Acid Base Balance And Liver Functions And Its Disorders

Question 1

What is acid base balance

Answer 1

Acid-base homeostasis involves maintenance of acidity of body fluids at optimal levels for proper functioning of the whole individual.

It employs chemical and physiological processes.

Question 2

What is the pH for blood

Answer 2

The pH of blood 7.35 - 7.45 7.40 (optimum pH) < 6.8 or > 8.0 can result in death

Question 3

What are the major sources of acid load

Answer 3

Cellular metabolism produces CO2 Incomplete Metabolism of Carbohydrates Increased oxidation of Fatty acids Acids produced by metabolism of proteins, phosphoprotein, phospholipids Acids taken in with foods Disease processes

Question 4

Why do you have to preserve acid base balance

Answer 4

Protein Denaturation & loss of biological function

• Enzyme- Optimal activity

• Hormones - Binding to receptors

• Changes in the distribution of electrolytes (Ca, Mg, Na+ , K+ , Cl- )

• Changes in excitability of nerve and muscle cells

• Decreases effectiveness of medications

Question 5

What are the three lines of defense of an acid base hemostasis

Answer 5

Buffer systems

• Respiratory system

• Renal system

Question 6

What are buffer systems

Answer 6

A buffer is a solution that can reversibly bind hydrogen ions

§A pH buffer works chemically to minimize changes in the pH of a solution §The body uses pH buffers in the blood to guard against sudden changes in acidity §Buffer systems act rapidly and constitutes the body’s first line of defense again

Question 7

What is the bicarbonate buffer system

Answer 7

Bicarbonate (HCO3 ) & carbonic acid (H2 CO3 ) An important ECF buffer. ~ 75% HCO 3 - : H2 CO 3- —-ratio maintained at 20:1

H + + HCO 3 - ⇄ H2 CO 3 ⇄ CO2 +H2 O

++ HCO 3-⇄ H2CO 3⇄ CO2+H2O H + is buffered Bicarbonate is consumed

Hyperventilation via the lungs H2 CO 3 ⇌ H2 O + CO2 ­

H+ + HCO 3 - ⇄ H2 CO 3 ⇄ CO2 +H2 O Any imbalance in CO 2 would lead to accumulation of H+ & HCO 3 which can be regulated by the kidneys

Question 8

What is the phosphate buffer system

Answer 8

Major ICF buffer –~5% HPO4 2 - /H2 PO4 -

H + + HPO 4 2- ⇄ H2 PO4-

Essential in the excretion of acids by the kidneys.

Question 9

What is the protein buffer system

Answer 9

~20 %

• Albumin accounts for 95 % of the non-bicarbonate buffercapacity of the plasma

•

• Haemoglobin –has a high hydrogen ion binding capacity effective buffer in the RBCs

Question 10

Describe physiological regulation

Answer 10

Buffering is but a temporal or short- term response to maintaining pH balance.

• Eventually all H + buffered must be excreted to maintain a normal pH balance.

Serves as the 2 nd line of defense.

The 2 main organs primarily responsible for acidbase regulation are:

LUNGS- Respiratory regulation KIDNEYS- Renal regulation

Question 11

What is respiratory regulation

Answer 11

Respiratory Regulation is primarily responsible for the volatile gas- CO ₂

• The lungs help regulate acid-base balance by eliminating or retaining CO ₂

Respiratory centers (Chemoreceptors) in the brain respond to changes in pH of blood by altering the rate of ventilation

• The respiratory centers and lungs are able to regulate the blood pH by adjusting the speed and depth of breathing

Question 12

What are the three main mechanisms for acid base regulation by the kidneys

Answer 12

The kidney regulates acid by 3 main mechanisms: ⁺

• Excretion of H

• Generation of HCO ₃ ⁻

• Reabsorption of filtered HCO ₃ ⁻

Question 13

What is renal regulation

Answer 13

With the net effect of eliminating the non-volatile acid load

ØA. H + secretion/excretion

Ammonia buffer Phosphate buffer

ØB. HCO 3 reabsorption

Proximal tubule – 90% the thick ascending limb, distal tubules & in the collecting tubule

Ø C. HCO 3 Reclamation or regeneration Distal tubule

Question 14

What is an acid base disorder

Answer 14

An acid-base disorder is a change in the normal pH of the blood that may result when:

• Renal or respiratory function is abnormal

• Acid or base load overwhelms excretory capacity

Question 15

What are the classifications of acid base disorders

Answer 15

Respiratory acidosis
Respiratory alkalosis
Metabolic acidosis
Metabolic alkalosis

Question 16

Describe acid base disorders

Answer 16

pCO 2 is regulated by respiration, abnormalities that primarily alter the pCO 2 are referred to as respiratory disorder.

