1

• RED BLOOD CELLS (RBC) COUNT, FUNCTIONS, STRUCTURE
• HEMOGLOBIN (Hb): CHEMISTRY, REACTIONS, FUNCTIONS, CONCENTRATION
• ERYTHROPOIESIS, CONTROL OF ERYTHROPOIESIS
• DESTRUCTION OF RBC, METABOLISM OF Hb AND IRON. HEMOSIDEROSIS
• JAUNDICE
• ERYTHROCYTE SEDIMENTATION RATE
• TYPES OF ANEMIA, SICKLE CELL DISEASE
• POLYCYTHEMIA
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Describe the functional consequence of the lack of a nucleus, ribosomes, and mitochondria for a) protein synthesis and b) energy production within the red blood cell.
Relate the three red blood cell concentration estimates, red blood cell count, hematocrit, and hemoglobin concentration.
Know the importance of MCV and be able to calculate the mean corpuscular volume.
Describe the structure of hemoglobin (Hb). Describe the differences between the major normal types of Hb (adult A and A2, glucosilated, fetal). Predict the changes in Hb types present in blood when synthesis of beta chains of globin is deficient. Describe the abnormal types of Hb (Hb S, thalassemias).
Describe the normal and abnormal Hb reactions (oxyHb, MetHb, carboxyHb). Calculate the mean corpuscular Hb concentration and the mean corpuscular Hb.
Identify the site of erythropoietin production, the adequate stimulus for erythropoietin release, and the target tissue for erythropoietin action. Describe the role of vitamin B12 & folic acid, and various hormones in regulation of RBC formation. Describe the dietary requirements for RBC production.
Relate the rate of red blood cell production and the percentage of immature reticulocytes in the blood.
Describe the metabolism of iron in the body.
Describe the metabolism of Hb (pre-hepatic, hepatic, post-hepatic).
Describe the three types of jaundice (pre-hepatic, hepatic and post-hepatic). Compare and contrast the laboratory findings and urine/stool color in the three types of jaundice.
Describe physiological jaundice of the newborn.
Discuss the normal balance of red blood cell synthesis and destruction, including how imbalances in each lead to anemia or polycythemia. Compare and contrast the main types of anemia (nutritional, hemolytic, aplastic, hemorrhagic). Be able to describe different types of anemia in terms of MCV and
MCHC. Describe the main effects of anemia and polycythemia on body functions.
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• Transport of O
2 direction from the lungs to the tissues and CO
2 in the opposite
– Hemoglobin
– Carbonic anhydrase
• Catalyses the reaction H
2
O + CO
2
↔ H
2
CO
3
• Maintenance of pH homeostasis (globin, phosphate and bicarbonate buffers)-hemoglobin in the cells is an excellent acid-base buffer
• Contribution to the blood viscosity
• ↓ blood oncotic P (by keeping Hb-protein inside the cells)
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• Normal values
– Adult males: 4 600 000 – 6 200 000/mm 3 (5.4million/mL)
– Adult females: 4 200 000 – 5 400 000/mm 3 (4.8million/mL)
• Abnormally high count – polycythemia
• Abnormally low count – anemia
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Small size
Excess of the plasma membrane & specific shape
RBC - biconcave discs with central depression on each side
High surfaceto-volume ratio
Deformation of the cells without stretching the plasma membrane
Rapid diffusion of respiratory gases to and from the cell
Easy passage through the small capillaries
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Figure 16-5

• Membrane contains special proteins and polysaccharides that differ from person to person – blood groups
• Lack of the nucleus and organelles
– Cannot undergo mitosis
– Generate ATP anaerobically → do not use oxygen they transport
– Can not synthesize new cellular components to replace damaged ones
Life span - 120 days
• Contain a red pigment, hemoglobin (red color of the blood)
– Occupies 1/3 of cellular volume
– 280 million Hb molecules/RBC
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MCV: 82-99 fL
• Mean volume of a RBC
• Values
– Normal range 82 – 99 femtolitre (fL)
– Low volume in microcytic anemia
– High volume in macrocytic anemia
• Calculation of the MCV
Hematocrit x 10
RBC count (in millions/mL blood)
• Sample calculation: Htc = 40, RBC count = 5 (x 10 6 /mL)
MCV = (40 x 10)/5 = 80 fl fL= 10 -15 L
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10

Pale cells (central pallor >1/3 dia) are referred to as hypochromic
(right), while cells without central pallor are called hyperchromic
(left).
