Jaundice Flashcards

1
Q

What’s jaundice?
Normal range of bilirubin
What level of jaundice is it clinical detectable

A

Definition:
Jaundice, also known as icterus, is a yellowish discoloration of the skin, sclera (the white part of the eyes), and mucous membranes. This occurs due to the accumulation of bilirubin in the bloodstream.

Normal Bilirubin Levels:
- Total Bilirubin Range: 3.4 to 20.0 micromol/L (0.2 to 1.2 mg/dL).
- Clinical Detection of Jaundice: Jaundice becomes noticeable when serum bilirubin levels exceed 51 micromol/L (3 mg/dL).

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2
Q

The causes of jaundice can be categorized into? With examples

A

Causes of Jaundice:
Jaundice can be broadly classified into three categories based on the underlying pathophysiology:

  1. Prehepatic (Hemolytic) Jaundice:
    • Mechanism: Increased production of bilirubin, usually due to excessive breakdown of red blood cells (hemolysis).
    • Examples: Hemolytic anemias, transfusion reactions, and sickle cell disease.
  2. Hepatocellular (Hepatic) Jaundice:
    • Mechanism: Impairment in the ability of hepatocytes (liver cells) to process and excrete bilirubin.
    • Examples: Viral hepatitis, alcoholic liver disease, cirrhosis, and drug-induced liver injury.
  3. Cholestatic (Post-hepatic) Jaundice:
    • Mechanism: Obstruction of bile flow within the biliary system, leading to the accumulation of bilirubin.
    • Examples: Gallstones, bile duct tumors, pancreatitis, and primary biliary cirrhosis.
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3
Q

How do you clinically evaluate jaundice? I. E history taking and physical examination

A

Diagnostic Evaluation:
To determine the cause of jaundice, a systematic approach involving history taking, physical examination, and specific investigations is essential:

  1. Focused History and Examination:
    • History: Inquire about symptoms like dark urine, pale stools, pruritus (itching), abdominal pain, weight loss, and changes in appetite. Ask about alcohol use, medication history, travel history, and family history of liver diseases.
    • Physical Examination: Look for signs like hepatomegaly (enlarged liver), splenomegaly (enlarged spleen), ascites (fluid in the abdomen), and spider angiomas.
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4
Q

What are the investigations carried out in a jaundice patient

A
  1. Initial Investigations:
    • Full Blood Count (FBC): To check for hemolysis or anemia.
    • Serum Liver Function Tests (LFTs): To assess liver function. This includes:
      • Serum Bilirubin (Total and Direct): Helps distinguish between conjugated (direct) and unconjugated (indirect) hyperbilirubinemia.
      • Alanine Aminotransferase (ALT) and Aspartate Aminotransferase (AST): Elevated levels suggest hepatocellular damage.
      • Alkaline Phosphatase (ALP) and Gamma-Glutamyl Transferase (GGT): Elevated in cholestatic jaundice.
      • Prothrombin Time (PT): May be prolonged in liver dysfunction.
    • Ultrasound of the Liver and Biliary Tract: Non-invasive imaging to assess liver parenchyma and detect biliary obstruction.
  2. Further Investigations:
    • Advanced Imaging: CT scan or MRI, especially if ultrasound suggests an obstruction or mass.
    • Additional Laboratory Tests: Depending on the clinical context, tests like viral hepatitis serologies, autoimmune markers, and liver biopsy may be necessary.

Jaundice is a clinical sign of an underlying pathology, usually related to bilirubin metabolism or liver function. Early and appropriate evaluation, including history, physical examination, and targeted investigations, is essential to identify the cause and guide further management.

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5
Q

Explain the process of bilirubin metabolism

A

Bilirubin Production:
- Source: Bilirubin is a waste product that originates from the breakdown of the heme molecule found in red blood cells (RBCs).
- Process:
- RBCs have a lifespan of about 120 days. After this, they are broken down by macrophages in the reticuloendothelial system, primarily in the spleen, liver, and bone marrow.
- Heme Breakdown: The heme portion of hemoglobin is broken down into biliverdin and then reduced to form unconjugated bilirubin.

Unconjugated Bilirubin:
- Characteristics: This form of bilirubin is lipid-soluble, which allows it to easily cross cell membranes. However, it is not water-soluble, so it cannot be excreted directly.
- Transport in Blood: Unconjugated bilirubin is transported in the bloodstream bound to albumin, which helps prevent it from diffusing into tissues.

Hepatic Processing:
- Uptake: Hepatocytes (liver cells) take up unconjugated bilirubin from the blood.
- Conjugation: Within hepatocytes, unconjugated bilirubin is conjugated with glucuronic acid by the enzyme UDP-glucuronosyltransferase. This process converts unconjugated bilirubin into conjugated bilirubin, which is water-soluble and can be excreted from the body.

