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(A) is the least worse among the other

if you are vaccinated for B then you will be protected from B and D

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This figure is only applicable for Hepatitis B

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Hepatitis C is the worst

it is asymptomatic

For hepatitis C, it is better for the patient to be listed on the transplantation list

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a. Fibrosis is the blue area
b. fibrosis is the red area
The spleen should be small

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There are vaccines only for Hepatitis A, B & E

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Blood supply enter through the liver helium

The hepatic artery, a branch of the coeliac axis, supplies 25% of the hepatic blood flow.

The portal vein drains most of the gastrointestinal tract and the spleen. It supplies 75% of hepatic blood flow

Acinus (functional hepatic unit)

1. consists of parenchyma (hepatocytes) supplied by the smallest portal tracts containing portal vein radicles, hepatic arterioles, and bile ductules

2. Cells in zone 1 more resistance to damage than those in zone 3

Sinusoids

It is a channel

Lacks a basement membrane and are loosely surrounded by specialist fenestrated endothelial cells and Kupffer cells (phagocytic cells).

Sinusoids are separated by plates of liver cells (hepatocytes).

The space of Disse is between sinusoids and hepatocytes, which contains a matrix of basement membrane constituents and stellate cells

Stellate cells: store retinoids in their resting state and contain desmin (intermediate filament). When activated (to myofibroblasts) they are contractile and regulate sinusoidal blood flow. Activated stellate cells produce signal proteins for synthesis or inhibition of degradation of extracellular matrix components, including collagen, as well as cytokines and chemotactic signals.

The biliary system

1. Bile canaliculi form a network between the hepatocytes.

2. These join to form thin bile ductules near the portal tract, which in turn enter the bile ducts in the portal tracts.

3. These then combine to form the right and left hepatic ducts that leave each liver lobe

4. The hepatic ducts join at the porta hepatis to form the common hepatic duct.

5. The cystic duct connects the gall bladder to the lower end of the common hepatic duct.

The common bile duct and pancreatic duct open into the second part of the duodenum most often through a common channel at the ampulla of Vater, which contains the muscular sphincter of Oddi

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1. Protein metabolism

1. Synthesis and storage

1. synthesis of proteins

1. such as albumin and fibrinogen

2. albumin has a role in oncotic pressure

2. The liver receives amino acids from the intestine and muscles and, by controlling the rate of gluconeogenesis and transamination, regulates plasma levels.

3. The liver also synthesizes all factors involved in coagulation

2. Degradation (nitrogen excretion)

1. degradation of aminoacids in the liver

2. Carbohydrate metabolism

1. Glucose homeostasis

2. It stores approximately 80 g of glycogen.

1. In the immediate fasting state, blood glucose is maintained either by glucose release from breaking down glycogen (glycogenolysis) or by synthesizing new glucose (gluconeogenesis).

3. Lipid metabolism

1. It synthesizes very-low-density lipoproteins (VLDLs) and high-density lipoproteins (HDLs).

2. Triglycerides can be synthesized in the liver

3. Cholesterol can be synthesized in the liver from acetyl-CoA

Formation of bile (look at the figure below!)

Bile consists of water, electrolytes, bile acids, cholesterol, phospholipids and conjugated bilirubin. Two processes are involved in bile secretion across the canalicular membrane of the hepatocyte – bile salt-dependent and bile salt independent processes.

Bile formation requires uptake of bile acids and other organic & inorganic ions across the basolateral (sinusoidal) membranes by transport proteins.

Bile acids are also synthesised in hepatocytes from cholesterol.

Secretion of a bicarbonate-rich solution is stimulated mainly by secretin and is inhibited by somatostatin.

Bile acids act as detergents; their main function is lipid solubilization. Bile acid molecules have both a hydrophilic and a hydrophobic end. In aqueous solutions they form micelles, with their hydrophobic (lipid-soluble) ends in the centre. Micelles are expanded by cholesterol and phospholipids (mainly lecithin), forming mixed micelles.

