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PATH  II  TUTORING!!!!  J  

Red  Blood  Cell  Pathology  

Chris  Hal3gin  
Wafa  Khadraoui  
Isael  Perez  
 Anemia  
•  S/S:  
–  Fa3gue,  headache,  dyspnea  
–  PALLOR!!!!  of  conjunc3va,  tongue,  nail  beds,  palms  
–  Mild  murmur  due  to  hypoviscosity  
–  Cardiomegaly  from  increased  O2  demand  by  3ssues  
•  Decreased  Hb  and  HCT!!!!  
•  Classified  based  on  RBC  indices:  
–  MCV  =  RBC  size  
•  Microcy3c,  Normocy3c,  Macrocy3c  
–  MCHC  =  Hb  content  
•  Hypochromic,  Normochromic,  Hyperchromic  
•  Area  of  central  pallor  is  normally  1/3  of  the  diameter  of  the  RBC  
–  ReHculocye  count  
•  Increased  (aka  Polychromasia)  =  marrow  response  to  premature  blood  loss  
or  increased  destruc3on  of  RBCs  (hemoly3c  anemia)  
•  Normal  or  Low  =  Anemias  of  underproduc3on  
–  RDW  =  uniformity  of  size  and  shape  of  RBCs  
 Morphologic Classification of Anemia

Microcytic Normocytic Macrocytic

MCV <80 MCV 80-96 MCV >98

Chronic disease
Aplastic anemia
Renal failure
Mild hemolytic
anemia B12/folate deficiency
Iron deficiency Drugs, Liver disease
Anemia  of  chronic  
Sideroblastic disease  is  most   Hypothyroidism
Thalassemia trait commonly  Normocy3c   Hemolytic anemia
Chronic disease Hemorrhage
 Functional Classification of Anemia
Low/Normal High
Reticulocyte Reticulocyte

Hypoproliferative/ decreased Hyperproliferative/ increased

production anemia destruction anemia

Hemolytic
Nutrition Marrow Ineffective Lack of anemia
Deficiency Suppres utilization EPO
Hemorrhage
-Fe -Aplastic Anemia of Renal
-B12 -MDS chronic Failure
disease
-Folate -Drugs
-Malignancy Sideroblastic
 Microcytic Normocytic MCV 80-96 Macrocytic
MCV <80 MCV >98
Low/normal retic
retic

Low/normal retic Chronic disease Mild

retic Aplastic anemia hemolytic
Renal failure anemia
Thalassemia
major Low/ normal retic
In  thal.  major  there  is  high  
re3culocytes  due  to  hemoly3c  anemia  
retic
because  of  the  precipita3on  of  the  
alpha  globin  pairs.  The  alpha  globin  
High Normal pairs  are  due  to  severe  deficiency  of  
Beta  globin,  so  the  alphas  start  pairing   B12/folate deficiency,
RDW RDW and  precipita3ng  in  the  RBCs…  
anything  that  precipitates  in  the  RBCs   drugs, liver disease
causes  them  to  be  sequestered  and  
destroyed  in  the  spleen   hypothyroidism,
Iron Thalassemia In  the  thalassemia  trait,  there  is   Hemolytic
s3ll  some  Beta  globin  around  so  
deficiency trait there  is  normal  re3culocyte   anemia
count  because  the  RBCs  aren’t  
Siderobalstic Chronic disease destroyed  by  the  spleen   Hemorrhage
 Anemia  of  Blood  Loss  
•  Acute  blood  loss  
–  Decreased  intravascular  volume  that  is  rapidly  restored  
by  intravascular  shiR  of  water  from  the  intersHHum  to  
blood  vesselsà  dilu3on  of  the  blood  
–  Hemodilu3onà  decreased  oxygenaHonà  increased  
EPO  secreHon  from  kidney  and  increased  bone  marrow  
acHvityà  ReHculocytosis  and  Thrombocytoisis  
–  NormocyHc  Normochromic  

