Cirrhosis Flashcards

Question

name some complications and prognosis of cirrhosis. What tools can be used (2)

Answer 1

MELD- every 6 months Child-Pugh score Malnutrition and muscle wasting Portal hypertension, oesophageal varices and bleeding varices Ascites and spontaneous bacterial peritonitis Hepatorenal syndrome Hepatic encephalopathy Hepatocellular carcinoma

Answer 2

Muscle wasting- due to loss of appetite. protein metabolism is affected. liver is unable to store glycogen inadequate ability for maintaining muscle tissue and muscle tissue is broken down for use as fuel. - regular meals - high protein and calorie intake reduced sodium intake to minimise fluid retention avoiding alcohol

Answer 3

superior mesenteric and splenic veins (portal veins)

Answer 4

liver cirrhosis can increase the resistance of blood flow into the liver and as a result there is increase pressure on the portal system and the back pressure of blood may result in splenomegaly.

Answer 5

where collaterals form between the portal and systemic venous systems. These collaterals can occur at several locations, notably the: Distal oesophagus (oesophageal varices) Anterior abdominal wall (caput medusae)

Answer 6

enlarged or dilated blood vessels in the oesophagus connecting the portal and systemic circulations. they form due to poor hypertension as a result of cirrhosis, resistance to portal blood flow and increased portal venous blood flow.

Answer 7

False. Prophylaxis of bleeding in stable oesophageal varices involves: Non-selective beta blockers (e.g., propranolol) first-line Variceal band ligation (if beta blockers are contraindicated)

Answer 8

Non-selective beta blockers (e.g., propranolol) first-line Variceal band ligation (if beta blockers are contraindicated)

Answer 9

Immediate senior help Consider blood transfusion (activate the major haemorrhage protocol) Treat any coagulopathy (e.g., with fresh frozen plasma) Vasopressin analogues (e.g., terlipressin or somatostatin) cause vasoconstriction and slow bleeding Prophylactic broad-spectrum antibiotics (shown to reduce mortality) Urgent endoscopy with variceal band ligation Consider intubation and intensive care Other options to control the bleeding include: Sengstaken-Blakemore tube (an inflatable tube inserted into the oesophagus to tamponade the bleeding varices) Transjugular intrahepatic portosystemic shunt (TIPS)

Answer 10

A wire under x-ray is inserted into the jugular vein down the vena cava and into the liver via the hepatic vein. A bypass is made from the hepatic vein and portal vein so the blood flow directly to relieve the pressure in the portal system. - Bleeding oeasophageal Varices - Refractory Ascites

Answer 11

- Fluid in the peritoneal cavity. Increased pressure in the portal system causes fluid to leak out of the capillaries in the liver and abdo organs into the peritoneal cavity. - The drop in the circulating volume results in a lower blood pressure in the kidneys. RAAS is activated therefore more absorption of fluid in the kidney and sodium retention.

Answer 12

False. Ascites is the leakage of fluid from the capilaries into the peritoneal cavity as a result of increased pressure in portal system. damaged liver means there is inadequate protein synthesis like albumin therefore oncotic pressure decreases, leading to fluid in the abdomen.

Answer 13

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

Answer 14

Spontaneous bacterial peritonitis (SBP) occurs in 10-20% of patients with ascites. It has a mortality of 10-20%. It involves an infection developing in the ascitic fluid and peritoneal lining without a clear source of infection (e.g., an ascitic drain or bowel perforation).

Answer 15

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

Answer 16

low. The infection can cause systemic inflammatory response where it can lead to vasodilation and increased vascular permeability resulting in decreased blood pressure. septic shock: overwhelms the body's ability to regulate BP. cirrhosis itself can cause vasodilation and reduced systemic vascular resistance leading to hypo.

Answer 17

Escherichia coli Klebsiella pneumoniae

Answer 18

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

Answer 19

Impaired kidney function caused by changes in the blood flow to the kidney relating to liver cirrhosis and portal hypertension. The exact pathophysiology is still being debated. A simplified version is that portal hypertension causes the portal vessels to release vasodilators, which cause significant vasodilation in the splanchnic circulation (the vessels supplying the gastrointestinal organs). Vasodilation leads to reduced blood pressure. The kidneys respond to the reduced pressure by activating the renin-angiotensin-aldosterone system, which leads to vasoconstriction of the renal vessels. Renal vasoconstriction combined with low systemic pressure results in the kidneys being starved of blood and significantly reduced kidney function. Hepatorenal syndrome has a poor prognosis unless the patient has a liver transplant.