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Blood tests

Liver "function" tests

serum albumin and bilirubin

Serum albumin: falling serum albumin is a bad prognostic sign.

prothrombin time (PT)

prothrombin time: Because of its short half-life, it is a sensitive indicator of both acute and chronic liver disease

Liver biochemistry

serum aspartate (AST) and alanine aminotransferases (ALT) - reflecting hepatocellular damage

AST: High levels are seen in hepatic necrosis

ALT: is a cytosol enzyme, more specific to the liver so a rise only occurs with liver disease.

serum alkaline phosphatase (ALP), gamma-glutamyl transpeptidase – reflecting cholestasis

raised in both intrahepatic and extrahepatic cholestatic disease of any cause

total protein

The proteins in the globulin fraction, raised in liver disease

gGT (see table)

obstruction of bile excretion

ammonia

degradation of aminoacids to urea

accumulation of ammonia in the brain is toxic and indicates (??? check)

Viral markers

Additional blood investigations: haematological, biochemical, immunological, markers of liver fibrosis and genetic analysis. (there is a figure for that!)

Urine tests – for bilirubin and urobilinogen

Imaging techniques – to define gross anatomy

Liver biopsy – for histology

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Acute liver disease

Signs:

jaundice → seen in the conjunctivae and sclerae

pale stools and dark urine

Spider naevi and palmar erythema

Symptoms:

malaise, anorexia and fever. Jaundice may appear as the illness progresses.

Chronic liver disease

Signs (see the figure)

Symptoms

Right hypochondrial pain due to liver distension

Abdominal distension due to ascites

Ankle swelling due to fluid retention

Haematemesis and melaena from gastrointestinal haemorrhage

Pruritus due to cholestasis

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(Look at the figure)

Blood changes

If the liver is fibrotic --> portal hypertension --> blood stream change splenomegaly caused by the blood builds up --> more breaking down --> bone marrow changes

caput medusea --> contributes to ascites

functional

coma caused by hyperammonemia

jaundice --> bilirubin

anemia --> iron deficiency

hyperestrogenism --> too much oestrogen caused by the liver dysfunction (the liver normally catabolizes that hormone)

The skin will be red

spider naevi (pic included)

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Ascites

Causes

Sodium & water retention

Portal hypertension

exerts a local hydrostatic pressure and leads to increased hepatic and splanchnic production of lymph and transudation of fluid into the peritoneal cavity

Low serum albumin

contribute by a reduction in plasma oncotic pressure.

________________________________________________________________

The skin

spider naevi on chest and upper body

telangiectases that consist of a central arteriole with radiating small vessels.

In haemochromatosis the skin may have a slate-grey appearance

The abdomen

hepatomegaly & Splenomegaly (due to portal hypertension)

The endocrine system

Gynaecomastia and testicular atrophy

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Protein metabolism

The liver is the principal site of synthesis of all circulating proteins apart from γ-globulins

Albumin

Controls plasma levels by controlling gluconeogensis and transamination

Transport of carrier proteins

Synthesises coagulation factors

Storage of vitamins and minerals

Degradation of amino acids produces ammonia -> urea

Carbohydrate metabolism

Glucose homeostasis and the maintenance of the blood sugar is a major function of the liver.

In the immediate fasting state, blood glucose is maintained either by glucose release from breaking down glycogen (glycogenolysis) or by synthesizing new glucose (gluconeogenesis).

In prolonged starvation, ketone bodies and fatty acids are used as alternative sources of fuel as the body tissues adapt to a lower glucose requirement

Lipid metabolism

It synthesizes very-low-density lipoproteins (VLDLs) and high-density lipoproteins (HDLs)

HDLs are the substrate for lecithin-cholesterol acyltransferase (LCAT), which catalyzes the conversion of free cholesterol to cholesteryl ester

MDLs remove triglycerides

Cholesterol may be of dietary origin but most is synthesized from acetyl-CoA mainly in the liver, intestine, adrenal cortex and skin.

Bile formation

Bile secretion & metabolism

Bile formation requires uptake of bile acids and other organic and inorganic ions across the basolateral (sinusoidal) membranes by multiple transport proteins; NTCP and sodium independent OATP2,

Two processes are involved in bile secretion across the canalicular membrane of the hepatocyte – bile salt-dependent and bile salt independent processes – each contributing about 230 mL/ day.