•  Chronic  Blood  loss  

–  Slow  loss  of  iron  over  3me  because  the  rate  of  blood  
loss  exceeds  the  rate  of  bone  marrow  genera3on  
–  Causes  an  acquired  iron  deficiency  anemia  
 Anemia  of  Increased  Destruc3on  
•  Elevated  EPO  and  compensatory  increase  in  bone  marrow  erythropoiesisà  
increased  reHculocytes  
–  Hypercellular  bone  marrowà  erythroid  hyperplasia  
–  If  the  anemia  is  severe  and  prolonged,  extramedullary  hematopoesis  may  occur  
 
•  Accumula3on  of  Hb  degrada3on  products  
–  Increased  bilirubinà  increased  risk  of  pigmented    gallstones  
–  Hemosiderosis  (Hemosiderin  accumula3on  in  macrophages)  in  spleen,  liver,  and  bone  
marrow  
 
•  Extravascular  Hemolysis  
–  Reduced  deformability  of  RBCs  makes  passage  through  spleen  harderà  sequestra3on  
and  destruc3on  by  splenic  macrophages  
–  SPLENOMEGALY!!!!,  Jaundice  
–  Increased  bilirubin,  LDH,  and  iron  
 
•  Intravascular  Hemolysis  
–  Destruc3on  of  RBCs  in  circula3on  (mechanical,  complement,  parasites)  
–  NO  SPLENOMEGALY!!!!,  Jaundice,  Hemoglobinemia,  Hemoglobinuria,  Hemosiduria  
–  Decreased  haptoglobin  (due  to  increased  Hb  in  blood),  increased  bilirubin,  increased  
LDH  
 Anemia  of  Increased  Destruc3on  
•  Hereditary  Speherocytosis            AD  
–  NormocyHc  Normochromic  
–  ****PaHent  will  have  had  anemia  since  childhood  
–  Deficiency  of  Ankyrin,  Spectrin,  Band  3,  or  Band  4.2  
–  Spherocytes  =  Small,  hyperchromic  RBCs  that  lack  the  zone  of  central  
pallor  
•  Spherical,  less  deformable,  and  increased  vulnerability  to  splenic  sequestraHon  
and  destrucHon  
–  Increased  reHculocytes,  SPLENOMEGALY,  BM  erythroid  
hyperplasia,  hemosiderosis,  jaundice,  nucleated  RBCs  
–  Increased  RDW  and  Increased  MCHC  (because  the  RBCs  are  smaller)  
–  OsmoHc  lysis  in  osmo3c  fragility  test  because  the  spherocytes  are  
sensi3ve  to  a  hypotonic  medium  
–  Tx  =  Splenectomy  
–  If  pa3ent  is  asplenic,  they  will  have  Howell  Jolly    
         bodies  in  RBCs  (but  just  remember  that  Howell    
         Jolly  Bodies  are  more  common  in  Sickle  Cell)  
 Anemia  of  Increased  Destruc3on  
•  G6PD  deficiency                    XR  
–  NormocyHc  Normochromic  
–  Abnormali3es  in  the  HMP  shunt  where  there  is  no  ability  to  
regenerate  reduced  glutathione  leading  to  decreased  NADPH  
and  increased  risk  of  oxidaHve  injuryà  EPISODIC  hemolysis  
due  to  exposure  to  increased  oxidaHve  stress  
–  Africans  (b/c  it  is  protecHve  against  malaria)  and  
Mediterranean  people  
–  InfecHons,  drugs  (Primaquine,  Chloroquine),  fava  beans  
•  Oxidants  cause  cross-­‐linking  of  globin  chainsà  membrane  bound  
precipitates  (Heinz  bodies)à  intravascular  and  extravascular  
hemolysis  that  occurs  about  2  to  3  days  aRer  exposure  to  oxidant  
–  Acute  onset,  faHgue,  red  urine,  back  pain,  decreased  
haptoglobin  
–  NO  SPLENOMEGALY!!!!,  hemoglobinemia,  
hemoglobinuria  
–  Bite  cells  =  Heinz  bodies  are  bi_en  out  of  RBCs  by  splenic  
macrophages  
–  Heinz  Body  =  denatured  hemoglobin  in  RBC  
 Anemia  of  Increased  Destruc3on  
•  Sickle  Cell  Anemia                    AR  
–  NormocyHc  Normochromic  
–  B-­‐globin  point  mutaHon  causes  polymerizaHon  of  deoxygenated  Hbà  
hemoly3c  anemia,  microvascular  obstruc3on,  and  ischemic  3ssue  damage  
•  Valine  for  a  Glutamine  
•  HbS  is  protec3ve  against  malariaà  prevalence  in  Africans  
–  SPLENOMEGALY!!!!  due  to  chronic  extravascular  hemolysis  and  
extramedullary  hematopoiesis  
•  There  is  also  extramedullary  hematopoiesis  in  facial  and  skull  bones  
–  HyperplasHc  bone  marrow  w/  erythroid  hyperplasia  and  increased  
reHculocytes  
–  Increased  bilirubin,  pigmented  gallstones,  hemosiderosis  
–  Sickled  cells,  Target  Cells,  Howell-­‐Jolly  bodies  in  Asplenic  
paHents  

