 Kidneys produce erythropoietin as a response to

ALTERATION IN OXYGENATION: reduced O2 levels in the blood (hypoxia, increase

BLOOD altitude, lung diseases)
 Homeostasis is maintained by negative feedback
BLOOD COMPOSITION from blood oxygen levels
1. Plasma= 55%
a. Water HEMATOPOIESIS
b. Salts  RBC Formation
i. Sodium osmotic balance
ii. Potassium pH buffer POINTS TO REMEMBER
iii. Calcium regulation of 1. It is not the relative amount of RBC in the blood that
iv. Magnesium membrane controls RBC production, but based on their ability
v. Chloride permeability to transport O2 to meet body’s demand
vi. Bicarbonate 2. Blood destruction & production occur at the same
c. Plasma proteins rate
i. Albumin osmosis & pH balance 3. Small amounts of erythropoietin circulates in blood to
ii. Fibrinogen clotting of blood fill up RBC losses
iii. Globulin defense & liquid transport
d. Substances transported by blood DISORDERS AFFECTING RED
e. Nutrients
f. Waste products BLOOD CELLS
g. Respi gases
h. Hormones 1. ANEMIAS
2. Formed elements=45% -A condition marked by a deficiency of RBCs or of
a. Erythrocytes hemoglobin in the blood, resulting in pallor &
i. 4-6 M weariness
ii. Transport O2 & help transport CO2
b. Leukocytes Etiology Classification
i. 4-11 k  Decreased production of healthy RBCs
ii. Defense & immunity due to:
Basophil o Iron, vit B12
Neutrophil o Folic acid, protein
c. Platelets o Pyridoxine, copper
i. 250-500 k o Defective bone marrow
ii. Blood clotting
 Increased destruction of RBCs (hemolysis)
*Extrinsic causes:
FUNCTION
o Physical trauma
1. Transportation
o Antibodies/ autoimmune
a. O2
b. Nutrients o Infectious agents (malaria)
c. Metabolic waste o Toxins (snake, venom)
2. Regulation *intrinsic causes:
a. Blood pH o Abnormal Hb (sickle cell)
b. Body temperature o Enzyme deficiency
3. Protection o Membrane abnormalities
a. Blood clot  Blood loss
b. Against diseases *Acute causes:
o Trauma
CLINICAL APPLICATION o Blood vessel rupture
 ↓ Retic Count *chronic causes:
o Bone marrow does not respond to erythropoietin o Gastritis
 ↑ Retic Count o Hemorrhoids
o Bone marrow respond to previous blood loss & o Menstruation
iron therapy Morphologic classification of ANEMIA
 Normocytic/ Normochromic
-normal in size & color
CONTROL OF ERYTHROCYTE PRODUCTION  Macrocytic/ Normochromic
 Rate is controlled by erythropoietin -larger in size & normal in color
  Microcytic/ Hypochromic  RBC count, hemoglobin level & hematocrit confirm
-smaller in size/ pale in color the presence of anemia

Pathophysiology Hemoglobin level

 When hemoglobin is lacking or RBCs are low to carry  Evaluate the hemoglobin content of erythrocytes.
O2 to tissues, hypoxia develops This measurement helps to indicate anemia &
 The body attempts to compensate for tissue hypoxia polycythemia
in four major ways  Normal hemoglobin varies c age
a) Redistribution of blood from tissues of low O 2 Men= 13.5-18.0 g/dl
need to tissues of high O2 need Women=12-16 g/dl
b) ↑ cardiac output & stroke volume
c) ↑ RBC production by erythropoietin Red blood cell indices
d) A shift in oxyhemoglobin curve to the right  The RBC indices are measures of erythrocyte size &
hemoglobin content
*O2 & CO2 Transport  Mean corpuscular volume (MCR)
-measures average size or volume of individual
Oxyhemoglobin Dissociation Curve RBC; differentiates Anemia into Microcytic,
 Represents the relationship between PaO 2 & the Normocytic & Macrocytic
saturation of hemoglobin. This saturation reflects the Formula: Hct/RBC
amount of O2 available to tissues Normal value: 80-95 um
 For normal curve to occur:  Mean Corpuscular Hemoglobin (MCH)
o T= 37 -measure hemoglobin content within one RBC of
o pH= 7.40 average size
o PCO2= 40 mmHg Formula: Hb/RBC
Normal value: 27-33 pg
Factors Affecting Oxyhemoglobin Dissociation Curve MCH<27 pg- hemoglobin deficiency, Hypochromic
 Temp RBC
 pH MCH>27 pg- Macrocytic cells c abnormal large
 PCO2 volume of hemoglobin
 2,3 diphosphoglycerate/DPG
Platelet count
 Presence of CO
 measures that no. of platelets (thrombocytes) per
 Abnormal hemoglobin
cubic millimeter of blood
Normal value: 150-450 k/mm3
What RIGHT SHIFT means
-there is an easier release (↓ affinity) of oxygen at
White blood cell count
tissue level but more difficulty in binding in the lungs
 evaluates body’s capacity to resist & overcome
-this protects the body by maintaining tissue
oxygenation infection, detecting & classifying leukemia, &
E.g. detecting allergies & parasitic infections
 Exercise
Peripheral blood smear
 Acidosis
 blood test used to look for abnormalities in blood cell
 Anemia
 determine variations in size & structure of RBC, WBC
 Hypoxia
& platelets
 Hyperthermia