Bile salt-dependent process:

the bile acid receptor, farnesoid X, blocks bile acid formation from cholesterol and also regulates the transport proteins (NTCP, OATP2) that increase bile acid uptake by the liver Na+ and water follow the passage of bile salts by diffusion across the tight junction between hepatocytes.

In the bile salt-independent process, water flow is due to other osmotically active solutes such as glutathione and bicarbonate.

The bile acids are excreted into bile and then pass via the common bile duct into the duodenum

Bilirubin metabolism

Bilirubin is produced from breakdown of mature red cells by Kupffer cells in the liver and reticuloendothelial system; 15% of bilirubin is formed from catabolism of other haem-containing proteins

Normally, 250–300 mg daily.

unconjugated bilirubin is water-insoluble, due to internal hydrogen bonding, and is transported to the liver attached to albumin.

Bilirubin dissociates from albumin and is taken up by hepatic cell membranes and transported to the endoplasmic reticulum by cytoplasmic proteins, where it is conjugated with glucuronic acid and excreted into bile.

conjugated bilirubin is water-soluble and is actively secreted into biliary canaliculi and excreted into the intestine within bile

not absorbed from the small intestine because of its large molecular size

In the terminal ileum, bacterial enzymes hydrolyse the molecule, releasing free bilirubin which is then reduced to urobilinogen, some of which is excreted in the stools as stercobilinogen.

The remainder is absorbed by the terminal ileum, passes to the liver via the enterohepatic circulation, and is re-excreted into bile. Then excreted kidneys

= When hepatic excretion of conjugated bilirubin is impaired, a small amount is strongly bound to serum albumin and is not excreted by the kidneys; it accounts for the persistent hyperbilirubinemia

Hormone and drug activation

The liver catabolizes hormones such as insulin, glucagon, oestrogens, growth hormone, glucocorticoids and parathyroid hormone.

It is also the prime target organ for many hormones (e.g. insulin).

It is the major site for the metabolism of drugs and alcohol.

Fat-soluble drugs are converted to water-soluble substances that facilitate their excretion in the bile or urine.

Cholecalciferol is converted to 25-hydroxycholecalciferol.

Immunological function

The hepatic reticuloendothelial system contains many immunologically active cells.

The liver acts as a ‘sieve’ for bacterial and other antigens carried to it by the portal vein from the gastrointestinal tract.

These antigens are phagocytosed and degraded by the Kupffer cells, which have specific membrane receptors for ligands and are activated by several factors, such as infection.

Antigens are degraded without the production of antibody, as there is very little lymphoid tissue and thus, they are prevented from reaching antibody-producing sites and thereby prevent generalized adverse immunological reactions

Cytokines also stimulate hepatic apoptosis.

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The bile is then reabsorbed in the intestines

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Bilirubin metabolism and elimination (important)

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Bilirubin metabolism and elimination (important)

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Hepatic encephalopathy, a condition that happens when the liver is too diseased or damaged to properly process ammonia. In this disorder, ammonia builds up in the blood and travels to the brain. It can cause confusion, disorientation, and coma. It can sometimes be fatal

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Types

Haemolytic jaundice

Increased bilirubin load for the liver cells

because there is more breakdown of red blood cells

Urinary urobilinogen is increased

congenital hyperbilirubinemias (non-haemolytic)

Unconjugated (lipid-soluble, bound to albumi)

Gilbert's syndrome

asymptomatic

Crigler-Najjar syndrome

Conjugated (soluble, addition of glucuronic acid to unconjugated in the liver.

