HEME/ONC Flashcards
Lab value used to monitor Heparin
PTT
Lab value used to monitor Warfarin
PT/INR
Lab value used to monitor Enoxaparin
Factor Xa activity
Test to dx beta-thalassemia minor
Hemoglobin electrophoresis – would find increased HbA2
Should be ruled out in male over 50 with new onset iron deficiency anemia
Colon cancer
8 causes of aplastic anemia
Radiation* Benzene Chloramphenicol Alkylating agents Anti-metabolites Viruses (e.g. parvo B19, EBV, HIV, HCV) Fanconi's anemia Immune-related
Main pathogenesis of aplastic anemia as well as distinguishing bone marrow findings.
Failure or destruction of myeloid stem cells – usually due to radiation.
Pancytopenia characterized by severe anemia, leukopenia, and thrombocytopenia. Normal cell morphology but hypocellular bone marrow with fatty infiltration (dry bone marrow tap).
5 etiologies of B12 deficiency
Insufficient intake (e.g. strict vegans) Malabsorption (e.g. Crohn's disease) Pernicious anemia Diphyllobothrium latum (fish tapeworm) PPIs
3 drugs that can cause folate deficiency
Methotrexate
Trimethoprim
Phenytoin
Lab findings in iron deficiency anemia
Decreased serum iron (PRIMARY)
Increased transferrin/TIBC
Decreased ferritin (iron stores depleted)
REALLY decreased % transferrin saturation (serum iron/TIBC)
Lab findings in anemia of chronic disease
Decreased serum iron
Decreased transferrin/TIBC because the body has adapted a system in which iron is stored within the cells of the body and prevents pathogens from acquiring circulating iron.
Increased ferritin (primary)
Lab findings in hemochromatosis
Increased serum iron (primary)
Decreased transferrin/TIBC
Increased ferritin
REALLY increased % transferrin saturation (serum iron/TIBC)
Lab findings in pregnancy/OCP use
Increased transferrin/TIBC (primary)
Decreased % transferrin saturation (serum iron/TIBC)
Findings in Hereditary Spherocytosis
Anemia Jaundice Pigmented gallstones* Splenomegaly \+ Osmotic fragility - Coomb's (Abs are not causing hemolysis)
Difference between HbS defect and HbC defect
HbS: subsitution of valine for glutamic acid at position 6 on beta globin
HbC: substitution of lysine for glutamic acid
Difference between Direct Coomb’s and Indirect Coomb’s
The Coombs test evaluates for RBC agglutination with the addition of antihuman antibody because RBCs are coated with Ig or complement proteins.
In a Direct Coomb’s, prepared Abs are added to a patient’s washed RBC to detect the presence of immunoglobulins already present on the RBC (using an Ab to detect an Ab).
In an Indirect Coomb’s, the patient’s serum is incubate with normal RBC to detect for the presence of Abs.
3 situations with a positive Direct Coomb’s
Hemolytic disease of the newborn
Drug-induced autoimmune hemolytic anemia
Hemolytic transfusion reactions
2 situations which use an Indirect Coomb’s
Tests blood prior to transfusion
Screening for maternal Abs to a fetus’ blood
It’s positive when there are Abs present to foreign blood.
Pathogenesis of Cold Agglutinins and 3 infections associated
Antibodies against RBCs that interact more strongly at low temps than at body temp.
Nearly always IgM.
Occur regularly in infections with Mycoplasma pneumonia, EBV, malignancies (CLL)
Problems/disease occurs when there is circulation to a cold extremity –> IgM binds RBC antigen –> complement fixation –> MAC lysis, opsonization –> phagocytosis
Pathogenesis of Warm Agglutinins and 4 disease associations
Antibodies that react against RBC protein Ags at body temperature.
Nearly always IgG.
Seen in viruses (EBV, HIV), SLE, malignancies (CLL), and congenital immune abnormalities.
2 protozoal diseases that can cause hemolytic anemia
Malaria
Babesiosis
4 diseases that cause basophilic stippling
Thalassemia
Anemia of chronic disease
Iron deficiency
Lead poisoning*
TAIL
4 conditions associated with target cells
HALT says the hunter to its TARGET. HbC disease Asplenia Liver disease Thalassemias
Anemia resulting from mechanical destruction of erythrocytes due to aortic stenosis or prosthetic heart valves
Macroangiopathic anemia
Mechanism and lab values seen in Bernard-Soulier syndrome
Defect in platelet plug formation due to decreased GpIb, causing a defect in platelet-to-vWF adhesion.