 ↓ 2,3 DPG Medical Management
I. alleviate & control the causes
 supplemental iron therapy
Clinical Manifestations  nutritional therapy
Manifestations differ depending on the severity:
 surgery to repair sites of hemorrhage
 Dyspnea, palpitations, diaphoresis c exertion &
 splenectomy
chronic fatigue
 removal of toxic agents that cause aplasia
 Appear pale particularly on palm lines, nail beds, &
(defective dev of RBC)
conjunctiva & circumoral area
 stem cell & bone marrow transplantation
 Fatigue
 corticosteroid/ immunosuppressive therapy
 Hypotension, if there is blood loss
II. relieve manifestations
 Tarry stools may be present if GI bleeding is present
 oxygen therapy
 i. O2 helps to prevent tissue hypoxia & collapse, bleeding, acute renal failure, shock
lessens the workload of the heart cardiac arrest
 Erythropoietin  M: stop transfusion, send blood samples to lab
i. To be effective, the pt must have a healthy for testing, send urine samples to lab, maintain
bone marrow & sufficient nutrients required BP, insert FBC, & measure output hourly ,
for RBC production dialysis
III. Iron replacement
 Ferrous sulfate & ferrous gluconate 4. NON IMMUNOLOGIC REACTIONS
i. Given c vit C for 6 months  Coronary overload
 IM iron dextran or iron sorbitol citrate complex Cause: too rapid infusion of blood in proportion
IV. Blood transfusions to size, cardiac status or clinical condition of
 BTs are valuable in treating Anemia resulting client
from: CM: cough dyspnea, pulmonary congestion
i. Acute blood loss (rales), headache, hypertension, tachycardia,
ii. Chronic anemia distended neck veins.
iii. Pt who respond poorly to other forms of M: place client in upright position c feet in
therapy dependent position. Administer diuretics, O2 &
V. Pretransfusion testing phlebotomy if necessary
 ABO & Rh type
 Indirect antiglobulin test 5. SEPTICEMIA
i. Test to determine the presence of  Cause: transfusion of blood contaminated c
antibodies other than Anti A / B. more than microorganisms
400 RBC antigens are identified in RBCs,  CM: rapid onset of chills, high fever, vomiting,
each of which can stimulate antibody diarrhea, hypotension & shock
production
 Cross matching 6. DELAYED TRANSUFION REACTIONS
i. CM is imprortant to pts who may have  HIV
multiple antibodies against RBCs, such as  Iron overload- occurs in pts receiving >100 units
those who receive multiple transfusions or of blood over a period of time
are known to have autoimmune antibodies -iron is deposited in heart, liver, pancreas &
 Correct labeling of blood samples joints
i. Lavel the sample at bedside after client -can be prevented by iron chelating therapy c
stated his/her name, exact date & sign by deferoxamine (Desferal)
phlebotomist  GVHD- occurs form replication of donor
lymphocytes (graft) in the transfusion recipient
TRANSUFION REACTIONS: (host)
1. FEBRILE
 Cause: sensitization to donor WBC, platelets & TRANSFUSION PROCEDURES:
plasma proteins  Obtain venous access
 CM: fever, pulmonary symptoms, sudden chills & -when packed RBCs are to be transfused, use
fever, headache, flushing, anxiety, muscle pain. gauge 20 or larger needle. If smaller needle must be
 M: if fever & pulmonary symptoms occur, stop used, the RBCs can be diluted c 0.9% saline, add
transfusion, give antipyretics but avoid aspiring no other solutions except normal saline to prevent
to thrombocytopenic pts hemolysis
2. ANAPHYLAXIS  Request blood release
 Cause: infusion of IgA proteins to IgA-deficient -certain procedures should be performed before
recipient who has developed anti-IgA antibodies blood is requested to prevent wasting a scarce
 CM: anxiety, urticarial, wheezing progressing to commodity, such as:
cyanosis, shock & possible cardiac arrest o The iv cath should be functional, flushed c
 M: stop transfusion, initiate CPR if needed, have normal saline & maintained at KVO rate
epinephrine ready for injection (0.4 ml @ 1:1 o Vital sign should be taken & recorded
SC) o Check for presence of fever
o Premeds may be given (acetaminophen,
3. ACUTE HEMOLYSIS antihistamine)
 Cause: ABO incompatibility  Confirm blood acceptability
 CM: chills, fever, low back pain, flushing, -80% of transfusion reactions are due to labeling
tachycardia, dyspnea, hemoglobinuria, errors
hemoglobinemia, hypotension, vascular o Check ABO & Rh compatibility
 o Check the bag label -radiographic studies, stool exam, for occult blood,
o Inspect units for leaks, clots, excessive air & esophagoscopy, & sigmoidoscopy are done to
bubbling, expiry date & serial no. identify the site of blood loss
 Infuse blood  Diet & supplemental iron preparations
-blood must be warmed to prevent hypothermia.