–  Microvascular  inclusionsà  dactyliHs,  leg  ulcers,  stroke,  renal  papillary  

necrosis,  priapism,  bone  necrosis,  blindness  
–  Autosplenectomy  in  adolescents  due  to  microvascular  inclusions  
•  Increased  risk  of  infecHons  w/  encapsulated  bacteria  
•  Salmonella  OsteomyeliHs  
 Anemia  of  Increased  Destruc3on  
•  Sickle  Cell  Anemia  conHnued  
–  Increased  sickling  due  to  Hypoxemia,  Acidosis,  
DehydraHon  
–  Painful  Crisis  
•  Back,  joint,  bone,  and  abdominal  pain  from  microvascular  
inclusions  causing  ischemia/infarc3on  
–  AplasHc  Crisis   Sickle Cell Anemia
•  Parvovirus  B19  shuts  dComplete
own  re3culocyte  
blood forma3onà  
count Sickle cell
decreased  re3culocytes  and  erythroid  precursors  in  bone  
marrow     – Normochromic normocytic
–  HemolyHc  Crisis   Peripheral smear
•  Increased  re3culocytes  and  
– jaundice  
Sickled RBC, targets,
–  SequestraHon  Crisis   Howell-Jolly bodies
Lab tests
–  Treatment  is  Hydroxyurea  –   Sickle test (screening)
– Hemoglobin electrophoresis, Howell-Jolly body
–  People  with  the  sickle  cell  trait  
DNA have  no  polymeriza3on  of  
the  globin  chains  un3l  they   are  exposed  to  a  hypoxic  
Treatment
state…  when  they  aren’t  in  a  hypoxic  state,  their  normal  
– Transfusion, iron chelation
HbA  interferes  with  HbS  polymeriza3on  
– Hydroxyurea
– Vaccine (prevention)
 Anemia  of  Increased  Destruc3on  
•  Thalassemias  in  general  
–  Decreased  synthesis  of  a-­‐globin  or  B-­‐globin  in  HbA  (α2β2)à  anemia,  3ssue  hypoxia,  and  
hemolysis  

–  Mild  deficiency  (Thal.  Minor/Trait)  

•  Mild  decrease  in  RBCs  and  Hb  
•  Mildly  microcyHc  hypochromic  
•  Normal-­‐low  reHculocyte  count  
•  Normal  RDW,  NORMAL  IRON  STUDIES  
•  Target  cells,  Basophilic  sHppling  

–  Marked  deficiency  (Thal.  Major)  