Excretion:
- Bile Secretion: Conjugated bilirubin is excreted into bile, which is then released into the intestines.
- Intestinal Processing:
- Conversion: In the intestines, gut bacteria convert conjugated bilirubin into urobilinogen and stercobilinogen.
- Excretion:
- Stercobilin: Most stercobilinogen is converted to stercobilin, which gives feces its brown color and is excreted in the stool.
- Urobilin: Some urobilinogen is reabsorbed into the blood, with a portion excreted by the kidneys as urobilin, which gives urine its yellow color.

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6
Q

Gilbert syndrome or Crigler-Najjar Syndrome causes what type of type of bilirubin elevation?

A

.
Conditions like Gilbert’s syndrome or Crigler-Najjar syndrome involve genetic defects in the conjugation process, leading to elevated unconjugated bilirubin.

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7
Q

What are the types of bilirubin elevation and conditions that can cause them

A

Types of Bilirubin Elevation and Related Conditions:

  1. Increased Unconjugated (Indirect) Bilirubin:
    • Causes:
      • Prehepatic (Hemolytic) Jaundice: Increased red blood cell destruction leads to an excess of unconjugated bilirubin, overwhelming the liver’s capacity to conjugate it. This can occur in conditions like hemolytic anemia, sickle cell disease, or transfusion reactions.
      • Impaired Conjugation: Conditions like Gilbert’s syndrome or Crigler-Najjar syndrome involve genetic defects in the conjugation process, leading to elevated unconjugated bilirubin.
    • Clinical Implications: Since unconjugated bilirubin is lipid-soluble, it can cross the blood-brain barrier, particularly in newborns, leading to conditions like kernicterus.
  2. Increased Conjugated (Direct) Bilirubin:
    • Causes:
      • Hepatocellular Jaundice: When hepatocytes are damaged, as in hepatitis or cirrhosis, their ability to excrete conjugated bilirubin into the bile is impaired, leading to its buildup in the blood.
      • Cholestatic (Obstructive) Jaundice: Obstruction in the bile ducts (e.g., due to gallstones, tumors, or strictures) prevents conjugated bilirubin from being excreted, causing it to back up into the bloodstream.
    • Clinical Implications: Elevated conjugated bilirubin typically presents with dark urine (due to excreted urobilinogen) and pale stools (due to reduced stercobilin).
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8
Q

What are the classification of jaundice

A

1. Prehepatic Jaundice:
- Location of Dysfunction: Before the liver, typically due to increased bilirubin production.
- Bilirubin Type: Increased unconjugated (indirect) bilirubin.
- Causes: Hemolysis, ineffective erythropoiesis.

2. Hepatocellular Jaundice:
- Location of Dysfunction: Within the liver, due to impaired bilirubin conjugation or excretion.
- Bilirubin Type: Increased conjugated (direct) bilirubin, but unconjugated bilirubin can also be elevated if hepatocyte function is severely compromised.
- Causes: Hepatitis, cirrhosis, alcoholic liver disease.

3. Cholestatic (Obstructive) Jaundice:
- Location of Dysfunction: After the liver, in the biliary system, due to obstruction of bile flow.
- Bilirubin Type: Increased conjugated (direct) bilirubin.
- Causes: Gallstones, biliary atresia, pancreatic cancer.

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9
Q

What are the causes of preheparic jaundice

A

Overview:
Prehepatic jaundice is characterized by an increase in unconjugated (indirect) bilirubin in the bloodstream. This occurs either due to increased production of bilirubin from excessive red blood cell (RBC) destruction or due to a dysfunction in the liver’s ability to conjugate bilirubin. The underlying causes of prehepatic jaundice primarily involve conditions that affect RBCs or the initial stages of bilirubin metabolism.

When RBCs are destroyed at an accelerated rate, the amount of heme released from hemoglobin increases. This leads to a higher production of unconjugated bilirubin, which can overwhelm the liver’s ability to conjugate it, resulting in elevated levels of unconjugated bilirubin in the blood.

A. Hereditary Hemolytic Anemias:
- Hemoglobinopathies:
- Sickle Cell Anemia: A genetic disorder where abnormal hemoglobin (HbS) leads to the deformation of RBCs into a sickle shape, making them more prone to hemolysis.
- Thalassemia: A group of inherited disorders characterized by abnormal hemoglobin production, leading to the destruction of RBCs and ineffective erythropoiesis.
- Membranopathies:
- Hereditary Spherocytosis: A condition where RBCs have a defective cell membrane protein, making them spherical and prone to rupture.
- Elliptocytosis: Similar to spherocytosis but with elliptical-shaped RBCs, also leading to hemolysis.
- Pyropoikilocytosis: A severe form of hereditary elliptocytosis with marked RBC shape abnormalities and significant hemolysis.
- Enzymopathies:
- Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency: A common enzymatic defect that renders RBCs vulnerable to oxidative stress, leading to hemolysis, particularly after exposure to certain drugs or infections.
- Pyruvate Kinase Deficiency: A metabolic disorder where the lack of pyruvate kinase enzyme causes energy depletion in RBCs, leading to their premature destruction.

