Hemeonc 4 Flashcards
If you have an anemia with normocytic MCV, what is the next test you should order? Why?
Reticulocyte count, to see if there is a production problem (organ dysfunction, chronic disease, HIV, myelosuppression) or bleeding problem (GI bleed, acute blood loss, hemolytic anemia)
What type of anemia is persistent for greater than 1 to 2 months in patients with the associated conditions:
Infection Malignancy Endocrine disorders Immune disorders (SLE, RA) Others: HIV, DM, Heart failure
Anemia of Inflammation
What signals the production of RBC’s? And where is it produced?
The hormone erythropoietin, produced in the kidneys
Causes of anemia of inflammation (2)
suppressed erythropoiesis (renal issue) inflammation (cytokines) results in poor iron metabolism/absorption
Do you expect ferritin to be low in an anemia of chronic disease? Why?
No, because ferritin is an acute phase reaction and it is often normal in chronic disease
What is the treatment for anemia of inflammation?
Treat the underlying cause
What type of anemia results in Bone Marrow Failure: (Global decrease in your stem cells and consequently there is a deficiency in all blood cells.)
PANCYTOPENIA
Aplastic Anemia
What is the major cause of aplastic anemia?
Other causes?
>50% AUTOIMMUNE (IDIOPATHIC) Also caused by drug reaction (sulfa, chloramphenicol, chemo) radiation genetic infection, pregnancy
What are common clinical features of aplastic anemia?
bleeding (thrombocytopenia)
infection (neutropenia)
fatigue/pallor (anemia)
For aplastic anemia,what would you expect to see on a PBS? BMbx?
pancytopenia
Hypocellular marrow with excess fat (normal cytology, just too few)
What is the treatment for aplastic anemia (after RFL to Hematologist)?
Immunosuppression
Allogenic BM transplant if 40 years
Temporary shutdown of erythropoiesis due to acute infection, commonly associated with Parvo/5ths Disease?
Aplastic Crisis
What changes lead to the aged (120 days) RBC being trapped and removed by the RE (reticuloendothelial) system (3)
1) Decrease in lipids in membrane
2) Less pliability
3) Shape becomes more spherocytic
Premature or accelerated destruction of RBCs (<100 days) beyond the ability of the bone marrow to fully compensate
Hemolytic Anemia
Clinical presentation of hemolytic anemia includes:
Jaundice, scleral ichterus, splenomegaly, gallstones, hypotension, hemoglobinuria
In hemolytic anemia, Would you expect an increase in indirect bilirubin? Why?
Yes, because bilirubin is the byproduct of lysed RBC’s
In hemolytic anemia, what would you expect to see on a PBS?
Nucleated red cells, high retic count, spherocytes, schistocytes
What test specifically looks at hemolysis?
Coombs test (Cross and screen is indirect Coombs test)
What genetic assay is associated with impaired metabolic pathways of RBC’s in hemolytic anemia?
G6PD assay (most common in males, blacks, Mediterraneans)
**Most common metabolic cause of hemolytic anemia, treat by avoiding oxidating drugs
Reason for hemolysis is due to the RBC itself
intrinsic factors (issue with membrane, metabolic, hemoglobin type)
Why would splenectomy often be effective tx for gallstones caused by hereditary spherocytes
because the spleen is breaking down the spherocytes rapidly and creating excess bilirubin that accumulates in the gallbladder
What are 3 pathways that the rbc’s utilize in order to create ATP and break down glucose?
1) Glycolysis (Embden-Meyerhof) Pathway produces majority of ATP
2) Hexose Monophosphate Shunt produces 10%
3) Nucleotide Salvage Pathway (very little)
Reason for hemolysis has nothing to do with properties of RBC itself:
Extrinsic factors (immune system, infection, mechanical destruction of RBC’s)
development of antibodies that target the RBC membrane
Autoimmune hemolytic anemia
When you think WARM autoimmune hemolytic anemia, think:
IgG, Fix complement weakly. Treat w/ steroids, splenectomy, immunosuppressants
When you think COLD autoimmune hemolytic anemia, think:
IgM, Fix complement strongly. (Underlying lymphoma common). Treat w/ avoidance of cold, cytotoxic meds, plasmapheresis
