1 MS HEMA

IRON DEFICIENCY ANEMIA

2. complete blood count (CBC)
RISK FACTORS: - RBC:
 N: 4.6-6 million cells/mm3
1. iron malabsorption
F- 4.6-5.4 mill
 Situations:
M- 5.2 – 6 mill
o diarrhea – nutrients pagawas tanan
 R: decrease RBC
o Infants – they are considered milk
babies (milks are considered as poor -Hgb: N: F: 12 -16 g/dl x 3 (pra makuha ang hema)
source of iron) = 36-48%
o Gastrectomy – removal of the stomach M: 14 – 18 g/dl x 3 = 42 – 53%
- Though Iron will be absorb in  Decrease ang hematocrit level pag
the small intestine dehydrated ang patient
 R: decrease Hgb and Hgt
2. iron loss
 Bleeding – surgery, ulcer (bleeding in the
mucosal walls, IBD NURSING MANAGEMENT
- menstruation (heavy-
menorrhagia), 1. decreased 02 demand
- labor and delivery - rest – balance activity and rest
 Parasites – worm, - plan activities (no to strenuous and physical
activities)
3. inadequate iron -administer oxygen as ordered
 Pregnant (adolescent)
2. diet
PATHOPYSIOLOGY - no to coffee, tea  decreases absorption of iron
- iron
Dec iron (helps In the HgB synthesis; decrease in Iron  vit.c (citrus) helps in the absorption of iron
decreases hgb synthesis production)  Liver
 eggs (yolks)
 lamb
 Beef & poultry
Rbc malformation  types: small:microcytic  brown rice
: pale: hypochromic  tofu
 Nuts & legumes
 dried fruit (raisins)
 green leafy veggies (spinach, broccoli,
O2 transportation – RBC purpose: transport 02 potato)

SIGN AND SYMPTOMS 3. administration of IRON

1. fatigue :tiredness, decrease activity - given with orange juice; vit C; citrus juices – best
 nsg dx: activity intolerance absorption with acidic environment
2. dyspnea - purpose: iron – helps in the Hgb synthesis
- SOB/BOD - route: oral (ferrous sulfate)
- dec RR (>30) Oral liquid – use straw (there is staining of teeth
3. Pallor if dli mag straw)
4. Nails  spoon shape (kaoilonychia) IM  Z track – prevents staining of skin
5, cheilosis  mouth (corner) ulceration -antidote: defaroxamine (desfera)
6. Pica  eating of non-edible things S/E: constipation
7. hair is brittle Stool color: black/greenish black
Staining on the teeth and skin
DIAGNOSTIC TEST
1. bone marrow aspiration
- confirmatory test
- definitive test
-Obtain bone marrow to the posterior iliac crest
- (R) – (+) RBC malformation
2 MS HEMA

PERNICIOUS ANEMIA MANAGEMENT

-only anemia that can affect the nerve 1. Vitamin B12
 lifetime – for the rest of the patient’s life
CAUSE/ RISK FACTOR  route: IM
 Monthly maintenance
1. surgery – gastroctomy (billroth 1 and 2) (1st 2 weeks: daily)
- intrinsic factor: gi produce sa stomach which can help 1st: every other day/weekly
in the absorption of vit b12 2. rest
2. Athrophy of lining (GI)  elderly
3. diet: strict vegetarian  the only source of B12 are SICKLE CELL ANEMIA
animal products
ASSESSMENT/ RISK FACTORS
1. race – African-American (blacks)
2. autosomal recessive
Problem: absence of intrinsic factor (helps in absorption - both parents are carrier
of B12) R: carrier: 2/4 50% (no manifestation but they
carry the genes, so ang anak naai chance
magka sakit ug sickle cells
Normal: ¼ = 25%
Affected: ¼ = 25%
No b12 absorption (b12: it is absorb in the ilium)
PATHOPHYSIOLOGY

CAUSE: dec o2 level in the blood (pag kulang ug o2

Defective cell maturation which is needed by the cell to live, this causes the blood
to sickle, or mag crescent shape cya)

SIGNS AND SYMPTOMS

Rbc  shape: sickling  crescent shape/s-shape
1.GIT Cells: red beefy tongue (classic sign of pernicious  Contains Hgb s
Anemia)
- Indigestion, nausea and vomiting