B. Acquired Hemolytic Anemias:
- Autoimmune Hemolytic Anemia:
- Causes: Conditions like Systemic Lupus Erythematosus (SLE), Rheumatoid Arthritis, and Scleroderma can cause the immune system to mistakenly attack RBCs, leading to their destruction.
- Infections:
- Malaria: A parasitic infection where the Plasmodium parasite invades RBCs, causing their rupture.
- Cytomegalovirus (CMV): A viral infection that can lead to hemolysis in some cases.
- Leishmaniasis: A parasitic disease that can cause hemolysis as part of its systemic effects.
- Infectious Mononucleosis: Caused by the Epstein-Barr virus, it can lead to mild hemolysis.
- Alloimmune Hemolytic Anemia:
- ABO Blood Group Incompatibility: Occurs when there is a mismatch in blood types between donor and recipient, leading to the immune-mediated destruction of transfused RBCs.
- Drug-Induced Hemolytic Anemia:
- Causes: Certain drugs can trigger hemolysis either through immune mechanisms or by directly damaging RBCs.
- Microangiopathic Hemolytic Anemias:
- Disseminated Intravascular Coagulation (DIC): A condition where widespread clotting in small vessels leads to RBC fragmentation (schistocytes) and hemolysis.
- Eclampsia: A severe complication of pregnancy characterized by hypertension and hemolysis, among other symptoms.
- Thrombotic Thrombocytopenic Purpura (TTP): A rare disorder where small blood clots form in blood vessels, leading to hemolysis and low platelet counts.
- Hemolytic Uremic Syndrome (HUS): Often triggered by infections (like E. coli), HUS leads to microangiopathic hemolysis, kidney failure, and low platelet counts.

In some cases, the liver’s ability to conjugate bilirubin is impaired, leading to an accumulation of unconjugated bilirubin in the blood. This can occur due to genetic defects affecting the enzymes responsible for bilirubin conjugation.

A. Gilbert Syndrome:
- Overview: Gilbert syndrome is a common, mild genetic disorder characterized by a reduced ability of the liver to conjugate bilirubin. This is due to a partial deficiency in the enzyme UDP-glucuronosyltransferase.
- Presentation: Patients may experience intermittent mild jaundice, often triggered by stress, fasting, or illness. The condition is typically benign and does not require treatment.

Prehepatic jaundice results from conditions that either increase the breakdown of RBCs (leading to excess unconjugated bilirubin production) or impair the liver’s ability to conjugate bilirubin. The causes range from hereditary disorders affecting hemoglobin, RBC membranes, or enzymes, to acquired conditions such as autoimmune diseases, infections, and drug reactions. Understanding the specific underlying cause is crucial for appropriate management and treatment of the jaundice.

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10
Q

Hepatocelluar case of jaundice causes the accumulation of what specific type of jaundice.

A

This results in the accumulation of both conjugated and unconjugated bilirubin in the blood

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11
Q

What are the infections that can cause hepatocelluar jaundice

A

Overview:
Hepatocellular jaundice arises when the liver’s hepatocytes (liver cells) are damaged or impaired, leading to a decrease in their ability to metabolize and excrete bilirubin. This results in the accumulation of both conjugated and unconjugated bilirubin in the blood. The underlying causes of hepatocellular jaundice can be diverse, including infections, toxins, malignancies, autoimmune disorders, genetic conditions, cardiac issues, and pregnancy-related complications.

A. Viral Infections:
- Hepatotrophic Viruses: These viruses specifically target the liver and are a common cause of liver inflammation (hepatitis) leading to jaundice.
- Hepatitis A, B, C, D, and E: These viruses cause varying degrees of liver damage, with Hepatitis B and C being notable for their potential to cause chronic liver disease and hepatocellular carcinoma.
- Non-Hepatotrophic Viruses: These are viruses that do not primarily target the liver but can cause liver damage as part of a systemic infection.
- HIV: While primarily an immune system virus, HIV can cause liver damage either directly or through co-infections (such as Hepatitis B or C) and the side effects of antiretroviral medications.

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12
Q

What are the parasites that can cause hepatocelluar jaundice

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B. Parasitic Infections:
- Ascaris lumbricoides: This intestinal roundworm can migrate to the bile ducts, causing biliary obstruction and hepatocellular damage.
- Clonorchis sinensis (Chinese Liver Fluke): This parasite resides in the bile ducts, causing chronic inflammation, fibrosis, and an increased risk of cholangiocarcinoma.
- Echinococcus granulosus (Hydatid Disease): This tapeworm causes cysts in the liver, which can lead to jaundice if they rupture or cause obstruction.
- Entamoeba histolytica: The cause of amoebic liver abscesses, which can result in hepatocellular damage and jaundice.
- Malaria: The Plasmodium parasite, particularly P. falciparum, can cause severe liver damage leading to jaundice, often as part of a broader systemic illness.