•  Severe  decrease  in  RBCs  and  Hb  
•  Severely  microcyHc  hypochromic  
•  Excess  unpaired  globin  chains  cause  precipitates  and  hemolyHc  anemia  
•  Increased  reHculocytes,  increased  RDW,  NORMAL  IRON  STUDIES  
•  Target  cells,  Basophilic  SHppling  
•  Transfusion  dependent  anemia  since  infancy  
•  Hepatosplenomegaly  and  Crew-­‐cut  appearance  from  massive  extramedullary  
hematopoesis  in  liver,  spleen,  facial,  and  skull  bones  
•  Hypercellular  bone  marrow  from  erythroid  hyperplasiaà  marrow  expansionà  skeletal  deformi3es  
and  grwoth  retarda3on  
•  SEVERE  IRON  OVERLOAD  due  to  suppression  of  hepcidin  and  increased  absorp3onà  
endocrine  dysfuncHon  and  cardiac  failure  
 Anemia  of  Increased  Destruc3on  
•  a-­‐thalassemia                    ****Asian  and  African  people  
–  Inherited  DELETIONS  that  cause  a  deficiency  in  a-­‐globin  

–  Silent  carrier  state  

•  DeleHon  of  single  a-­‐globin  gene  that  is  essen3ally  negligible  and  asymptoma3c  
 
–  a-­‐thal.  trait  
•  DeleHon  of  2  a-­‐globin  genes  from  a  single  chromosome  or  one  from  each  of  
the  two  chromosomes  
•  Mild  microcy3c  anemia  with  normal  HbA2  levels  
 
–  HbH  
•  DeleHon  of  3  a-­‐globin  genes  with  forma3on  of  B4  tetramers  because  of  an  
excess  of  unpaired  B  globin  chains  
•  Moderate-­‐severe  anemia  
 
–  Hb  Barts  or  Hydrops  Fetalis  
•  DeleHon  of  all  4  a-­‐globin  genes  with  excess  unpaired  y-­‐globin  forming  y4  
tetramers  
 Anemia  of  Increased  Destruc3on  
•  B-­‐thalassemia                    ****Mediterranean  people  
–  POINT  MUTATIONS  that  cause  decreased  B-­‐globin  synthesis  
–  Produc3on  of  underhemoglobinized  microcyHc  hypochromic  RBCs  with  
decreased  O2  transport  capacity  and  decreased  survival  of  RBCs  and  
their  precursors  from  a-­‐globin  and  B-­‐globin  imbalance  
–  Precipita3on  of  unpaired  a-­‐globin  chains  in  RBC  precursors  

–  B-­‐thal.  Minor  
•  Usually  asymptoma3c  
•  Peripheral  smear  may  show  microcy3c  hypochromic  RBCs,  with  basophilic  
s3ppling  or  target  cells  
•  Increased  HbA2  (which  differen3ates  it  from  iron  deficiency)  

–  B-­‐thal.  Major  
•  IneffecHve  hematopoiesis  due  to  aggregates  of  unpaired  a-­‐globin  chainsà  a4  
tetramersà  severe  extravascular  hemolysis  
•  No  HbA,  Increased  HbF,  and  increased  HbA2  
•  Crew  Cut  appearance  
•  Progressive  iron  overload,  secondary  hemochromatosis,  and  cardiac  disease  
 Anemia  of  Increased  Destruc3on  
•  Paroxysmal  Nocturnal  Hemoglobinuria  
–  NormocyHc  normochromic  
–  ACQUIRED  PIGA  gene  mutaHon  that  causes  loss  of  the  GPI  anchoring  protein  
(regulatory  complement  protein)  in  stem  cellsà  complement-­‐mediated  
intravascular  hemolysis  by  the  MAC  
–  Deficient  GPIs  =  CD55  (DAF)  and  CD59  (inhibits  C3  convertase  and  prevents  
ac3va3on  of  alterna3ce  pathway)à  increased  C3  convertase  acHvity  
•  RBC  lysis  occurs  at  night  because  when  we  sleep  our  pH  decreases,  which  makes  
complement  more  ac3ve  
–  GPI  defect  in  hematopoie3c  stem  cellsà  deficiency  of  GPI  on  RBCs,  WBCs,  and  
plateletsà  Pancytopenia  
–  Increased  risk  of  venous  thrombosis,  especially  portal,  cerebral,  and  
hepa3c  veins  
–  Red  urine  IN  MORNING,  hemoglobinemia,  hemoglobinuria,  hemosidiuria  
–  Increased  reHculocytes,  decreased  Haptoglobin  
 
