Bikman - Anemia Flashcards
What are the two main components of complete blood count (CBC)? Why?
- Hemoglobin
- More red when oxygenated means more hemoglobin - Hematocrit
- How much of what’s in the tube is made of RBCs
What is the most common anemia worldwide?
Iron-deficiency
Anisocytosis
Size variation
Poikilocytosis
Shape variation
What is anemia?
A reduction below normal in Hb or RBC #.
Symptoms:
- Pale skin
- Mucus membranes
- Jaundice (if hemolytic)
- Breathlessness
- Tachycardia
- Dizziness
- Fatigue
Not enough of RBCs or Hb or not enough vitamin B12 (aids in cell formation) or if it’s not moving around as it should
What are the three causes of anemia?
- Blood loss
- Excessive RBC destruction
- Extracorpuscular reasons
- Intracorpuscular reasons - Insufficient RBC production
- Too little material
- Too little RBCs
- Not enough room
Anemia induced by blood loss
Cause: trauma resulting in acute blood loss
- After 2-3 days, reticulocytes spike (normal is 1%)
Kidneys release erythropoietin and goes to bone marrow and activates erythropoiesis, releasing reticulocytes (RBC precursors) which mature in the blood to erythrocytes
Anemia induced by excessive RBC destruction - what are some signs of destruction and some signs of production?
Destruction
- Increased bilirubin (breakdown of RBCs)
- Increased LDH (where RBCs get their energy b/c no mt)
- Reduced haptoglobin
Production
- Increased reticulocytes
- Nucleated red cells in blood
Erythrocyte destruction
- Lifespan of RBC is ~120 days
- RBC destroyed by macrophages in spleen and liver
- RBC recycling
- – Globin (into AA)
- – Heme (Fe-containing part) used in liver, spleen, bone marrow
- – Remainder converted to bilirubin
Unconjugated bilirubin is toxic
- Bilirubin + Albumin complex
- Lipid soluble
- Damage cell membranes
Bilirubin elimination
- Unconjugated bilirubin is taken up by the liver and other cells
- Conjugated via glucuronyl transferase (makes bilirubin water soluble)
- Conjugated bilirubin is excreted with bile to the small intestine
- – Can be eliminated from body in feces
- Some bilirubin in the intestine is converted into urobilinogen by intestinal bacteria
- – Most excreted via feces
- – Some reabsorbed into the blood and liver can further metabolize urobilinogen and excrete it as bile
- Small amounts of urobilinogen are excreted from the body in the urine
What is jaundice? How can we treat it?
Excess bilirubin accumulation in the body
- Skin, nails, whites of eyes
Toxic to brain cells.
Tx:
- Tx cause of condition
- Blood transfusion
- Sun/UV rays make bilirubin water soluble
What is jaundice caused by?
Excess bilirubin production due to RBC destruction
- Surpasses liver’s ability to conjugate
OR
- Decreased bilirubin excretion
- Reduced hepatic uptake (hepatitis, cirrhosis)
- Decreased conjugation (hepatitis, cirrhosis, enzyme deficiency)
- Bile duct obstruction (tumor, stone)
Dx and Tx of Jaundice
Location determined by
- Color of feces and urine
1. Light or clay-colored feces and dark urine- Extrahepatic obstructive jaundice = obstruction of bile duct
- Normal to light colored feces and light urine
- Intrahepatic obstructive jaundice = damaged hepatocytes; cirrhosis, hepatitis, liver failure - Dark feces and urine
- Hemolyic anemia
- X-ray, CT scan, liver biopsy can provide evidence of presence of stone, tumor, hepatitis, cirrhosis
Extrahepatic obstructive jaundice
Light or clay colored feces, dark urine
Obstruction of the bile duct
Intrahepatic obstructive jaundice
Normal to light-colored feces, light urine
Damaged hepatocytes from cirrhosis, hepatitis, liver failure
Hemolytic anemia
Dark feces and urine
Overloading the process, destroying too much
What are the extracorpuscular hemolytic anemias?
- Microangiopathic hemolytic anemia
- Autoimmune hemolytic anemia
Microangiopathic hemolytic anemia
Extracorpuscular hemolytic anemia
- Physical trauma to RBCs
- Schistocytes (RBC fragments)
Causes:
- Artificial heart valve
- Malignancy
- Obstetric complications
- Sepsis
- Trauma
Autoimmune hemolytic anemia
Extracorpuscular
Warm
- IgG - more active at higher temp
- Spleen
- Spherocytes
Cold
- IgM, complement - more active at lower temp
- Intravascular hemolysis
- Agglutination
Type II
What are the intracorpuscular hemolytic anemias?
- Sickle cell anemia
- Thalassemia
- Hereditary spherocytosis
- Howell-Jolly bodies
- G6PDH deficiency
Sickle Cell Anemia
Intracorpuscular
- Hemoglobinopathy
- Single aa substitution in beta chain (Val for Glut Acid)
- Heter vs homozygous
- African ethnicity
Aggregates and polymerizes, clogging the vessels -> ischemic necrosis or spleen infarction
Thalassemia
Intracorpuscular
Hypochromic, microcytic anemia
- Can’t make enough alpha or beta chain
- Increased RBC synthesis (EPO)
- Medullary expansion due to increased erythropoiesis
alpha: SE asian
beta: Mediterranean
Hereditary Spherocytosis
Intracorpuscular
- Many spherocytes
- Caused by a spectrin defect
- Splenectomy is curative
- RBCs form polymers and get trapped in the spleen = SPLENOMEGALY