Respiratory acidosis (high PCO2 ) & Respiratory alkalosis (low PCO2 ).

Question 17

What is compensation as used in acid base balance

Answer 17

The physiological response of the respiratory system or the renal system to restore pH or to limit change in pH induced by a primary acid-base disorder is termed COMPENSATION

respiratory disorders, the kidney modifies serum bicarbonate to return pH toward normal.

In metabolic disorders, breathing is altered to change the pCO2 in order to Return pH toward normal.

Complete compensation: if [H ]or pH is brought back within normal limits

⁺

• Partial compensation: if [H ] or pH range is still outside reference limit.

Respiratory compensation – alteration in ventilation allows immediate adjustment for metabolic acid-base disorders

• Renal compensation –adaptation of the kidneys to alterations in pH by changing the amount of generated/reabsorbed.

HCO3

-

• Full renal compensation might take 2-5 days

Question 18

WhT is respiratory acidosis

Answer 18

Respiratory acidosis is a clinical disorder characterized by:

• a low arterial pH ; an elevation in arterial pCO2

• Respiratory acidosis develops when the lungs does not expel CO 2 adequately

• Primarily due to hypoventilation never to increased CO2 production

Question 19

What is respiratory alkalosis

Answer 19

Respiratory Alkalosis is characterized by

• elevated arterial pH,

• hyperventilation resulting in a low pCO2

Hyperventilation:

Leads to eliminating excessive amounts of CO2 Increased loss of CO 2 from the lungs at a rate faster than it is produced

Question 20

What is metabolic acidosis

Answer 20

characterized by :

• low arterial blood pH

• reduced plasma [HCO3 -]

• Excess H+

An acid-base imbalance not attributable to CO2

Recognizable by assessing levels of [HCO3 ]

Broadly, causes of metabolic acidosis are:

• Increased endogenous production

• Increased exogenous acid administration

• Accumulation/decreased excretion of Acids loads

• Excessive loss of Bases or HCO 3 - rich fluids

Question 21

What is metabolic alkalosis

Answer 21

characterized by:

• an elevation in the arterial pH,

• an increase in the plasma [HCO3 - ]

Increase in pH which has a non-respiratory origin

characterized by:

• an elevation in the arterial pH,

• an increase in the plasma [HCO3 - ]

Increase in pH which has a non-respiratory origin

Question 22

What are ABG investigations

Answer 22

In the laboratory a patient’s acid-base status is evaluated by an blood-gas analysis and parameters used are:

An arterial blood gas (ABG) is a sample of arterial blood that reports: pH / pO 2 / pCO 2 / HCO3

• pH: 7.4 (H ion concentration)

• PCO2 : 40 mmHg (dissolved CO 2 in blood or ventilatory effectiveness)

• HCO3 : 24 mEq/L (metabolic effectiveness)

• PO2 : 80-100 mmHg (O 2 content of blood)

Question 23

What is bilirubin metabolism

Answer 23

Haem is converted to bilirubin in the reticuloendothelial system by two enzymes, haem oxygenase and biliverdin reductase.
•Haem oxygenase converts the porphyrin ring to biliverdin IXα
•Biliverdin IXα undergoes biotransformation via biliverdin reductase to form bilirubin IXα.
•Bilirubin IXα is referred to as unconjugated bilirubin
•Most of it is transported in the blood reversibly bound to albumin to the liver.
At the hepatic sinusoidal membrane, the bilirubin-albumin complex dissociates, with selective uptake of bilirubin into the cell.
•It is then reversibly bound to cytosolic proteins, ligandin Y and Z - transport proteins associated with intracellular binding and transport of bilirubin which function to prevent the of efflux of bilirubin from the cell.
•In the hepatocytes, bilirubin is conjugated to two molecules of glucuronic acid in the smooth endoplasmic reticulum catalyzed by UDP glucose dehydrogenase, UDP-glucuronyl transferase I and II.
•Bilirubin diglucuronide is actively secreted into the bile canaliculi.

