

  • LFT deranged in decompensated
  • albumin and prothrombin (synthetic function of the liver)
  • hyponatraemia if fluid retention
  • urea and creatinine (hepatorenal syndrome)
  • viral markers
  • alpha feta protein (tumor marker for hepatocellular carcinoma) (check every 6 months)
  • ultrasound
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17
Q

Enhanced Liver Fibrosis (ELF) blood test

A

first line recommended investigation for assessing fibrosis in non-alcoholic fatty liver disease but it is not currently available in many areas and cannot be used for diagnosing cirrhosis of other causes. It measures three markers (HA, PIIINP and TIMP-1) and uses an algorithm to provide a result that indicates the fibrosis of the liver:

< 7.7 indicates none to mild fibrosis
≥ 7.7 to 9.8 indicates moderate fibrosis
≥ 9.8 indicates severe fibrosis

18
Q

ultrasound cirrhosis

A

Nodularity of the surface of the liver
A “corkscrew” appearance to the arteries with increased flow as they compensate for reduced portal flow
Enlarged portal vein with reduced flow
Ascites
Splenomegaly
Ultrasound is also used as a screening tool for hepatocellular carcinoma. NICE recommend screening patients with cirrhosis for HCC every 6 months.

19
Q

Fibroscan

A

check the elasticity of the liver by sending high frequency sound waves into the liver. It helps assess the degree of cirrhosis. This is called “transient elastography” and should be used to test for cirrhosis. NICE recommend retesting every 2 years in patients at risk of cirrhosis:

Hepatitis C
Heavy alcohol drinkers (men drinking > 50 units or women drinking > 35 units per week)
Diagnosed alcoholic liver disease
Non alcoholic fatty liver disease and evidence of fibrosis on the ELF blood test
Chronic hepatitis B (although they suggest yearly for hep B)

20
Q

liver cirrhosis imaging

A

Endoscopy
Endoscopy can be used to assess for and treat oesophageal varices when portal hypertension is suspected.

CT and MRI scans
CT and MRI can be used to look for hepatocellular carcinoma, hepatosplenomegaly, abnormal blood vessel changes and ascites.

Liver Biopsy
Liver biopsy can be used to confirm the diagnosis of cirrhosis.

  • Child Pugh’s score
  • MELD score
21
Q

general management of lier cirrhosis

A

Ultrasound and alpha-fetoprotein every 6 months for hepatocellular carcinoma
Endoscopy every 3 years in patients without known varices
High protein, low sodium diet
MELD score every 6 months
Consideration of a liver transplant
Managing complications as below

22
Q

complications of liver cirrhosis

A

Malnutrition and muscle wasting (increased use of muscle tissue as fuel an reduces the protein avaiabiliy in the body for muscle growht) (disruption of the ability to store glucose as glycogen and release when its required))

Portal Hypertension, Varices and Variceal Bleeding
Ascites and Spontaneous Bacterial Peritonitis (SBP)
Hepato-renal Syndrome
Hepatic Encephalopathy
Hepatocellular Carcinoma

  • regular meals
  • low sodium
  • high protein, high calorie
  • avoid alcohol
23
Q

what delivers blood to the liver?

A 
portal vein (from the superior mesenteric vein) 
splenic vein
24
Q

portal hypertension and varices

A

liver cirrhosis= high resistance of blood flow in the river so there is a backpressure into the portal system

back pressure causes the vessel a the sites where portal system anastomoses with systemic venous system
swollen, tortuous vessels

Gastro oesophageal junction
Ileocaecal junction
Rectum
Anterior abdominal wall via the umbilical vein (caput medusae)

high blood flow= exsanguinate quickly

25
Q

treatment of stable varices:

A

Propranolol reduces portal hypertension by acting as a non-selective beta blocker
Elastic band ligation of varices
Injection of sclerosant (less effective than band ligation
TIPS

26
Q

TIPS

A

a technique where an interventional radiologist inserts a wire under xray guidance into the jugular vein, down the vena cava and into the liver via the hepatic vein. They then make a connection through the liver tissue between the hepatic vein and the portal vein and put a stent in place. This allows blood to flow directly from the portal vein to the hepatic vein and relieves the pressure in the portal system and varices. This is used if medical and endoscopic treatment of varices fail or if there are bleeding varices that cannot be controlled in other ways.

27
Q

management of bleeding oesophageal varices

A

Resuscitation

Vasopressin analogues (i.e. terlipressin) cause vasoconstriction and slow bleeding in varices
Correct any coagulopathy with vitamin K and fresh frozen plasma (which is full of clotting factors)
Giving prophylactic broad spectrum antibiotics has been shown to reduce mortality
Consider intubation and intensive care as they can bleed very quickly and become life threateningly unwell
Urgent endoscopy

Injection of sclerosant into the varices can be used to cause “inflammatory obliteration” of the vessel
Elastic band ligation of varices
Sengstaken-Blakemore Tube is an inflatable tube inserted into the oesophagus to tamponade the bleeding varices. This is used when endoscopy fails.