Normal peripheral blood RBCs are normochromic normocytic .
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• Protein – globin
– 4 polypeptide chains
• Normal adult Hb – HbA,
Hbα
2
β
2
– A pair of α chains (141 AA)
– A pair of β chains (146 AA)
• Adult Hb – HbA2 (2.5% of Hb),
Hbα
2
δ
2
– β chains are replaced by δ chains
• Fetal Hb – HbF, Hbα
2
γ
2
– β chains are replaced by γ chains
(146 AA)
• Adult Hb glucosilated – HbA
Ic
– Has a glucose attached to each β chain
Adult Hb
– HbA, Hbα
2
β
2
• Nonprotein pigment bound to each of the 4 chains – hem
– Each hem ring has 1 iron ion (Fe 2+ ) that can combine reversibly to 1 O
2 molecule
– Each Hb molecule can bind 4 O
2 molecules
Hb A 2 α 2 β
HbA2 2 α 2 δ
HbF 2 α 2 γ
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• Inherited disease
• High prevalence in the malaria belt
• Mutation causes formation of HbS instead of HbA
– HbS precipitates into long crystals when oxygen tension is low
(hypoxia) → cell elongation (sickling) and damage to the cell membrane → hemolysis
→ hypoxia (vicious cycle)
 Rigid sickled RBCs occlude the microvasculature leading to vasoocclusive crisis.
HbS
– HbαA2βS2
Negatively charged glutamate is substituted for nonpolar valine at position 6 in the
β chain)
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• Oxyhemoglobin: Hb + 4 O
2
(O
2 attaches to Fe
– Is produced in the lungs (oxygen loading)
2+ in hem)
• Reduced Hb (deoxyHb)
– Is produced in tissue capillaries after dissociation of O
2
(oxygen unloading)
– Combines with H+ acts as a buffer
– Combines with CO2 → Carbaminohemoglobin: Hb + CO
2 hem)
(CO2 binds to globin, not to
OxyHb
O
2 carrying function
Buffering function
COOH/COO -
NH
2
/NH
3
+
CO
2 carrying function
NH-COO -
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• Methemoglobin (MetHb):
– Hb iron is oxidized from the ferrous (Fe 2+ ) to the ferric state (Fe 3+ )
– Is incapable of carrying O
2 and has a bluish color → cyanosis
– Limited amount of metHb can be converted back to Hb by methemoglobin reductase present in the RBCs
– In normal state, 1.5% of Hb is in MetHb state
– Methemoglobinemia: Met-Hb > 1.5% (results from oxidation by nitrates, drugs like phenacetin or sulfonamides and congenital deficiency of methemoglobin reductase).
• Carboxyhemoglobin: Hb + CO(carbon monoxide) → cherry-red color of the skin and mucous membranes
– CO has 200-250 times the affinity to Hb as does O
2 molecule
– CO ↓ the functional Hb concentration
→ HbCO is a very stable
• HbCO is unavailable for O
2 anemia transport →
CO poisoning
, acute onset
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Concentration per unit volume of whole blood
Mean corpuscular Hb concentration concentration of Hb per unit packed cell volume
MCHC = Hb amount / Volume of packed RBC
Hb concentration
= Hb amount
(g)/Volume of whole blood
(dL, L )
Plasma
Calculation :
MCHC = Hb concentration x 100
Htc
Sample calculation :
[Hb] = 14.5 g/dL, Htc = 45 mL/dL
MCHC = (14.5/45) x 100 = 32.2 g/dL packed cells
RBC
Normal range :
31-37 g/dL packed cells
↓ value – hypochromia (i.e., Hb deficiency)
↑ value – hyperchromia (i.e., spherocytosis)
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• Is the total Hb content of a RBC
• Values
– Normal range – 27-31 pg
– ↓ value – hypochromia (i.e., iron deficiency anemia)
– ↑ value – hyperchromia (i.e., vit B12 deficiency)
• Calculation
MCH = Hb in grams/100 mL blood x 10
RBC count in million/L blood
• Sample calculation: [Hb] = 12 g/dL, RBC count = 4 x 10 6 /mL
MCH = 12/4 x 10 = 30 pg
MCH
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


CFU ： colonyforming unit
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 the committed red cell precursor undergoes several divisions.
