Liver Disorders Flashcards
What is the lifespan of Red blood cells?
120 days
What is the breakdown components of Haemoglobin? (3)
- Globin -> amino acids
- Haem -> iron + protoporphyrin
- Protoporphorin -> converted into unconjugated bilirubin (lipid soluble)
Describe the process of bilirubin production from Haemoglobin? (5)
- Haem -> iron + protoporphyrin
- Protoporphorin -> converted into unconjugated bilirubin (lipid soluble)
- Albumin binds to unconjugated bilirubin and transports it to the Liver
- Hepatocytes conjugate UCB to produce conjugated bilirubin which is now water soluble
- This is then secreted via the bile ducts and stored in the Gall bladder as a component of bile.
What are the steps following Bilirubin secretion from the Gallbladder? (4)
- Gall bladder secretes bile into the duodenum to help with food digestion
- Bacteria in the intestine convert Bilirubin —> Urobilinogen
Urobilinogen; - Some gets reabsorbed by the blood, reaching the kidneys and excreted into the urine - giving it a yellow colour
- Remaining urobilinogen —> further converted —> stercobilinogen which remains in the colon and excreted into the faeces giving it a distinct brown colour
What is the pathophysiology of Jaundice?
- Disruption of hepatocytes preventing conjugation of the bilirubin
- Bilirubin leaks out of the cells
- Eventually enter the blood stream,
- Leading to a yellowing of the skin and sclera - which is high in elastin and binds to bilirubin with a higher affinity, thus can be the earliest sign.
What is the pathophysiology of neonatal jaundice?
- High rate destruction of fetal red blood cells at birth
- Leads to high level of unconjugated bilirubin
- New born livers also have a lower amount of UGT enzyme to convert and conjugate bilirubin
Neonatal jaundice : complications
Kernicterus - unconjugated bilirubin builds up its the basal ganglia leading to brain damage
Neonatal jaundice : Management
** Phototherapy **- targets bilirubin molecules and causes them to change shape, making them more soluble and able to be excreted in the urine
Jaundice : Causes in children
- Haemolytic anaemia or ineffective haemopeisis
- High volume of RBC degradation thus high levels conjugated bilirubin and aunconjugated bilirubin as hepatocytes may not be able to conjugate at this capacity - Gilbert’s syndrome - low levels of UGT enzyme activity, thus process of conjugation is much slower
- Unable to respond to physiological stress such as infection, increased hemolysis leading to a build up of Unconjugated bilirubin and jaundice.
What feature indicates high levels of unconjugated bilirubin in the blood?
**Pale urine **
* Uncojugated bilirubin cannot be excreted by the kidneys as it is not water soluble
Describe the anatomy of the Hepatic portal system? (5)
- Superior mesenteric vein + Inferior mesenteric vein : venous blood from small and large intestine
- Splenic vein : venous blood from spleen
- Right + Left gastric vein : venous blood from stomach
- Combine to form } Hepatic portal vein which contains all the nutrients absorbed from the GI tract and toxins for breakdown by liver and excretion from the kidneys
- Hepatic portal vein; enters the liver to form -
- Right and Left hepatic veins } enter the Inferior vena cave
Portal hypertension : Pathophysiology of disease
- Increased blood pressure in the hepatic portal venous system - largely due to hepatic cirrhosis which is when the liver tissue is replaced by fibrotic tissue.
- Blood is diverted from the liver - diminished liver function, decreased blood detoxification leads to a build up of toxic metabolites like ammonia.
- This can enter the blood stream and causes hepatic encephalopathy.