Dubin-Johnson & Rotor syndromes

Benign recurrent intrahepatic cholestasis

Progressive familial intrahepatic cholestasis (PFIC) syndromes

Cholestatic jaundice (acquired)

Extrahepatic: is due to large duct obstruction of bile flow at any point in the biliary tract distal to the bile canaliculi

Intrahepatic: occurs owing to failure of bile secretion

Differential diagnosis:
You ask for the history of the patient to see whether it is possible to get infected by trevelling.

we look at age

a young person is more likely to have hepatitis, so questions should be asked about drug and alcohol use, and sexual behaviour

An elderly person with gross weight loss is more likely to have a carcinoma

Clinical features

Hepatomegaly: seen in hepatitis and with extrahepatic obstruction

Splenomegaly: indicates portal hypertension

Ascites: found in cirrhosis but can also be due to carcinoma

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Acute hepatitis

Acute parenchymal liver damage can be caused by many agents

Chronic hepatitis

is defined as any hepatitis lasting for 6 months or longer

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Incidence

affects 3–6% of the population in the USA

25% according to the lecture (check this p: )

Histological changes

from simple fatty change to fatty inflammation to fibrossi

Risk factors

Oxidative stress injury

Diagnosis

ultrasound, with the exclusion of other causes of liver injury

Liver biopsy allows staging of the disease but when this should be performed is unclear

Elastography is being used to evaluate the degree of fibrosis.

Management

weight loss, exercise, strict control of hypertension, diabetes and lipid levels are the only treatments

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Aetiology

Alcohol

Viral infections

NASH

Autoimmune disorders

Cholestatic disorders

Metabolic diseases

Pathogenesis

Injury -> cirrhosis can take 5-50 years, affected by risk factors

Injury -> fibrosis (resolvable!)

Inflammatory damage

Matrix deposition

Parenchymal necrosis

Angiogenesis

Fibrosis -> Cirrhosis (can regress)

Disrupted architecture

Loss of function

Aberrant hepatocyte regeneration

Pathology

Destruction of extracellular matrix

formation of micro and macro nodules

Micronodular

Macronodular

aggregated cells, clumps

Redistribution of blood supply in liver

Investigations - to check prognosis & liver function

Severity

Type

Imaging

Biopsy

Management

Transplant

Reversing damage by removing underlying cause

Course and prognosis

5 year survival rate of 50%

Depends on influencing factors

Genetic

Environment

Liver transplantation

Indications

Mainly: cirrhosis or conditions which result in this

Contraindication

sepsis

rate of recurrence of carcinoma is high

Preparation

Rejection

Prognosis

90% 1 year, 70-85% 5 year survival

Carcinoma's can recur

Complications and effects

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aetiology: alcohol, viral infection, hepatitis B and C

there is also a table for the causes

Pathogenesis

Chronic injury to the liver results in inflammation, necrosis and, eventually, fibrosis

Fibrosis is initiated by activation of the stellate cells.

Kupffer cells, damaged hepatocytes and activated platelets are probably involved.

Stellate cells are activated by many cytokines and their receptors, reactive oxygen intermediates and other paracrine and autocrine signals

Inflammatory cells contribute to fibrosis via cytokine secretion

In the space of Disse, the normal matrix is replaced by collagens

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Investigations

Severity

Liver function – serum albumin & prothrombin time are the best indicators of liver function. Prognosis poor with albumin below 28 g/L.

Liver biochemistry – All biochemistry deranged in decompensated cirrhosis. Can be normal, depending on severity.

Serum electrolytes – Low sodium indicates severe liver disease.

Serum creatinine – Elevated concentration = worse prognosis.

Type

Viral markers

Serum autoantibodies

Serum immunoglobulins

Iron indices and ferritin

Copper, ceruloplasmin

Alpha1-Antitrypsin

Imaging

Ultrasound – can demonstrate change in size & shape. Useful in detecting hepatocellular carcinoma.

to measure fibrosis we use elastography

CT scan – shows hepatosplenomegaly and dilated collaterals. Can detect hepatocellular carcinoma.

Endoscopy – detection and treatment of varices and portal hypertensive gastropathy.

MRI scan – Diagnosis of both benign and malignant tumours.

Liver biopsy – usually necessary to confirm the type & severity of disease.

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management of complications seen in decompensated cirrhosis.

Patients with compensated cirrhosis should lead a normal life.

Reduce dietary salt intake

avoid aspirin and NSAIDs, and avoid alcohol.

Course is varaible depending on severity and locations

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Liver Transplantation –

Indications for transplantation – acute: fulminant hepatic failure of any cause. Chronic: complications of cirrhosis no longer responding to therapy.