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13
Q

What are the bacterial infections and toxins that causes hepatocelluar jaundice

A

C. Bacterial Infections:
- Leptospirosis: A bacterial infection that can cause Weil’s disease, characterized by severe jaundice, renal failure, and hemorrhage.

A. Alcohol:
- Chronic alcohol consumption can lead to a spectrum of liver diseases, including fatty liver, alcoholic hepatitis, and cirrhosis, all of which can impair hepatocyte function and cause jaundice.

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14
Q

What are the drugs that can cause B. Drug-Induced Liver Injury (DILI): leading to hepatocelluar J

A

B. Drug-Induced Liver Injury (DILI):
- Certain medications can cause hepatocellular damage, leading to jaundice. Common culprits include:
- Antibiotics: Some, like amoxicillin-clavulanate and isoniazid, are notorious for causing liver injury.
- Acetaminophen (Paracetamol): Overdose is a well-known cause of acute liver failure.
- Estrogen: Hormonal medications can cause cholestatic jaundice.
- Antiepileptics: Drugs like valproate and phenytoin can lead to hepatotoxicity.
- NSAIDs: Non-steroidal anti-inflammatory drugs, particularly diclofenac, can cause liver injury in susceptible individuals.

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15
Q

Malignancies and autoimmune dxs that can damage the liver function

A

A. Hepatocellular Carcinoma (HCC):
- This is the most common primary liver cancer, often arising in the context of chronic liver disease. It can cause jaundice either by direct hepatocyte damage or by obstructing the biliary tree.

B. Metastatic Liver Disease:
- Metastases to the liver from cancers elsewhere in the body (e.g., colon, breast, lung) can impair liver function, leading to jaundice.

C. Lymphoma:
- Both Hodgkin’s and non-Hodgkin’s lymphomas can infiltrate the liver, causing hepatocellular dysfunction and jaundice.

A. Autoimmune Hepatitis:
- A chronic inflammatory condition where the body’s immune system attacks hepatocytes, leading to progressive liver damage and jaundice.

B. Primary Biliary Cholangitis (PBC):
- A chronic disease where the immune system slowly destroys the bile ducts within the liver, leading to cholestasis, fibrosis, and cirrhosis.

C. Primary Sclerosing Cholangitis (PSC):
- A disease characterized by inflammation and scarring of the bile ducts, leading to liver damage and jaundice. PSC is often associated with inflammatory bowel disease (IBD), particularly ulcerative colitis.

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16
Q

What are the genetic conditions and cardiac causes that can cause hepatocelluar jaundice

A

A. Wilson Disease:
- A rare inherited disorder where copper accumulates in the liver, brain, and other organs, leading to hepatocellular damage, neurological symptoms, and jaundice.

B. Hemochromatosis:
- A genetic condition where excessive iron is absorbed and stored in the liver and other tissues, leading to liver damage, cirrhosis, and jaundice.

C. Alpha-1-Antitrypsin Deficiency:
- A genetic disorder that results in a lack of the protein alpha-1-antitrypsin, leading to liver damage (due to accumulation of abnormal protein in the liver) and lung disease.

A. Heart Failure:
- Chronic heart failure can lead to congestive hepatopathy, where reduced cardiac output causes hepatic congestion and hypoxia, leading to liver dysfunction and jaundice.

B. Ischemic Hepatitis:
- Also known as “shock liver,” this occurs due to a sudden decrease in blood flow to the liver, often from heart failure or sepsis, leading to hepatocyte necrosis and jaundice.

17
Q

What are the pregnancy related conditions that can cause hepatocelluar jaundice

A

A. Acute Fatty Liver of Pregnancy (AFLP):
- A rare but serious condition in the third trimester where the liver accumulates fat, leading to liver failure and jaundice.

B. HELLP Syndrome:
- A severe form of preeclampsia characterized by Hemolysis, Elevated Liver enzymes, and Low Platelet count, often accompanied by jaundice.

C. Intrahepatic Cholestasis of Pregnancy (ICP):
- A condition where hormonal changes during pregnancy impair bile flow, leading to jaundice, itching, and increased risk of fetal complications.

18
Q

What are the benign causes of cholestetic jaundice

A

Overview:
Cholestatic jaundice, also known as post-hepatic jaundice, occurs when there is an obstruction in the bile ducts, preventing bile from draining properly from the liver to the intestines. This blockage leads to the accumulation of conjugated bilirubin in the blood, resulting in the yellow discoloration seen in jaundice. The obstruction can be caused by benign (non-cancerous) or malignant (cancerous) conditions.