- Blood gets backed up into the systemic veins
Portal Hypertension : Clinical features (3)
Portal vein hypertension may be asymptomatic until complications occurs
1. Ascites, Caput medusa
1. GI bleeding 2nd to oesophageal varices
1. Jaundice if 2nd to liver dysfunction
Portal hypertension : Prehepatic causes
- Portal vein thrombosis
Portal hypertension : Hepatic causes
- Liver cirrhosis
- Sarcoidosis : granulomas develop inside the liver
Portal hypertension : Posthepatic causes
- Right sided heart failure, constrictive pericarditis : restrict the blood flow from the heart to lungs, causing blood to accumulate downwards including into the portal circulation
Portal hypertension : Investigations for diagnosis
- Gold standard - measure of a hepatic venous pressure gradient, Liver US,
- CT scan or MRI, Endoscopy - reveals varices.
Portal hypertension : Management
- TIPS procedure - intrahepatic protosystemic shunt to decrease hepatic portal pressure and prevent complications
- Betablockers e.g Propanolol - decreases portal venous pressure
Portal Hypertension : Complications
- Oesophageal varices
- Haeorrhoids
- Hypersplenism
- Ascites
Variceal haemorrhage : management
- Resuscitation :Blood + clotting agent transfusion, IV fluid resus
- Vasoactive agent : Telipressin for haemostats and rebreeding
- Prophylactic antibiotics in liver cirrhosis (reduced mortality)
- Endoscopy;
First line : Band ligation
Second line: Sengstaken-Blakemore tube
Third line : TIPPS procedure
ALT enzyme : Where is it found?
- Origin : found in high concentrations in the liver.
- ALT is usually higher than AST in most types of liver disease in which the activity of both enzymes is predominantly from the hepatocyte cytosol.
AST enzyme : origin?
- Origin : found in the liver, cardiac muscle, skeletal muscle, kidneys, brain, pancreas, lungs, leucocytes, and red cells.
- It is not as sensitive or specific for the liver as ALT and elevation in AST may be seen as secondary to nonhepatic causes as well.
ALT : Causes of elevation?
- Acute or chronic viral hepatitis
- Steatohepatitis
- acute Budd-Chiari syndrome,
- ischemic hepatitis,
- autoimmune, hemochromatosis, medications/toxins, alpha1-antitrypsin deficiency, Wilson disease, Celiac disease
Alkaline phosphatase : Origin?
Origin : highly concentrated in the microvilli of the bile canaliculus as well as several other tissues (e.g., bone, intestines, and placenta)
GGT : Origin?
Origin : on membranes of cells with high secretory or absorptive activities.
GGT : significance of rise?
- More specific for biliary disease when compared to alkaline phosphatase because it is not present in bone
Liver enzymes : Cholestatic pattern?
- Cholestatic pattern : indicates osbtruction of the biliary tract
- Elevated alkaline phosphatase + gamma glutamyl transferase + bilirubin > out of proportion to AST and ALT
Whta is cholestatic disease?
- Disorder chracterised by impaired bile flow within the liver or from the liver to the small intestine
- Distruption normal flow of bile
ALP + GGT + Bilirubin > AST and ALT : Hepatobiliary causes
- Bile duct obstruction
- primary biliary cirrhosis,
- primary sclerosing cholangitis
- infiltrating diseases of the liver (sarcoidosis, amyloidosis, lymphoma, among others), cystic fibrosis, hepatic metastasis, cholestasis
ALP + GGT + Bilirubin > AST and ALT : Non hepatic causes?
- Bone disease,
- Pregnancy,
- Chronic renal failure
- .Lymphoma or other malignancies, congestive heart failure, childhood growth, infection, or inflammation
Liver Cirrhosis : Pathophysiology of disease (5)
- Repeated insult to the liver due to excess alcohol or toxins can cause fibrosis
- process mediated by stellate checks that sit between the sinusoid and hepatocytes known as the pre sinusoidal space. - Stellate cells main function is to store vitamin A
- Hepatocytes damage causes them to release paracrine factors which activates changes in stellate cells.
- Stellate cells lose vitamin A, and secrete growth factor which causes them to produce collagen resulting in fibrosis
- Fibrotic tissue starts to build up and compress the central veins and sinusoids - resulting in Portal vein hypertension.
