HEMA IMMUNO

BLOOD

LIQUID SOLID
60% 40%
Plasma Blood cells (rbc,wbc,platelets)
Fluid- H2O Hematopoiesis
Electrolytes: Na 135-145 mEq/L
K 3.5-5.2 mEq/L
Ca 8.5-10.5 mg/dL KIDNEY > Erythropoietin > Bone marror
a. Yellow Bone marrow: responsible for production
CHON (Protein) > of fat globules
 Albumin (responsible for oncotic b. Red bone marrow: Responsible for blood cell
pressure) production (hematopoiesis)
- Oncotic pressure is a pressure that attracts fluids form
intracellular to intravascular Possible complications for long bone Fracture
 Hydrostatic: pushes fluid from intravascular to
intracellular  FAT EMBOLISM:
 Intracellular (Edema)  Petechial rashes on chest
 Sudden sharp pain during inspiration
 Prothrombin/ Fibrin : responsible for hemostasis.  HEMORRHAGE: shock
 Immunoglobulin (Ig)  Hypotension
 Kwashorkor: Protein deficiency  Tachycardia
 Marasmus: Caloric deficiency  Tachypnea
 Types of Ig (GAMED)
- G : Activated during pregnancy (placental transfusion) Different blood cells
-
- A: found in all secretions found in body.(colostrum) RBC (Erythromycin)
 Gas exchange
- M: Activated during acute phase of infection (<14  4-6million (normal)
days) (adenovirus a common colds)  Annucleated (no cells)
 Biconcave
 Essential nutrients need to promote maturation of
- E: Activated during allergy (hypersensitivity) RBC
 Detects Allergic substance and - Iron:
activates basophils. - responsible for hemoglobin synthesis
- D: Activated during chronic infection (last 6 months - Cyanocobalamin(B12): responsible for DNA synthesis
and beyond) - Folic Acid: responsible for DNA synthesis

Vitamins and Minerals Increase RBC: Erythrocytosis  hyperviscosity  HTN

Decrease RBC  Anemia (qualitative/quantitative)

If cellular destruction occurs and RBC destroyed all

components can go outside that can lead to these
complications:
 Hyperkalemia:
 Iron Toxicity
 Hyperbilirubinemia

MANAGEMENT
 Hyperkalemia
- Kayexalate  PO  slow acting

- Insulin with Dextrose DOC in emergency situation

because it is fast acting. It is combined with Dextrose to
prevent hypoglycemia.

- Na Bicarbonate hyperkalemia + Acidosis

 Pottasium is Acid in nature.

- Diuretics Given only to those who has hyperkalemia

 with fluid overload.
 Potassium wasting

- Ca Gluconate An emergency medications if the

patient already suffering from Arryrthmia.

 Iron Toxicity
- Chelating Agent DOC  Deferoxamin(Dispersal)
(it binds in iron to execrate in urine)

 Hyperbilirubinemia
- Adult: sunlight
- Infants: Phototherapy (cover the eyes because it can lead
to blindness and genitals because it can lead to
infertility)

WBC(Leukocytes)
 Responsible for infection/immunity.
 Steroid : Stress hormone in the body.
 5000-10000  Normal
 13000  Normal in pregnant
 Increasing  Leukocytosis  Infection
 Decrease  Leukopenia  immunocompromised
- Long term steroid therapy
- Chemotherapy/radiation therapy
- HIV under AIDS
- People with blood Dyscrasia (Blood abnormalities) 
Agranulocytosis
- Leukemia/ Multiple myeloma
- Plasmapheresis  it removes all antibodies present in
the body.
Components of WBC

Polymorphonuclear Mononuclear
AKA Agranulocytes AKA
Agranulocytes

 Neutrophils (Segmenters)  Lymphocytes

 Acute infection
 First to increase in - B cells
inflammatory response. Burbusa (it
 The most abundant matures in Bone
(70% of overall WBC) marrow)

 Basophils AKA Humoral

 Responsible for allergic mediated
reaction. immunity
 Activated by IgE during
allergic reaction. Fast acting type
of immunity

 Eosinophils
 Responsible for - T cells
Parasitic infection. Matures in
 Thymus. (Adult
has no thymus
gland because as
we reached
puberty thymus
gland shrinks. So,
to become mature
it will go back to
bone marrow to
mature.)

Cell mediated.

Slow acting
immunity.

