RBCs Flashcards
Burr cells
Seen in liver disease and end stage renal disease.
Howell Jolly bodies
basophilic remnants of the nucleus that appear as small black pellets in RBCs. Pts with hx of splenectomy or functionl asplenia.
Spur cells
Liver disease
Target cells
Hemoglobinopathies (e.g., thalassemia) or chronic liver disease, esp obstructive liver dz.
Bite cells and Heinz bodies
G6PD deficiency. G6PD is an enzyme involved in creating NADPH, a cofactor required to create glutathione and prevent the oxidation of hemoglobin. Without G6PD, hemoglobin becomes oxidized and denatures into Heinz bodies. The denatured Hgb disrupts RBC membranes and causes hemolysis. This reaction typically occurs in response to oxidant drugs like antimalrials and sulfas and infection. X linked recessive.
Why might a patient with sickle cell get nocturne?
Nocturia is most likely secondary to an impairment in his kidney’s ability to concentrate urine, a condition called hyposthenuria. Hyposthenuria is found in patients with sickle cell but is also common in patients with sickle cell trait. Hyposthenuria is thought to result from RBC sickling in the vasa rectae of the inner medulla, which impairs countercurrent exchange and free water reabsorption.
Clinical mx of PNH
Hemolysis – > fatigue
Cytopenias (impaired hematopoiesis)
Venous thrombosis (intra-abdominal, cerebral veins)
Pathophys of PNH
PNH is an autoimmune hemolytic disorder characterized by intravasc and extravasc hemolysis and hemoglobinuria. The disease is due to an acquired genetic defect that results in lack of the glycosylphosphatidylinositol anchor which connects proteins, including CD55 and CD59, to the cell surface. These proteins normally inhibit the activation of complement on red blood cells, but their absence allows the complement MAC to form and results in hemolysis.
Lab signs of intravascular hemolysis
Low haptoglobin accompanied by elevated bill and LDH
CLinical presentation of hereditary spherocytosis
Increased MCHC, hemolytic anemia, jaundice and splenomegaly in a patient of Northern European descent.
Why are pts with hereditary spherocytosis susceptible to acute cholecystitis?
Short life span of spherocytes and chronic hemolysis cause high Hhgb turnover and excess bill that overwhelm conjugation and elimination from the body. Resulting hyperbole manifests as jaundice, dark urine, and pigment (calcium blurb) gallstones.
Prophylactic tx of pts with hereditary spherocytosis
Cholecystectomy, folate supplementation aas chronic hemolysis consumes folate. Many pts also require splenectomy to minimize hemolysis.
Major cause of anemia in patients with ESRD
Deficiency of erythropoietin. The anemia is normocytic and normochromic.
Tx of choice in ESRD anemia and the most common side effects
recombinant epo which is started if the Hb
How does CO poisoning cause increased hematocrit?
CO binds hemoglobin with an affinity approximately 250 times that of oxygen. The presence of CO-bound hemoglobin significantly decreases the blood’s oxygen-carrying capacity. To compensate for decreased oxygen delivery, the body increases RBC production.