The activity of UDP-glucuronyl transferase may be induced by phenobarbitone and inhibited by novobiocin.
•Bacterial flora in the gut reduce the bilirubin conjugates to urobilinogens mesobilinogen and stercobilinogen which are mainly excreted in the faeces.
•The pigments contribute to the colour of the stool.
•A portion of the urobilinogens are reabsorbed back into the blood stream and later re-excreted by the liver (enterohepatic circulation).
•Small amount urobilinogens excreted through the kidneys (70 μmol/ day)
•Normal adults do not excrete bilirubin in the urine and stool

The liver - main site of bilirubin conjugation but may occur in the kidney and intestinal mucosa
•Bilirubin diglucuronide actively secreted into the bile
•When conjugated bilirubin gets to the terminal ileum and the large intestines, the intestinal flora deconjugates the bilirubin
•Bilirubin is then converted to urobilinogen, mesobilinogen and stercobilinogen
•Some of the pigments undergo enterohepatic circulation

Question 24

What is bilirubin

Answer 24

Urobilinogen is a normal constituent of the urine
•The pigments contribute to the colour of the stool
•Normal adults do not excrete bilirubin in the urine and stool.

Question 25

What causes elevated bilirubin

Answer 25

(Pre-hepatic) - Overproduction by RES due to hemolytic anaemias and internal hemorrhage.
•(Hepatic) - Failure to conjugate or excrete due to cirrhosis and viral hepatitis.
•(Post hepatic) - Obstruction of biliary excretion into intestine

Question 26

What is jaundice/icterus

Answer 26

It is a yellowish pigmentation of the skin the conjunctival membranes over the sclerae and other mucous membranes caused by hyperbilirubinemia.
•Jaundice indicates a hyperbilirubinaemia in excess of 40 μmol/L.
•It becomes overt when levels are about 55-70 µmol/l
•Jaundice is not a disease but a symptom of an underlying disease.
•It may be due to pre-hepatic, hepato-cellular and post-hepatic causes

The reference range of bilirubin in adults is up to 17.1 µmol/l
•Jaundice is characterized by the yellowish colouration of the tissues due to retention of pigments
•Experienced physicians discern when blood [bilirubin] is about 35 µmol/l
•It becomes overt when levels are about 55-70 µmol/l
•Jaundice is a symptom of an underlying disease
•It may be due to pre-hepatic, hepato-cellular and post-hepatic causes

Question 27

What is pre-hepatic jaundice

Answer 27

Known as unconjugated hyperbilirubinaemia
•is caused by anything which causes an increased rate of haemolysis.
•Impaired binding of bilirubin to Ligandin or impaired conjugation with glucuronate.
•Malaria and certain genetic diseases, such as sickle cell anaemia, sperocyotsis, thalassemia and G6PD deficiency.

Defects in bilirubin metabolism also present as pre-hepatic jaundice, as in Gilbert’s syndrome and Crigler-Najjar syndrome.
•Bilirubin is not usually found in the urine because unconjugated bilirubin is not water-soluble.
•There is a combination of increased urine-urobilinogen with no bilirubin.

Laboratory findings include:
•Urine: no bilirubin present, urobilirubin > 2 units (except in infants where gut flora has not developed).
•Serum: increased unconjugated bilirubin.

Question 28

What is hepatocellular jaundice

Answer 28

Biphasic hyperbilirubinaemia.
•When the liver is diseased affecting its architecture, conjugation ability is affected.
•Caused by liver pathologies including acute hepatitis, hepatotoxicity and alcoholic liver disease
•Less common causes include primary biliary cirrhosis, Gilbert’s syndrome, Criggler-Najjar syndrome

Defects in conjugation may result from diffuse hepatic injury which may occur in the following:
•Acute, sub-acute, chronic, fulminant hepatitis, hepatotoxicity, and alcoholic liver disease.
•Effects of drugs or toxins such as paracetamol, alcohol, CCl4 and halothane
•Jaundice seen in the newborn, known as neonatal jaundice
•Defects in uptake may result from the effects of flavispidic acid

Question 29

What are some causes of unconjugated high bilirubin levels (or bilirubin that is formed by the breakdown of red blood cells and can’t be excreted in urine, include)

Answer 29

Hemolytic anemia: When red blood cells are rapidly destroyed, often as a result of cancer (such as leukemia or lymphoma), autoimmune diseases (like lupus), or medications (such as acetaminophen, ibuprofen, interferon, and penicillin), it can cause high bilirubin levels.
•A lack of digestive bacteria in newborns: This can cause jaundice in newborns due to impaired breakdown of bilirubin.
•Gilbert syndrome: This is a genetic disorder that causes the liver to process bilirubin slowly.
•Liver disease: This can occur if the liver is not functioning as it should.