Liver cirrhosis : complications (5)
- Inability to metabolise and break down oestrogen : high levels of oestrogen in the blood can lead to gynecosmastia
- Inability to conjugate bilirubin : increase level of unconjugated bilirubin in the blood, leads to jaundice
- Inability to produce proteins : hypoalbuminaemia
- Inability to produce coagulation factors : coagulopathy
- Hepatic encephalopathy - release of toxins and ammonia in the blood.
Liver cirrhosis : Scoring system
- Model for end stage liver disease (MELD) - ( Child-Pugh classification was previously used)
- Used to assess severity of liver cirrhosis particularly for patients on list for liver transplant
- MELD - combination of bilirubin, creatinine and INR used to calculate 3 month mortality likelihood.
Liver cirrhosis : Investigation for diagnosis
Fibroscan - transient elastography a type of US to measure stiffness of the liver
Liver cirrhosis : Who should be offered screening and what does it entail?
** NICE Recommendations for :**
1. Upper endoscopy to check for varices in newly dx liver cirrhosis
2. Liver US every 6 months +/- alpha-feta protein to check for hepatocellular cancer
Screening should be offered to;
1. People with hepatitis C infection
2. Hx of severe alcohol excess
3. Alcoholic liver disease
Liver cirrhosis : Lab results?
- Elevated bilirubin
- Elevated liver enzymes
- Low platelet count
Acute liver failure : Definition
- Rapid onset of heaptocellular dysfunction leading to a variety of systemic complications
Acute Liver failure : Causes
- Paracetamol overdose
- Alcohol
- Viram hepatitis (A or B)
- Acute fatty liver of pregnancy
Acute Liver failure : Clinical features
- Jaundice
- Coagulopathy
- Hypoalbunaemia
- Hepatic encephalopathy
- Renal failure - hepatorenal syndrome
Liver disease : Explain the coaagulopathy seen?
Increases risk of thrombosis AND risk of bleeding
- In liver disease - all clotting factors are low except for ‘Factor VIII’
- Factor VIII - synthesis in the endothelial cells through out the body and not exclusively by the hepatocytes
- Poor function of the Liver - Factor VIII is nor cleared from the blood stream by the liver
- Higher levels of circulation Factor VIII, increases risk of thrombosis.
- Also - poor hepatic function reduces synthesis of anticoagulants such as Protein C, Protein S and anti-thrombin : increased risk of thrombosis
Non alcoholic fatty liver disease : Definition
- Fat deposition in the liver which is unrelated to alcohol or viral causes
- Associated with metabolic syndrome - obesity, diabetes, high cholesterol and hyperlipidaemia
Non alcoholic fatty liver disease : Pathophysiology
- Insulin resistance develops in various tissues including the liver
- Reduced response to insulin by the liver causes it to increase fat storage and decrease fatty acid oxidation.
- This results in decreased secretion of lipids into the blood and increased uptake of fatty acids from the blood, in a process called steatosis.
- Fat droplets form within the hepatocytes, resulting in inflammation - known as steatohepatitis.
- The chronic seato-hepatitis causes the stellate cells to lay down fibrotic tissue resulting in fibrosis.
- Chronic inflammation can cause fibrosis to progress into cirrhosis.
Non alcoholic fatty liver disease : Investigations for diagnosis
- US liver : Hepatomegaly and increased echogenicity
- Liver biopsy : to confirm the diagnosis
What is the management if an incidental finding of NAFLD?
ELF - Enhanced liver fibrosis test : blood test to check for advanced fibrosis
Non alcoholic fatty liver disease : Lab results of liver enzymes
Destruction of hepatocytes lead to release of liver enzyme into the blood;
* ALT (alanine transaminase) levels > AST (aspartate transaminase) of > 2
Alcoholic liver disease : Pathophysiology
- Ethanol —> (enzyme alcohol dehydrogenase) —> acetaldehyde
NAD+ —> NADH - High NADH and low NAD+ levels stimulate hepatocytes to produce more fatty acids, resulting in steatosis.