Systemic circulatory cooling can cause THALASSEMIA
intravascular agglutination  Inherited blood disorder which the body makes an
-the blood can be warmed by placing it between 2
abnormal hemoglobin
aluminum heating plates, or using warmed water
(37oC)  Results in excessive destruction of RBC which leads
to anemia
Nursing Diagnosis  IDA affects heme synthesis, thalassemia disrupts
 Fatigue, lack of energy, dyspnea, pallor, tachycardia globin synthesis
or cognitive dysfunction Types:
 Imbalanced nutrition  Alpha- benign & asymptomatic condition
 Beta- minor, mild to mod microcytic anemia
ANEMIA CAUSED BY (thalassemia trait)
 Beta- major, sever microcytic, hypochromic anemia
DECREASED ERYTHROCYTE Etiology & Risk Factors
 Common in Mediterranean, African & southeast
PRODUCTION Asian origin
a) Thalassemia minor
Due to: -People who inherited either alpha gene (most
 ↓ synthesis of normal hemoglobin common form) or beta gene (carrier state of
Iron & protein deficiency thalassemia)
 Defective DNA synthesis b) Thalassemia major
Defective bone marrow -Inherited both (life threatening anemia)
 ↓ availability of erythrocyte precursor Pathophysiology
B12, iron, folic acid  Disorders in the goblin genes.
Goblin protein (2 alpha, 2 beta polypeptide)
1. IRON DEFICIENCY ANEMIA *Alpha thalassemia- mutation of alpha goblin gene
-when iron, hemoglobin concentration in RBC is ↓ & *Beta thalassemia- mutation of beta goblin
appear pale *Thalassemia major- mutation of 2 beta gene
-microcytic, Hypochromic resulting to reduction in hemoglobin production
Pathophysiology  Unpaired alpha/ beta changes aggregate to form a
 Iron is used in the bone marrow to form heme, which precipitate that damage RBC membranes
is required to synthesize hemoglobin. Clinical manifestations
 Without iron, hemoglobin is not formed  Affected children appear normal at birth. However, as
Clinical manifestations HbF switches to HbA, manifestations of sever
 Fatigue anemia begin to appear.