Answer 20

Hepatic encephalopathy is also known as portosystemic encephalopathy. It is thought to be caused by the build-up of neurotoxic substances that affect the brain. when proteins are broken down by intestinal bacteria it releases ammonia which is absorbed by the intestine.

Answer 21

Firstly, the liver cells’ functional impairment prevents them from metabolising the ammonia into harmless waste products. Secondly, collateral vessels between the portal and systemic circulation mean that the ammonia bypasses the liver and enters the systemic system directly.

Answer 22

Constipation Dehydration Electrolyte disturbance Infection Gastrointestinal bleeding High protein diet Medications (particularly sedative medications)

Answer 23

confusion and reduced consciousness

Answer 24

Lactulose (aiming for 2-3 soft stools daily) Antibiotics (e.g., rifaximin) to reduce the number of intestinal bacteria producing ammonia Nutritional support (nasogastric feeding may be required) Lactulose works in several ways to reduce ammonia: Speeds up transit time and reduces constipation (the laxative effect clearing the ammonia before it is absorbed) Promotes bacterial uptake of ammonia to be used for protein synthesis Changes the pH of the contents of the intestine to become more acidic, killing ammonia-producing bacteria Rifaximin is the usual choice of antibiotic as it is poorly absorbed and stays in the gastrointestinal tract. Neomycin and metronidazole are alternatives.

Answer 25

Non-alcoholic fatty liver disease Non-alcoholic steatohepatitis (NASH) Fibrosis Cirrhosis

Answer 26

Triglyceride

Answer 27

Non-alcoholic fatty liver disease shares the same risk factors as cardiovascular disease and diabetes: Middle age onwards Obesity Poor diet and low activity levels Type 2 diabetes High cholesterol High blood pressure Smoking

Answer 28

Obesity diabetes hypertension

Answer 29

-Raised ALT if the first indication

Answer 30

NO. US can show hepatic steatosis (fatty liver).

Answer 31

The enhanced liver fibrosis (ELF) blood test is the first-line investigation for assessing fibrosis in non-alcoholic fatty liver disease. It measures three markers (HA, PIIINP and TIMP-1) and uses an algorithm to provide a result that indicates whether they have advanced fibrosis of the liver: 10.51 or above – advanced fibrosis Under 10.51 – unlikely advanced fibrosis (NICE recommend rechecking every 3 years in NAFLD)

Answer 32

NAFLD Fibrosis Score (NFS) is another option for assessing liver fibrosis in NAFLD. It is based on an algorithm of age, BMI, liver enzymes (AST and ALT), platelet count, albumin and diabetes. Transient elastography (“FibroScan”) can be used to assess the stiffness of the liver using high-frequency sound waves. It helps determine the degree of fibrosis (scarring) to test for liver cirrhosis. It is used where the enhanced liver fibrosis (ELF) test indicates advanced fibrosis. Liver biopsy may be required to confirm the diagnosis and exclude other causes of liver disease. TOM TIP: Both the NFS and FIB-4 scores use the AST:ALT ratio to assess the severity of liver fibrosis. The normal ratio is less than 1. A ratio greater than 0.8 in NAFLD suggests advanced fibrosis. An AST:ALT ratio greater than 1.5 (meaning a disproportionately high AST) indicates alcohol-related liver disease rather than NAFLD.

Answer 33

The diagnosis requires the presence of ultrasound findings of a fatty liver, risk factors and excluding other causes of liver disease with a careful alcohol history and full non-invasive liver screen. Liver biopsy is the gold standard test.

