wk 1-3 Flashcards
What are the three main functions of blood?
Transportation (oxygen, nutrients, waste)
Balance (pH, temperature, water)
Protection (immune defense, clotting).
What are the percentages of blood components?
55% plasma, 1% buffy coat (WBCs, PLTs), 45% RBCs.
What hormone stimulates RBC production? Where is it made?
Erythropoietin (EPO), made by the kidney; stimulates bone marrow stem cells.
Reduced in kidney failure, HIV/AIDS, cancers, RA.
What is the structure of fetal hemoglobin (HbF)?
HbF = 2 alpha, 2 gamma chains; higher oxygen affinity than adult hemoglobin (2 alpha, 2 beta chains).
What are the roles of WBC types?
Neutrophils = bacteria;
Eosinophils = parasites, allergies;
Lymphocytes = viruses + tumors;
Monocytes = macrophages;
Basophils = small %, hypersensitivity reaction with food or drugs, ATTRACT OTHER WBCS
What are atypical lymphocytes a key indicator of?
Infectious mononucleosis, often the first sign of EBV infection.
What is the CBC Rule of 3s?
RBC x 3 ≈ Hemoglobin x 3 ≈ Hematocrit.
What does MCV measure, and why is it important?
Measures RBC size; microcytic (<80), normocytic (80-100), macrocytic (>100).
What does RDW indicate?
Variation in RBC size (anisocytosis); high RDW = greater variation, often seen in anemia.
Who is the universal blood donor and recipient?
O- = universal donor; AB+ = universal recipient.
What happens if an Rh-negative mother carries an Rh-positive baby?
Antibodies against Rh+ develop, leading to erythroblastosis fetalis in later pregnancies.
RH negative mother has Rh positive baby = antibodies can build against Rh + blood =
erythroblastosis fetalis (hemolytic disease of the newborn) = problem for 2nd Rh + baby,
Rhogam is given after delivery to prevent development of these antibodies
Prevented with Rhogam postpartum or during pregnancy.
What is TRALI, and how is it managed?
Transfusion-related acute lung injury:
- transfused product has anti-HLA or anti-neutrophil antibodies
sx: FEVER, HYPOTENSION, dyspnea, hypoxemia, bilateral chest infiltrates
Stop transfusion immediately, manage airway, supplemental O2
MCC of death associated with transfusions
MCC of transfusion-related death.
What is TACO, and how does it differ from TRALI?
Transfusion-associated circulatory overload: dyspnea, edema, HYPERTENSION (volume overload signs, no immune reaction)
- Manage with slow transfusion, diuretics.
- often occurs in
elderly and chronically anemic
- TRALI= hypotension; FEVER
Common in elderly, chronically anemic.
What defines anemia?
Decreased RBC count, hemoglobin, or hematocrit, reducing oxygen-carrying capacity of blood.
What are reticulocytes, and what do they indicate?
precursor to RBC, have remnant genetic material. Retic counts measure
the rate of RBC production by the bone marrow, appear as polychromasia on a wright
stained blood smear
Appear as polychromasia on Wright stain.
How are platelets (PLTs) formed?
From megakaryocytes in the bone marrow.
What organ is at greatest risk in hemolytic anemia?
The kidney, due to hemoglobinuria.
What is the recommended hemoglobin level for transfusion?
<7 grams per deciliter in asymptomatic patients.
What are the lab findings in iron deficiency?
Serum Iron = low
Ferritin = Low *
Transferrin = High, TIBC = High,
*
Tsat = low,
UIBC = high,
RDW = high*
MCV < 80 -> microcytic hypochromic anemia.
What is iron deficiency anemia (IDA)? cause
MC type
causes: decreased intake, hemolysis, hemorrhage (most cases), increased utilization.
What are the symptoms of IDA?
Fatigue, pallor, poor concentration, syncope, weakness, dyspnea, angular cheilitis, koilonychia, pica, atrophic glossitis, aphthous ulcers, RLES.
What is the best treatment for iron replacement in IDA?
Oral ferrous sulfate is best for treating IDA.
What are the features of lead poisoning?
Mimics IDA; features Burton lines on gums, elevated ICP, learning/IQ issues, basophilic stippling; history of lead exposure critical.
What is hereditary hemochromatosis?
Autosomal recessive HFE mutation -> inc iron absorption, high ferritin, high Tsat.
Triad: hepatomegaly, skin hyperpigmentation, diabetes.
Managed with phlebotomy.
What is cold agglutinin disease?
IgM-mediated (‘Mittens = cold’).
- against I antigen
Causes: primary = idiopathic; secondary = lymph disorders, infections.
Features: Raynaud’s, no splenomegaly.
Positive Coombs test ( C3+)
Tx: immunosuppressants (NO STEROIDS OR SPLENECTOMY)
What vaccinations are required pre-splenectomy? what happens post splenectomy and how does this relate to howell jolly
Pre-splenectomy: pneumococcal, meningococcal, Hib vaccines (2 weeks prior).
(this is bc you are more susceptible to strep pneumoniae, Hae influenzae, and neisseria meningitidis)
Post splenectomy (asplenism) = pt. Is found to have Howell-Jolly bodies (or if they’re hyposplenic = sickle cell)
Howell jolly bodies:
- small dense basophilic RBC includsions (usually removed by spleen)
- found in things with decreased splenic function: sickle cell ds, severe hemolytic anemia, megaloblastic anemia
Post-splenectomy: Howell-Jolly bodies.
What are the features of thrombotic thrombocytopenic purpura (TTP)?
TTP = FAT RN”
Thrombocytopenia, microangiopathic hemolytic anemia.
- Primarily in Adults
- Presents with classic pentad = anemia, thrombocytopenia, renal failure, neuro findings, fever.
- Related to deficiency of ADAMTS13 which cleaves VWF, levels < 10% more clearly assosc with idiopathic TTP.
- ADAMTS13 deficiency -> increase in von Willebrand factor (like sticky paper) -> more platelet adhesion -> microthrombosis in vessels
- ADAMTS13 tests are required for confirming dx,
- < 10% is diagnostic of TTP, peripheral smear can have schistocytes and polychromasia.
- Plasma exchange therapy is Tx of choice, Rituximab if that fails.
