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Haematology. Group A. Patient X. A 61 year old male Presents with: generalised weakness & increasing dyspnoea on exertion for 3/52. Medical History: Alcoholism Social History Divorced for 2 years Lives Alone Retrenched 6 years ago; has not worked since. Mr X cont…. On Examination:

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patient x
Patient X
  • A 61 year old male
  • Presents with:
    • generalised weakness & increasing dyspnoea on exertion for 3/52.
  • Medical History:
    • Alcoholism
  • Social History
    • Divorced for 2 years
    • Lives Alone
    • Retrenched 6 years ago; has not worked since
mr x cont
Mr X cont…
  • On Examination:
    • Pallor and scleral icterus were noted
    • Clinical evidence of chronic alcoholic liver disease with portal hypertension
    • Spleen was palpable (2cm).
mr x s biochemistry fbc
Mr X’s Biochemistry - FBC
  • Initial biochemistry:
  • Blood flim:
        • Marked anisocytosis (oval macrocytes +++)
        • Poikilocytes (tear drop & fragmented cells ++)
        • Red cells normochromatic
        • Neutropenia with marked neutrophil hypersegmentation
        • Thrombocytopenia.
portal hypertension
Portal Hypertension
  • Pressure in the hepatic portal vein is increased
  • Most common cause is cirrhosis, but any liver disease can cause it
  • In cirrhosis, hepatocytes regenerate more slowly than scar-tissue forms
    • As the scar tissue shrinks, it obstructs blood flow through the hepatic portal system
symptoms of portal hypertension
Symptoms of Portal Hypertension
  • Common portal hypertensive complications include:
    • Hepatic encephalopathy
    • Bleeding esophageal varices
    • Ascites & spontaneous bacterial peritonitis
    • Hepatorenal syndrome
alcoholic liver disease
Alcoholic Liver Disease
  • A spectrum of clinical syndromes & pathologic changes in the liver caused by alcohol. The spectrum includes fatty liver, alcoholic hepatitis & alcoholic cirrohsis.
  • Approximately 15% to 20% of those who abuse alcohol develop alcoholic hepatitis and/or cirrhosis, which may develop in succession or exist concomitantly
  • The level of alcohol consumption necessary for the development of these advanced forms of alcoholic liver disease is probably 80 g of alcohol per day, the equivalent to 6 to 8 drinks daily for several years
  • BUT, the threshold of alcohol necessary for the development of advanced alcoholic liver disease varies substantially among individuals
alcoholic fatty liver
Alcoholic Fatty Liver
  • Also called steatosis
  • Predominantly an asymptomatic condition that develops in response to a short duration (a few days) of alcohol abuse
  • Up to 15 drinks a day for 10 days
  • Entirely reversible with abstinence
alcoholic hepatitis
Alcoholic Hepatitis
  • Prolonged alcohol abuse results in alcoholic hepatitis.
  • Patients with this condition have various constitutional symptoms, such as fatigue, anorexia, weight loss, nausea and vomiting.
  • Severe alcoholic hepatitis may be evident by advanced symptoms due to portal hypertension, including gastrointestinal (GI) bleeding, ascites, and hepatic encephalopathy.
  • Other findings depend on the severity of liver insult and may include jaundice, splenomegaly, hepatic bruits, collateral vessels, and ascites.
  • Reversible if patients stop drinking
alcoholic cirrhosis
Alcoholic Cirrhosis
  • Alcoholic cirrhosis may occur before, concomitant with, after, or independent of a bout of alcoholic hepatitis