Contraindications – active sepsis, malignancy outside the liver, liver metastases, no psychological commitment. Patients 70 or older are not usually transplanted.

Prognosis – in low-risk patients, 90% 1-year survival. 5-year survival is as high as 70-85%.

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https://www.webmd.com/hepatitis/digestive-diseases-liver-transplantation

Criteria MELD (look at them in the  article/lecutre)

you need to know this

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What Is a Liver Transplant?

A liver transplant is a surgical procedure that replaces someone's diseased liver with all or part of a healthy one from another person, who's called a donor.

When Is a Liver Transplant Needed?

The liver is your largest internal organ. An adult's weighs about 3 pounds. It's just below your diaphragm on the right side of your belly. Your liver does many important things, including making proteins and breaking down nutrients from food to help your body make energy.

You might need a transplant if your liver doesn't work the way it should. This is called liver failure.

Liver failure can happen suddenly as a result of viral hepatitis, drug-induced injury, or infection. This is called acute or fulminant hepatic failure.

It can also be the end result of a long-term problem (chronic). Conditions that can cause chronic liver failure include:

Chronic hepatitis with cirrhosis

Primary biliary cholangitis, a rare condition in which your immune system destroys your bile ducts

Sclerosing cholangitis, scarring and narrowing of the bile ducts inside and outside your liver, causing bile to back up

Biliary atresia, a rare liver disease that affects newborns

Alcohol overuse

Liver cancers such as hepatocellular carcinoma

Wilson's disease, which causes unusual levels of copper throughout your body, including in your liver

Hemochromatosis, in which your body has too much iron

Alpha-1 antitrypsin deficiency, an unusual buildup of a protein called alpha-1 antitrypsin in your liver, resulting in cirrhosis

How Do People Get Selected for Liver Transplants?

Your doctor may recommend a liver transplant if they've ruled out all other treatments for your condition and if they think you're healthy enough for surgery. They'll refer you to a transplant center. There, you'll talk with specialists and have tests to find out whether you can get a transplant.

Each center has different rules about who can have a transplant. You might not be able to get one if you have:

A severe infection

Problems with alcohol or drug use

Cancer outside your liver

Serious heart or lung disease

You or your caregivers will also need to understand and follow your doctor's directions after the surgery, including medications that you'll take for the rest of your life.

Your Liver Transplant Team

A team of specialists will help you every step of the way. They include:

A liver specialist (called a hepatologist)

A transplant surgeon

A transplant coordinator, usually a registered nurse who specializes in the care of liver transplant patients. This person will be your main contact with the transplant team.

A social worker to discuss your support network of family and friends, employment, and financial needs

A psychiatrist to help you deal with issues that might come along with a transplant, such as anxiety and depression

An anesthesiologist

A chemical dependency specialist to help if you have a history of alcohol or drug use

A financial counselor to act as a go-between for you and your insurance company

Which Tests Are Required Before Getting a Liver Transplant?

Bring all medical records, X-rays, liver biopsy slides, and a record of your medications to your evaluation for a liver transplant. The team might do tests including:

CT, which uses X-rays and a computer to make pictures of your liver. CTs and chest X-rays will also check your heart and lungs.

Doppler ultrasound to find out whether the blood vessels to and from your liver are open

Echocardiogram to check your heart

Pulmonary function studies to look at how well your lungs exchange oxygen and carbon dioxide

Blood tests to learn more about your blood and to check how well your liver is working. You'll also be screened for HIV, other viruses (such as herpes and Epstein-Barr), and hepatitis.

How Does the Liver Transplant Waiting List Work?

If you meet the criteria for a transplant but don't have a donor lined up, the center will put you on a waiting list. It lists patients according to their blood type, body size, and medical condition (how ill they are). Each patient is given a priority score based on three blood tests ( creatinine, bilirubin, and INR). The score is known as MELD (model of end-stage liver disease) in adults and PELD (pediatric end-stage liver disease) in children.

Patients who have the highest scores and acute liver failure get top priority for a liver transplant. If their condition gets worse, their scores rise, and their priority for transplant goes up. This way, the transplants go to people who need them the most.

It's hard to say how long you might have to wait to get a liver. Your transplant coordinator is always available to discuss where you are on the waiting list.