Answer 34

False. Management involves: Weight loss Healthy diet (Mediterranean diet is recommended) Exercise Avoid/limit alcohol intake Stop smoking Control of diabetes, blood pressure and cholesterol Refer patients where scoring tests indicate liver fibrosis to a liver specialist Specialist management may include vitamin E, pioglitazone, bariatric surgery and liver transplantation

Answer 35

1. Alcoholic fatty liver (also called hepatic steatosis) Drinking leads to a build-up of fat in the liver. This process is reversible with abstinence. 2. Alcoholic hepatitis Drinking alcohol over a long period causes inflammation in the liver cells. Binge drinking is associated with the same effect. Mild alcoholic hepatitis is usually reversible with permanent abstinence. 3. Cirrhosis Cirrhosis is where the functional liver tissue is replaced with scar tissue. It is irreversible. Stopping drinking can prevent further damage. Continued drinking has a very poor prognosis.

Answer 36

14 units binge drinking is 6 or more units for women and 8 or more for men in a single session

Answer 37

Alcohol-related liver disease Cirrhosis and its complications (e.g., hepatocellular carcinoma) Alcohol dependence and withdrawal Wernicke-Korsakoff syndrome (WKS) Pancreatitis Alcoholic cardiomyopathy Alcoholic myopathy, with proximal muscle wasting and weakness Increased risk of cardiovascular disease (e.g., stroke or myocardial infarction) Increased risk of cancer, particularly breast, mouth and throat cancer

Answer 38

Smelling of alcohol Slurred speech Bloodshot eyes Dilated capillaries on the face (telangiectasia) Tremor

Answer 39

Raised mean cell volume (MCV) Raised alanine transaminase (ALT) and aspartate transferase (AST) AST:ALT ratio above 1.5 particularly suggests alcohol-related liver disease Raised gamma-glutamyl transferase (gamma-GT) (particularly notable with alcohol-related liver disease) Raised alkaline phosphatase (ALP) later in the disease Raised bilirubin in cirrhosis Low albumin due to reduced synthetic function of the liver Increased prothrombin time due to reduced synthetic function of the liver (reduced production of clotting factors) Deranged U&Es in hepatorenal syndrome

Answer 40

Liver ultrasound may show early fatty changes with “increased echogenicity”. Later, it can show changes related to cirrhosis. Ultrasound is used to screen for hepatocellular carcinoma in patients with cirrhosis. Transient elastography (“FibroScan”) can be used to assess the elasticity of the liver using high-frequency sound waves. It helps determine the degree of fibrosis (scarring). Endoscopy can be used to assess for and treat oesophageal varices when portal hypertension is suspected. CT and MRI scans can be used to look for fatty infiltration of the liver, hepatocellular carcinoma, hepatosplenomegaly, abnormal blood vessel changes and ascites. Liver biopsy can be used to confirm the diagnosis of alcohol-related hepatitis or cirrhosis, particularly in patients where steroid treatment is being considered for alcohol-related hepatitis.

Answer 41

Stop drinking alcohol permanently (drug and alcohol services are available for support) Psychological interventions (e.g., motivational interviewing or cognitive behavioural therapy) Consider a detoxication regime Nutritional support with vitamins (particularly thiamine – vitamin B1) and a high-protein diet Corticosteroids may be considered to reduce inflammation in severe alcoholic hepatitis to improve short-term outcomes (but not long-term outcomes) Treat complications of cirrhosis (e.g., portal hypertension, varices, ascites and hepatocellular carcinoma) Liver transplant in severe disease (generally 6 months of abstinence is required)

Answer 42

The CAGE questions can be used to quickly screen for harmful alcohol use: C – CUT DOWN? Do you ever think you should cut down? A – ANNOYED? Do you get annoyed at others commenting on your drinking? G – GUILTY? Do you ever feel guilty about drinking? E – EYE OPENER? Do you ever drink in the morning to help your hangover or nerves?

Answer 43

AUDIT Questionnaire. The Alcohol Use Disorders Identification Test (AUDIT) was developed by the World Health Organisation to screen people for harmful alcohol use. It involves 10 questions with multiple-choice answers and gives a score. A score of 8 or more indicates harmful use.

Answer 44

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

Answer 45

Delirium tremens is a medical emergency associated with alcohol withdrawal. There is a 35% mortality rate if left untreated.

Answer 46

alcohol is a depressant substance. It stimulates GABA receptors in the brain. GABA receptors relaxes the electrical activity of the brain whilst alcohol inhibits the glutumate receptors (NMDA) which further relaxes brain's activity. Chronic alcohol use results in the GABA system becoming down-regulated and the glutamate system becoming up-regulated to balance the effects of alcohol. When alcohol is removed, the GABA system under-functions and the glutamate system over-functions, causing extreme excitability of the brain and excessive adrenergic (adrenalin-related) activity.