  • Characterized anatomically by widespread nodules in the liver combined with fibrosis
  • Most common of specific organ damage in alcoholics
  • The clinical history is similar to that of alcoholic hepatitis, & symptoms are similar to those observed with other forms of end-stage liver disease
bilirubin
Bilirubin
  • Bilirubin: A break-down product of haemoglobin
  • Dying RBCs are engulfed & destroyed by macrophages
  • Heme is split from globin & the iron core is salvaged
  • The remaining heme molecule is degraded to bilirubin
bilirubin13
Bilirubin
  • Unconjugated bilirubin is transported in the plasma bound to albumin
  • This free bilirubin is conjugated with glucuronic acid in the liver.
  • The conjugated bilirubin is then secreted in the bile as an orange-yellow pigment
bilirubin liver disease
Bilirubin & Liver Disease
  • Generally, liver disease leads to mixed hyperbilirubinemia, i.e., high levels of both circulating (unconjugated) and conjugated bilirubin. (Total=84, range: 2-20) and conjugated 44 micro mol/L, range: 1-4
  • This is due to impaired liver uptake of unconjugated, and impaired excretion of conjugated bilirubin from bile duct perhaps due to gallstones, hepatitis, trauma or long term alcohol abuse
  • Also, an increase in bilirubin may mean too many RBC are getting destroyed
mr x are his bilirubin results consistent with alcoholic liver disease
Mr X – are his bilirubin results consistent with alcoholic liver disease?
  • Hyperbilirubinemia: excess of bilirubin in the blood
      • Visible jaundice occurs at ~20-30μmol/L
      • The patient has jaundice (scleral icterus)
  • History of alcoholism
  • Mr X has mixed hyperbilirubinemia
lactate dehydrogenase ld
Lactate Dehydrogenase (LD)
  • Cytoplasmic enzyme
  • Its function is to catalyze the oxidation of L-lactate to pyruvate
    • Assayed as a measure of anaerobic carbohydrate metabolism
  • Present in heart, liver, kindey, lungs, skeletal muscle and brains
  • Used as a diagnostic marker for MI, muscular disorders, malignancy and liver disease
  • Not a specific marker
increased levels indicate
Increased Levels Indicate:
  • MI
  • Stroke
  • Anaemia
  • Hypotension
  • Liver disease
  • Megaloblastic anaemia
  • Perniciour anaemia
when is ld testing performed
When is LD testing Performed
  • Possible diagnosis:
    • Anaemia of Vitamin B12 deficiency
    • Megaloblastic anaemia
    • Perniciour anaemia
  • LD isoenzyme levels may be requested
lactate dehydrogenase liver disease
Lactate Dehydrogenase & Liver Disease
  • LD has several isoenzymes (LD-1 to LD-5)
  • LD-1 and 2
    • MI, Renal infarction, megaloblastic anaemia
  • LD-2 and 3
    • Acute leukaemia
  • LD-5
    • Liver and skeletal muscle damage
what this tells us
What this tells us:
  • Tissue damage
  • Possible liver disease
  • Possible anaemia
  • Muscle injury
  • MI
haptoglobins
Haptoglobins
  • Plasma proteins that carry “free” haemoglobin (i.e., Hb NOT in RBCs)
  • Blood levels used to detect haemolysis (intravascular destruction of RBC)
    • Normally ~10% of haemolysis is handled by haptoglobins and haemopexin
    • Haemolysis > Haptoglobin synthesis  decrease in serum haptoglobin
  • Lower than normal levels may indicate chronic liver disease, haemolytic anaemia, primary liver disease, AMI and some cancers
  • Increased levels in certain chronic diseases and inflammatory disorders
mr x are his haptoglobin results consistent with alcoholic liver disease

