 Reticulocyte (Immature) converted to
ANEMIA
•It is a condition characterized by a decrease
in hemoglobin or RBC mass which results to
decreased oxygen carrying capacity of the
blood.
•It may decrease due to blood loss, increased
destruction of RBCs or decreased production
of RBCs
•It is measured according to the amount Of
hemoglobin.
•Hemoglobin the protein within red blood
cells that carries oxygen from the lungs to the
body’s tissues.
ANEMIA
-There is a reduction in the absolute
number of RBC/ erythrocytes
-We observe a decrease in
Hemoglobin (Hgb) as well as a
decrease in hematocrit (Hct)
Erythrocytes
- are responsible for the oxygen-
carrying capacity of the blood.
Hemoglobin
- pertains to the protein component
of RBC
-O2 carrying capacity
Hematocrit
measures how much of your blood is RBC
Normal hematocrit 35% - 50%
Female hematocrit 36.1% - 44.3%
We can say the patient is anemic if his/her
hemoglobin
Female <120 g/L
Male <140 g/L
Mechanism of Erythropoiesis
- Synthesis of RBC
-synthesis happens in bone marrow
Starts from STEM CELL  converted to
Proerythroblastconverted into Early
Erythroblast (this where can happen the
Ribosome synthesis) late Erythroblast (this
happened the formation of Hemoglobin)
will now convert to Normoblast (trophoblast)
Erythrocyte  matured erythrocyte enters
systemic circulation for about 24-48 hrs. 
Will now deliver o2 to different organs. 
Erythrocytes will die after 120 days.  dead
erythrocyte will go to “graveyard” Spleen,
some will go to Liver and Bone marrow) 
Macrophage  Hemoglobin will divide into;
Globin composed of protein will undergo to
catabolism and will converted into simpler
Amino acid, then Amino acid will reabsorb
from our body and will go back to bone
marrow, and it will repeat the cycle of
Erythropoiesis. and Heme has two
components: Iron (Fe2+) and Unconjugated
Bilirubin
-Reticulocyte is the immature type of RBC
-on a cellular level we can observe that on
reticulocyte stage is the beginning of removal
of nucleus of the reticulocyte, which means
that the cell is matured
-RBC is an anucleated cell (means lack of
nucleus)
-in production of Hgb kailangan sa early
erythroblast stage palang marami na agad na
production ng Ribosomes kasi siya yung
organelle na responsible for protein
synthesis.
-anucleate is still immature, reticulocyte stays
in bone marrow for approx. 3 days.
- conversion of Normoblast into reticulocyte
is facilitated by hormone Erythropoietin,
Thyroid hormone, and Androgen
-Erythropoietin is secreted by the Kidney.
Spleen
will divide the erythrocytes some will
reabsorb, and some will excrete out
of the body.
-Has macrophage, it will ingest
old/dead erythrocytes and will absorb
the hemoglobin the component of
RBC.
IRON: transferrin will carry out the iron to
circulation and then will go to the bone
marrow to happen the erythropoiesis.
Unconjugated Bilirubin: Is a Lipid soluble
-it must be excreted out of the body.
-since it is lipid soluble, it will go to the liver
by the transporter of Albumin, then will be
converted into Conjugated bilirubin (water
soluble) then it can easily be excreted from Laboratory perspective to know if the patient
our body via bile. (yellow pigment) can develop anemia is by:
Conducting CBC (Complete Blood count)
- MCV (Mean Corpuscular Volume- It
GENETIC ETIOLOGY measures the average size of RBC
•Hemoglobinopathies  - Microcystic (small) size is <80 fl
•Thalassemias  (femtoliter)
•Enzyme abnormalities of the glycolytic o Condition under
pathways  Microcystic
•Defects of the RBC cytoskeleton  -Iron deficiency
•Congenital dyserythropoietic anemia  -Thalassemia
•Rh null disease -Anemia caused by chronic
•Hereditary xerocytosis  diseases
•Abetalipoproteinemia  -Pb poisoning
•Fanconi anemia - Normocystic 80-100 fl (focalic)
o Base on Reticulocyte level
NUTRITIONAL and CHRONIC o Increase Reticulocyte:
DISEASE ETIOLOGIES Bleeding, Hemolytic anemia
•Iron deficiency o Decrease Reticulocyte: Bone
•Vitamin B-12 deficiency marrow failure (aplastic
•Stravation and Generalized Malnutrition anemia)
•Renal disease - Macrocystic >100 fl
•Hepatic disease o Nutrient deficiency
•Chromic infections  B12 deficiency
•Neoplasia  B9 Deficiency
•Collagen Vascular disease (Macrcystic anemia)
- Other conditions
PHYSICAL ETIOLOGY o Fanconi’s anemia
•Trauma o Kidney damage (consumption
•Burns of expire drug antibiotics)
•Frostbite
•Prosthetic valve and surface

INFECTIOUS ETIOLOGIES
•Viral RBCs CHARACTERISTIC
•Hepa, Infectious mononucleosis, •RBC is highly deformable and increase size
Cytomegalovirus from 7um to 13 um when they transverse
•Bacterial capillaries with 3um diameter.
•Clostridia, GM(-) sepsis •They have negative charge on their surface
•Protozoal which deflects the phagocytosis.
•Malaria, Leishmaniasis, Toxoplamosis3 •They don’t have nucleus that’s why they
didn’t undergo Krebs’s cycle.
•RBC relies on glycolysis via Embden
Meyerhof and Pentose Phosphate Pathway