PLATELETS
 250,000-450,000
 Responsible for coagulation
 Increase  Thrombocytosis.
Risk for clot formation
 Decrease Thrombocytes Thrombocytopenia
bleeding tendencies
DIFFERENT BLOOD DISORSDERS

A. IRON DEFICIENCY ANEMIA (IDA)

 PREDISPOSING FACTOR
 Sex: Female has higher risk due to menstruation and pregnancy.
 Bleeding/ Hemorrhage
 Anorexia
 Psychological problems: Pica (eating of inedible substance)
 Excessive menstruation (menorrhagia)  normal:80mL(2-3pads) // Spotting (metrorrhagia)

 SIGNS AND SYMPTOMS

 Asymptomatic
 Hypoxemia
 Fatiguability
 Restless/ Lightheaded
 Agitation  initial manifestation
 Tachycardia
 SOB

 Cyanosis
 Chest retraction due to severe SOB (usage of accessory muscles)
 late manifestation
 Clubbing of fingers

 Angular Cheilosis: Cracking on the edge of lips HALLMARK SIGN

 DIAGNOSTIC TEST
 RBC
o <4 million (in quantity)
o Check RBC with differential and cellular analysis (Qualitative) Microcytic Anemia

 Hemoglobin
o 12-14grams  Female
o 14-16 grams  Male

 Hematocrit
o Hemoglobin x3
o 36-42%  Female  ratio of liquid and RBC
o 42-48%  Male

 MANAGEMENT

 Green leafy vegetables, red meat

 Iron supplement
o Take with Vitamin C for fast absorption (Ascorbic Acid, citrus fruits)
o Remind for episode of gastric upset because it can increase acidity of the stomach and patient is at risk of peptic
ulcer disease.
o Remind patients about constipation.
o Observe black tarry stool  it requires further investigation because it could be a normal side effect because the
patient is taking iron supplement and result of gastric upset, or the patient might have internal bleeding and
suffering from peptic ulcer disease.
o No PO solution  it can promote staining of the teeth.
o Always use straw for solutions to avoid staining of the teeth.
  Blood transfusion  if hemoglobin is <8grams/dL
o Blood typing and Crossmatch
o Universal Donor  Type O+
o Universal Recipient  Type AB
o If the patient does not have any history or signs of bleeding, we only give Pack RBC. But if the patient has history
or signs of bleeding, we give whole blood. Because if we give Whole blood without any bleeding it can lead to Iron
overload.

B. PERNICIOUS ANEMIA (Megaloblastic Anemia)

 Loss of intrinsic factor  lack of the ability to absorb Vitamin B12.

 Characteristics:
 Vitamin B12 is responsible for maturation of brain cells  it can lead to intellectual disability/ mental retardation.

 PREDISPOSING FACTOR
 Heredity
 Autoimmunity  triggered by:
severe case of stress
infection
trauma  aggravating farctor

 Surgical Intervention  Gastrectomy/ antrectomy (Billroth)

 SIGNS AND SYMPTOMS

 Hypoxemia
 Neurologic impairment
o Pediatric  mental retardation/ intellectual disability
o Adults  numbing, paresthesia, psychosis.
 Beefy red tongue  HALLMARK SIGN

 DIAGNOSTIC TEST
 Biopsy  To check the parietal cells.
 Schilling’s Test  patient is given oral radioactive vitamin B12, once absorbed 30min-1hour we will now give
unlabeled vitamin B12 (non-radioactive) via IM. It will be now excreted to the kidney.
 In normal individuals, once radioactive Vitamin B12 is taken, it will go to the GI tract to the Intravascular to
the cells and it will filter by the kidneys. Within 24 hours vitamin B12 in urine output should be increased at
>6%. What we reflect is the radioactive vitamin b12. Since the patient has no intrinsic factor the Vitamin B12
that will reflect in the urine is the unlabeled Vitamin b12 and the patient will have the possibility to have
pernicious anemia. The confirmatory test is the biopsy.
Once seen that the unlabeled Vitamin B12 is increased in the urine, the MD will administer intrinsic factor.
Once seen that the radio-active vitamin B12 is increased in the urine that is confirmatory for pernicious anemia.

 Gastric test (Gastric aspirate)  parietal cells is responsible for production of hydrochloric acid. It would become
alkaline in nature.