- Acetaldehyde can bind to molecules and proteins within the liver - forming acetaldehyde adducts which are recognised by the immune system as a foreign bodies, causing inflammation.
What is the disease progress in Alcoholic Liver disease?
Alcoholic fatty liver disease —> alcoholic hepatitis —> Alcoholic cirrhosis
Alcoholic liver disease : Investigation for diagnosis
Histology on biopsy : In Alcoholic hepatitis, mallory bodies which are damaged filaments of proteins are found in the histology.
Alcoholic liver disease : Labs result of liver enzymes
Liver enzymes : AST:ALT > ratio of 3, Gamma-GT is elevated
Alcoholic liver disease : Management
- Life style advice - avoid excess alcohol consumption
- Glucocorticoids e.g. Prednisolone - use to suppress immune system in the management of acute episode of alcoholic hepatitis
Hepatitis : Definition
Inflammation of the liver secondary to a virus
Hepatitis : Pathophysiology
- Viruses target hepatocytes causing them to display their antigens on the MHC class 1 molecules
- Triggers immune cell to infiltrate the liver and cause destruction of the infected hepaocytes
- Cytoxic destruction of the hepatocytes causes liver inflammation and hence hepatitis
Hepatitis : Clinical features
- Fever, malaise, nausea
- Hepatomegaly
- Hepatocyte damage - release of a mix of both conjugated and unconjugated bilirubin into the bloodstream
-Dark urine : due to rise in urobiinogen and conjugated bilirubin leaking into the blood and entering the urine
Hepatitis : Lab results of LFTs
Labs : raised ALT, raised AST, raised WCC
Heptatitis A : transmission and presentation
Transmission : through ingestion of contaminated food and water.
Presentation : Only presents as an acute episode - not chronic.
Heptatitis A : Lab results?
HAV-IgM antibody : indicates active infection
HAV-IgG : indicates previous infection or vaccination
Hepatitis A : Management
Option for immunisation
Heptatitis E: transmission and presentation
Transmission : trasmitted via oral-fecal route, acquired through undercooked sea food or contaminated water
Presentation : Only presents as an acute episode - not chronic.
Can be very serious in pregnant women
Hepatitis E : Lab results?
HEV-IgM antibody : indicates active infection
HEV- IgG : indicates previous infection or vaccination
Hepatitis E : Management
No option for immunisation
Heptatitis C : Transmission and presentation
Transmission : mostly via blood but low chance also via bodily fluids through sex e.g. IVDU,transfusion, childbirth, sex
Presentation : Can develop into chronic hepatitis
Heptatitis C : Lab results
HCV-IgG - is not regarded as a protective antibodies
HCV RNA test (gold standard) -can detect it within 1-2 weeks
Heptatitis B: Transmission and presentation
Transmission :mostly via sex/exchange of bodily fluids and blood
Presentation : develop into chronic hep B in 20% of cases, chronic Hep B is known to be linked to liver cancer.
What is the main complication of Hepatitis B?
Chronic Hepatitis B can develop into Hepatocellular cancer
Hepatitis B : HBsAg (HBV surface antigen)?
Key marker for HBV infection, present in acute infection then cleared in recovery.
If present for >6 months this indicates a chronic infection
Hepatitis B : HBcAg (HBV core antigen)
- Antigens from the core of the virus, present in active infection for 6 months, if present longer, individual is a carrier
Hepatitis B : Anti- HBe
Anti- HBe - secreted by infected cell ad marker of active viral replication, indicates active infection
Hepatitis B : Anti- HBs
Implies immunity either through exposure or immunisation
Hepatitis B : Anti- HBc
Anti-HBc - implies previous or current infection
* IgM anti-HBc : appears during acute or recent hepatitis B infection and is present for around 6 months
* IgG anti-HBc : persists following infection >6 months ago
Hepatitis B : In pregnancy?
- If pregnancy with Hep B - given vaccination + Hep B immunoglobulin
- Cannot be transmitted via breastfeeding (unlike HIV)
Primary biliary cirrhosis/cholangitis : Pathophysiology (4)
- Immune reaction, antibodies are created against the mitochondria of the cells within the bile ducts.