–  Associated  with  aplas3c  anemia,  AML,  and  myelodysplas3c  syndrome  
–  Increased  sensi3vity  to  complement  RBC  lysis  in  Sucrose  lysis  or  Ham  test  
–  Tx  =  HSC  transplanta3on  
 Anemia  of  Increased  Destruc3on  
•  Autoimmune  hemolyHc  anemias  
–  NormocyHc  normochromic  
–  Warm  Ab  
•  IgG,  37oC,  extravascular  hemolysis  from  IgG  RBC  opsonizaHon  
•  Opsoniza3on  of  RBCs  by  IgG  causes  par3al  phagocytosis  of  RBC  membraneà  generaHon  
of  spherocytesà  sequestra3on  and  destruc3on  by  spleenà  SPELENOMEGALY  
•  Primaryà  Idiopathic  
•  Secondaryà  SLE,  Drugs  (penicillin,  cephalosporins,  an3malarials,  methyldopa),  CLL  
•  Peripheral  smear  looks  like  hereditary  spherocytosis,  so  pay  ajenHon  to  the  paHents  
age  and  presentaHon…  HS  pa3ent  will  be  younger!!!!  

–  Cold  AggluHnin  
•  IgM,  <37oC,  usually  0oC-­‐4oC,  intravascular  hemolysis  from  IgM  acHvaHon  of  
complementà  clumping  of  RBCs  
•  Acuteà  post-­‐infec3on  (Mycoplasma  pneumoniae,  infec3ous  mononucleosis)  
•  Chronicà  idiopathic,  lymphoid  neoplasms  
•  Associated  with  Raynaud’s  phenomena  in  the  digits  when  they  are  exposed  to  cold  
temperatures  

–  Cold  Hemolysin  
•  IgG  to  P-­‐group  Ag,  <37oC,  intravascular  hemolysis,  Children,  aRer  viral  infecHons  
 Non-­‐immune  Hemoly3c  Anemias  
•  Mechanical  arHficial  heart  valves  
•  Malignany  HTN  
SCHISTOCYTES!!!!  
•  MAHAs  
–  DIC  
•  Elevated  D-­‐dimer,  increased  PT  and  PTT  
•  Massive  ac3va3on  of  coagula3on  cascadeà  consump3on  of  
coagula3on  factorsà  systemic  microthrombi  
–  TTP  
•  ADAMTS13  muta3on  
•  Fever,  neurological  symptoms,  renal  failure,  TCP,  hemoly3c  anemia  
•  Normal  PT  and  PTT  
–  HUS  
•  E.coli  O157:H7  
•  Fever,  no  neurological  symptoms,  profound  renal  failure,  TCP,  
hemoly3c  anemia  
•  Normal  PT  and  PTT  
 Anemia  of  Decreased  Produc3on  
•  MegaloblasHc  Anemia  
–  MacrocyHc  normochromic  
–  B12  or  Folate  deficiencyà  impaired  DNA  synthesisà  
ineffec3ve  hematopoiesis  and  abnormally  large  erythroid  
precursors  and  RBCs  
•  Folate  deficiencyà  ALCOHOLIC,  pregnancy  (hopefully  not!!!!),  
drugs  (Methotrexate),  hemodialysis  
–  No  neurological  problems,  normal  methylmalonic  acid,  increased  
homocysteine  
•  B12  deficiencyà  Pernicious  anemia  (due  to  autoimmune  gastri3s  
an3-­‐IF  or  an3-­‐parietal  cell  Abs),  Crohn  disease,  gastrectomy,  ileal  
resec3on,  the  good  old  fish  tapeworm  diphylobothrium  latum,  strict  
vegans  
–  Neurological  problems,  increased  methylmalonic  acid,  increased  
homocysteine  
–  DemyelinaHon  of  dorsal  and  lateral  spinal  tractsà  subacute  combined  
neurological  degeneraHonà  Hngling,  loss  of  touch,  vibraHon,  
propriocepHon,  depressed  reflexes,  ataxia  
 