 The daughter cells becomes progressively smaller,
 the cytoplasm changes color from blue to pink as hemoglobin is synthesized,
 the nucleus becomes small and dense and then extruded.
Proerythroblast Polychromatophilic Reticulocyte
(Pronormoblast)
Basophilic
Normoblast
Orthochromatophilic
Normoblast Normoblast



Proerythroblast
(Pronormoblast)
Polychromatophilic
Basophilic
Normoblast
Normoblast
Reticulocyte
Orthochromatophilic
Normoblast
Erythrocyte
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



 a, Stimulates the proliferation and differentiation of the committed red cell precursor
 b, Accelerates hemoglobin synthesis
 c, Shortens the period of red cell development in the bone marrow.
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Hypoxia stimulates production of EPO by the kidneys - the tubular epithelial cells and juxtaglomerular cells
(90% of EPO) & the liver
↑
↓
Tissue oxygenation is the most powerful regulator of the
RBC production
(but not the RBC count in the blood)
↑
Biological effects of EPO:
1. ↑ production of proerythroblasts from hematopoietic stem cells
2. ↑ speed of erythropoietic stages
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Morpho-functional changes (proerythroblast → RBC)
Appearance of Hb
Some Hb is present in the early erythroblasts
Late erythroblasts are saturated with Hb
Degeneration of the nucleus
Starts in the late erythroblast stage
Disappeared by the reticulocyte stage
Degeneration of the cell organelles
Progressi ve ↓ in the cell size
Reticulocytes enter the blood and within 1-2 days develop into mature RBC.
Only mature RBC and reticulocytes are present in the blood 25

– 1-4% of the circulating RBC in adults
– 2-6% in newborns
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CLINICAL FOCUS: BLOOD DOPING AND EPO
• Beneficial effects of EPO
– ↑ RBC count and O2 carrying capacity of the blood → ↑ O2 delivery to tissues, ↑ muscular performance, ↓ muscular fatigue
– Recombinant EPO (rhEPO) is used for treatment of anemias associated with chronic renal failure, AIDS and cancer chemotherapy
• Dangers of excessive EPO
– Genetically engineered EPO (i.e., darbepoetin) has increased life time
– ↑ Htc → ↑ blood viscosity, ↑ peripheral resistance, ↑ blood pressure, ↓ heart rate (secondary to increased blood pressure), ↑ blood clotting
– Genetically engineered EPO often cause production of antibodies against natural EPO and destruction of the RBC
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• Are required for maturation of the RBC
– ↑ Synthesis of DNA
(synthesis of thymidine triphosphate – DNA building block) → rapid proliferation of the erythroblastic cells
Dietary B12
Parietal/oxyntic cells of gastric mucosa produce intrinsic factor (IF)
B12 binds with the IF
– protection from digestion by GIT secretions
• Vitamin B12
(cyanocobolamin)
– Is required for action of folic acid on erythropoiesis
Complex of Vit B12 +IF complex binds to the mucosal receptors in the ileum → transport across mucosa
Release of B12 into the portal blood freed of IF
Binding to the plasma globulins
(transcobolamin I, II and III) → red bone marrow or storage in the liver (very large quantities – 3-4 years reserve)
B12+IF
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• Testosterone
– Stimulates the release of EPO
• Adrenal cortical steroids and ACTH
– In physiological concentrations stimulate EPO production
– Large doses are inhibitory
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• Sites of destruction
– Circulating blood (10% of senescent RBCs)
– Macrophage system (spleen and liver)