- Autoimmune disease where T cells attack the cells that line the smaller sized bile ducts in the liver
- As cells are damaged by immune attack, they start letting bile leaking into the hepatocytes and the blood.
- Inflammation of the bile ducts results in cholangitis, can cause progressive cholestasis, over time chronic inflammation can result in cirrhosis.
Primary biliary cirrhosis/cholangitis : Which other diseases is it associated with?
Associated with other immune disorders;
* Sjoren’s syndrome (seen in 80% of patients)
* Rheumatoid arthritis
* Systemic sclerosis
Primary biliary cirrhosis/cholangitis : Clinical feature
- Pruritus and itching - due to bile salts
- Cholestatic jaundice - bile and conjugated bilirubin leaking into the blood
- Xanthomas, xanthelasmas: Cholesterol within the bile - deposits within the skin,
- RUW, Hepatomegaly - can lead to liver failure
- Sx of sjoren’s syndrome and rheumatoid arthritis
Primary biliary cirrhosis/cholangitis
Itching in middle aged women
Primary biliary cirrhosis/cholangitis : Demographic
- Middle aged females 9:1
Primary biliary cirrhosis/cholangitis : Investigations for diagnosis (blood tests and imaging results)
- Immunology;
* Anti-mitochondrial (AMA) antibodies present in 98% of patients
* Raised IgM antibodies
Imaging - Ultrasound or MRCP of the liver/biliary tract to exlcude extrahepatic biliary obstruction
Autoimmune hepatitis : definition
Chronic inflammatory liver disease where antibodies are produced against hepatocytes
Unknown etiliology
Autoimmune hepatitis : Epidemiology
- Young females
- Associated with HLA-DR3 and HLA-DR4 which are both MHC class II surface receptors.
Autoimmune hepatitis (Type 1) : Which antibodies are found?
Type 1 - 80% of autoimmune hepatitis cases
* Anti-nuclear antibodies (ANA present)
* Anti-smooth muscle antibodies (ASMA present)
Autoimmune hepatitis (Type 2) : Which antibodies are found?
Type 2 - 20%
Defined as presence of antibodies to microsomes of the kidney or liver
1. Anti-liver/kidney microsomal antibody (ALKM antibody)
Autoimmune hepatitis : Clinicall features
- Amenorrhea (common)
- Acute/Chronic liver disease } jaundice, fever
Autoimmune hepatitis : Management
- Steroids and immunosuppressants e.g. Azathiprine
- Liver transplantation
Primary sclerosis cholangitis : Definition
- Sclerosis refers to hardening of tissues and cholangitis is the inflammation of the bile ducts
- Fibrosis and inflammation of both the intrahepatic and extra hepatic ducts
Primary sclerosis cholangitis :Pathophysiology
Autoimmune disease attacking and destroying the bile ducts epithelial cells - link with HLA B8 and HLA-DR3.
Primary sclerosis cholangitis : Which other diseases is it associated with?
Ulcerative colitis (80% of patient)
Crohns
Primary sclerosis cholangitis : Main complication?
Risk of cholangiocarcinoma
Primary sclerosis cholangitis : Clinical features
- Fibrosis obstructs the flow of bile, thus sx of obstructive jaundice
- Pruritus - bile salts and acids deposit in the skin\
- Jaundice
-Dark urine - conjugated bilirubin is filtered out via the kidneys
RUQ pain
Primary sclerosis cholangitis : Investigations for diagnosis
- ERCP/MRCP - Gold standard with biosy may show ‘onion skin’
Primary sclerosis cholangitis : Lab results?
Immunology;
1. Perinuclear anti-neutrophil cytoplasmic antibody (pANCA positive)
2. Elevated IgM
Lab results;
1. Raised bilirubin - bilirubinuria
2. Raised ALP and GGT
Primary sclerosis cholangitis : Management
Immunosupression
What are the differences between Primary Biliary Cholangitis and Primary Sclerosing cholangitis?