–  Macroovalocytes,  HYPERSEGMENTED  NEUTROPHILS  >5  
lobes,  decreased  to  normal  reHculocytes  
–  Hypercellular  bone  marrow  due  to  increased  hematopoe3c  
precursors  and  megaloblasHc  erythroid  hyperplasiaà  
crowding  of  bone  marrowà  slower  producHon  of  
RBCsà  anemia  
–  Atrophic  glossiHs  
 Decreased Production
Anemia   of  Decreased  Produc3on  
Peripheral smear
Iron deficiency anemia
Peripheral smear

•  Iron  deficiency  anemia  

– Microcytic Hypochromic
–  Most  common  nutriHonal  disorder  in  the  world  
RBC
–  MicrocyHc  hypochromic  
– Variation
–  Infants,  young  females   is psize
with  heavy   and
eriods,   shape
pregnancy  
women  
– Increased RDW
–  Dietary  deficiency,  decreased  absorp3on,  increased  
demand,  CHRONIC  
Lab BLOOD  
TestLOSS  
•  Chronic  blood  loss  can  be  due  to  heavy  periods  or  malignancy  
– Iron (Fe) studies
like  COLON  CANCER  
•  In  an  elderly  paHent  with  iron  deficiency  anemia  Decreased
and  occult   Production
blood  in  their  stool,  assume  colon  cancer  unHl  proven  
otherwise   Iron deficiency anemia
Serum Fe Ferritin* TIBC %Bone
transferrin sat
–  Spoon  nails,  beefy  red  tongue,  Plummer-­‐Vinson   Marrow Fe Stain
syndrome  (esophageal  webs),  Pica   Bone marrow
(weird   cravings  like   Normal Fe Deficiency
Fe
ea3ng  dirt,  chewing  on  ice,  craving  –pMildly
encil  lead,   or  even  
hpercellular
deficiency
PAINT  CHIPS…  ya  this  happens!!!!)  – Absent iron (Fe) stores
–  Absent  bone  marrow  iron  stores  Treatment
and  disappearance  of  
*Ferritin acute phase reactant
sustainable  iron  from  bone  marrow  macrophages  
– Investigate cause
–  Decreased  reHculocytes,  increased  Stool RDW   occult blood
–  Decreased  serum  Fe,  decreased  FerriHn,   increased  TIBC,  
Endoscopy
decreased  Transferrin  saturaHon  
•  Ferri3n  is  decreased  because  all  the  storage   Urinalysis
iron  has  been  used  
up.  TIBC  increases  because  the  liver  –mReplaceakes  as  much  
irontransferrin  
as  possible  to  try  and  bind  up  any  iron  that  is  available,  but  the  
trasnferrin  satura3on  is  decreased  b–ecause   Transfuse there  is  so  li_le  iron  
 Decreased Production

