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Erythrocytes: Functions and Dysfunctions

By: Kirk Odrey O. Jimenez
Erythrocytes
o Also called Red Blood Cells or RBC’s
o Function primarily to ferry Oxygen in the blood to
all cells in the body
o Also transports Carbon dioxide out of the body
o Lifespan of 120 days only
 Hemoglobin in the RBC binds with the Oxygen as it is transported in
the blood
 Female : 12 – 16 g/100ml
 Male : 13 – 18 g/100ml
 Normal RBC count: about 4 – 6 million/mm³
 Hematocrit (HCT) – percentage of RBC per given volume of blood and
is an important indicator of the Oxygen-carrying capacity of the blood
 Female : 37 – 48%
 Male : 45 – 52%
Hematopoiesis (Blood Cell Formation)

 Occurs in the Red Bone Marrow, chiefly in flat bones

like Skull, ribs, pelvis, sternum and proximal
epiphyses of the humerus and femur
 Erythropoiesis – RBC production, is a very active
process
 RBC are continuously being destroyed by the liver &
spleen
 RBC’s have a lifespan of 120 days
 As RBC’s are destroyed, iron is recycled to the
bone marrow for use in the formation of new
RBC’s
 Erythropoietin – secreted by the kidneys &
released when blood levels of Oxygen begins to
decline for any reason; which stimulates the Red
Bone Marrow to produce more RBC’s
ERYTHROPOIESIS - RBC production
 Requirements :

 Erythropoietin
 Iron
 Folic Acid
 Vitamin B6, Vitamin B12
 Vitamin C

Liver and Spleen - Graveyard of the RBC

ERYTHROCYTES Destruction
 destruction- mature cells removed chiefly by spleen & liver

 * BILIRUBIN = byproduct of Hgb released when RBC’s

destroyed

 * IRON = freed from Hgb during bilirubin formation

 = transported to bone marrow via TRANSFERIN &
reclaimed for new Hgb production
Glucuronic
acid
Blood Groups
Compatible Blood Types
DONOR

  O A B AB

AB        
Recipient
B        

A        

O        
ERYTHROCYTE
DISORDERS
ANEMIA
Anemia
• Conditions in which the number of RBC’s or amount of hemoglobin is lower than
normal
• leads to hypoxia and ischemia
Classifications of Anemia According to Etiology
Bleeding Hypoproliferative Hemolytic
Resulting from RBC Loss low RBC production increased RBC destruction

accidents / trauma Iron deficiency enlarged spleen

surgery Vit. B12 deficiency sickle cell
childbirth Folic acid deficiency thalassemia
ruptured blood vessel Vit. C deficiency G6PD
menorrhagia chronic disease drug-induced
epistaxis low erythropoietin
hemorrhoids cancer
GI bleeding / ulcers
cancer
 most common type of anemia
 Iron stores are depleted, resulting in a
decreased supply of iron for the
manufacture of hemoglobin in RBC’s
 Commonly results from blood loss, increased metabolic
demands, syndromes of gastrointestinal malabsorption,
and dietary inadequacy
 cause :
 inadequate absorption or excessive loss of iron
 Bleeding – principal cause in adults
 Vegetarian diets
 Low Vitamin C diet – increases iron absorption
 Pathophysiology
Stage 2
Stage 1 Fewer RBC are produced
Iron loss exceeds
intake, depleting
iron reserves Stage 3
Anemia develops
RBC – normal but few in number
Hgb & Hct – normal levels
Stage 4
Bone marrow compensates : Stage 5
Speeds up production – Microlytic /
Symptoms of anemia
Small red blood cells
worsens
Most definitive way to diagnose anemia :
Bone marrow aspiration
 Assessment Findings
Mild cases - asymptomatic
fatigue
dyspnea
Palpitations & dizziness
Pallor
Brittle hair and nails
Pica
Glossitis
Cheilosis
Irritability
Koilonychia
Glossitis
Cheilosis
Koilonychia
Laboratory findings :
 RBC’s are small / microcytic and pale

 decreased hemoglobin decreased

hematocrit
 decreased serum iron decreased ferritin
Nursing Interventions
1. Identify the cause

2. Monitor S/Sx of bleeding – stool, urine and GI

contents
3. Provide rest
4. Give iron preparations ( 6 – 12 months )
 Ferrous Sulfate, Ferrous Gluconate, Ferrous Fumarate

a. always give after meals or snacks

b. dilute liquid preps and give thru straw
c. give with orange juice (Vitamin C enhances absorption)
d. warn clients the stool will become black and can cause
constipation
5. For clients with poor absorption or continuous blood
loss
IM or IV of Iron Dextran
a. Use 1 needle to withdraw and another for
injection
b. Use z-track method
c. don’t massage but encourage ambulation
d. usually, deep IM at buttocks
6. Give dietary teaching – liver, meats, nuts, egg yolk,
shellfish, legumes, etc.