A. Choledocholithiasis:
- This refers to the presence of gallstones in the common bile duct (CBD). These stones can block the flow of bile, leading to jaundice. It’s a common cause of cholestatic jaundice and can result in biliary colic, cholangitis, or pancreatitis if not treated.

B. Postoperative Biliary Stricture:
- After surgeries involving the bile ducts or gallbladder (such as cholecystectomy), scar tissue can form and narrow the bile ducts, leading to a stricture. This can obstruct bile flow and cause jaundice.

C. Immunoglobulin G4 (IgG4)-Related Cholangiopathy:
- A rare autoimmune condition where the bile ducts become inflamed and scarred due to the infiltration of IgG4-producing plasma cells. This can mimic other causes of biliary obstruction, like primary sclerosing cholangitis or bile duct cancer.

D. Parasitic Infections:
- Strongyloides stercoralis: This parasite can cause inflammation and obstruction of the bile ducts.
- Ascaris lumbricoides: This roundworm can migrate into the bile ducts, causing obstruction.
- Clonorchis sinensis (Chinese liver fluke): A parasite that resides in the bile ducts, leading to chronic inflammation and obstruction.

19
Q

What are the malignant causes of cholestetic jaundice

A

A. Pancreatic Cancer:
- Tumors in the head of the pancreas can compress the common bile duct as it passes through or near the pancreas, leading to obstructive jaundice. This is often associated with weight loss, abdominal pain, and Courvoisier’s sign (a painless, palpable gallbladder).

B. Cholangiocarcinoma:
- A cancer of the bile ducts, which can occur within the liver (intrahepatic) or outside the liver (extrahepatic). This malignancy leads to obstruction of the bile ducts, resulting in cholestatic jaundice.

C. Metastasis:
- Cancers from other parts of the body (such as breast, lung, or colon cancer) can spread (metastasize) to the liver or bile ducts, causing obstruction and jaundice.

D. Lymphoma:
- Lymphomas, particularly those involving the lymph nodes near the bile ducts or within the liver, can cause compression and obstruction, leading to jaundice.

20
Q

How do you approach a patient for jaundice i.e clerking

A

Diagnosis:
The diagnosis of jaundice is typically straightforward based on the history and physical observation of yellowing of the sclera (the whites of the eyes), skin, and mucous membranes. The key challenge lies in determining the underlying cause of jaundice, which involves careful clinical assessment and investigations.

A. Duration and Progression:
- Rapid Onset (Within Days): This suggests acute hepatitis, often due to infections (e.g., viral hepatitis), alcohol use, or drug-induced liver injury.
- Subacute Onset (Within a Few Weeks): More likely to be caused by subacute hepatitis or bile duct obstruction, such as from gallstones or tumors.
- Fluctuating Jaundice: Could indicate a recurrent or intermittent obstruction, often seen with gallstones, drug-induced liver injury, or ampullary carcinoma.

B. Associated Symptoms:
- Fever: May suggest an infectious cause (e.g., viral hepatitis, cholangitis) or malignancy.
- Pale Stools and Dark Urine: Indicate obstructive jaundice, where bile flow is blocked.
- Anorexia, Weight Loss, Fatigue: These are more suggestive of malignancy or chronic liver disease.
- Nausea and Vomiting: Common in many forms of liver disease or biliary obstruction.
- Pruritus (Itching): Often seen in cholestasis due to the buildup of bile salts in the skin.

C. Past Medical History:
- Inflammatory Bowel Disease (IBD): Increases the risk of primary sclerosing cholangitis, a cause of chronic cholestasis.
- Inherited and Acquired Hemolytic Disorders: Important for differentiating prehepatic causes of jaundice.
- Previous Malignancy: Raises suspicion for metastatic disease.
- History of Blood Transfusions: Important in assessing the risk of viral hepatitis (e.g., Hepatitis C).
- Any Abdominal Surgery: Could lead to postoperative biliary strictures or other complications.

D. Drug History:
- Prescription and Non-Prescription Drugs: Certain medications, including herbal remedies and illegal drugs, can cause liver damage or cholestasis.

E. Travel History:
- Important for assessing the risk of infectious causes, especially parasitic infections or viral hepatitis.

F. Social History, Including Sexual History:
- Alcohol Use: A major risk factor for liver disease.
- Sexual History: Relevant for assessing the risk of sexually transmitted infections that can affect the liver, such as Hepatitis B and C.

G. Family History:
- A family history of liver disease or hemolytic disorders can provide clues to genetic conditions like Wilson disease or hereditary spherocytosis.

21
Q

What’s Courvoisier’s Law?

