hematology Flashcards
lifespan of blood cells
o Erythrocytes=120d
o Granulocytes=0.5d
o Platelets=9d
sites of hematopoeisis throughout the lifespan
o Prenatal: yolk sac
o 4months gestation—birth: liver, spleen
o Childhood: bone marrow (all over, incl tibia/femur)
o Adult: bone marrow shifts to vertebrae, sternum, and ribs predominantly
o *w/ inc. demand for blood cells, hematopoeisis can persist or be reestablished in normally inactive marrow sites (even liver/spleen)
bone marrow architecture
o Cords (niches)
• Mixture of cell types in various stages of maturation
o Sinuses
o Bone marrow-blood barrier
o Adipose and fibroblast cells and their secretions (adhesive molecules and chemokines, like CXCL12) provide the special microenvironment that allow HSC to survive (homing)
3 requirements for hematopoiesis
o Stem cells
o Stroma/extra-cellular matrix (microenvironment)
o Growth factors (regulators)
growth factors in hematopoiesis
o Stem cells (stem cell factor factors)
o Myeloid cells (GM-CSF, G-CSF, M-CSF)
o Erythroid cells (erythropoietin)—epo synthesized by kidney cells in response to hypoxia
o Megakaryocytes (thrombopoietin)
o Lymphoid cells (interleukins, cytokines)
o Growth factors (except EPO) exhibit redundancy (overlappin functions), pleiotrophy (multiple functions; stimulate multiple cells), and synergy (combo are more effective than individual factors)
o Synthesis is high localized w/ GF tethering
o Myeloid GF influence primitive progenitor cells and mature progeny
o Act to: maintain cell viability, initiate cell cycle, activate effector functions
hematopoietic stem cells
o Multi-potent (produce all different cell lines and possible endothelial cells)
o Self-renewing (can maintain its own cell pool)
- Asymmetric vs symmetric
o Capable of repopulating (bone marrow transplant)
o Capable of differentiation into mature precursors
o Are present in very low numbers and are morphologically indistinct
o Capable of mobility and redistribution through the circulation
red cell maturation
o Normally 50,000 in circulation
o If have severe RBC deficiency, can lose 1g Hb/week
o Decrease in cell size
o Decreasing nuclear-cytoplasmic ratio
o Nuclear maturation (chromatin clumping and extrusion)
o Cytoplasmic maturation (hemoglobin)
erythrocyte characteristics
o Non-nucleated biconcave disc
o Slightly smaller than normal lymphocyte nucleus
o Central pallor (1/3 cell diameter)
o Released into blood as reticulocytes
o 120 day lifespan (1/120 replaced every day = 0.8-1.0 % reticulocytes)
o main function is oxygen transport. Hemoglobins:
• Hb A (a2b2)—main adult hemoglobin (95%)
• Hb F (a2g2)—1% (but main Hb in fetuses)
• Hb A2 (a2d2)—2-3%
reticulocyte characteristics
o Newly produced red cells
o Slightly larger, diffusely basophilic cytoplasm
o Supra-vital staining of RNA-ribosomal complexes (still hemoglobin synthesis)
o Increased numbers reflect increased production. Markedly increased in hemolytic processes
erythropoietin
• Erythropoietin (EPO) is main regulator of RBC production:
o Made by interstitial cortical renal cells
o HIF (hypoxia inducible factor) regulates Epo txn
o Clinical uses:
• Anemia of renal failure
• Anemia of prematurity
• Myelodysplasia (refractory anemia, sideroblastic anemia)
• Anemia of chronic disease (inflammatory or malignant)
• w/ surgical procedures (autologous transfusion)
Lab values: RBC
• RBC – Total number
o Reported as number of cells per liter of blood
o Adult male 4.5-6 x1012/L, adult female 4-5.5 x1012/L
Lab values Hemoglobin
• Hemoglobin (Hb) – Concentration
o Measured as gram per deciliter of blood
o Adult male 14-18g/dL, Adult female 12-16g/dL
o Anemia: decreased Hb
o Polycythemia: increased Hb
Hematocrit Lab values
• Hematocrit (Hct) – Volume
o Volume of red blood cells to volume of whole blood cells
o Calculated from RBC and MCV: Hematocrit = RBC (cells/liter) X MCV (liter/cell)
o Adult male 40%-54%, adult female 35%-47%
Mean copuscular volume (MCV)
• Mean corpuscular volume (MCV)
o Determined as mean of red blood cell distribution histogram, Normal range: 82-100 um3
o Microcytosis: decreased MCV