• Senescent RBC
– ↓ metabolic rate → ↑ fragility → rupture of the membrane when
RBC pass through tight spots of the circulation (i.e., red pulp of the spleen)
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• Prehepatic
– Takes places in the macrophages
– Results in formation of bilirubin – a bile pigment
• Hepatic
– Takes place in the liver (hepatocytes)
– Conjugation of bilirubin with glucuronic acid – bilirubin mono- or bi-
glucuronide and secretion of conjugated bilirubin into the bile
• Posthepatic
– Takes place in the GI and kidneys
– Formation of urobilinogen and stercobilinogen and excretion
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RBC or remnant
Cell remnants
Hem
Conversion of the hem pigment into the bile pigment biliverdin + CO
→ bilirubin → blood plasma
Pigment
CO Biliverdin
Bilirubin
Exhaled
In the plasma water insoluble bilirubin combines with albumin to form water soluble complex → liver
Albumin
Bilirubin-albumin
Liver
Hemoglobin
Fe++
Fe++ pool
Macrophages
Blood
Globin
Removal of the globin from Hb in macrophages
→ protein pool of the body
Protein pool
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• In the liver
– Replacement of albumin with glucuronic acid – bilirubin mono- or bi-glucuronide (water soluble)
– Excretion of conjugated bilirubin into the small intestine via the bile
• In the small intestine
– Conversion of bilirubin to urobilinogen by the intestinal bacteria
• Conversion to stercobilinogen → oxidation and excretion in the feces as stercobilin
• Absorption from the small intestine & either reexcretion by the liver or oxidation & excretion by the kidneys as urobilin.
Transport of bilirubin from plasma into the hepatocytes
Glucuronic acid
Liver
Reabsorption
Re-excretion in bile
Albumin
Bilirubin-glucuronide
Urobilinogen (in the small intestine)
Stercobilinogen
Excretion as urobilin in urine
Excretion as stercobilin in feces
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Bilirubin
Free bilirubin = unconjugated bilirubin
Conjugated bilirubin
Total bilirubin
Concentration in plasma, mg/dL
0.1 – 1
0 – 0.3
0.3 – 1.2
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Refers to the yellow color of the skin, conjunctivae and mucous membranes caused by the presence of excessive bilirubin in the plasma and body fluids ( jaune (French) = yellow)
Blood bilirubin level must exceed three times the normal values, for the coloration to be easy visible
Types of jaundice:
Pre-hepatic – the pathology occurs prior to the liver
Hepatic – the pathology is located in the liver
Post-hepatic – the pathology occurs after the conjugation of bilirubin in the liver
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Excessive hemolysis of the RBCs
– hemolytic jaundice
 bilirubin production
↑ unconjugated (indirect) bilirubin
Normal conjugated (direct) bilirubin
N
 urobilinogen formation
  urobilinogen → dark urine
Capacity of the liver to conjugate bilirubin is exceeded
(saturation of enzyme glucuronyl transferase)
↑ stercobilinogen
→ dark feces
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Results from infective or toxic damage to the liver cells (hepatocellular damage)
Uptake, conjugation and/or excretion of bilirubin is affected
↑ unconjugated bilirubin
Normal/decreased conjugated bilirubin
↑ urobilinogen in blood
(↓ enterohepatic circulation and hepatic extraction of blood urobilinogen by damaged hepatocytes)
↑ urobilinogen filtration and excretion in urine
Dark urine
Pale/N stool
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Results from obstruction of the bile ducts by stones, tumors, etc.