Platelet count is decreased, bleeding time is increased.
Mechanism and lab values seen in Glanzmann’s Thrombasthenia
Defect in platelet plug formation due to decreased GpIIb/IIIa, causing a defect in platelet-to-platelet aggregation.
On labs, there is no platelet clumping on blood smear.
This causes increased bleeding time with no change in platelet count.
Mechanism and lab values seen in Idiopathic Thrombocytopenic Purpura (ITP)
Anti-GpIIb/IIIa Abs attached to platelets cause the splenic macrophages to sequester and destroy these complexes. This obviously decreases platelet survival, causing a decrease in platelet count and an increase in bleeding time.
Labs show increased megakaryocytes.
Mechanism and lab values seen in Thrombotic Thrombocytopenia Purpura (TTP) –SX associated (hint: mneumonic)
A deficiency of ADAMTS 13 (vWF metalloprotease) causes decreased degradation of vWF multimers. These huge multimers cause increased platelet aggregation and thrombosis, causing decreased platelet survival with schistocytes and increased LDH present.
SX are HUS + neurologic sx and fever.
FAT RN = Fever, Anemia (hemolytic), Thrombocytopenia, Renal failure (uremia), Neurologic sx
Mechanism, triad of sx and most common cause of HUS
Hemolytic anemia + thrombocytopenia + renal failure
Preceded by E. coli 0:157 H:7
Endothelial cells are damaged predomianntly in the kidney causing paltelets to aggregate, forming microthrombi. This causes renal injury leading to uremia.
The clot formation consumes platelets, causing thrombocytopenia.
The thrombi shear RBCs causing schistocytes and anemia.
2 locations of vWF synthesis
megakaryocytes (alpha granules inside platelets) endothelial cells (Weibel-Palade bodies)
Pathogenesis of von Willebrand’s disease
Qualitative or quantitative deficiency in vWF. In its absence, stability of factor VIII is lost causing an intrinsic pathway coagulation defect and increasing PTT. vWF is also involved in platelet adhesion to vessel wall and other platelets. Thus, its deficiency leads to an increased bleeding time due to the defect in platelet-to-vWF adhesion.
AUTOSOMAL DOMINANT.
Dx of von Willebrand’s disease uses …
Ristocetin cofactor assay
Lifespan of a platelet
8-10 days
Pathogenesis of DIC
Pathological activation of coagulation mechanisms in response to a variety of diseases. DIC leads to the formation of small blood clots inside the blood vessels throughout the body. As the small clots consume coagulation proteins and platelets, normal coagulation is disrupted and abnormal bleeding occurs from the skin (e.g. from sites where blood samples were taken), the GI tract, the respiratory tract and surgical wounds. The small clots also disrupt normal blood flow to organs (such as the kidneys), which may malfunction as a result.
4 neoplasms associated with AIDS
Kaposi sarcoma
Invasive SCC
CNS lymphoma
NHL
4 diseases associated with Marginal Cell Lymphoma
Hashimoto Thyroiditis
Sjogren disease (salivary gland)
Stomach in H. pylori - gastritis
GI tract in MALToma
Most common lymphoma in US
Diffuse large B cell lymphoma
2 lymphomas associated with EBV
Burkitt lymphoma
Hodgkin lymphoma
Lymphoma equivalent of CLL
Small lymphocytic lymphoma
STarry sky pattern due to phagocyotsis of apoptotic tumor cell
Burkitt lymphoma
Age distribution of Hodgkin’s vs. Non-Hodgkin’s lymphoma
Hodgkin’s: bi-modal (under 20 or over 65)
NHL: widely variable
Most common type of NHL in adults; NHL in children
Adults: diffuse large B cell
Children: lymphoblastic lymphoma
Epidemiology of ALL
White male children
Leukemia associated with the enzyme terminal deoxynucleotide transferase (TdT)
ALL
Leukemia that is PAS +
ALL
Characteristic auer rods
AML (M2, M3)
AML that are CD13 and CD33+
M0-M6 AML
AML associated with Down syndrome
M7 AML
Myelodysplastic and myeloproliferative d/o may both progress to
AML
Acute leukemia vs chronic leukemia blast count
Acute: >20%
Chronic: <5%
Numerous basophils, splenomegaly, and negative for leukocyte alkaline phosphatase
CML
Always positive for philadelphia chromosome t9;22
CML