o Macrocytosis: increased MCV
MCH lab value
• Mean corpuscular hemoglobin (MCH)
o Hemoglobin concentration per cell
o Normal range: 27-34 pg
o Hemoglobin divided by RBC
o Limited clinical use
MCHC lab values
• Mean corpuscular hemoglobin concentration (MCHC)
o Average hemoglobin concentration per total red blood cell volume, Normal range 32-36%
o Hemoglobin divided by hematocrit
o Limited clinical use
RDW lab values
• RDW: Red cell distribution width:
o Coefficient of variation of red cell histogram distribution curve
o Measure degree of variation of red blood cell size (or anisocytosis)
o Normal range: 11-15%
o Increase of RDW is associated with anemia from various deficiencies: Iron, B12, folate
o Normal or low RDW is associated with thalassemia or anemia of chronic disease
o Not specific, must be interpreted in conjunction of other CBC and red cell indices
lab values reticulocytes
• Reticulocytes:
o Immature red blood cells containing residual ribosomes
o Indicator of red cell production
o Normal range: 0.5-1.5% (20-76 B/L)
o Clinically used to evaluate anemia
• Low reticulocyte count: iron deficiency, folate/B12 deficiency, bone marrow failure
• High reticulocyte count: acute blood loss, hemolysis
ESR lab values
o Measures distance of red blood cells fall in a vertical tube over a given period of time
o Normal range: 0-15 mm/hr
o Negative charges on red blood cells prevent stacking
o Inflammatory proteins (such as fibrinogen, a-, b-, g-globins) increase red cell sedimentation.
o A more rapid fall of red cells in the test tube, resulting higher stack of red cells – elevated ESR
o Elevated ESR indicates inflammatory process
• useful in monitor disease process, esp. temporal arteritis, polymyalgia rheumatica
o Not recommended for screening test or diagnostic purpose
o False positive and false negative common
MCV low, RDW normal
thalassemia trait
MCV low, RDW high
iron deficiency
MCV normal, RDW normal
chronic disease
MCV normal, RDW high
homozygous hemoglobinopathy
MCV high, RDW normal
aplastic anemia
MCV high, RDW high
folate and B12 deficiency
iron deficiency anemia lab characteristics
o Microcytic hypochromic anemia: reduced hemoglobin, reduced MCV, increased RDW
o Serum iron profile: reduced iron, reduced ferritin, increased total iron binding capacity
o Normal to low reticulocytes count, lack of polychromasia on blood smear
o Microcytic hypochromic red blood cells in blood smear: smaller red cells with increased central pallor
anisocytosis
variation of cell size
poikilocytosis
variation of cell shape
Polychromasia – Increase of reticulocytes
Spherocytes – Smaller, round shaped red blood cells which lack central pallor.
- Acquired immune hemolytic anemia
- Post transfusion
- Hemolytic anemia due to oxidant drugs
- Hemolysis due to a large spleen
- Hereditary spherocytosis
Elliptocyte (aka ovalocyte) - an elongated red blood cell with blunt end
Shape varies from slightly oval or egg-shaped to long pencil-like.
- Hereditary elliptocytosis
- Smaller number can be seen in iron deficiency, thalassemia, hemoglobinopathy, and other anemia.
Target cell - A dense central area surrounded by a relatively clear area and a peripheral rim of hemoglobin
Thalassemia
Sickle cell disease (esp. hemoglobin C disease)
Liver disease
Post splenectomy
Iron deficiency
Sickle cell – Sickle shaped red cells, pointed at both ends, caused by molecular aggregation of hemoglobin S
Sickle cell disease, not present in sickle cell trait
Caused by a point mutation in b-globin chain
Mutated b-globin polymerizes with low oxygen
Cause changes of red cell shape
Echinocyte (Burr cells) – short, evenly space spicules and preserved central pallor
Uremia
Bleeding ulcer
Gastric cancer
Artifact
Distinguish from Acanthocyte (Spur cell) mostly seen in lipoproteinemia
Schistocyte – Distorted, fragmented cells with 2 to 3 pointed ends
Microangiopathic hemolytic anemia (DIC, TTP)
Severe burns
Prosthetic heart valves
Teardrop cells – Distorted, drop-shaped cell
Myelophthisis – bone marrow fibrosis caused by various etiologies such as primary myelofibrosis, metastatic carcinoma etc.