Question 30

What are some causes of conjugated hyperbilirubinemia (or bilirubin that has been altered by the liver and is more readily passed in urine and bile, include)

Answer 30

Liver disease: This can occur when blood flow through the liver is impaired.
•Bile duct obstruction: Bilirubin cannot be delivered to the small intestine in bile, often as a result of cirrhosis, gallstones, pancreatitis, or tumours.

Question 31

What is post-hepatic jaundice

Answer 31

This is usually due to mechanical obstruction of the biliary tree as a result of:
–Gallstones
–Carcinoma of the head of the pancreas
–Scarring from infection
•Also called obstructive jaundice.
•Caused by an interruption to the drainage of bile in the biliary system.
•Common causes are pancreatic cancer, “liver flukes” and strictures of the common bile duct and biliary atresia.
•Two broad varieties are recognised: intra-hepatic and extra-hepatic cholestasis.

Intra-hepatic cholestasis
•Associated with structural liver damage: Acute hepatocellular disease, primary biliary cirrhosis, sclerosing cholangitis
•This may occur in subacute or chronic hepatitis
•It may also be due to the effects of drugs such as
–17 α-alkylated steroids e.g methyltestosterone or norethisterone
–Phenothiazine e.g chlorpromazine
–Antibiotics e.g oleandomycin and erythromycin
–Penicillin sensitivity
•It may also occur in some forms of cirrhosis, especially primary biliary

Extra-hepatic
•Biliary obstruction caused by stones, strictures, malignancy (e.g., carcinoma of the head of the pancreas), pancreatitis, biliary atresia, cholangitis.
•Also, a group of parasites known as “liver flukes” can live in the common bile duct, causing obstructive jaundice.
•In complete obstruction of the bile duct, no urobilinogen is found in the urine.
Laboratory findings
•The presence of pale stools and dark urine.
•Elevated serum cholesterol

Question 32

What are some inherited hyperbilirubinemia diseases

Answer 32

This may be classified into unconjugated and conjugated types
•The congenital unconjugated hyperbilirubinemia’s are Gilberts and Criggler-Najjar Syndromes
•The congenital conjugated hyperbilirubinemia’s are Dubin Johnson and Rotor Syndromes

Question 33

What is Gilbert’s syndrome

Answer 33

A heterogenous condition caused by abnormal gene formed due to mutation on promoter region of a gene for the enzyme (UGT1A1 gene) which results in decreased activity of the bilirubin uridine diphosphate glucuronosyltransferase enzyme.
• It is typically inherited in an autosomal recessive pattern and occasionally in an autosomal dominant pattern depending on the type of variant characterized by the defective uptake of bilirubin by the hepatocytes
•There may be an associated reduction in the life span of the erythrocytes
•Serum [bilirubin] is usually between 20-40 µmol/l and rarely exceeds 80 µmol/l
•Their serum bilirubin levels may rise during intercurrent illness or during

Characterized by mild jaundice due to increased unconjugated bilirubin.
• Is found in up to 5% of the population.
•Arises from several different genotypic variants of the gene for UDP-glucuronosyltransferase which is responsible for conjugating bilirubin.
• Characterized by a 70%-80% reduction in the action of the enzyme.
•Other factors such as increased red cell turnover and decreased hepatic uptake of bilirubin have been observed.
•May present at any age but it commonly presents in the second decade of life.