Answer 47

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

Answer 48

The CIWA-Ar (Clinical Institute Withdrawal Assessment for Alcohol, revised) tool can be used to score the patient on their withdrawal symptoms and guide treatment.

Answer 49

Chlordiazepoxide (Librium) is a benzodiazepine used to combat the effects of alcohol withdrawal. Diazepam is a less commonly used alternative. It is given orally as a reducing regime titrated to the required dose based on the local alcohol withdrawal protocol (e.g., 10 – 40 mg every 1 – 4 hours). The dose is reduced over 5-7 days. High-dose B vitamins (Pabrinex) is given intramuscularly or intravenously, followed by long-term oral thiamine. This is used to prevent Wernicke-Korsakoff syndrome.

Answer 50

thiamine (vitamin B1) poorly absorbed in the presence of alcohol.

Answer 51

wernicke's encepholopathy, Korsakoff syndrome

Answer 52

Confusion Oculomotor disturbances (disturbances of eye movements) Ataxia (difficulties with coordinated movements)

Answer 53

Memory impairment (retrograde and anterograde) Behavioural changes

Answer 54

Wernicke’s encephalopathy is a medical emergency with a high mortality rate. Korsakoff syndrome is often irreversible and results in patients requiring full-time institutional care. Prevention and treatment involve thiamine supplementation and abstaining from alcohol.

Answer 55

Copper deposition can lead to cirrhosis, affecting the CNS can lead to neurogloical and psychiatric problems. Neurological symptoms can include tremor, dysarthria (speech difficulties) and dystonia (abnormal muscle tone). Copper deposition in the basal ganglia causes Parkinsonism (tremor, bradykinesia and rigidity). Psychiatric symptoms can include abnormal behaviour, depression, cognitive impairment and psychosis.

Answer 56

autosomal recessive where there is excessive amount of copper in the body tissues, mainly in liver . caused by mutation in the Wilson disease protein gene on chrom-13. This copper protein-transporting protein is important in helping removing excess copper from the body via the liver. copper is excreted in the bile.

Answer 57

Teenagers or young adults. It is rare for symptoms to start after age 40. The presenting features vary significantly between individuals.

Answer 58

Kayser-Fleischer rings in the cornea (deposition of copper in Descemet’s membrane) may be seen in Wilson’s disease. These are green-brown circles surrounding the iris of the eye. They can usually be seen by the naked eye but proper assessment is made using slit lamp examination. Haemolytic anaemia (low haemoglobin caused by red blood cell destruction) may also be a feature.

Answer 59

Serum caeruloplasmin is the initial screening test for suspected Wilson’s disease. A low serum caeruloplasmin is suggestive of Wilson’s disease. Caeruloplasmin is the protein that carries copper in the blood. It can be falsely normal or elevated in cancer or inflammatory conditions. A 24-hour urine copper assay will show high urinary copper. Liver biopsy can be used to assess the liver copper content and assess liver disease. Scoring systems that consider various features and laboratory results are used to establish the diagnosis. Other investigations: Kayser-Fleischer rings on slit lamp examination MRI brain may show changes, including the characteristic “double panda sign” Low haemoglobin with haemolytic anaemia (negative Coombs test) Genetic testing (including screening family members)

Answer 60

Treatment is with copper chelation using either: Penicillamine Trientine It's to remove copper accumulated in tissues and to prevent further accumulation. Other treatments include: Zinc salts (inhibit copper absorption in the gastrointestinal tract) Liver transplantation,

Answer 61

NAFLD Alcoholic liver disease drug induced autoimmune disease

Answer 62

hepatitis B and D

Answer 63

Hepatitis A RNA Faecal-oral route Yes Supportive Hepatitis B DNA Blood/bodily fluids Yes Supportive/antivirals Hepatitis C RNA Blood No Direct-acting antivirals Hepatitis D RNA Always with hepatitis B No Pegylated interferon alpha Hepatitis E RNA

Answer 64

Hep A- supportive (doesn't lead to cirrhosis) Hep E- supportive (doesn't lead to cirrhosis) Hep B- supportive/ antivirals Hep C- direct-acting antivirals Hep D- Pegylated infer alpha

Answer 65

Hep A- faecal-oral- travelling Hep B- Blood, Bodily fluids Hep C- Blood Hep D- Always with Hep B Hep E- faecal-oral- seafood travelling

Answer 66

Hep A- yes Hep B- Yes Hep C- NO Hep D- No Hep E- No.