Rouleaux – cell aggregates resembling stack of coins, caused by increased paraprotein in serum
Paraproteinemia – monoclonal or polyclonal gammopathy
Artifact – thick smear
Agglutination – Cell clumping
Cold agglutinin disease
Mostly IgM againt I/i antigens on red cells
No reactive in body temperature, maximum reactivity at 4°C
May cause extravascular or intravascular hemolysis
Also artifact
Howell-Jolly bodies – Small discrete basophilic dense inclusions usually single, nuclear remnants
Post splenectomy
Hemolytic anemia
Megaloblastic anemia
Basophilic stippling – Punctate basophilic inclusions, precipitated ribosome RNA
Various anemia – fine stippling
Thalassemia – coarse stippling
Lead intoxication – coarse stippling
microangiopathic hemolytic anemia
Include thrombotic thrombocytopenic purpura (TTP), disseminated intravascular coagulation (DIC), hemolytic uremic syndrome, uremia with hypertension, sickle cell anemia with pulmonary emboli.
Red blood cells are fragmented by intravascular fibrin deposit in TTP and DIC
Red cell morphology includes helmet, burr, acanthocyte, spur, spiculated, fragmented, pinched etc.
50-65% of leukocytes
Segmented nucleus (3-4 lobes)
Granular, pale pink cytoplasm
Circulate only briefly (12 hours)
Released into blood at band stage
Recruited into tissues (acute inflammation)
neutrophilia
Absolute neutrophil count > 7,000/ml
- *Etiology:**
1) Infectious diseases (especially bacterial)
2) Acute stress (trauma, recent surgery)
3) Acute tissue necrosis (acute MI)
4) Medications (steroids, lithium, growth factors)
5) Pregnancy (third trimester)
6) Underlying malignancy (tumor products)
Pathophysiology: Increased mobilization of neutrophils from
1) Bone marrow storage pool
2) Marginal pool of circulating blood
Increased bone marrow production secondary to colony stimulating factors
reactive morphologic findings
1) Left shift (increased number of bands)
2) Toxic granulation (increased primary granules)
3) Döhle bodies (blue cytoplasmic inclusions, aggregated rough ER)
4) Vacuolization
neutrophil leukemoid reaction versus chronic myelogenous leukemia
1) Stages of myeloid cells present (reactive has more mature cells)
2) Alkaline phosphatase activity (present in reactive)
3) Morphologic findings (toxic changes) (present in reactive)
4) Basophilia (present in CML, NOT IN REACTIVE)
5) Philadelphia chromosome (BCR-ABL)–CML
Neutropenia
- Absolute neutrophil count < 1800/ml
- Increased susceptibility to infection as neutrophil count drops below 1000/ml
- Agranulocytosis - virtual absence of neutrophils (depletion of blood and marrow storage pools)
- May need to use antibiotic prophylaxis
Pathophysiology:
- Decreased marrow production (aplastic anemia, viral suppression, drug-related, Kostmann syndrome, cyclic neutropenia)
- Ineffective marrow production (megaloblastic anemia, myelodysplasia)
- Increased peripheral destruction (antibody mediated, overwhelming infection, hypersplenism)
Pelger-Huët anomaly: hyposegmented neutrophils
inherited (autosomal dominant)
- acquired (myelodysplasia)
hypersegmented neutrophils: >5 segments
megaloblastic anemia, hydroxyurea
lymphocytes
25-40% of leukocytes (higher in children)
Round/oval non-segmented nucleus
Scant basophilic cytoplasm
80% are T cells (CD4:CD8 = 2:1)
Large granular lymphocytes (cytotoxic T cells, NK cells)
Function in humoral and cell-mediated immunity
lymphocytosis
Absolute lymphocyte count > 5000/ml (>7000/ml - children, >9,000/ml - infants)
Etiology:
1) Infectious diseases (especially viral)
2) Lymphoproliferative disorders
3) Immunologic reactions (drugs, serum sickness)
Types
Small mature lymphocytes (pertussis)
Reactive “atypical” lymphocytes (EBV)
1) Increased size, smudgy chromatin, may have nucleoli, abundant basophilic cytoplasm
2) Spectrum of atypical cells (CD8 T cells)
Large granular lymphocytes (HIV, rheumatoid arthritis, clonal proliferations)
Monocytes
- 5-12% of leukocytes
- Irregular non-segmented nucleus
- Abundant blue-gray cytoplasm with some granules and vacuolization
- Migrate into tissues, become macrophages
- Function in acute and chronic inflammation
Monocytosis
Absolute monocyte count > 800/ml
Etiology:
1) Chronic inflammatory disorders
2) Chronic infectious diseases (TB)