 Pain
 Headache
 Failure to thrive
 Dyspnea
 Frequent infection
 Palpitations
 Splenomegaly
 Pallor in the face, palm, nail bed, mucus membrane
of mouth & conjunctiva  Hepatomegaly
Laboratory results shows  Jaundice from hemolysis
 Peripheral blood smears reveals microcytic &  Bone marrow hyperplaxia
hypochromic RBCs Management
 Hemoglobin levels ↓ A. Provide adequate normal hemoglobin
 Moderately ↓ total RBC count a. Chronic transfusions are administered to
correct anemia c target Hb @ 9-10 g/dl
 ↓ MCV, MCHC
B. Alleviate the effects of iron overload
 ↓ serum iron level to 0 mg/dl (normal 50-150 mg/dl)
a. Iron chelation c Deferoxamine is necessary
 Complete absence of hemosiderin (insoluble form of to prevent iron overload
storage iron from bone marrow) b. Iron supplementation should not be used
Management c. Increase vit C to improve iron excretion
 Diagnosis & correction of underlying cause d. Splenectomy to decrease transfusion
requirements
 e. Allogenic hematopoietic transplantation  Iron deficiency anemia can develop
f. Genetic counseling & testing for families during treatment of pernicious
should be encouraged anemia
 Injections of B12 cause a rapid
regeneration of RBC that depletes
MEGALOBLASTIC ANEMIA iron, causing IDA
 Large & premature RBCs are found in the blood &  IVTT B12
bone marrow. o Treat neurologic complications
 Caused by deficiencies of vit B12 and folic acid  Multidrug combinations of folate,
Types: cobalamin & pyridoxine (B complex)
1. PERNICIOUS ANEMIA (Cobalamin / B12 deficiency) have been proposed to help prevent
-autoimmune disorder characterized by the absence neurologic cimplications
of intrinsic factor in gastric secretions, leading to  Paresthesis of both hands &
malabsorption of B12 feet
-macrocytic anemia  Memory loss, cognitive
Etiology problems & depression
 Failure of absorption of vit B12 from absence of 2. FOLLIC ACID DEFICIENCY ANEMIA
intrinsic factor (IF) in gastric secretion From:
 90% of people c PA have antibodies that react o Diet lacking in green leafy veggies, liver,
against the parietal cells where IF is produced citrus, nus, grains & yeast
Pathophysiology o Anorexia in chronic alcoholism (blocks
 Normally cobalamin (extrinsic) is bound to intrinsic response of bone marrow to folic acid)
factor. Without cobalamin results to: o Anticonvulsant
 Impairs DNA synthesis & replication o ↑ demands of folate during pregnancy
 Reticulocytes do not divide normally Clinical manifestations
 Large poorly functioning RBCs  Slow & insidious onset anemia
 Myelin sheath production affected  Client often thin & emaciated, appears quite ill
Clinical manifestations  Clint’s malnourishment leads to other deficiencies
 ↓ Hb, hematocrit & RBC levels (iron, protein, minerals & vitamins)
 GI manifestations include:  Electrolyte imbalance
o Weight loss
o Appetite loss APLASTIC ANEMIA
o Nausea & vomiting  Failure of the bone marrow to produce hematopoietic
o Distended abdomen cell
o Diarrhea, constipation & steatorrhea  Hypoplastic bone marrow results in anemia,
 Neurologic manifestations: leukopenia, & thrombocytopenia or known as
o Paresthesia of hands & feet Pancytopenia
o Poor gait Etiology
o Memory loss, cognitive problem &
 Hereditary
depression
Laboratory test  Acquired
 Schillings test (definitive test) o Radiation
-whether absorption of B12 is proper or not o Drugs
-measures the absorption of orally administered
radioactive B12 before & after parenteral o Autoimmune disorders
administration of intrinsic factor o Infectious agents
 Gastric secretion analysis o Disease of bone marrow
-more pts c PA anemias have ↓ volume gastric
secretions c ↑ pH, even after the administration of Laboratory findings
histamine, chich normally stimulates gastric  Pancytopenia
secretions o ↓ RBC
Medical management:
o Cobalamin therapy o ↓ WBC
 PO 1,000 ug daily for 2 weeks o ↓ platelet
 72 hrs response
o Iron supplements o Bone marrow- hypoplastic
Clinical manifestations
  Infection on mouth  Low O2 tension
 Bleeding, rash Risk factors
 Melena  ↑ prevalence rate is in West Africa
Medical management  In US 75,000 people have SCD; 1 in 500 African
 Withdrawal of offending agent American infants is affected
 Transfusion therapy  Cold- slows blood flow
 Treatment of infection  ↑ blood viscosity- impairs O2 delivery
 Bone marrow transplantation Clinical manifestations
 Immunosuppressive therapy  Anemia-sickled cells have a shorter life span (10-20
Medical management days)
 Diet adjustment  Painful vaso-occlusive crisis
 Client education  Jaundice
 Renal medullary ischemia- ↓ concentration urine
GLUCOSE-6 PHOSPHATE  Aseptic necrosis
 Folate deficiency
DEHYDROGENASE DEFICIENCY
 Bone marrow hyperplasia