Functioning of the hepatic cells is normal
 plasma level of conjugated bilirubin due to the bile entry into the blood from ruptured congested canaliculi and
↑ total bilirubin
N Normal unconjugated bilirubin
 urobilinogen formation
Conjugated bilirubin in urine (kidney can excrete small quantities of highly soluble conjugated bilirubin) → dark urine
↓ or absent urobilin in urine in feces →
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Hemolysis of the excess RBC when the infant is suddenly exposed to a high oxygen environment and hence does not need so many RBC as in the uterus
Immaturity of the liver (inability to conjugate significant quantities of bilirubin with glucuronic acid for excretion into the bile) to handle the excess bilirubin (especially in premature babies)
↑ plasma total bilirubin concentration (less than 1 mg/dL → 5 mg/dL )
Mild jaundice (yellowness) of the infant’s skin and the sclerae for 1-2 weeks
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1.
2.
3.
4.
Dissociation of Fe from the hem
→ plasma → binding to transferrin, transport in the blood →
2
Detachment from transferrin & storage in the liver, muscle cells
& macrophages attached to ferritin or hemosiderin →
1 3
Release from the storage sites, transport in the blood by transferrin
4
↓ quantities of transferrin → ↓ Hb content in the RBC
– hypochromic anemia
Transport into the RBC precursor cells by receptor mediated endocytosis → Hem synthesis
Synthesis of transferrin increases with iron deficiency but decreases with any type of chronic disease.
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• Recommended daily intake - 15 – 18 mg (250-330 μmol)
• Minimal absorption to balance iron loss
– Adult males - 35 μmol
– Adult females - 175 μmol
• Distribution of body iron in an average man
– Hb , 2100 mg
– Ferritin - water soluble protein-iron complex , 700 mg (in the liver, spleen, marrow and plasma)
– Hemosiderin - water insoluble complex (macrophages of the liver and bone marrow), 300 mg
– Myoglobin - local oxygen reserve, 200 mg
– Tissue (heme and nonheme) enzymes , 150 mg
– Transport-iron compartment in plasma ( transferrin ), 3 mg.
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• Reasons
– Primary - one of the most common autosomal recessive genetic disorders characterized by excessive absorption of dietary iron resulting in a pathological increase in total body iron stores
• Failure to reduce iron reabsorption in response to increased iron level in the body
– Secondary – is not genetic (results from anemia, alcoholism, transfusion iron overload – hemosiderosis, etc.)
• Consequences
– Deposition of iron in the body tissues (liver, heart, pancreas, pituitary, joints, and skin) initially as ferritin and than as hemosiderin
– Toxic action on organs and damage of cells due to action as a pro-oxidant (↑ formation of free radical formation, i.e., the hydroxyl radical and the superoxide radical) → DNA cleavage, impaired protein synthesis, and impairment of cell integrity and cell proliferation, leading to cell injury and fibrosis.
• Cirrhosis, hyperpigmentation of skin, diabetes mellitus, impotence, joint diseases, etc.
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• Specific weight of the RBC is higher than that of the plasma
 in a stabilized blood, RBC slowly sink towards the bottom of the test tube sedimentation Males
– 3-6 mm/h
Females – 8-10 mm/h
• Factors increasing ESR
– ↓ Htc, ↓ blood viscosity
– ↑ concentration of fibrinogen (i.e., pregnancy, vascular diseases, heart diseases), haptoglobulin, lipoproteins, immunoglobulins
– Macrocytic RBC
– Extreme elevation of WBC count (leukemia)
ESR
• Factors decreasing ESR
– ↑ Htc
– Change in the RBC shape (i.e., sickle-cell anemia, poikilocytosis – nonuniformity of shape)
– ↑ albumin concentration
Clumps of RBCs
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• Deficiency of blood Hb due to
– ↓ RBC count (too rapid loss or/and too slow production)
– ↓ Hb quantity in the RBC
WHO's Hemoglobin thresholds used to define anemia (1 g/dL = 0.6206 mmol/L)
Age or gender group Hb threshold
(g/dl)
Children (0.5-5.0 yrs) 11,0
Children (5-12 yrs) 11,5
Children (12-15 yrs) 12,0
Women, nonpregnant (>15yrs)
12,0
Women, pregnant 11,0
Men (>15yrs) 13,0
6,8
7,1
Hb threshold
(mmol/l)
7,4
7,4
6,8
8,1
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• ↓ oxygen-carrying capacity of the blood → hypoxia → vasodilation
• ↑ in pulse and respiratory rates (effort to supply sufficient oxygen to tissues)
• ↓ exercise & cold tolerance
• Pale skin (↓ red colored oxyHb)
• ↑ fatigue and lassitude
• ↓ blood viscosity → ↓ peripheral vascular resistance → ↑ blood flow, venous return, cardiac output and work load on the heart
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Classification according to etiological ground
Anemia: classification according to MCV
• Nutritional
• Aplastic
• Hemorrhagic
• Hemolytic
Macrocytic anemia
(MCV>100)
Normocytic anemia
(80<MCV<100)
Deficiency of vit
B12, folic acid, or IF.