 MANAGEMENT
 Lifetime administration of B12 (IM)  main management
monthly basis
 Administer by MD. Z track administration
 Blood transfusion  if hemoglobin is <8gr/dL
C. SICKLE CELL ANEMIA
 RBC has abnormal shaped cells  Cresent shape

 PREDISPOSING FACTORS
 Afro American
 Heredity/congenital problems
 Common in male

 SIGNS AND SYMPTOMS

 Vasoocclusive crisis  to prevent this Increase oral fluid intake.
Immature RBC  compensatory mechanism is to stimulate Red bone marrow to increase RBC  blood becomes
hyperviscous  hypertensive reaction

Clumping occur due to aggregation of the blood

 obstruction

Pale, cold to touch  hand and foot syndrome.  HALLMARK SIGN

ischemia

Pain

 necrosis

 Splenic sequestration
o Immature RBC  Cellular death is 6-20days (Normal life span of RBC is 80-120 days)
 Spleen (will accommodate all the dead RBC)
 Splenomegaly

Management: Avoid

 Strenuous activity
 Bending waist
 Contact sport
 Palpation
 Constrictive clothing

 Rupture

 Bleeding  shock (Hypo, tachy, tachy)

 Peritonitis  Board-like/ rigid abdomen
 Management: Blood transfusion  whole blood
  Aplastic Crisis
o Bone Marrow  Exhaustion  due to over production of RBC
 Bone marrow depression (Demineralization)
 pancytopenia

 Anemia
 Leukopenia
 Thrombocytopenia

 MANAGEMENT
 HHOPIA
o Hydrate the patient (Increase Oral fluid intake  2-3L
o Hydroxy Urea  It is a oncologic medication(cancer) that prevent sickling of cell  side effect is megaloblastic
anemia
o Oxygen  o increase perfusion
o Pain relief  Narcotics  Morphine  No meperidine Demerol because it could further promote sickling of the
cells.
o IV fluids  Blood Transfusion
o Antimicrobials  antibiotics  perform culture and sensitivity first before giving antibiotics.

 Difference between:
o Aplastic crisis  triggering factor is exhaustion of Bone marrow due to over production of RBC

o aplastic anemia  Triggering factor is myelotoxic substances  medications (oncologic meds/management) that
directly damage the bone marrow.  epileptic meds, radiation therapy, Chemotherapy
 Signs and Symptoms  Pancytopenia
 Diagnostic  Bone marrow aspiration
 Management  Bone marrow transplant

 autologous  specimen is coming from patient

Allogenic  coming from family members.

 Syngenic  Identical twins (monozygotic twins)

D. HEMOPHILIA
 Sex linked disorder  mother  carrier
 male  disease
 Hemophilia A  Loss of clotting factor 8
 Hemophilia B  Loss of clotting factor 9

 SIGNS AND SYMPTOMS

 Bleeding of gums
 Epistaxis
 Ecchymosis
 Petechial
 Hemarthrosis
 Hemoptysis
 Hematemesis
 Hematochezia/ melena
  MANAGEMENT
 Razors (electric)
 ASA  avoided.
 No needle prick injuries
 Decrease size of the needle by increasing gauge.
 Injury prevention
 Pressure in the affected area (external injury)
 Rest
 Immobilize the affected area
 Cold compress
 Elevate the affected area
 Splint
 Medication
o Administer clotting factor, cryoprecipitate, plasma expanders, fluid.

IMMUNOLOGY

ANAPHYLACTIC REACTION (severe allergic reaction)

Basophils  IgE  Chemical mediators activated.
Histamine, bradykinin, leukotriene, prostaglandin, serotonin

SIGNS AND SYMPTOMS

 Bronchoconstriction  priority
 Urticaria
 Rashes
 Pruritus
 Edema
 Decrease sensorium.


DOC
 Antihistamine (side effects(Benadryl): Pedia  Hyperactivity/ Adult  drowsiness).
 Antileukotriene  montelukast
 Bronchodilators
 Corticosteroids
 Decongestants  never give beyond 3-5 days it will give rebound congestion.
 Epinephrine  EMERGENCY
CYTOTOXIC REACTION  body identifies the blood as foreign and destroys it
 Hemolytic Anemia(ABO incompatibility)
 Erythroblastosis Fetalis  Rh incompatibility Rh negative mother  1st baby is normal and
the triggering factor  succeeding babies will be affected and dies within 24 hours

DIAGNOSTIC TEST
 Coomb’s Test
 Vaccine  Rhogam  Administer to mother with Rh negative to help not developed antibodies.  given 28
weeks during pregnancy and within 24 hours after delivery
IMMUNE COMPLEX RELATED DISORDER  Autoimmune disorders

 SLE  connective tissue (Butterfly rashes hallmark)

 Systemic Sclerosis  Hardening of tissues  tumitigas ang smooth muscle  Calcium
 Rheumatoid Arthritis  Inflammation of joint  Swan neck, boutonniere’s and ulnar drift  Hallmark

DOC (2C’s)
 Cortecosteriods  SONE/LONE
 Chemotherapy  methotrexate, sadimmune

Delayed hypersensitivity

 T cell activation causing delayed activation.