 Deficiency of glucose-6 phosphate dehydrogenase
causes red blood cells to break down prematurely  Tachycardia
 Genetic disorder mostly in males  Skeletal & joint involvement
 G-6-PD enzyme, is the catalyst for glycolysis in RBC  Priapism- leads to impotence
& protects the cell from oxidative agents  Impaired circulation
Clinical manifestations  Ophthalmologic manifestations
 Hemochromatosis(bronze skin tone)  Splenomegaly
 Hemoglobinuria (dark urine)  Hepatomegaly
 Fever, neurologic signs, petechiae Complications
 Renal failure from ↑ load of RBC degradation  Infection
products  Stroke
 Jaundice, leg ulcers, hepatosplenomegaly, folate  Renal failure
deficiency, hemosiderosis  Impotence
Management  Heart failure
 Transfusion therapy  Pulmonary hypertension
 Adequate fluids to flush the kidney Pathophysiology
 Folic acid may be given to offset the consumption of  After 6 mos, when HbF is changed to HbA, & when
folate the defective RBC is exposed to ↓ O2 tension, the
 Iron replacement RBC losses its round, pliable, biconcave disk shape,
becomes dehydrated, rigid, & sickle shape
 Corticosteroids for hemolysis caused by autoimmune
disorder  The sickle RBCs adhere to smaller blood vessels
causing obstruction to blood flow
 Educate client to recognize the manifestations of
hemolysis & to seek immediate treatment  May lead to the ff:
o Dark urine o Sickle cell crisis- obstruction of blood flow by
o Jaundice the sickled cells
3 types
o Heart murmur
1. acute vaso-occlusive crisis
o ↑ HR
-entrapment of erythrocytes & leukocytes in the
o Enlarged spleen microcirculation, causing tissue hypoxia,
o Enlarge liver inflammation, & necrosis due to inadequate blood
flow to specific region or organ
SICKLE CELL DISEASE 2. plastic crisis
 Severe hereditary form of anemia in w/c a mutated -results from infection w/ the human parvovirus B-
form of hemoglobin(Hbs) distorts the RBC into a 19. Hemoglobin falls rapidly & the bone cant
crescent shape at low oxygen levels compensate, as evidence by an absence of char
 Most common among african descent 3. sequenstration crisis
Etiology -sickled cells become trapped obstructing blood flow
 Autosomal-recessive disorder in w/c the person is w/ pooling & enlargement of an organ
homozygous for Hbs -common in infants & children
 Heterozygous form, known as sickle cell trait is a Common sites:
milder form of the disease & the carrier state of the a. spleen
Hbs b. liver
 c. lungs  Chronic pain & substance abuse
S/S:
a. rapid enlargement of spleen
COAGULATION PROBS
b. circulatory collapse HEMOPHILIA
Triggers of SCD  X-linked genetic disorder
1. ↓ O2 levels  Deficiency of coagulation factors
a. High altitude  Passed from mother to son
b. Strenuous exercises Types
c. Respi infections 1. Hemophilia A- factor VIII
d. Undergoing anaesthesia w/o receiving 2. Hemophilia B- factor IX
adequate O2
2. It may be induced by:
a. Stress VON WILLEBRAND’S DISEASE
b. Exposure to cold water or temp  Inherited factor VIII deficiency & defective platelet
c. Hypoxia or infection function
Assessment  To both sexes
 Pt w/ SCD has ↓ hemoglobin, ↓ hematrocrit & sickled Lab findings
cells on smear  ↓ platelet adhesiveness
 Pt w/ SCTrait has normal all 3  ↑ coagulation time & bleeding time\
 Note: child w/ SCT will develop manifestations of the Clinical manifestations
disease when expose to ↓ oxygen tension  Hemarthrosis
Laboratory exam
 A strained blood smear DISSEMINATED INTRAVASCULAR
o Examined for presence of sickle cell COAGULATION
after deoxygenation of the blood  Accelerated intravascular coagulation
 Sickle turbidity tube test  Consumptive coagulopathy
o Blood is mixed w/ sickledex solution in a
test tube. 5 min after, the specimen is
observed for cloudiness, w/c indicates
the presence of Hbs
ANEMIA CAUSED BY
 Hb electrophoresis INCREASED RBC
o Blood test used to measure & identify DESTRUCTION
the diff types of hemoglobin
 If Hbs is 75-100% of the total & the rest HbF or
HbA, the pt is homogenous & has sickle cell HEMOLYTIC ANEMIA
anemia  Bone marrow fails to replace RBCs at the rate they
Prognosis are destroyed
 Life expectancy 50 years Etiology
 Intrinsic (hereditary)
Medical management
o Spherocytosis (most common)
 Hematopoietic stem cell transplant-only known o G-6-PD
cure o Thalassemia
 Transfusion therapy o Sickle cell anemia
Pharmacologic therapy  Extrinsic (most common type)
 Hydroxyurea- ↑ HbF o Toxins
 Arginine- ↑ nitri oxide o Prosthetic heart valves
Supportive therapy o Trapping of RBC w/in liver/ spleen
 Reduce pain
 Non-pharmacologic measures
Nursing interventions ANEMIA CAUSED BY
 Manage pain
 Manage fatigue
INCREASED RBC
 Prevent infection PRODUCTION
 Promote coping skills
 Priapism leading to impotence POLYCYTHEMIA VERA
 Ruddy complexion