Hypothyroidism.
Alcoholism. Liver diseases. Drugs that inhibit DNA replication (i.e., methotrexate, zidovudine)
Acute blood loss, chronic diseases, bone marrow failure, hemolysis
Microcytic anemia
(MCV<80)
Hem synthesis defect (i.e., iron deficiency, chronic diseases)
Globin synthesis defect (i.e., thalassemia)
Sideroblastic defect
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Iron deficiency
• Is the most common type
• Reasons
– Premenopousal women: Blood loss during menses (20% of all women of childbearing age have iron deficiency anemia, compared with only 2% of adult men)
– Males and postmenopausal females: Excessive iron loss due to chronic occult bleeding (peptic ulcer, tumor, etc.)
– Increased iron demands (i.e., pregnancy and lactation)
– Inadequate iron intake or absorption (i.e., vit. C deficiency)
– Parasitic infestation (hookworm, amebiasis, schistosomiasis)
– Chronic intravascular hemolysis (if the amount of iron released during hemolysis exceeds the plasma iron-binding capacity)
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• Low serum ferritin (serum iron) level
– Plasma ferritin concentration is an excellent indicator of the iron stored in the body, because of a dynamic balance between intraand extracellular ferritin iron
• ↓ bone marrow iron stores (ferritin and hemosiderin)
• ↓ saturation of transferrin
• ↓ RBC count & Htc
• RBC are small and look pale microcytic hypochromic anemia
• Abnormal fissuring of the angular (corner) the lips (angular stomatitis).
• Abnormal craving to eat substances paint). sections of
(eg, ice, dirt,
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• Inadequate marrow utilization of iron for
Hb synthesis despite the presence of adequate or increased amounts of iron
• Reasons: Hereditary or acquired, including lead and ethanol toxicity, pyridoxine deficiency
• Deficient reticulocyte production, intramedullary death of RBCs, and bone marrow erythroid hyperplasia (and dysplasia)
• Presence of polychromatophilic, stippled
RBCs ( siderocytes )
• Hipochromic, microcytic RBCs, variations in RBC size Ring sideroblasts are erythroid precursors whose mitochondria
(located around the nucleus) are loaded with nonheme iron.