Anemia  of  Decreased  Produc3on  

Anemia of chronic disease
Bone Marrow Fe
Bone marrow
•  Anemia  of  Chronic  Disease   – Normocellular
–  Most  commonly  NormocyHc  normochromic,   – Increased iron  
         but  can  be  microcy3c  hypochromic  stores
–  InflammaHon,  malignancy   Treatment
–  IneffecHve  iron  uHlizaHonà  ineffecHve    
– Underlying cause
         hematopoiesis  and  increased  Hepcidin  acHvity  
•  Chronic  inflamma3on  causes  increased  Hepcidin  acHvity,  which  blocks  
transferrin  acHvityà  abnormal  storage  of  iron  
–  Decreased  reHculocytes  (because  all  the  iron  is  stored),  Normal  
RDW  
–  Normocellular  bone  marrow  with  markedly  increased  iron  stores  
–  Decreased  serum  Fe,  increased  FerriHn,  decreased  TIBC,  decreased  
Transferrin  saturaHon  
•  Increased  hepcidin  ac3vity  causes  increased  iron  storage  in  3ssue  macrophages  
leading  to  increased  ferri3n  levels  and  decreased  serum  iron  levels.  TIBC  
decreases  because  hepcidin  blocks  transferrin  from  binding  to  iron,  which  also  
decreased  Trasnferrin  satura3on  
–  DO  NOT  TREAT  WITH  IRON  SUPPLEMENTATION  because  there  is  
already  enough  iron  in  the  body…  it  is  just  hiding.  Thanks  Hepcidin!  
 Anemia  of  Decreased  Produc3on  
•  Aplas3c  anemia                    should  be  called  “Aplas3c  Pancytopenia”  
–  NormocyHc  normochromic  
–  Chronic  primary  hematopoieHc  failureà  pancytopenia  
(anemia  neutropenia,  TCP)  
–  Toxins,  drugs,  viruses  (EBV,  HCV,  CMV),  autoimmune  
(majority  of  idiopathic  cases)  
–  Markedly  hypocellular  bone  marrow  
–  No  splenomegaly,  decreased  reHculocytes\  
 
–  Pa3ent  will  present  with  petechiae,  
       ecchymosis,  and  bleeding  (from    
       decreased  platelets),  pallor,    
       dyspnea  (from  decreased  RBCs),    
       and  increased  infec3ons  (from    
       decreased  neutrophils)  
 BONUS  SLIDE  1  J  
Basophilic
stippling

•  SideroblasHc  anemia  
–  MicrocyHc  hypochromic  
–  Heme  (porphyrin)  synthesis  defect  in  
mitochondria  and  failure  of  iron  uHlizaHon  
–  Hereditaryà  ALAS  gene  deficiency                  XR  
–  Acquiredà  ALCOHOL,  drugs,  B6  deficiency,  Lead  
poisoning,  MDS  
–  May  also  be  idiopathic   Basophilic  s3ppling  
Ringed
–  Normocellular  bone  marrow   with  increased  iron    
Basophilic
Sideroblast
stores   stippling                Ringed  sideroblasts  
–  Increased  RDW,  Basophilic  sHppling,  Ringed  
sideroblasts  (mitochondrial  iron  overload)  
–  Increased  serum  Fe,  increased  FerriHn,  
decreased  TIBC,  increased  Transferrin  saturaHon  
•  Decreased  iron  u3liza3on  causes  increased  iron  in  
the  blood  and  increased  iron  storage  with  ferri3n.  
TIBC  is  decreased  because  transferrin  levels  are  
decreased  due  to  increased  iron  bound  to  the  
transferrin.  This  will  increase  the  transferrin  
satura3on.  
 BONUS  SLIDE  2  J  
•  Pure  Red  Cell  Aplasia  
–  NormocyHc  normochromic  
–  Primary  bone  marrow  disorder  where  only  erythroid  
precursors  are  suppressed  
– Parvovirus  B19,  Thymoma  
–  Decreased  or  absent  RBC  precursors,  Decreased  
reHculocytes  
 Microcy3c  Anemia  Summary  
Microcytic Anemias
Serum Fe Ferritin TIBC %sat RDW

Fe def

ACD NL NL NL

Thal NL NL NL NL NL

Siderob NL
•  I  tones  it  down  this  3me  with  the  Canadian  
flags  because  there  is  something  in  each  
disease  that  is  very  testable.  So  to  make  up  for  
it…  J    
 Ques3ons?    
Comments?    
Concerns?    
Any  good  jokes?  
Thanks  for  coming!!!!  J