3) Associated with neutropenia (relative)
4) Clonal disorders (monocytic leukemias)
Eosinophils
- 3% of leukocytes
- Segmented nucleus (2 lobes)
- Numerous orange-red cytoplasmic granules (basic proteins)
- Migrate into tissues (mucosal surfaces)
- Function in allergic reactions, parasitic infections
eosinophilia
Absolute eosinophil count > 350/ml
Etiology (specific growth factors - IL-5):
1) Infectious diseases (tissue parasites)
2) Allergic reactions
3) Asthma
4) Collagen vascular diseases
5) Neoplastic processes
Hypereosinophilic Syndrome
- Persistent eosinophilia (> six months) with no apparent underlying cause
- Eosinophil count often > 1500/ml
- Eosinophils have abnormal morphology
- Tissue infiltration (heart, lungs, CNS)
- Treat with steroids and/or chemotherapy
Basophil
- Up to 1% of leukocytes
- Segmented nucleus
- Numerous purple cytoplasmic granules (inflammatory mediators, e.g. histamine)
- Distinct cell from mast cell (tissue cell)
- Immediate type hypersensitivity
chronic granulomatous disease
functional leukocyte defect
1) X-linked deficiency of NADPH oxidase
2) Impaired respiratory burst and H2O2 production
3) Recurrent bacterial infections (especially catalase-positive organisms)
microcytic anemia
causes
clinical work-up
o Iron deficiencies
o Hemoglobinopathies
• Thalassemia (α-thalassemia, β-thalassemia)
• Sickle cell disease
o Membrane defects
• Hereditary spherocytosis
o Work up:
• History and physical exam
• Overt bleeding
• Symptoms of anemia
• Symptoms of systemic disease
• Labs
• CBCD and smear
• Iron studies: Fe, TIBC, ferritin
• Hemoglobin electrophoresis (Genetic studies for α thalassemia)
characteristics of iron deficiency anemia
microcytic
o Bleeding
o Cigar shaped cellso
Hypochromic
o MCV usually 70s
o May be symptomatic or asymptomatic
o Platelet count may be high.
characteristics of sickle cell disease causing anemia
• Sickle Cell Disease (microcytic)
o Associated with joint pain
o Sickle shaped cells
o Usually MCV 70s or low 80s
o Not hypochromic
anemia d/t red cell memrbane abnormalities
• Membrane abnormalities (microcytic anemia)
o Hereditary spherocytosis
• Small cells without central pallor
• MCV <70
• May have large RDW
o Hereditary elliptocytosis
o Stomatocytosis
anemia due to thalassemias
• Thalassemia (microcytic anemia)
o Usually very low MCV
o Hypochromic
o Range of symptoms from completely asymptomatic to transfusion dependent
o May have normal RBC
anemia due to B12 deficiency
macrocytic
o Associated with macroglossia, neuropathies
o May have very low h/h
o Usually indicates absorption issue
o May present with multilineage cytopenias and hemolysis
anemia due to myelodysplasia
macrocytic
o Usually presents in middle aged or older patient
o Normal or high B12 and folate
o Usually slow onset
o Bone marrow biopsy needed to diagnose
anemia of chronic inflammation/kidney disease
o Renal insufficiency or inflammation can lead to normocytic normochromic anemia
o May be macro- or microcytic
o Exogenous erythropoietin can be given with caution (Thrombotic risk!!)
o Consider whether treatment is needed/helpful
o Poor prognostic sign (esp in older patients) but not clear that treatment is helpful in the absence of symptoms
anemia d/t bone marrow infiltration
o Hematologic malignancy
• Leukemia
• Multiple myeloma
• Lymphoma
o Solid tumor
o Scar tissue
• Myelofibrosis (primary or secondary)
• HIV
o Aplastic anemia (primary or secondary)
o Pure red cell aplasia (parvovirus)
anemia d/t meds or drugs
o Can be d/t basically any med
o Hemolysis (G6PD deficiency—malarials, sulfa drugs, nitrates; lidocaine)
o Underproduction:
• Chemo (methotrexate, cyclosporine, hydroxyurea)
• OTC, supplements
anemia due to parvovirus
o Hypoplastic anemia
o Pure red cell aplasia
pt presents with fatigue, dyspnea on exertion, and dizziness on standing
he is found to have a microcytic, hypochromic anemia
He also reports cravings for ice.
on PE he is tachycardic, tachypnic, has othrostasis and appears pale
labs show dec ferritin
DX: iron deficiency anemia
Tx: oral replacement for those who can tolerate (constipation and nausea are side effects); otherwise IV replacement (anaphylaxis)
60yo woman presents with fatigue, SOB, and syncope. She also reports decreased sensation in feet.