A

According to Courvoisier’s Law, an enlarged gallbladder with jaundice is more likely due to a malignancy (e.g., pancreatic cancer) than a stone in the common bile duct. Stones usually result in a scarred, non-distensible gallbladder.

22
Q

What are the things to look out for in general examination of a jaundice patient

A

When examining a patient with jaundice, a thorough physical examination is essential, focusing on signs that can indicate the severity, cause, and complications of the underlying liver disease or obstruction. Below is a breakdown of key components to assess during the examination.

  • Scleral Icterus and Skin Examination:
    • Scleral Icterus: Yellow discoloration of the sclera is often the first sign of jaundice.
    • Skin Examination: Check for yellow discoloration, which can range from a subtle yellow tinge to deep orange. Look for signs of chronic liver disease:
      • Track Marks: May indicate intravenous drug use, a risk factor for viral hepatitis.
      • Ecchymosis or Petechiae: These are signs of coagulopathy, often seen in advanced liver disease.
      • Fever: Suggests an infectious cause of jaundice, such as cholangitis or viral hepatitis.
      • Spider Angiomata: Small, spider-like blood vessels seen in the upper body, commonly associated with cirrhosis.
      • Palmar Erythema: Reddening of the palms, another sign associated with chronic liver disease.
  • Muscle Wasting: Chronic liver disease often leads to muscle wasting:
    • Temporal Wasting: Loss of the fat pads in the temples.
    • Thenar Eminence: Wasting of the muscle at the base of the thumb.
  • Finger Clubbing: Bulbous enlargement of the tips of the fingers, associated with chronic liver disease, biliary cirrhosis, and other chronic conditions.
  • Pedal Edema: Swelling of the feet and ankles, common in liver failure due to hypoalbuminemia.
  • Flapping Tremors (Asterixis): A sign of hepatic encephalopathy, often seen in severe liver dysfunction.

.

23
Q

What are the things to watch out for during abdominal examination in a jaundice patient

A

A. Inspection:
- Asymmetry: Could indicate an underlying mass or enlarged organ.
- Distension: May suggest ascites (fluid accumulation in the abdomen), a common complication of cirrhosis.
- Scarifications: Previous surgical scars could provide clues to past surgeries, such as cholecystectomy or liver biopsy.
- Collateral Veins: Prominent veins on the abdomen could indicate portal hypertension.
- Umbilicus: Check for hernias or an everted umbilicus, which may occur with ascites.
- Inguinal Hernia: Common in patients with increased intra-abdominal pressure due to ascites.

B. Palpation and Percussion:
- Liver and Spleen:
- Palpation: The liver and spleen should be palpated during both inspiration and expiration to assess for enlargement, tenderness, or nodularity.
- Percussion: Helps to estimate liver size and check for dullness over the spleen.
- Nodular Liver: A nodular liver with decreased size often suggests cirrhosis.
- Collateral Vessels: Suggestive of portal hypertension, which occurs in chronic liver disease.
- Ascites: Check for fluid by percussion (shifting dullness or fluid wave).
- Gallbladder:
- Palpation: Note if the gallbladder is palpable. According to Courvoisier’s Law, an enlarged gallbladder with jaundice is more likely due to a malignancy (e.g., pancreatic cancer) than a stone in the common bile duct. Stones usually result in a scarred, non-distensible gallbladder.

24
Q

A. Lung Examination:
- Pleural Effusion (Hepatic Hydrothorax): In some patients with advanced liver disease, fluid may accumulate in the pleural space, especially on the right side. Listen for decreased breath sounds or dullness on percussion.

B. Cardiovascular Examination:
- Right Heart Failure: Signs of congestion from right heart failure can suggest liver dysfunction due to cardiac causes. Look for:
- Elevated jugular venous pressure (JVP).
- Hepatojugular reflux (enlargement of the liver when pressing on the abdomen).
- Peripheral edema.

C. Rectal Examination:
- Gastrointestinal Bleeding: A rectal examination may reveal signs of gastrointestinal bleeding, such as melena (black, tarry stools) or hematochezia (fresh blood), which can be a complication of portal hypertension leading to variceal bleeding.

The physical examination in a patient with jaundice provides vital clues to the underlying cause and the presence of complications. This includes inspecting for signs of chronic liver disease, assessing nutritional status and extremities, and conducting a thorough abdominal examination to evaluate the liver, spleen, and gallbladder. Additionally, a lung and cardiovascular examination, along with a rectal exam, can provide further insights into potential complications related to liver dysfunction and portal hypertension

A
25
Q

What are the patterns that can be seen in LFTs serum Liver Function Test.