28
Q

Ascites- clinical features

A

fluid in peritoneal cavity
increased pressure in portal system causes fluid to leak out of capillaries in the liver and bowel into peritoneal cavity

drop in circulating volme
reduction in BP
RAAS
reabsoorption of fluid and sodium in kidneys

transudative (low protein) content ascites

29
Q

ascites mx

A

Low sodium diet
Anti-aldosterone diuretics (spironolactone)
Paracentesis (ascitic tap or ascitic drain)
Prophylactic antibiotics against spontaneous bacterial peritonitis (ciprofloxacin or norfloxacin) in patients with less than 15g/litre of protein in the ascitic fluid
Consider TIPS procedure in refractory ascites
Consider transplantation in refractory ascites

30
Q

SBP spontaenous bacterial peritonitis

A

This occurs in around 10% of patients with ascites secondary to cirrhosis and can have a mortality of 10-20%. It involves an infection developing in the ascitic fluid and peritoneal lining without any clear cause (e.g. not secondary to an ascitic drain or bowel perforation).

- asymptomatic
fever
- abdo pain
- deranged bloods (WBC, CRP, creatinine, metabolic acidosis)
- ileus
- hypotension

common organisms:
E.coli, Klebsiella pneumoniae,

31
Q

SBP management

A

Take an ascitic culture prior to giving antibiotics

Usually treated with an IV cephalosporin such as cefotaxime

32
Q

Hepatorenal syndrome

A

occurs in liver cirrhosis

hypertension in portal system leads to dilation of the portal blood vessel

leads to a loss of blood vessels in circulation including kidneys. leads to hypotension = RAAS= renal vasoconstriction

the low circulation volume starves the vblood to the kidney

33
Q

hepatic encephalopathy

A

portosystemic encephalopathy

build up of toxins (ammonia)

ammonia is produced by break down of proteins by intestinal bacteria

builds up when:

  1. functional liver cells are impaired so unable to metabolise ammonia into hrmelss waste products
  2. collateral vesels between portal and systemic circulation means ammonia is bypassed the liver and therefore enters the systemic directly!
34
Q

hepatic encephalopathy presentation and precipitating factors

A

acute- reduced consciousness and confusion

chronic- changes to personality, memory and mood

Precipitating Factors:
Constipation
Electrolyte disturbance
Infection
GI bleed
High protein diet
Medications (particularly sedative medications)
35
Q

hepatic encephalopathy management

A

mx:
1. laxatives (lactulose) to promote the excretion of ammonia from gut. aim for 2-3 soft motions daily. may require enema initially.

  1. antbiotic (rifaximin) to reduce the amount of bacteria in the gut producing ammonia. poorly absorbed so stays in GI tract
  2. nutritional support - NG feeding
36
Q

NAFLD

A

metabolic syndrome
increased risk of CVD, stroke, diabetes

fat deposits in liver cells
fat can interfere with functioning liver cells
can progress to hepatitis and cirrhosis

37
Q

NAFLD stages

A

Non-alcoholic Fatty Liver Disease
Non-Alcoholic Steatohepatitis (NASH)
Fibrosis
Cirrhosis

38
Q

NAFLD risk factors

A 
Obesity
Poor diet and low activity levels
Type 2 diabetes
High cholesterol
Middle age onwards
Smoking
High blood pressure
39
Q

investigate abnormal LFT’s

A

non invasive liver screen

  1. us liver
  2. hep b and c serology
  3. autoantibodies
  4. immunoglobulins (autoimmune hepatitis)
  5. wilsons disease (caeruloplasmin)
  6. alpha 1 antitrypsin
  7. ferritin and transferrin saturation (hereditary haemachromatosis)
40
Q

NAFLD autoantibodies

A 
Antinuclear antibodies (ANA)
Smooth muscle antibodies (SMA)
Antimitochondrial antibodies (AMA)
Antibodies to liver kidney microsome type-1 (LKM-1)
41
Q

investigations for NAFLD

A

first line:

  1. liver US to confirm hepatic steatosis (fatty liver) but does not indicate severity
2. enhanced liver fibrosis (ELF)
measures 3 markers
HA PIINP and TIMP-1
< 7.7 indicates none to mild fibrosis
≥ 7.7 to 9.8 indicates moderate fibrosis
≥ 9.8 indicates severe fibrosis

second line:
NAFLD fibrosis score (if ELF is unavailable) based on an algorithm of age, BMI, liver enzymes, platelets, albumin and diabetes and is helpful in ruling out fibrosis but not assessing the severity when present.

third line:
fibroscan
US that measures the stiffness of the liver and gives indication fo fibroiss.

42
Q

NAFLD management

A

Weight loss
Exercise
Stop smoking
Control of diabetes, blood pressure and cholesterol
Avoid alcohol
Refer patients with liver fibrosis to a liver specialist where they may treat with vitamin E or pioglitazone.

Hepatology (6 decks)

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