RBC life cycle

 PREGNANCY
WHILE 9 mg
BREASTFEEDING

DAILY INTAKE FOR AGE OVER 14 Y/O

MEN 400 mcg
WOMEN 400 mcg
DURING 600 mcg
PREGNANCY
BREASTFEEDING 500 mcg

DAILY INTAKE FOR ADULT

ADULT (MEN AND 2.4 mcg
WOMEN)
DURING 2.6 mcg
PREGNANCY

BREASTFEEDING 2.8 mcg

CLINICAL MANIFESTATION
•Palor (Pale)
•Feeling of coldness
•Lightheadedness or dizziness
•Unusual cravings
•Trouble concentrating (low lvl of O2 in
FACTORS THAT DECREASES RBC brain)
PRODUCTION •Constipation

•Inadequate erythropoietin COMPLICATIONS

•Inadequate dietary intake •The most serious complications of severe
•Hypothyrodism anemia arise from tissue hypoxia. (decrease
lvl of O2 in brain)
FACTORS THAT INCREASE RBC •Shock, hypotension, or coronary and
DESTRUCTION pulmonary insufficiency can occur.
•This is more common in older individuals
•Hemorrhaging with underlying pulmonary and cardiovascular
•Endometriosis disease.
•Accidents
•GI lesions CLINICAL MANIFESTATION
•Menstruation •Severe form:
•Childbirth •Brittle nails
•Excessive Uterine Bleeding •Shortness of Breath
•Surgery •Chest pains
•Cirrhosis •Fainting
•Fibrosis
•Hemolysis Diagnosis
•Disorder of spleen and liver •Personal Health history
•Genetic disorders (G6PD, Thalassemia, •Family health history
Sickle cell anemia) •Physical Exam
•Laboratory Assessment
DAILY NUTRITIONAL
REQUIREMENTS  PHYSICAL DIAGNOSIS
•Optic Fundi evaluation
IRON DAILY INTAKE FOR ADULTS (19- 50 •Blood pressure
Y/O) •Heart rate
MEN 8 mg •Heart murmur
WOMEN 18mg •Enlarged lymph nodes, spleen, and liver
DURING 27 mg •Atrophic glossitis of tongue
•Color of the skin •Hb SC -2nd most common SCD. Less severe
• Pale anemia.
• Jaundice  •Hb SB+ thalassemia -defected beta globin
gene production resulted in reduced cell size.
LABORATORY ASSESSMENT Not severe anemia
•CBC (Complete Blood Count) •Hb SB 0 thalassemia -defected beta-globin
•Serum Iron Levels gene. Same with Hb SS, severe anemia
•Ferritin test
•Vitamin B-12 test CLINICAL MANIFESTATION
•Folic acid test
•Stool test for occult •It appears in babies as early as 4 months old
•Measuring of RBC mass but generally occurs around the 6-month
• These are time-consuming and expensive mark.
and usually require transfusion of radiolabeled •They usually experience:
erythrocytes. •Excessive fatigue or irritability
•Fussiness (in babies)
ADDITIONAL ASSESSMENT •Bed wetting (due to kidney problems)
•Upper GI •Jaundice (yellow eyes and skin)
Barium enema •Swelling and pain in hands and feet (called
•Chest X-rays Dactylitis)
•CT scan of the abdomen •Frequent infections
•Chest pain, back pain, pain in arm and legs

CLINICAL INTERVENTION AT RISK FOR SCD

•Nutritional supplements •Children with both parent carriers.
•IV of Vitamin B12 •Regions that have endemic malaria:
•Erythropoietin •Africa
•Blood transfusion • India
• the Mediterranean
SICKLE CELL ANEMIA •Saudi Arabia
•SCD is a genetic disease of RBC.
•Crescent shaped like RBCs which gives the
flexibility to travel through even the smallest CIRCUMSTANCES THAT CAN
blood vessel. INDUCE SCD
•However, this shape makes them sticky and •Illness
rigid and prone to getting trapped in small •Changes in temperature
vessels. •Stress
•It blocks the blood which causes pain and •Poor hydration
tissue damage •altitude
•SCD is an autosomal recessive condition.
•Hemoglobin in RBC is easily displaced. COMPLICATION THAT induces SCD
•Hb has 2 alpha chains and 2 beta chains. •Severe anemia
•SCD has 4 main types: •Hand-Foot Syndrome
•Hemoglobin SS •Splenic sequestration
•Hemoglobin SC •Delayed growth
•Hemoglobin SB+ (beta) thalassemia •Neurological complication
•Hemoglobin SB 0 (beta-zero) thalassemia •Eye Problems
• Sickle cell trait- a.k.a: sickle cell carrier •Skin Ulcers
No health problem unless exposed to extreme •heart disease and Chest syndrome
conditions: •Lung disease
-dehydration •Priapism
-high altitude area •Gallstones
•Sickle cell chest Syndrome (manageable
Endemic are Malaria (Plasmodium using antibiotic: penicillin)
falciparum)
(Heterozygote advantage) DIAGNOSIS
SICKLE CELL SUBTYPES •Hemoglobin electrophoresis
•Hb SS - Most common type of SCD. Severe -measures different Hb level
anemia. •Sickle cell gene from amniotic fluid
•Detailed patient history
•Blood test

CLINICAL INTERVENTION
•Rehydration
•Symptomatic management (opioid)
•Blood transfusion
•Supplemental Oxygen (may experience
acidosis)
•Pain Medication
•Bone marrow transplant
May recommend Hydroxyurea 
increase gamma globulin.
SKD: having problem with Hgb A (2
alpha globin chains) and 2 beta globin
chain

Pag may SKD ang problema ay sa 2 beta

chains so pag nag administer ng
hydroxyurea magiging 2 alpha globin
chains at 2 gamma globin chains.

NON-PHARMACOLOGIC
•Heating pads for pain
•Folic acid-rich food
•Diet regulation
•More fluids
•Exercise
•Less stress
•Contact your family doctor