A

The investigation of jaundice involves a comprehensive assessment to determine the underlying cause and assess the extent of liver dysfunction. Below is a detailed explanation of the key investigations:

Liver function tests provide critical information on the type and extent of liver injury. Three patterns of liver function derangement can be identified:

  • Cholestatic Pattern:
    • Characterized by a predominant elevation of bilirubin, alkaline phosphatase (ALP), and gamma-glutamyl transferase (GGT).
    • This pattern indicates a possible obstruction in bile flow, either intrahepatic (within the liver) or extrahepatic (outside the liver).
  • Hepatocellular Pattern:
    • Marked by elevated bilirubin, aspartate aminotransferase (AST), and alanine aminotransferase (ALT).
    • Indicates damage to hepatocytes (liver cells), which is typical in conditions like viral hepatitis, drug-induced liver injury, and alcoholic liver disease.
  • Mixed Pattern:
    • Features of both cholestatic and hepatocellular injury, indicating a complex or overlapping pathology.
    Important Considerations:
    - ALT and AST Levels: In advanced liver disease, such as cirrhosis, ALT and AST may be normal despite significant liver damage because the liver has lost much of its functional tissue.
26
Q

What test result can be indicative of Alcohol abuse

A
  • AST/ALT Ratio: An AST/ALT ratio >2 is suggestive of alcoholic liver disease and is observed in approximately 70% of patients with this condition.
27
Q

What are they investigations carried out in a jaundice patient

A

LFTs
Prothrombin Time
Urinalysis
FBC
Reticulocyte count and Peripheral Blood Smear
Hemoglobin Genotype
E/U/Cr
Haptoglobin and LDH
Infection Screening

28
Q

For each of the step mentioned previously why are they done?

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  • Increased PT/INR:
    • Indicates impaired synthesis of clotting factors due to liver dysfunction.
    • Coupled with low serum albumin, it is suggestive of cirrhosis or acute liver failure.
    • However, elevated PT/INR can also occur in cholestasis due to vitamin K malabsorption, as bile is necessary for fat-soluble vitamin absorption.
  • Bilirubinuria:
    • The presence of bilirubin in the urine typically indicates conjugated (direct) hyperbilirubinemia, as unconjugated bilirubin is not water-soluble and cannot be excreted in urine.
  • Thrombocytopenia:
    • A low platelet count is common in chronic liver disease, particularly cirrhosis, due to splenic sequestration of platelets and reduced thrombopoietin production.
  • Anemia:
    • Anemia can result from chronic disease, bleeding (e.g., variceal bleeding), or hemolysis.
  • Leucocytosis:
    • Elevated white blood cell count might suggest infection, especially in the context of sepsis or cholangitis.
  • Reticulocyte Count:
    • Elevated in hemolytic anemia as the bone marrow responds to increased red blood cell destruction.
  • Peripheral Blood Smear:
    • Can reveal abnormal red blood cell morphology, such as spherocytes in hereditary spherocytosis or schistocytes in microangiopathic hemolytic anemia.
  • Sickle Cell Disease:
    • Screening for sickle cell disease is essential in populations with a high prevalence, as this can lead to hemolytic anemia and subsequent jaundice.
  • Acute Kidney Injury (AKI):
    • May occur in acute liver failure, acute-on-chronic liver failure, or decompensated cirrhosis.
  • Hyponatremia:
    • Common in cirrhosis due to fluid retention and dilutional hyponatremia.
  • Elevated Urea and Urea:Creatinine Ratio:
    • May indicate upper gastrointestinal bleeding, which is common in patients with portal hypertension and varices.
  • Hemolytic Anemia:
    • Decreased haptoglobin and increased LDH are indicative of hemolysis. Haptoglobin binds free hemoglobin, so levels decrease when hemolysis is occurring.

Patients with suspected or confirmed liver dysfunction, particularly in the context of decompensated cirrhosis or alcoholic liver disease, should undergo a thorough infection screen:

  • Viral Hepatitis Serology:
    • Anti-HAV IgM: To screen for acute hepatitis A.
    • Hepatitis B Serology and Viral Load: To detect active hepatitis B infection.
    • Anti-HCV IgM and Viral Load: For hepatitis C infection.
    • Anti-HDV Antibody: For hepatitis D infection, especially in those with hepatitis B.
    • Anti-HEV Antibody: If hepatitis E is suspected.
  • Leptospirosis Testing:
    • If leptospirosis is suspected, use ELISA for leptospiral IgM, blood cultures, microscopic agglutination test (MAT), and leptospiral DNA PCR.
  • Blood and Urine Cultures:
    • Particularly important in patients with cirrhosis or suspected sepsis.

Investigations in a patient with jaundice are aimed at identifying the underlying cause, assessing the degree of liver dysfunction, and screening for potential complications. These tests include liver function tests to determine the pattern of liver injury, coagulation studies to assess synthetic function, and additional tests such as urinalysis, full blood count, and infection screening to evaluate for hemolysis, kidney injury, and possible infections.