Where Does a Liver for a Transplant Come From?

You might get a liver from a donor who's alive or one who's died.
Living donor
In a living donor liver transplant, your doctor will take part of a healthy person's liver and implant it in you. Both liver segments will grow back to their regular size in a few weeks.
Deceased donor
A donor who's died may have had an accident or head injury. Their heart is still beating, but they're legally dead because their brain has stopped working permanently. The donor is usually in an intensive-care unit. The team turns off life support in the operating room during the transplant.

The donor's identity and the details of their death are confidential.

Depending on your condition, you might have a "domino" liver transplant. This is when a young person who has a metabolic liver disease gets a liver from a healthy donor. But rather than destroying the young person's liver, doctors give it to an older patient who has a more diseased liver. It can take decades for the older person to have signs of the metabolic disease. Or they may never get it at all. Domino transplants help widen the pool of people who can donate organs.

Who Can Be a Liver Transplant Donor?

A living donor may be a relative, a spouse, a friend, or an unrelated "Good Samaritan." They'll have complete medical and psychological tests to keep risks as low as possible. Blood type and body size are crucial to finding a match. A donor younger than 60 years old is ideal.

Hospitals will check possible donors for liver problems or other things, including:

Liver disease

Overuse of alcohol or drugs

Cancer

Infections

Hepatitis

HIV

What Happens When They Find a Liver Transplant Match?

A transplant coordinator will contact you when they've found a possible donor liver. Don't eat or drink anything after they tell you to go to the hospital. When you get there, you'll probably have more blood tests, an electrocardiogram, and a chest X-ray. You also may meet with the anesthesiologist and a surgeon. If the donor liver is approved, the transplant will go ahead. If not, you'll go home.

What Happens During the Liver Transplant Operation?

Liver transplants usually take 6 to 12 hours. Your surgeons will take out your liver and replace it with the donor liver. Because a transplant is a major procedure, the surgeons will put several tubes in your body. These tubes are necessary to help your body do certain things during the operation and for a few days afterward.

What Complications Are Associated With Liver Transplant?

A liver transplant is a complex procedure that may have complications soon afterward or many years later.

Rejection
Your immune system destroys things that invade your body. But it can't tell the difference between your transplanted liver and unwanted invaders, such as viruses and bacteria. So your immune system may attack your new liver. This is called a rejection episode. About 64% of liver transplant patients have some kind of organ rejection, most within the first 90 days. You'll get anti-rejection medications to prevent an immune attack.
Infection
The drugs that you take to keep your body from rejecting your new liver weaken your immune system. They're called immunosuppressants. They make you more likely to get an infection. This problem goes away over time.
Liver function problems
About 1% to 5% of new livers don't work as well as they should or don't work at all. If it doesn't get better quickly, you might need a second transplant.
Surgical risks
Complications related to the operation include:

Clots in the artery that takes blood from your heart to your liver (called hepatic artery thrombosis) or in the vein that takes blood from your intestines, pancreas, and spleen to your liver (portal vein thrombosis)

Bile leaking out of your bile ducts and into your belly

Narrowed bile ducts

Bleeding

Infection of the surgical wound

Return of disease
Some conditions that cause liver failure can still damage or destroy your new liver. These include:

Hepatitis C

Primary sclerosing cholangitis

Fatty liver disease

Cancer
People who have an organ transplant have a 25% higher chance of getting skin cancer than the rest of the population. Immunosuppressant drugs can also make you more likely to get other cancers, including a rare condition called post-transplant lymphoproliferative disorder (PTLD).

What Are Anti-Rejection Medications?

You'll need to take at least one immunosuppressant for the rest of your life. You might get a mix of a calcineurin inhibitor (CNI) such as cyclosporine ( Neoral) or tacrolimus ( Prograf); a glucocorticoid such as prednisone ( Medrol, Prelone, Sterapred DS); and a third agent such as azathioprine ( Imuran), everolimus (Afinitor, Zortress), mycophenolate mofetil (CellCept), or sirolimus ( Rapamune).