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Deficiency of vitamin B12 and/or folic acid
• Reasons
– Inadequate intake (a strict vegetarian diet excluding all meat, fish, dairy products, and eggs; chronic alcoholism)
– Inadequate GI absorption
• Lack of IF pernicious anemia
– Autoimmune destruction of parietal cells (atrophic gastric mucosa) or AB against IF
– Removal of the functional portion of the stomach, such as during gastric bypass surgery
• Crohn's disease intestinal malabsorption disorders
• Resection (or inflammation) of the ileum (site of B12 reabsorption)
• Consequences
– Maturation failure
• Failure of DNA synthesis with preserved RNA synthesis, restricted cell division of the progenitor cells. which result in
• Production of large precursor cells – megaloblasts and larger irregular oval erythrocytes – macrocytes fully saturated with Hb – macrocytic (megaloblastic) anemia
• ↑ fragility of the plasma membrane → ↓ life span → anemia
– Vitamin B12 deficiency only results in peripheral neuropathy and spinal cord degeneration
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• Results from abnormal blood loss (mild or severe; acute or chronic)
– Replacement of lost fluid within 1 – 3 days (much faster than the replacement of lost RBC) → dilution of the RBC
• Is normocytic
• Prolonged but mild loss of the blood causes microcytic hypochromic anemia (iron deficiency)
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• Results from suppression or destruction of the bone marrow (i.e., overexposure to ionizing radiation, adverse drug reaction, toxic chemicals, severe infections)
• Is usually normocytic
• Panhypoplasia of the marrow is associated with leukopenia and thrombocytopenia
52

• Is caused by an abnormally high rate of the RBCs destruction
(hemolysis) due to:
– Structural abnormalities of the RBC (more fragile cells)
• Hereditary spherocytosis – cells are spherical and can not be compressed
• Sickle cell anemia – cells have sickle shape → hemolysis
– Bacterial toxins, parasitic infections (i.e., malaria)
– Adverse drug reactions
– Autoimmune reactions
• The bone marrow is unable to compensate for premature destruction of RBC by increasing their production.
Thalassemias (α, β)
• Hereditary hemolytic anemia
• Abnormal or nonfunctional genes → globin chains are normal in structure but are produced in reduced amounts
• Cells are microcytic and hypochromic
Spherocytosis
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• Occurs as part of a chronic disorder (i.e., infection, inflammatory disease, or cancer)
• Pathophysiologic mechanisms
– Shortened RBC survival
– ↓ EPO production and marrow responsiveness to EPO
– Impaired intracellular iron metabolism
• Is microcytic or marginal normocytic
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• ↑ RBC count, Htc and Hb concentration
• Reasons
– Hypoxic erythropoietic drive (i.e., high altitudes, chronic pulmonary or cardiac disease)
– Hemoconcentration - dehydration (i.e., heavy sweating, vomiting or diarrhea)
– Polycythemia vera or erythremia – uncontrolled RBC production (i.e., neoplastic disease condition of hemocytoblastic cells)
• Results in
– ↑ blood viscosity
– ↑ peripheral resistance → ↓ venous return to the heart
– ↑ blood volume tends to ↑ venous return
– ↑ arterial BP
– Ruddy skin and mucosa membranes with cyanotic tint
(sluggish blood flow → ↑ blood deoxygenation in the skin circulation)
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A 14-year-old girl complained of fatigue and loss of stamina. Her appetite was marginal, as she was very conscious of maintaining her body weight at 96 pounds. Her monthly menstrual flow was always heavy and long from its onset at twelve years of age.
Relevant laboratory findings included the following:
– Hematocrit (Hct) - 28%
– Hemoglobin (Hgb) - 9 g/dL
– Iron 16 µg/dL
– Bone marrow iron - absent
– Erythrocytes - small and pale
Suggested treatment included ferrous sulfate or ferrous gluconate for six months orally between meals, since food may reduce absorption. A well-balanced diet was also suggested, as well as a gynecological examination.
Questions.
1. What is the primary disorder of this individual?
2. What does the ferrous sulfate or ferrous gluconate provide? Why is it necessary?
3. What dietary inclusions would you suggest?
4. Why is the gynecological examination important?
5. Why is bone marrow iron an important clinical indicator in this individual?
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A 51-year old male complains of generalized weakness and weight loss over the past 6 months. His blood pressure and pulse rate are elevated. Laboratory values revealed a hematocrit of 35% and hemoglobin level of 10.9 g/dL. A blood smear shows hypochromic and microcytic cells. A stool test for occult blood is positive. Which of the following would be the most likely cause of the findings?
a.
Acute blood loss b.
Iron deficiency c.
Spherocytosis d. Folic acid deficiency e.
Autoimmune reactions
B.
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