7. Increase intake of roughage and fluids to prevent

constipation.
 Vitamin B12 Deficiency Anemia

 caused by inadequate Vit. B12 intake or deficiency in

intrinsic factor

 Vit. B12 combines with intrinsic factor so it can be

absorbed in the ileum into the bloodstream`
 the result is abnormally large erythrocytes and
hypochlorhydria ( a deficiency of hydrochloric acid in
gastric secretions).
 Lack of intrinsic factor is caused by gastric mucosal
atrophy (possibly due to heredity, prolonged iron
deficiency, or an autoimmune disorder), can also result in
client who have had a total gastrectomy
 Usually occurs in men and women over age 50, with an
increase in blue eyed persons.
Pathophysiology
Intrinsic factor + Vit. B12 for absorption

Result : decreased or no Vit. B12

Lead to : decreased RBC production

 Assessment :
Anemia - symptoms are :
Fatigue, weakness
dyspnea
Palpitations & dizziness
Pallor
confusion
Decreased intellectual fxn
Sore tongue : Beefy red tongue
Paresthesias
Weight loss
Lab Results
Decrease RBC
Decreased free Hydrochloric acid
Large RBC / Megaloblast
Positive Schilling Test – definitive test for
Pernicious anemia
- used to detect lack of intrinsic
factor
 Positive schilling test
 Measures absorption of radioactive vitamin B12 both before and
after parenteral administration of intrinsic factor.
 Definitive test for pernicious anemia.

 Used to detect lack of intrinsic factor.

 Fasting client is given radioactive vitamin B12 by mouth and

nonradioactive vitamin B12 IM to saturate tissue binding sites and to
permit some excretion of radioactive vitamin B12 in the urine if it is
absorbed.
 24-48 hour urine collection is obtained; client is
encouraged to drink fluids.
 If indicated, a second stage Schilling test will be
performed 1 week after first stage.
 Fasting client is given radioactive vitamin B12
combined with human intrinsic factor and the test
will be repeated.
Nursing Interventions / Treatment
 1. Drug Therapy
a. Vit. B12 injections monthly for life
b. Iron Preparations
c. Folic Acid
 2. Transfusion therapy
 3. Bed rest
 4. Mouth care
 5. Dietary teaching
 6. Teach about importance of lifelong Vitamin B12 therapy
Nursing Interventions / Treatment
 7. Provide a nutritious diet high in iron, protein, and
vitamins (fish, meat, milk/milk products and eggs).
 8. Avoid highly seasoned, coarse or very hot foods if client
has a mouth sores.
 9. Provide mouth care before and after meals using a soft
toothbrush and non irritating rinses.
• increase rate of RBC destruction
• short life span of RBC
a.G6PD
b.Sickle cell anemia
c. Thalassemia
d.DIC
e. Transfussion incompatibilities
 Most common inherited disease among black Americans.
 Also found in Arabian, Mediterranean and Caribbean

descent
 Hgb S ( abnormal hemoglobin ), which has reduced

oxygen carrying capacity, replaces all or part of the

hemoglobin in the RBC’s.
 Life span is 6-20 days instead of 120, causing hemolytic

anemia.
 Death often occurs in early adulthood due to occlusion or
infection.
 During decreased O2 tension, lowered pH, dehydration

and severe infections, RBC’s change from round to sickle

or crescent shape
 Sickled cells don’t slide thru vessels as normal RBC’s do,

causing clumping, thrombosis, arterial obstruction,

increased blood viscosity, hemolysis and eventual tissue
ischemia and necrosis
Sickle Cell Crisis :
 Cause : infection, dehydration, fever, cold
exposure, hypoxia, strenuous exercise,
extreme fatigue or extreme changes in
altitude
VASO-OCCLUSIVE CRISIS:
A. most common and most painful type of crisis
caused by stasis of blood with clumping of the cells in the
microcirculation leading to ischemia & infarction.
B. signs include fever, pain, and tissue engorgement
C. Treatment
– hydration, electrolyte replacement, bed rest, broad
spectrum antibiotics, transfusions and oxygen therapy.
SPLENIC SEQUESTRATION:
 A. Life - threatening crisis caused by the pooling of
blood in the spleen. (from congestion of sickled cells)