These drugs can have serious side effects. Along with a higher chance of infection, they can cause:

Bone loss

Diabetes

High blood pressure

High cholesterol

Kidney damage

Weight gain

Other drugs and supplements can affect how these medications work. Talk to your doctor before taking anything new or if you have concerns about side effects.

When Will I Be Able to Go Home After a Liver Transplant?

The average hospital stay after a liver transplant is 2 to 3 weeks. Some patients go home sooner, but others have to stay longer.

The nursing staff and your transplant coordinator will start to get you ready for discharge soon after you move from the intensive care unit (ICU) to the regular nursing floor. They'll give you a discharge manual, which reviews much of what you need to know before you go home.

You'll learn how to take new medications and how to check your blood pressure and pulse. You'll also learn the signs of rejection and infection, and you'll know when it's important to call your doctor.

Many people have to be admitted to the hospital again, especially within the first year after a transplant. This is usually for treatment of a rejection episode or infection.

After a Liver Transplant
Follow-up care
Your first return appointment will probably be about 1 to 2 weeks after you leave the hospital. You'll see your transplant surgeon and transplant coordinator. A social worker or a member of the psychiatric team may also be available. After that, you'll have follow-ups 3, 6, 9, and 12 months after the transplant and then once a year for the rest of your life.

Your primary care doctor should be notified when you have your transplant and when you're discharged. Though your transplant center will handle most problems related to the transplant, your primary care doctor will remain an important part of your medical care.

Self-care
Some lifestyle changes can protect your overall health after a liver transplant.

Eat a healthy, balanced diet. Limit salt, cholesterol, fat, and sugar. A dietitian or nutritionist can help you make a meal plan.

Don't eat grapefruit or drink grapefruit juice. They can affect how some immunosuppressants work.

Don't eat unpasteurized milk products or raw eggs, meat, or fish.

Don't drink alcohol or use it in food if you have a history of alcohol use disorder.

Get regular exercise.

Don't smoke.

Limit your contact with things that can carry germs, such as soil, mosquitoes, ticks, rodents, reptiles, birds, and water from lakes or rivers.

If you're planning to travel, especially to a developing country, talk to your care team about how to lower risks at least 2 months before you leave.

Liver Transplant Outlook

Your outlook after a liver transplant depends on several things, including the condition that caused your liver failure. About 88% of patients live at least a year after their transplant, and 73% live at least 5 years.

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You might need a liver transplant if your liver doesn't work the way it should. This is called liver failure. Learn more about liver transplantation, including when it may be needed, how candidates are picked, what to expect from the procedure, and what happens after surgery.

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Complications that could kill the patient:

renal failure

bleeding

carcinoma

heptopulmonary syndrome

vasorenal system

Portal hypertension & gastrointestinal haemorrhage

Prehepatic – due to blockage of the portal vein before the liver

Intrahepatic – due to distortion of the liver architecture, which can be presinusoidal or post-sinusoidal (cirrhosis)

Post-hepatic – due to venous blockage outside the liver (rare)

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Secondary liver tumours – secondary (metastatic) tumours, most common.

Clinical features – variable but usually include weight loss, malaise, upper abdominal pain, and hepatomegaly, with or without jaundice.

Diagnosis – ultrasound is primary, with CT or MRI to look for primary. Serum alkaline phosphatase is elevated.

Treatment – Depends

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Hepatocellular carcinoma – 5th most common cancer worldwide

Aetiology – carriers of HBV or HCV. Also associated with cirrhosis.

Pathology – single or occurs in multiple nodules. Histologically consists of cells resembling hepatocytes.

Clinical features – weight loss, anorexia, fever, ache in the right hypochondrium, and ascites.

Investigations – Ultrasound scans show filling defects in 90% of cases. CT, MRI, biopsy.

Treatment & prognosis – median survival rate of 5 years if surgical resection is possible. Transplantation is usually limited due to the underlying cause of HCC. Conventional chemotherapy and radiotherapy unsuccessful.

Prevention – vaccination against HBV.

this reduces the annual incidence of the disease

Cholangiocarcinoma – increasing in incidence. Can be intra- or extrahepatic. Not associated with HBV or cirrhosis. Clinical features similar to primary HCC. Patients usually die within 6 months.