Question 34

What is Crigler-Najjar syndrome

Answer 34

An autosomal recessive disorder, usually presents at birth
•Defective UDP-glucuronosyltransferase activity but of greater severity than in Gilbert’s syndrome.
•Two types of the condition have been described
•Type I : Absolute deficiency of the transferase which results in kernicterus and death soon after birth.
•Type 2: Partial deficiency of the transferase which is not fatal.
•serum [bilirubin] may be reduced by drugs which induce hepatic enzyme synthesis e.g phenobarbitone

Question 35

What is type 1 Criggler-Najjar syndrome

Answer 35

This is a very rare disease
•Consanguinity/kinship increases the risk of this condition
•Intense jaundice appears in the first days of life and persists thereafter.
• UGT1A1 (UDP glucuronosyltransferase 1 family, polypeptide A1) expression cannot be detected in hepatic tissue.
•Hence, there is no response to treatment with phenobarbital (which causes CYP450 enzyme induction)
•Characterised by a serum bilirubin usually above 345 µmol/L (310–755)

Question 36

What is the treatment for type 1 Criggler-Najjar syndrome

Answer 36

Exchange transfusions in the immediate neonatal period
•12h/d phototherapy
• Haem oxygenase inhibitors to reduce transient worsening of hyperbilirubinemia (although the effect decreases over time)
•Oral calcium phosphate and carbonate to form complexes with bilirubin in the gut

Question 37

How does type II Criggler-Najjar syndrome differ from type I

Answer 37

Type II differs from type I in several aspects:
•Bilirubin generally below 345 µmol/L (100–430; thus, there is overlap), and some cases are only detected later in life.
•Lower serum bilirubin, kernicterus is rare in type II.
•Bile is pigmented, instead of pale in type I or dark as normal, and monoconjugates constitute the largest fraction of bile conjugates.
•UGT1A1 is present at reduced but detectable levels (typically <10% of normal), because of single base pair mutations.
•Treatment with phenobarbital is effective, generally with a decrease of

Question 38

What is Dubin-Johnson syndrome

Answer 38

It is an autosomal recessive disorder that causes an increase of conjugated bilirubin.
•There is no elevation of liver enzymes (ALT, AST)
•associated with a defect in the ability of hepatocytes to secrete conjugated bilirubin into the bile.
•Due to a defect in the multi-specific anion transporter (cMOAT) gene
• It is usually asymptomatic but may be diagnosed in early infancy based on laboratory tests

A rare and benign condition which is characterized by defective excretion of bilirubin but not bile salts
•It is associated with a slightly raised serum conjugated [bilirubin]
•Affected subjects present with bilirubinuria but the ALP is normal
•There may be hepatomegaly
•The liver of affected persons has orange-yellow granules
•Liver of subjects is usually dark brown due to the deposition of a melanin-like pigment.

•There is also an associated abnormality in porphyrin metabolism.
•Most patients are asymptomatic with plasma bilirubin levels ranging from 30 to 90 μmol/L.
•Prognosis is good, and treatment of this syndrome is usually unnecessary.
•Most patients are asymptomatic and have normal life spans.
•Some neonates will present with cholestasis.
•Hormonal contraceptives and pregnancy may lead to overt jaundice and icterus (yellowing of the eyes and skin).

Question 39

What is rotor syndrome

Answer 39

•RS named after the Filipino internist, Arturo Bellez Rotor (1907–1988).
•First described in the Philippines, is similar to the Dubin-Johnson syndrome.
•The liver of affected subjects does not have orange-yellow granules
•Rare, relatively benign autosomal recessive bilirubin disorder - unknown origin.
•Characterized by defective excretion of conjugated bilirubin into the biliary tree.

Question 40

What is neonatal jaundice

Answer 40

Neonatal jaundice is a yellowing of a baby’s skin and eyes
•Very common and can occur when babies have a high level of bilirubin, a yellow pigment produced during normal breakdown of red blood cells.
•The reference range of bilirubin in neonates is 8-67 µmol/l
•In the first week of a neonates life, there may be a physiological hyperbilirubinaemia
•The serum [bilirubin] may rise to as high as 200 µmol/l and is usually prolonged in preterm neonates

Question 41

What are some causes of neonatal jaundice

Answer 41

Can be classified as physiological or pathological
•Haemolytic disease e.g blood group incompatibility and G6PD deficiency
•Immaturity of the hepatic processes for uptake and excretion of bilirubin
•Interference with hepatic transport functions by drugs e.g progesterone or steroids with progesterone-like activity
–Drugs such as salicylates and sulphonamides which compete for binding to Alb
–Novobiocin which inhibits the glucuronyl transferase system

Question 42

What are some manifestations of liver injury

Answer 42

Manifestations
–Cell necrosis
–Immune cell infiltration
–Fatty change
–Mixed necrosis and fatty change
–Later, fibrosis