Answer 67

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

Answer 68

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

Answer 69

Type 1 typically affects women in their late forties or fifties. It presents around or after menopause with fatigue and features of liver disease on examination. It takes a less acute course than type 2. Type 2 usually affects children or young people, more commonly girls. It presents with acute hepatitis with high transaminases and jaundice.

Answer 70

Investigations will show high transaminases (ALT and AST) and minimal change in ALP levels (a “hepatitic” picture). Raised immunoglobulin G (IgG) levels are an important finding. Autoantibodies in type 1 autoimmune hepatitis are: Anti-nuclear antibodies (ANA) Anti-smooth muscle antibodies (anti-actin) Anti-soluble liver antigen (anti-SLA/LP) Autoantibodies in type 2 autoimmune hepatitis are: Anti-liver kidney microsomes-1 (anti-LKM1) Anti-liver cytosol antigen type 1 (anti-LC1)

Answer 71

Anti-nuclear antibodies (ANA) Anti-smooth muscle antibodies (anti-actin) Anti-soluble liver antigen (anti-SLA/LP)

Answer 72

Anti-liver kidney microsomes-1 (anti-LKM1) Anti-liver cytosol antigen type 1 (anti-LC1)

Answer 73

Liver biopsy forms part of the diagnosis. Key histology findings are interface hepatitis and plasma cell infiltration.

Answer 74

Treatment is with high-dose steroids (e.g., prednisolone). Other immunosuppressants are also used, particularly azathioprine. Immunosuppressant treatment is usually successful at inducing remission (controlling the disease). Liver transplant may be required in end-stage liver disease. Autoimmune hepatitis can reoccur in the new liver.

Answer 75

autosomal recessive resulting in iron overload. The human haemochromatosis protein (HFE) gene is located on chromosome 6. The majority of cases of haemochromatosis relate to C282Y mutations in this gene. Mutations are required in both copies of the gene (homozygous) since it is an autosomal recessive condition. This gene is important in regulating iron metabolism.

Answer 76

age ove 40, when iron overlaod become symptomatic. Chronic tiredness Joint pain Pigmentation (bronze skin) Testicular atrophy Erectile dysfunction Amenorrhoea (absence of periods in women) Cognitive symptoms (memory and mood disturbance) Hepatomegaly

Answer 77

It presents later in females due to menstruation acting to eliminate iron from the body regularly.

Answer 78

Serum ferritin is the initial investigation.

Answer 79

Haemochromatosis Infections (it is an acute phase reactant) Chronic alcohol consumption Non-alcoholic fatty liver disease Hepatitis C Cancer

Answer 80

Genetic testing for mutations in the HFE gene is used when the serum ferritin and transferrin saturation are both high in haemochromatosis.

Answer 81

Liver biopsy with Perl’s stain can be used to establish the iron concentration in the liver. Genetic testing means that a liver biopsy is not usually necessary for establishing a diagnosis. It may help stage the fibrosis and exclude other liver pathology.

Answer 82

Secondary diabetes (iron affects the functioning of the pancreas) Liver cirrhosis Endocrine and sexual problems (hypogonadism, erectile dysfunction, amenorrhea and reduced fertility) Cardiomyopathy (iron deposits in the heart) Hepatocellular carcinoma Hypothyroidism (iron deposits in the thyroid) Chondrocalcinosis (calcium pyrophosphate deposits in joints) causes arthritis

Answer 83

Venesection (regularly removing blood to remove excess iron – initially weekly) Monitoring serum ferritin Monitoring and treating complications

Answer 84

hypothyrodism- iron deposit in the thyroid cardiomiopathy- iron deposits in the heart secondary diabetes- iron affects the functioning of the pancrease.

Cirrhosis Flashcards

(115 cards)