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Men- 14-18 g/dL Women 12-16 g/dL 90-95% of the cytoplasm of RBC



Men- 42-52% Women- 37-47%



Mean red blood cell volume/size estimate Hct/Rbc 80-100 fL (10^-15 L) 100 macrocytic 80-100- normocytic


Mean cell Hb concentration

Hb/ Hct Differentiate bt hypo and normo chromatic 32-36 g/dL



Red cell distribution width Std of MCV Tells how much cells differ in size, low = uniform / minimal anisocytosis 12-13.5 %




4,500 to 11,000/mm3



45-70% 2-8 *10^9




1-4 *10^9



1-8% 0.1-0.8



0-6% 0-0.5



0-1% 0-0.3


Platelet count



Mean platelet volume

Depends on count Low count body tries to compensate by making platelets bigger


Common causes of iron deficiency anemia

1. Infants/Children: diet, breastfeeding

2. Adults: GI bleed, peptic ulcer, menorhhagia, pregnancy, colon polyps, carcinoma

3. Tropical: hookworm (nicator and anstilastima)

4. Celiac/ Malabsorption

5. Gastrectomy ( acidity of stomach maintains iron as fe2+ which binds to heme better so loss of some of stomach means less fe2+)


Megloblastic anemia

Impaired DNA synthesis 

B12 or folate deficiency (methotrexate, folate anagonist) 

Other rapidly dividing cells effected too - enlarged epithelial cells in gut; macrocytic RBCs and hyper segmented PMNs (greater than 5 lobes) giant red cells and neutrophil precursors (band cells) also seen in bone marrow ; increased lactic acid dehydrogenase (LDH-2); glossitis 


Pathophysiology of hereditary spherocytosis

Autosomal Dominant; Extravascular normocytic anemia

RBC cytoskeleton membrane tethering protein defect in spectrin or ankyrin, band 3.1, which causes instability and breakage of RBCs

Change in shape makes cells less able to navigate splenic sinusoids and consumed by macrophages in spleenic sinusoids



G6PD deficiency

X linked recessive disorder that reduces half life of RBC that renders cell vulnerable to O2 stress; common in black males 

RBCs use glutathione to protect against oxidative stress (H2O2 +GSH (reduced glutathione)--> GS-SG; needs to be reduced back to GSH via NADPH which is produced by G6PD) 

In red cells African variant: mildly reduced half life G6PD; older cells destroyed

Mediterranean variant: marked reduced G6PD half life; when ox stress more cells die

Protective against falciparum malaria

Infections, drugs (antimalarials, sulfadrugs, aspirin, vit K), fava beans

The increased free radicals denature the bonds between heme and glob in making globin form a glob --> Heinz bodies--> bite cells by spleen --> intravascular hemolysis,  Hemoglobinuria,  and back pain (nephrotoxic) 

Enzymatic studies after disease has resolved (during crisis all the cells without the enzyme are dead)


Sickle cell anemia mutation 

Autosomal recessive point mutation at residue 6 in beta globin gene where glutamic acid gets replaced with valine

Protective against Plasmodium falciparum malaria




Decreased production of a globin chain, leading to decreased hemoglobin production and also tetramers due to unpaired chains

Common in Mediteranian/Greek, Asian, and African populations


Warm antibody Immunohemolytic Anemia 

IgG anti red blood cells antibodies that bind well at 37 Celsius (central body) and are consumed by macrophages in the spleen; slow loss of membrane from cell results in spherocytosis

1. Idiopathic 

2. Secondary immune system disease: SLE, RA, or Drugs (PCN- haptens, methyldopa- production of antibodies and binds existent antigens) 

Chronic mild anemia with moderate splenomegaly

Diagnosis: Coomb + 

Treat: IVIG (splenic marcophages will eat IVIG instead of red cells); Steroids, removal of drug; splenectomy (removes antibodies and destruction) 


Microangiopathic Hemolytic Anemia

Pathology in small blood vessels that results in a hemolytic anemia (some sort of thrombus that blocks the vessel partially)

Tear up blood cells --> Schitocytes ( pointy red cell fragments)

Causes: TTP ; HUS; DIC; Maligant hypertension, SLE, disseminated cancer 



Pathophysiology of anemia of chronic disease

Associated with chronic disease or cancer (inflammation, infection, malignancy)

Inflammation (IL6) produce acute phase reactant Hepcidin (made in liver) that sequesters iron by blocking ferroportin and also suppresses EPO; protective mechanism because bacteria need iron to proliferate (body thinks any inflammation is bacterial) 


Aplastic anemia

Multipotent myeloid stem cells are supressed resulting in pancytopenia 

1. Idiopathic

2. Myelotoxic agent (choramphenicol, benzene, alkalating agents, antimetabolites, or idiosyncratic hypersentitivity rxn) 

3. Viral agents (parvovirus b19, EBV, HIV, HCV)

4. Congenital: Fanconi anemia

Empty marrow on marrow biopsy (>90% fat)

Cessation of causative drugs, transfusion, marrow stimulating factors (EPO, GM-CSF, G-CSF); immunosuppression (if etiology is autoimmune); bone marrow transplant



Decrease in the oxygen -transporting capacity of the blood usually steming from a decrease in the red blood cell mass to subnormal levels

Measure of mass of rbcs Less than 13.5 g/dl males and 12.5 g/dl females


Iron metabolism

In meat( heme derived, better absorb) and veg Absorbed in duodenum by enterocytes, reduce to Fe2+ in lumen, dimethyltransferase brings it into enterocyte and then transported into blood via ferroportin on the basolateral side ; and oxidized to Fe3+ (hephestin) no way for body to get rid of iron so regulates fe through enterocytes Bound to transferrin in blood ( bc can make free radicles via Fenton rxn) and then transported to liver or bone marrow macrophages for storage and stored bound to ferritin


Fe lab measures

For every three transferrin molecules one will carry an iron and then bound to ferritin in macrophage Serum iron- iron in blood Transferrin in blood- tibc. Total iron binding capacity %sat- how much transferrin is bound to fe Serum ferritin- how much iron is present in bone marrow macrophages and liver


Stages of iron deficiency

1.) bone marrow uses up stored fe making new rbcs ( serum ferritin decreases; tibc increases - liver recognizes fe is down and pump out transferrin) 2.) serum iron consumed ( serum iron goes down, percent saturation of iron decreases) 3.) normocytic anemia- bone marrow continues to make rbcs, but has less fe, so make less of them 4.) microcytic, hypochromic anemia- so severe that can't produce normal rbcs so has to send out cells smaller than normal with less color , expanded central area of pallor


Clinical features of iron deficiency


Koilonychia- spoon shaped nails



Plummer Vincent syndrome

Iron deficiency anemia with esophageal web ( outfold of mucosa obstructs lumen of the esophagus that can cause dysphasia),  and atrophic glottis

Presents with anemia, dysphasia, and beefy red tongue


Sideroblastic anemia

Defective protoporphyrin synthesis

Pp synthesized by a series of rxns that occur within cytoplasm and mitochondria in the erythroblasts

Gives you ringed sideroblast cells with ring of blue in a Prussian blue stain representing iron in the mitochondria