Primary biliary cholangitis
* - Associated with autoimmune disorder
* - Primarily affects the small bile ducts in the liver and causes accumuation of bile in the liver
* - Most common in middle afed wineb
Primary sclerosing cholangitis
* Immune and genetic factors - associated with Ulcerative colitis
* Characterised by inflammation and scarring inside and outside of the liver - can cause strictures and also affects larger bile ducts
* More common in younger men
Name the drugs which may induce/contribute to Liver damage and disease?
- Paracetamol
- Anti-epileptics : Sodium valproate, phenytoin
- Psychiatric drugs : Methyldopa
- Tuberculosis drugs : Isoniazid, rifampicin, pyrazinamide
- Statins
- Alcohol
Name the drugs which can cholestasis +/- hepatitis?
- Combine oral contraceptives - increases risk of gall stones forming
- Antibiotics - Flucloxacillin,** co amoxiclav**
- Phenothiazine - prochlorperazine
- Sulphonylureas
Name the drugs which can cause Liver Cirrhosis?
- Methotrexate
- Methyldopa
- Amiodorone
Cholangiocarinoma : Definition?
- Rare cancer of the bile duct arising from the epithelial cells of the intrahepatic and extra hepatic bile ducts
- High fatality due to late diagnosis and highly proliferative
Cholangiocarinoma : Risk factors?
- Primary sclerosis cholangitis (main risk factor),
- Chronic liver disease such as hepatitis or cirrhosis,
- Obesity
Cholangiocarcinoma : Clinical symptoms (3)
- Systemic : general malaise, weight loss, abdominal pain
- Extra hepatic disease - obstruction of drainage of bile from the liver
Jaundice, pruritus, dark urine - Intra hepatic disease : dull RUQ pain, malaise, weight loss
Cholangiocarcinoma : Clinical signs
- ‘Courvoisier sign’ - palpable mass in the RUQ
- ‘Sister Mary Joseph nodes’ - periumbilical lymphadenopathy
Cholangiocarcinoma : Investigations for diagnosis
Abdominal US with biopsy
Cholangiocarcinoma : Tumor marker
Tumor markers : CA 19-9, CEA
Cholangiocarcinoma : Lab results
Raised LFTs : elevated GGT, ALP
Elevated bilirubin
Cholangiocarcinoma : Management
Surgery for resection + chemotherapy
Ascities : Definition
abnormal accumulation of fluid in the abdomen
Ascites : What are the two categories?
- Serum ascites albumin level >11g/L
-normal level of protein in the blood, fluid in the abdomen is due to fluid load - Serum ascites albumin level <11g/L Due to low protein in the blood,
- reduced oncotic pressure
- Hypoalbunaemia - Nephrotic syndrome, severe malnourishment
Ascites : Causes of serum ascites albumin level <11g/L
- Hypoalbunaemia - Nephrotic syndrome, severe malnourishment
- Infections - tuberculosis
- Other - pancreatitis, bowel obstruction, biliary ascites
Ascites : Causes of serum ascites albumin level >11g/L
- Liver disorders e.g. cirrhosis, acute liver failure, liver metastases
- Cardiac disorders e.g. Right heart failure, constrictive pericarditis
- Other : Budd-Chiari syndrome, Portal vein thrombosis
Ascites : Management
- Reduce dietary sodium
- Fluid restriction if sodium <125
- Aldosterone antagonists e.g. Spirnolactone to reduce sodium- can add loop diuretics if not sufficient response
- Prophylactic antibiotics - reduce risk of spontaneous bacterial peritonitis
- Abdominal paracentesis - for large volume ascites
Ascites : Guidelines for Abdominal paracentesis
- Albumin cover : as removal of large volume of fluid >5L is associated with high rate of ascites recurrent, development of hepatorenal syndrome and higher rates of mortality
Spontaneous bacteria peritonitis : Definition
Bacterial infection of the peritoneal cavity of the abdomen
Commonly seen in patient sight ascites 2nd to liver cirrhosis
If due to Alcoholic liver disease - poor prognosis
Spontaneous bacteria peritonitis : Clinical features
Abdominal pain and tenderness,
Fever
Worsening ascite
Spontaneous bacteria peritonitis : Investigations for diagnosis
Paracentesis - neutrophil count >250 cells,
-most common organism is E.coli
Spontaneous bacteria peritonitis : Management
IV Ceforaxime
Spontaneous bacteria peritonitis : When are prophylactic antibiotics indicated and which?