PE: chelitis around edges of mouth, glossitis
Lab: macrocytic, megaloblastic anemia; elevated homocysteine and MMA; low–normal B12 and normal Folate
Dx:
Tx?
causes?
Dx: anemia d/t B12 deficiency
Tx: IV replacement therapy followed by oral replacement
Causes: vegan, malabsorption (esp. pernicious anemia, lack of terminal ileum etc.)
Pt presents w/ SOB, fatigue, and chest pain
PE: conjutiva are pale, tachycardic, tachypnic, orthostasis
Lab: macrocytic megaloblastic anemia, elevated homocysteine;
Dx?
Tx?
Causes?
dx: anemia d/t folate deficiency
Tx: folate replacement
Causes: inadequate intake (vegans are fine), malabsorption, alcohol, IBD, bowel resection, amyloid, scleroderma
inc. loss: CHF, dialysis, severe liver disease
hemagglutinin
IgM vs IgG
o antibody causes RBC aggregation
• forms basis for blood bank testing
o IgM antibodies:
• large pentamer is big enough to overcome repellant forces between RBCs
o IgG antibodies:
• CANNOT cause hemaglutination: its not big enough
• AHG = anti human globulin
- = blood bank laboratory reagent
- reacts with IgG antibody on RBCs → hemaglutination
- AHG bridges the gap between IgG antibodies
- allows blood bank to detect RBCs coated with IgG antibodies
direct antiglobulin test (DAT)
- determines what is on RBCs
- = DAT or direct coomb’s test
- detects IgG or C3 on RBC (C3 = footprint of IgM)
- used to determine immune hemolysis by in vivo red cell sensitization
- autoimmune hemolytic anemia, hemolytic disease of newborn, drug induced hemolytic anemia, transfusion reactions
indirect antiglobulin test (IAT)
- determines what is in serum
- = IAT or indirect coomb’s test
- detects IgG in serum
- used to determine RBC compatibility prior to transfusion
mechanism of intravascular hemolysis
• intravascular hemolysis: usually due to IgM antibodies
o cause hemaglutination in circulation
o IgM cause mechanical destruction of RBCs + complement fixation/lysis → RBC lysis causes free RBC stroma release → free RBC stroma stimulates vasoactive peptide + clotting cascades + anaphylatoxins release
o symptoms:
• back pain
• hemoglobinemia: red plasma
• hemoglobinuria: red urine
(these are not seen in extravascular hemolysis)
• fever; coagulopathy; hTN; pulmonary compromise → DIC, vascular collapse, renal failure → death
mechanism of extravascular hemolysis
• extravascular hemolysis: usually due to IgG antibodies
o no lysis of RBCs because IgG is inefficient at complement mediated lysis
o IgG coats RBCs → allows faster clearance by reticuloendothelial system
o symptoms:
• paucity of signs and symptoms
• low grade fever
• hallmark = drop in RBC count due immune destruction of RBCs
Lab findings in intra and extravascular hemolysis
o spherocytes
o circulating nucleated RBCs
o reticulocytosis
o ↑ LDH; ↑ bilirubin; ↓ haptoglobin
ABO antibodies
o IgM antibodies (some IgG can be made)
o arise naturally in individuals lacking corresponding antigen
o arise after infancy after stimulation by cross reacting environmental antigens (bacteria colonizing gut)
• (NOT inherited!)
o cause hemaglutination of antigen positive RBCs @ body T
• ABO incompatible RBC transfusion → fatal complication
• sold organ transplant rejection
Rh antibodies
o do not occur naturally, usually IgG
o alloimmunized to Rh antigens by exposure to RBC
o Rh negative patient may make IgG anti-D antibodies
• following:
- transfusion with D positive blood
- pregnancy with an Rh positive fetus
• occurs in 80% of normal, Rh negative patients when exposed to D positive RBCs
Rh factor
D antigen
D antigen + is Rh positive
D antigen - is Rh negative
Rh negative mother pregnant with and Rh positive fetus. This is her second pregnancy.
What are the potential complications?