 B. signs include profound anemia, hypovolemia, and

shock

 C. treatment : blood transfusions and splenectomy

APLASTIC CRISIS:
 A. Occurs infrequently and is caused by:
diminished production of RBC
increased destruction of RBC’s
triggered by a viral infection or the
depletion of folic acid.
 B. signs include profound anemia, pallor, and
PANCYTOPENIA.
 C. Treatment – Transfusion of packed RBC’s
 Frequent infection esp. with H. influenzae
 Infants may have Dactylitis (hand – foot syndrome)
symmetrical painful soft tissue swelling in the hands and
feet in the absence of trauma
 Signs and symptoms of anemia – pallor, weakness
 Hepatospleenomegaly
 Dactylitis (Symmetric swelling of the hands and feet) – called hand-
foot syndrome
 Other problems :
 CVA
 MI
 Growth retardation – initial manifestation
 Decreased fertility
 Priapism
 Recurrent severe infections
MEDICAL MANAGEMENT
A. Drug therapy
> analgesic/narcotics to control pain
 Avoid meperidine (Demerol) due increased risk of seizures in

children
> antibiotics to control infection.
B. Blood transfusions
C. Hydration:oral and IV
D. Bed rest
E. Surgery: splenectomy
INTERVENTIONS
 Administer O2 & Blood Transfusion as Rx
 Maintain adequate hydration
 Avoid tight clothing that could impair circulation.
 Keep wounds clean and dry.
 Provide bed rest to decrease energy expenditure and
oxygen use.
 Encourage patient to eat foods high in calories, CHON,
with folic acid supplementation.
 Analgesics:
 Acetaminophen
 Morphine
 avoid aspirin as it enhances acidosis,which promotes sickling
 Avoid anticoagulants( sludging is not due to clotting ).
 Antibiotics.
 Avoid activities that require so much energy.
 Keep arms and legs from extreme cold.
 Decrease emotional stress.
 Provide good skin care
THALASSEMIA MAJOR
(Cooley’s anemia)
 B - thalassemia refers to an inherited hemolytic anemia,
characterized by reduction or absence of the B-globulin
chain in Hgb synthesis
 Fragile RBC & short life span
 Autosomal recessive pattern of inheritance
 Insufficient B-globulin chain synthesis allows large
amounts of unstable chains to accumulate
 Precipitates of alpha chains that form cause
RBC’s to be rigid & easily destroyed, leading
to severe hemolytic anemia = chronic hypoxia
 Skeletal deformities: pathologic fractures

 Hemosiderosis – excess iron supply, which

leads to iron deposits in the organ tissues

leading to decreased function
 CLINICAL
MANIFESTATIONS
 onset is usually insidious
 Sx are primarily related to progressive anemia, expansion
of marrow cavities of the bone & developmemnt of
hemosiderosis
 Early Sx often include progressive pallor, poor feeding &
lethargy
 Further signs: hemorrhage, bone pain, exercise
intolerance, jaundice, & protuberant abdomen
 DIAGNOSTIC EVALUATION
 Decrease hemoglobin
 RBC= increase in number
 Hgb elctrophoresis
 elevated levels of HgF ( doesn’t hold O2 well )
 limited amount of HgA
Management
 Frequent and regular transfusion of packed
RBC’s to maintain Hgb levels above 10 g/dL
 Iron chelation therapy with deferoxamine
(Desferal) – reduces toxic effects of excess iron &
increases iron excretion thru urine & feces
 Splenectomy
 Supportive management of symptoms
 Bone marrow transplant