Prophylactic Abx (Ciprofloxacin) should be given after ascites resolves if;
1. previous episode of SBP, Fluid protein <15
2. Child-Pugh of 9<
3. Hepatorenal syndrome
Primary Hepatocellular carcinoma : Pathophysiology (2)
- Mutation of the hepatocytes, observed when liver cells are forced to repair at a high frequency,
- This can be caused by any diseases which leads to cirrhosis and scarring of the liver tissue such as alcoholic hepatitis etc.
What is the most common cause of heaptocellular carcinoma
- In the world?
- In the UK?
- World :Chronic hepatits B
- Europe : Chronic hepatits C
Primary Hepatocellular carcinoma : Risk factors
- Heptitis B and C
- Alcohol
- Hemochromatosis
- Primary billiary cirrhosis
Primary Hepatocellular carcinoma : Tumor marker
Alpha feta protein tumor marker - raised as can be produced by the tutor or proliferating cells
Hepatocellular carcinoma : Clinical features
Symptoms present late
General sx of liver cirrhosis and liver failure:
1. RUQ pain
2. Hepatosplenomegaly
3. Pruritus
4. Ascites
Primary Hepatocellular carcinoma : 2WW criteria
If upper abdominal mass consistent with enlarged liver : 2WW Ultrasound scan
Primary Hepatocellular carcinoma : Lab results
Labs;
1. Destruction of hepatocytes - raised ALP and GGT
2. Alpha feta protein tumor marker
Primary Hepatocellular carcinoma : Screening protocol
Screening with US +/- alpha-fetoprotein for high risk groups such as ;
* Patients with liver cirrhosis 2nd to Hep B/C
* haemochromatosis
* alcohol abuse
Primary Hepatocellular carcinoma : Management
- Surgical resection with chemotherapy
- Radiofrequency ablation
- Liver transplantation
Hepatorenal syndrome ; Definiton
- Serious and potentially life-threatening complication of advanced liver disease, particularly cirrhosis.
- Characterized by the development of acute kidney injury in individuals with severe liver dysfunction
Hepatorenal syndrome : Pathophysiology
-
Portal Hypertension and Systemic Vasodilation:
-Liver cirrhosis causes liver scarring which increases resistance to blood flow through the liver, leading to portal hypertension.
-Portal hypertension can result in the dilation of blood vessels (vasodilation) in other parts of the body, including the kidneys.
- Activation of the Renin-Angiotensin-Aldosterone System (RAAS): The decreased blood flow to the kidneys due to vasodilation triggers the activation of the RAAS
- This activation leads to increased retention of sodium and water by the kidneys, further contributing to fluid overload.
- Sympathetic Nervous System Activation: The sympathetic nervous system, which plays a role in the body’s “fight or flight” response, is activated in response to reduced renal perfusion.
- This activation leads to vasoconstriction of renal blood vessels, which can exacerbate renal dysfunction.
- Circulatory Changes and Renal Ischemia: reduced blood flow to the kidneys lead to ischemia (inadequate blood supply), impairing the kidney function
Hepatorenal syndrome : Clinical features
Signs of Kidney injury
1. Decrease in urine output, increased levels of creatinine,and electrolyte imbalances
Signs of advanced liver disease
1. Ascites (fluid accumulation in the abdomen)
1. Hepatic encephalopathy (a decline in brain function due to liver dysfunction), may also be present.