Question 43

What are some common types of liver injury

Answer 43

Viral hepatitis
–Hep A, B, C, etc
•Alcoholic hepatitis
•Non Alcoholic Fatty Liver disease
•Cirrhosis
–Scarring, which is end result of acute injury
–Fatty Liver: Symptoms, Causes, and Treatment (healthline.com)
–Non-Alcoholic fatty liver disease - Symptoms and causes - Mayo Clinic

Question 44

What is acute liver disease

Answer 44

Acute liver failure is loss of liver function that occurs rapidly — in days or weeks — usually in a person who has no preexisting liver disease. This may be caused by:
–Poisoning
–Infection
–Inadequate perfusion

Poisoning
Poison: a substance that is capable of causing the illness or death of a living organism when introduced or absorbed
•Examples of such drugs are sodium valproate (an anticonvulsant) and halothane (an anaesthetic agent).
•The capacity of the liver to withstand toxic insults is impaired if there is an underlying liver damage due to alcohol, malnutrition or any chronic disease.
This may result from:
–Paracetamol
–Carbon tetrachloride
–Some plant and fungal toxins
•Toxins or drugs which give rise to hepatocellular damage in some individuals

Infection:
Both bacteria and viruses may give rise to infective hepatitis
•Viral hepatitis may be associated with viral infections such as infectious mononucleosis (Epstein Barr virus), rubella and cytomegalovirus.
•Clinically, viral hepatitis is usually associated with infection by the hepatitis viruses

Inadequate perfusion:
This may result from:
•Severe anaemia

•Trauma

•Dehydration which will result in hypovolaemia

Question 45

What is the outcome of acute liver damage

Answer 45

Acute liver damage may progress in three ways as follows:
•It may resolve (majority of cases).

•It may progress to acute hepatic failure.

•It may lead to chronic hepatic damage

Question 46

What is cirrhosis of the liver

Answer 46

Any condition leading to persistent or recurrent hepatocyte death may lead to hepatic cirrhosis.
•Cirrhosis may also develop in children as a result of α1- antitrypsin deficiency or Wilson’s disease.
• In adults it may also develop secondary to haemochromatosis which is characterized by the deposition of iron in the hepatocytes and other tissues.
•Ascites due to reduced albumin synthesis which may result in hypovolaemia and hypotension

Question 47

What is chronic liver disease

Answer 47

Diffuse scarring (Cirrhosis) of the liver from any cause:
•Alcoholic fatty liver - Alcoholic liver disease
•Chronic active hepatitis.
•An episode of severe liver necrosis
•Other drugs and chemicals
•Primary biliary cirrhosis - Longstanding bile duct obstruction

Question 48

What are some conditions associated with chronic liver disease

Answer 48

Viral causes
• Hepatitis B
• Hepatitis C
• Cytomegalovirus (CMV)
• Epstein Barr Virus (EBV)

Toxic and drugs
• Alcoholic liver disease
• Amiodarone
• Methotrexate
• Nitrofurantoin

Metabolic
• Non-alcoholic fatty liver disease
• Haemochromatosis
• Wilson’s Disease

Autoimmune
• Autoimmune Chronic Hepatitis
• Primary Biliary Cirrhosis
• Primary Sclerosing Cholangitis

Other
• Right heart failure

Question 49

What are some manifestations to cirrhosis of the liver

Answer 49

The outcome of chronic liver disease is Cirrhosis of the Liver characterized by the shrinking of the liver with the disorganization of its architecture. The remaining hepatocellular tissue develop fibrosis.
•Liver failure
•Liver unable to inactivate estrogen in males
•Testicular atrophy, loss of sex drive, breast hypertrophy
•Portal hypertension
•Ascites, collateral circulation formation

Question 50

What are some complications of chronic liver disease

Answer 50

Portal Hypertension
• Ascites
• Hypersplenism (with or without splenomegally)
• Varices (lower oesophageal and rectal)

Synthetic Dysfunction
• Hypoalbuminaemia
• Coagulopathy

• Hepatopulmonary Syndrome
• Hepatorenal Syndrome
• Encephalopathy

Question 51

What are the faces of cirrhosis

Answer 51

In the early phase
•there may be no abnormal biochemical findings.

In the terminal phases the features include:
•Jaundice.
•Encephalopathy which may be related to toxins which are not removed from plasma
•Terminal liver failure
•Cirrhosis - Symptoms and causes - Mayo Clinic