 Prognosis and Survival rate is poor because

of no known cure
 Often fatal in late adolescence or early

adulthood
Complications
 Splenomegaly
 Growth retardation in the second decade
 Endocrine abnormalities :
 delayed development of secondary sex characteristics –

most boys fail to undergo puberty, girls – menstruation

problems
 DM – due to iron deposits in the pancreas

 Hypermetabolic rates
 Skeletal complications
 Frontal & parietal bossing (Enlargement)

 Maxillary hypertrophy – leading to occlusion

 Premature closure of epiphyses of long bones

 Osteoporosis & pathologic fractures

 Cardiac problems: pericarditis & CHF – usual cause of

death
 Complications
 Gallbladder disease
 Gallstones that often require surgery

 Skin – bronze pigmentation caused by iron deposits in the

dermis
 Leg ulcers
ERYTHROBLASTOSIS FETALIS
Rh Incompatibility
 Destruction of RBCs that result from Ag-Ab
rxn
 Characterized by hemolytic anemia or
hyperbilirubinemia
 Possibly caused by Rh incompatibility

between the mother & the fetus (Ag & Ab

reaction)
ERYTHROBLASTOSIS FETALIS
 Sensitization of Rh (-) woman by
transfusion of Rh (+) blood
 Sensitization of Rh (-) woman by presence

of Rh (+) RBCs from her fetus conceived

with Rh (+) man

Approximately 65% of infants conceived by this
combination of parents will be Rh (+)
 Mother is sensitized by passage of Rh (+) RBCs

thru placenta, either during pregnancy

(break/leak in membrane) or at the time of
separation of the placenta after delivery.
RH INCOMPATIBILTY

FIRST PREGNANCY
 - mother may become sensitized, baby rarely affected
 INDIRECT COOMB’S TEST
 - Tests for anti-Rh(+) Ab in mother’s circulation
 - performed during pregnancy at first visit & again
about 28 week’s gestation.
RESULTS:
 - If (-) at 28 weeks, a small dose of (MicroRhogam) is
given prophylactically to prevent sensitization in the 3rd
trimester.
 - Rhogam may also be given after 2nd trimester
amniocentesis
 - If (+), levels are titrated to determine potential
effects on the fetus
RH INCOMPATIBILTY
 DIRECT COOMBS’ TEST
 - Tests done on the cord blood at delivery
to determine presence of (+) Ab on fetal
RBCs
 RESULTS
 - If both indirect & direct Coombs’ test is NEGATIVE &
infant is Rh(+):
 - NEGATIVE: No formation of Anti-Rh (+) Ab
 - Rhogam (Rho[D] human immune globulin is given to the
Rh(-) mother to prevent development of anti-Rh(+) Ab as
the result of sensitization from present or just terminated
pregnancy.
RH INCOMPATIBILTY
 In each pregnancy, an Rh(-) mother who carries
an Rh (+) fetus receives Rhogam if both the
mother and infant is (-) to both direct & indirect
Coombs’ test.


RH INCOMPATIBILTY
 If mother is has been sensitized:
 anti-Rh(+) Ab are present

- Rhogam is not indicated

 Rhogam must be injected into unsensitized

mother’s system within 72 hours of delivery of
Rh(+) infant
ERYTHROBLASTOSIS FETALIS
CLINICAL FINDINGS
 Anemia
 Jaundice that develops rapidly after birth and before 24

hours or that occurs within 24 - 36 hours

 Enlarged placenta

 Edema

 Ascites
ERYTHROBLASTOSIS FETALIS
NURSING INTERVENTIONS
 Determine blood type and Rh early in pregnancy.
 Determine results of direct Coomb’s test early in
pregnancy & again at 28 week’s.

ERYTHROBLASTOSIS FETALIS
 Determine results of direct Coomb’s test on cord
blood.
- type & Rh, Hgb, Hct
 Implement phototherapy or exchange
transfusion.
ERYTHROBLASTOSIS FETALIS
NURSING INTERVENTIONS
 Administer Rh0 (D) immune globulin to the mother
during the first 72 hrs. after delivery if the Rh(-)
mother delivers an Rh (+) fetus but remains
unsensitized
 Assist with exchange transfusion as prescribed.
ERYTHROBLASTOSIS FETALIS
 The baby undergoes transfusion of blood to stop
the destruction of the baby’s RBC
- the transfused blood is replaced with the baby’s
own blood gradually
 Reassure the mother that the newborn will suffer
no untoward effects from the condition