2. RBC: macrocytic  macrocytic Sickling  RBC becomes more fragile, rigid, easily
 immature – (+) anemia; large but destroyed (risk for hemolysis – destruction of RBC)
immature
3. Nerve cells:
s/sx: tingling (pins and needles) RBC clumping – which then causes the blood to not flow
prickling  paresthesia easily
numbness
confusion
Occlusion/obstruction – the problem of sickle cell
DIAGNOSITIC TEST - Nursing diagnosis: impaired
1. Schilling’s test circulation / impaired tissue
- administer vit b12 PO (oral) perfusion
- urine collection: 24 hours
- R: if urine: (-) B12  R: suspect

 if ang urine naa sa ihi meaning na absorb cya sa Ischemia = (+) pain
body but since negative man or positive ang patient sa
pernicious anemia so negative sa uring ang b12
SIGNS AND SYMPTOMS
-administer b12 with Intrinsic factor
- route: IM -occurs about 4 months: Hgb replaces fetal Hgb
- urine collection: 24 hours 1. Pain: arms, joints,
R: (+) b12  confirm!! 2. dyspnea
3. Fatigue, tiredness, poor muscle tone
4. Jaundice – increase bilirubin (r/t RBC destruction)
assess on the skin or sclera
3 MS HEMA

TYPES OF CRISIS

1. Vaso – occlusive APLASTIC ANEMIA

Cause: obstruction of blood vessel
Problem: decrease O2 to area RISK FACTORS
Result: necrosis (cell death to area
PRIMARY – Congenital  inborn
2. sequestration
Secondary – acquired  no exact cause
Problem: massive pooling of RBCs
 Most cases: unknown (idiopathic)
S/Sx: splenomegaly (the cemetary of dead RBC) ,
Autoimmune – self-destruction – own antibody attacks
hepatomegaly
own cells
Blood transfusion reaction – incompatibility
DIAGNOSTIC TEST
Chronic infection
1. CBC Drugs and chemicals toxicity: chemo therapy, benzene,
- RBC  (+) Hgb S (there is sickling mao present ang S; Arsenic
dapat Exposure to radiation (nuclear plants)
- reticulocyte: increase immature RBC
PATHOPHYSIOLOGY
2. sickledex morbidity
- specimen: blood
Damage: bone marrow stem cells
- place in test tube
- centrifuge machine
- check blood specimen in microscope
Aplasia: decrease in RBC, WBC, PLATELET
R: (N) = clear
(+) = cloudy  (+) sickle cells; s shape or sickle
Pancytopenia
shape
Decrease in RBC - anemia
Decrease in WBC – leukopenia  risk for infection
NURSING MANAGEMENT
decrease in PLATELET – thrombocytopenia  risk for
bleeding
1. prevent sickling
Hydration  increase fluid intake via oral or iv DIAGNOSTIC TEST
(priority ni if dli ubos ang o2 sat)
1. Bone marrow aspiration
If mag offer ug snack offer popsicle
Position: posterior iliac crest
R: bone marrow is suppressed
O2  as prescribed (R): suppression  decrease in RBC, WBC,
Pain management  mild: NSAIDS, tylenol, Asperin PLATELET
Child: Tylenol
Severe pain: morphine (opioids- adult) 2. CBC
Caution: merpedine (Can cause Seizure) (R): decrease in RBC, WBC, PLATELET
Avoid iron (increases HgB synthesis) – increase
TREATMENT
clumping
Give Vit B  maturation of cell
1. Bone marrow transplant
Donor: 500 mL bone marrow
2. health teachings
Site: posterior iliac crest
- position; legs extended (for circulation)
- avoid: stress
 high altitude – rocky mountains
Bone marrow: filtered
cold weather
infection and trauma
Transfused to the patient
Activities for the patient with sickle cell anemia
should consist of non-stress activities like going to
Priority: risk for infection
the museum and such
2. therapy: immunosuppressive
 cyclosporine and prednisone
action: suppress autoimmunity
4 MS HEMA

NSG MGT s/sx: Abdominal pain, bloody diarrhea, confusion

Refer to chemo or leukemia mgt (dec LOC), changes in skin: bronze/gray

THALASSEMIA Antidote for iron overload: deferoxamine

(desferal) bedside meds
2. BMT
RISK FACTORY
1. Genetics
MANAGEMENT
- autosomal recessive  both parents are carrier

2. race 1. Minimize fatigue (decrease O2 demand)

 Asian (middle east): alpha thalassemia - balance activity and rest
Mediterranean: beta thalassemia - no activities
- no cold environment
PATHOPHYSIOLOGY
2. prevent infection (BMT)
- reverse isolation
Globulin chain: impaired synthesis production
- wear mask
- no to crowded places
- no to fresh fruits
Milder: thalassemia minor
- no to fresh flowers
Severe: thalassemia major
(fresh fruits and flowers sometimes harbors
microorganism that can cause infection to the pt)
- no to vaccine (if live)
Compensation:
 Hemochromatosis: excess iron
 Abnormal increase of Hgb production 3. diet: decrease iron intake