29
Q

When evaluating a patient with jaundice and suspected liver dysfunction, several specific tests may be necessary to further investigate underlying conditions. Here’s a detailed explanation:

  • Indication: Suspected Wilson’s disease.
    • Wilson’s disease is a genetic disorder that leads to the accumulation of copper in the liver, brain, and other organs due to defective copper metabolism.
    Key Tests:
    - Serum Ceruloplasmin: Typically decreased in Wilson’s disease because ceruloplasmin, a copper-carrying protein, is either low or dysfunctional.
    - Urinary Copper Excretion: Elevated in Wilson’s disease due to increased copper release from damaged liver cells into the bloodstream and subsequent excretion in urine.
  • Indication: Suspected Alpha-1 Antitrypsin Deficiency.
    • Alpha-1 antitrypsin deficiency is a genetic disorder that can cause liver and lung disease. It leads to abnormal accumulation of alpha-1 antitrypsin in the liver, which can cause liver damage.
    Key Test:
    - Serum Alpha-1 Antitrypsin Levels: Typically reduced in this condition. Additionally, genetic testing may be required to confirm the diagnosis.
  • Indication: Suspected Hereditary Hemochromatosis.
    • Hereditary hemochromatosis is a genetic disorder characterized by excessive iron absorption, leading to iron overload and potential damage to the liver, heart, pancreas, and other organs.
    Key Tests:
    - Total Iron, Total Iron Binding Capacity (TIBC), Transferrin Saturation, and Ferritin:
    - Transferrin Saturation: The ratio of serum iron to TIBC is crucial; a level >45% suggests iron overload.
    - Ferritin: Elevated levels can indicate iron overload but are also raised in inflammation, so it’s important to interpret in context.
    - Genetic Testing: If transferrin saturation is elevated, genetic testing for the HFE gene mutation (C282Y and H63D) is recommended.
  • Indication: All patients with decompensated cirrhosis.
    • An ascitic tap (paracentesis) is performed to analyze the fluid in the abdomen for signs of infection, malignancy, or other underlying causes.
    Key Tests:
    - Absolute Neutrophil Count: A count >250 cells/mm³ is diagnostic for Spontaneous Bacterial Peritonitis (SBP).
    - Gram Stain and Microbiological Culture: To identify any bacterial infection in the ascitic fluid.
    - Serum Ascitic Albumin Gradient (SAAG): Helps distinguish between portal hypertension-related ascites and other causes like malignancy.
  • Indication: Suspected Autoimmune Liver Diseases.
    • Autoimmune liver diseases involve the immune system attacking the liver, leading to inflammation and damage.
    Key Tests:
    - Antinuclear Antibody (ANA): Non-specific but often positive in autoimmune hepatitis.
    - Anti-Smooth Muscle Antibody (ASMA): Highly suggestive of autoimmune hepatitis.
    - Anti-Liver-Kidney Microsome Type 1 (Anti-LKM-1) Antibody: Specific for autoimmune hepatitis, particularly in children.
    - Anti-Soluble Liver Antigen (Anti-SLA) Antibody: Also associated with autoimmune hepatitis.
    - Anti-Mitochondrial Antibody (AMA): Diagnostic of Primary Biliary Cholangitis (PBC).
    - Serum IgG4: Elevated in IgG4-related cholangiopathy, a condition causing bile duct inflammation and obstruction.
  • Indication:
    • Screening for pneumonia in patients with alcoholic liver disease or decompensated cirrhosis.
    • Assessing for hepatic hydrothorax (pleural effusion related to cirrhosis) and signs of heart failure such as cardiomegaly or pulmonary edema.
  • Indications: Evaluate liver and biliary tract pathology.Key Imaging Modalities:
    - Abdominal Ultrasound: First-line imaging for liver size, texture, and the presence of masses, as well as for detecting gallstones or biliary duct dilation.
    - Abdominal CT Scan: Provides detailed imaging of the liver and surrounding structures, useful for detecting masses, liver lesions, and complications like ascites.
    - MRI (Magnetic Resonance Imaging): Provides more detailed imaging than CT, especially useful for characterizing liver lesions or assessing biliary tract abnormalities.
    - Endoscopic Ultrasound (EUS): Combines endoscopy and ultrasound to evaluate the pancreas, bile ducts, and surrounding areas for tumors or stones.
    - Endoscopic Retrograde Cholangiopancreatography (ERCP): Both diagnostic and therapeutic, used to visualize the bile ducts and pancreatic ducts, remove stones, or place stents.

In addition to standard liver function tests, specific investigations such as serum ceruloplasmin, urinary copper excretion, serum alpha-1 antitrypsin levels, iron studies, ascitic tap, immunological tests, and advanced imaging techniques are crucial in diagnosing and managing complex liver conditions like Wilson’s disease, alpha-1 antitrypsin deficiency, hereditary hemochromatosis, autoimmune hepatitis, and related liver diseases.

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