Parameter

Value

Reference Range

Haptoglobin

0.3g/L

0.3-2.0g/L

Mr X – are his haptoglobin results consistent with alcoholic liver disease?
  • 0.3g/L is boarder-line low for the normal range (0.3 – 2.0g/L)
ferritin
Ferritin
  • An iron compound synthesised in response to erythrophagocytosis
  • Ferritin is stored in the liver, spleen & bone marrow for eventual encorporation into haemoglobin
  • Ferritin iron is the principle form of iron storage therefore serum ferritin levels indicate the body’s iron stores
ferritin24
Ferritin
  • Two main functions:
    • sequester potentially toxic iron into the apoferritin protein shell
    • provide a readily accessible store of iron
  • Can be used to diagnose iron deficiency anaemia
    • In combination with serum iron and total iron-binding capacity tests, it can differentiate and classify different types of anaemia\'s
mr x are his ferritin results consistent with alcoholic liver disease

Parameter

Value

Reference Range

Ferritin

442μg/L (H)

33-330μg/L

Mr X – are his ferritin results consistent with alcoholic liver disease?
  • 442μg/L is significantly higher than the upper normal range (33-330μg/L)
  • This suggests a high level of erythrophagocytosis, most likely due to severe inflammatory liver disease
folate vitamin b 9
Folate (Vitamin B9)
  • Obtained from green, leafy vegetables
  • Total body folate is ~70mg
    • 1/3 of this is stored in the liver
  • In folate deficiency anaemia, the red cells are abnormally large (“megalocytes”)
    • Precursors, in the bone marrow are “megaloblasts”
    • Thus, this anaemia is referred to as megaloblastic anemia
folate deficient anaemia
Folate–Deficient Anaemia
  • Causes of the anaemia are poor dietary intake of folic acid as in chronic alcoholism
  • Causes of folic acid depletion include:
    • Poor intake (e.g., chronic alcoholism, diet lacking in fresh vegetables)
    • Inadequate absorption/malabsorption syndrome (e.g, drug-induced by phenytoin, primidone, barbiturates; celiac disease)
    • Inadequate utilisation via antagonists such as methotrexate and trimethoprim
  • Alcohol also interferes with its intestinal absorption, intermediate metabolism & entero-hepatic salvage
megaloblastic anemia
Megaloblastic Anemia
  • Results from defective DNA synthesis. RNA synthesis continues  increased cytoplasmic mass & maturation
    • I.e., All cells have dyspoiesis: cytoplasmic maturity > nuclear maturity  production of megaloblasts
    • Dyspoiesis  increased intramedullary cell death  hyperbilirubinemia & hyperuricemia
    • All cell lines are affected, so leukopenia & thrombocytopenia may occur
  • Main causes: defective utilisation of folic acid or vitamin B12 deficiency; cytotoxic drugs; Di-Guliemo Syndrome
mr x are his results consistent with megaloblastic anaemia

Parameter

Value

Reference Range

Serum B12

138 pmol/L

120-680

Serum folate

0.7 nmol/L (L)

7-45

Red cell folate

125 nmol/L (L)

360-1400

Mr X – are his results consistent with megaloblastic anaemia?
  • The patient’s Hb is low, indicating anaemia, while his elevated MCV indicates macrocytic anaemia.
  • The patient has a serum folate of 0.7nmol/L, & a RBC folate level of 125nmol/L which are well below the normal ranges. His serum B12 is within the normal range
    • Normal serum B12 assay with a low RBC folate level are consistent with alcoholism
  • Both of these results

also support the diagnosis of

megaloblastic anaemia due

to folic acid deficiency.

mr x s biochemistry fbc30
Mr X’s Biochemistry - FBC
  • Initial biochemistry:
  • Blood flim:
        • Marked anisocytosis (oval macrocytes +++)
        • Poikilocytes (tear drop & fragmented cells ++)
        • Red cells normochromatic
        • Neutropenia with marked neutrophil hypersegmentation
        • Thrombocytopenia.
mr x are his results consistent with megaloblastic anaemia31
Mr X – are his results consistent with megaloblastic anaemia?
  • Mr X’s neutrophils are below the normal range.
    • This tends to occur in chronic disease states and megaloblastic anaemias
  • Hypersegmentation of neutrophils occurs in 91% of cases megaloblastic anaemia
conclusions
Conclusions
  • Mr X is experiencing multiple biochemical changes due to his chronic alcohol intake.
  • Treatment for him is primarily supportive. He needs to improve his diet, and ideally, should cease alcohol intake.
  • Corticosteroids may be indicated.
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