POLYCYTHEMIA VERA
RBC destruction  hemolysis
RISK FACTOR
SIGN AND SYMPTOMS Race: jewish
1. anemia: fatigue/tiredness, pallor, hypoxia age: middle age (>50)
2. jaundice: increase bilirubin r/t hemolysis gender: male
3. organ enlargement: excessive iron deposit in tissue

Spleen splenomegaly stem cell: proliferation (over production of RBC)

Liver  hepatomegaly
4. face
> cheek: flat bone marrow: over production of RBC, PLATELET,
>philtrum: smooth WBC
>jaw: under develop
>upper lip: thin SIGNS AND SYMPTOMS
>eye opening: small Increase RBC  complexion: ruddy (flushed)
>nose: short Marked increase HCT (>55 %)
HGB (>18 g/dL)
DIAGNOSTIC TESTS Increased platelet  increase blood clotting
 Hyper: coagulation
1. CBC  Increase viscosity (thick blood)
a. RBC:  N: 4.6-6 million cells/mm3  Complication: CVA (stroke)
F- 4.6-5.4 mill MI
M- 5.2 – 6 mill DVT r/t thrombus/clot
R: small (microcytic) Increase WBC  Increase Basophils (release
pale (hypochromic) histamine)
unequal size (anicytosis)  Late sign: itchiness (pruritus)
b. HgB R: excessive HGb: aBn
does not depend on the beta chains COMPLICATION
Increase blood volume  hypervolemia
TREATMENT s/sx: 1. Ache “headache” r/t HPN
1. Blood transfusion 2. BP increase (HPN)
frequent (regular)  goal: to maintain (N) Hgb level 3. CHF
risk: iron overload 4. DOB SOB (dyspnea), orthopnea (DOB when
5 MS HEMA

Supine)
5. dizziness
6. blurred vision – disturbance in vision
DIAGNOSTIC TEST

1. CBC  increase RBC, WBC, PLATELET, Hgb, HCT Pancytopenia

2. UTZ Decrease in RBC - anemia
Decrease in WBC – leukopenia  risk for infection
TREATMENT decrease in PLATELET – thrombocytopenia  risk for
1. Phlebotomy bleeding
 removing of blood – goal: to decrease blood volume
to decrease patients iron  to prevent Hgb and RBC
synthesis WBC infiltration:
repeated 2 – 3x week Organs: joints, liver, Lymph nodes, bones
decrease to every 2-3 months CNS: early: decrease LOC: confusion, disorientation,
Restlessness
MANAGEMENT Late: increase ICP
1. Circulation Long term: infection
> increase fluid (hydration) 3L/day
> no to constrictive clothing socks, belt, clothing SIGN AND SYMPTOMS
For venous return: 1. Anemia: fatigue, pallor, tiredness
>elevate the feet
> support hose  antiembolic stocking 2. Thrombocytopenia: bleeding (bruises, ecchymosis,
purpura, hematuria, hematochezia, melena, petechia)
2, health teaching
>Increase fluid 3. Leukopenia
>Diet: decrease iron  caution:multi vits risk for infection  watch out for cough and fever
>For pruritus  tipid Water
>No to alcohol DIAGNOSIS

LEUKEMIA 1. cbc
R: decrease wbc, rbc, platelet
Increase immature WBC (malignant)
RISK
1. AGE 2. bone marrow biopsy
ALL  4-12 (PEAK: 4 YEARS OLD) confirmatory test
AML  60 yrs old  R: (+) malignancy
CLL  after 60 years old Site: adult: iliac crest
CML  45 – 55 years old Infant: tibia
2. Gender: Male TREATMENT
1. Chemotherapy
3. Exposure to chemicals  radiation  job related
DOC: asparaginase (ELSPAR); anti leukemia
S/Sx: gouty – increase uric acid
4. Diseases: viral infection
Anaphylaxis
Pancreatitis
PATHOPHYSIOLOGY
MANAGEMENT
Problem: WBC  malignant proliferation of immature
1. prevent infection  lowest WBC: NADR
WBC (cancer)
-isolation: reverse
-Room: private
Wear mask
Immature/malignant:
Handwashing
Increase lymphocytes: ALL, CLL
Procedure  aseptic technique
Increase myeloblast: AML, CML
No to raw food, fresh flowers, long standing water
(pitcher), crowded places
Malignant WBC: overcrowding; infiltration  spead
2. prevent bleeding
X injury – no to contact sports
Caution: invasive procedure
Inhibits N hematopoiesis
6 MS HEMA

Toothbrush: soft
No to rectal procedures
Stool softeners  route: oral
V/S: temperature
3. health teaching
Rest (balance activity and rest)
Oral hygiene  rinse: NSS
 Cotton swabs
 If there is lesions: dry tea bag
No to lemon glycerin
No raw foods (unpeeled fruits)