How should she be treated?
complications: erythroblastosis, hydrops fetalis (hemolysis, anemia, hyrops, fetal demise)
Prevention:
-Rh (-) women sensitized during pregnancy with Rh (+) fetus → fetal maternal hemorrhage (FMH) during delivery → all subsequent pregnancies with Rh (+) fetuses would be at risk
• anti-D from sensitized donor plasma
- → injected into Rh (-) mothers
- RhIG = Rh immune globulin
- ↓ HDN incidence of Rh incompatible pregnancies
- only effective if Rh(-) mother is naïve to D-antigen
- ( alloimmunized Rh (-) mothers gain no benefit from RhIG)
- give @ 3rd trimester and at delivery to prevent FMH alloimmunization
ABO hemolytic didsease of newborns
o cause by caused by antibodies to other Rh antigens, the ABO system, other antigens
o milder than anti-D HDN, can occur in first pregnancy
o seen if IgG component of maternal ABO antibodies is present
• usually group O mother and group A or B fetus
o no method for prevention
basic principles of ABO compatability for RBC transfusion vs platelet transfusion
- RBC transfusion: avoid incompatibility with patients ABO hemagglutinin
- plasma transfusion: avoid incompatibility with patients antigens
basic principles for Rh compatibility
• Rh (+) can get either Rh (+) or (-) blood
• Rh (-) should only get Rh (-)
- if supply is low, reserve for females of childbearing age
- ignore Rh for plasma transfusion
- honor Rh for platelet transfusion
- platelets produce some RBCs in them
- platelet production may often be ABO incompatible but generally accepted as safe
Blood products are tested for…
o anti-HIV 1 and 2( lowest risk of transfusion transmission(1/ 2 million))
o HbsAg
o anti-HBc
o anti-HCV
o anti-HTLV 1 and 2
o syphilis
o nucleic acid testing: HIV, HBV, HCV, west Nile virus
o antibodies to trypanosomes, Chagas disease
**immunocompromised pts: must test for CMV or provide leukocyte reduced preparation
Adverse reactions to transfusions
- Acute hemolytic transfusion reaction
- delayed hemolytic transfusion reaction: pt antibodies did not show up at time of screening
- delayed serologic transfusion reaction: pts develop new antibody after transfusion
- Febrile, Non-hemolytic transfusion reaction: pt has anti-leukocyte antibodies to donor leukocytes; 1% transfusions; rigors
- Transfusion associated circulatory overload: excessive rate/volume of transfusions, CV disease, overload system
- Acute hypotensive reaction: pts taking ACE-I
- Transfusion related acute lung injury (TRALI): donor has anti-leukocyte antibodies that react w/ pt leukocytes; acute lung injury
- Transfusion associated graft vs host disease: immunocompromised pts, very severe
characteristics of hemolytic anemia (3)
- decreased RBC life span
- membrane damage
- Hb release (intravascular or extravascular)
clinical signs and symptoms of hemolytic anemia
o general symptoms of anemia
• pallor, ↓ exercise tolerance, fatigue, palpitations, dyspnea
• compensated anemia: no anemia unless complications of hemolytic anemia
o specific:
• jaundice: icterus
• dark colored urine
o splenomegaly +/- hepatomegaly seen in
• congenital chronic hemolytic anemias
- hereditary spherocytosis
- PK deficiency
- thalassemia
• acquired hemolytic anemia
- autoimmune hemolytic anemia
Lab signs of hemolytic anemia
o reticulocytosis = polychromasia
o unconjugated hyperbilirubinemia
o ↑ fecal and urine urobilinogen
o ↓ serum haptoglobin
o ↑ LDH (lactate dehydrogenase)
o ↑ AST (amino transferase)
o hemoglobinemia
- • hemoglobinuria
- • hemosiderinuria
o ↓ survival of autologous RBC labeled with Cr
Signs of chronic hemolysis
o cholelithiasis: brown bilirubin gallstones
o leg ulcers
• especially in sickle cell anemia and hereditary spherocytosis
o aplastic crises
• precipitated by infection: parvovirus B19
o hyperhemolysis
• precipitated by infection
o skeletal abnormalities
• characteristic of severe thalassemia major and sickle cell disorders
• hair on end appearance of x ray @ skull
• jaw and dental abnormalities
types of erythrocytes in hemolytic anemia (3)
discocyte: SA:V ratio>1 (normal)
Spherocyte: SA:V ratio is decreased (lose membrane)
Target cell: SA:V ratio is increased (lipid bilayer expands)
Clinical features
platelet defect vs coagulopathy
*
coombs test
direct: positive test indicates presence of Ab on RBC
indirect: postiive test indicates presence of Ab in serum
essential nutrients iron vs folate vs B12
