Risk factors for ↓ PLT

 Idiopathic Thrombocytopenic purpura (ITP): bleeding disorder,

immune system destroys PLTs
 Thrombotic Thrombocytopenic disorder (TTP): blood disorder
causing blood clots to form in small blood vessels around
body→ ↓ PLT
 Hypercoagualtion disorder (DIC, Thrombosis)
 Hypocoagulation disorder (Liver Dz, Vitamin K deficiency)
 Chemotherapy—nadir day+7-14 recovery within 2-6 weeks
 Radiation tx
 Medications( ASA, digoxin, furosemide, phenytoin, quinidine,
sulfonamide, tetracycline)
 Mgmt Thrombocytopenia

 PLT transfusions PLT<10,000

 Colony stimulating factors, eg IL 11 (Neumega)
 Steroids
 Progesterone ↓ menstrual bleeding
 Nursing interventions
 Avoid tight BP cuffs when PLT<20,000
 Avoid invasive procedures
 Avoid sharp objects/no barefoot
 Apply firm pressure to venipuncture sites for 5 minutes
 Treat nose bleeds with high fowler’s position-icepack
 Prevent constipation
 Encourage soft toothbrushes
 Why do we evaluate WBC?
 To assess body's response to significant bacterial
insult, such as appendicitis, Pelvic inflammatory
disease, pneumonia, pyelonephritis, and SEPSIS
 WHITE BLOOD CELLS
 Segmented Neutrophil
(60%)
 Lymphocytes(30%)
 Monocytes(6%)
 Eosinophils(3%)
 Basophils(1%)
SEGMENTED NEUTROPHIL
 1ST line of defense
 Normal 50-70%
 Survive 1-2 DAYS
 LYMPHOCYTES
 2 Types by appearance:
Large granular and small
 Large granular are NK
cells
 Small are T & B cell
 T cell mediated
immunity
 B cell humoral immunity
 MONOCYTE
 5-10 % Circulating
WBCs
 When stimulated become
Macrophages and
dentritic cells in the
tissue
 Clean up the debris
 EOSINOPHIL
 1-5% Circulating WBCS
 Involved in parasitic
infections
 Involved with
mechanism associated
with allergy and asthma
 ↑In case of w.w.w.
 BASOPHIL
 < 1% circulating WBCS
 Involved with allergic
and inflammatory
response
 Release histamines and
cytokines
Hematological
Symptoms
 Hematological Symptoms
 Neutropenia—defined as ANC<1000/mm3
 Anemia--↓RBC & Hgb
 Thrombocytopenia—low PLT <100,000
 Leukopenia—decrease in WBC, below the lower
limit
 Pancytopenia-an abnormal deficiency in all
blood cells, RBC, WBC, & PLT; usually
associated with bone marrow tumor or with
aplastic anemia)
 Risk factors for febrile neutropenia
 Previous Hx Chemo/Type of chemo/prior radiation
Tx
 Age>65/ female gender
 Poor nutritional status
 Advanced cancer and bone marrow involvement
 ↑LDH, ↓Hgb
 Leukemia/lymphoma/lung cancer
 Open wounds
 DM
 COPD
 Prevention of Neutropenia
 Growth stimulating factors activate production
of bone marrow cells. It can be given
prophylactically or therapeutically
 BMT give GCSF on day+4 of stem cell SCT
 GCSF-/filgrastim 5mcg/kg
 Pegfilgrastim--Neulasta 6mcg/kg
 Neutropenic Precautions
 Limit exposure of pts to infections
 Hand washing ↓spread
 Avoid crowds
 Avoid fresh fruits /vegetables/flowers
 Avoid caring for animals esp. cleaning excretes
 Avoid gardening
 Infections
 Mechanical barriers—skin, mucous membranes
 Chemical barriers-pH of tissues
 Inflammatory and immune responses
 Risks of Infections
 High risk
 Intermediate risk
 Low risk
 High Risk for infection
 Allogeneic BMT
 Acute Leukemia's
 GVHD tx ↑dose steroids
 Neutropenic lasting >10 days
 Break in skin/mucosal barrier
 Prolonged ABX or steroid use
 Poor nutrition
 Invasive procedure
 Poor personal hygiene
Intermediate Risks for infections
 Autologous BMT
 Lymphoma/MM/CLL
 Neutropenic anticipated to last >7-10 days
 Low Risk for infections
 Standard Chemotherapy
 Neutropenia <7 days
 PT AND PTT
 PT (PROTIME) Test the extrinsic pathway
 PTT Tests the intrinsic pathway
 COUMADIN (WARFARIN) Affects the
Vitamin K factors (II,VII,IX,X ) of which
factor VII is the most labile
 Hemophilia is a factor VIII deficiency
 INR: Method for standardizing Protimes. It is a
ration of tested results : control
 COAGULATION PRODUCTS
 Fresh Frozen Plasma
 Cryoprecipitate: Factor VIII, Fibrinogen
 Activated Products: Factor IX
 Chemistry Tests
 Liver Function Studies
 Renal Function
 Electrolytes—Na, K, Ca, Mg, Po4, Co2
 LIVER FUNCTION
Hepatocelluar Enzymes:
 AST (ASPARTATE AMINOTRANSFERASE)

 ALT (ALANINE AMINOTRANSFERASE)

 SGGT (very specific)

 LDH (Lactate Dehydrogenase)
 LIVER FUNCTION
ALKALINE PHOSPHATASE-AP not specific to liver
AP= LARGE COMPONENT IN BONE
BILIRUBIN -2 TYPES
DIRECT OR CONGUGATED AND INDIRECT OR
UNCONGUGATED.
 AP / BILIRUBIN the first enzymes to rise
with liver GVHD
 INDIRECT BILIRUBIN associated with
hemolysis
 LDH
 Nearly every type of cancer, as well as many other
diseases, can cause LDH levels to be ↑, cannot be used
to dx a particular type of cancer.
 LDH levels can be used to monitor treatment of some
cancers, including testicular cancer, Ewing's sarcoma,
non-Hodgkin's lymphoma, and some types of leukemia
 Elevated LDH levels can be caused by a number of
noncancerous conditions, including heart failure,
hypothyroidism, anemia, and lung or liver disease.
 RENAL
 BUN (BLOOD UREA NITROGEN)
Elevated with:
Kidney dysfunction, Dehydration, excess protein in
blood such as TPN, High protein diet, GI bleeding
 Creatinine: chemical waste is generated from
muscle metabolism. Creatinine is produced from
creatine, a molecule of major importance for energy
production in muscles. Creatinine is transported
through the bloodstream to the kidneys. The kidneys
filter out most of the creatinine and dispose of it in
the urine.
 CREATININE CONT.
 The ratio of BUN : creatinine determines renal dysfunction
VS pre-renal dysfunction such as dehydration.

 CALCULATED CREAT. CLEARANCE:

in ml/min---CRCL=(140-AGE) x ideal B.W./Scr. x 72 (x 0.85
for females)
 ELECTROLYTES
 SODIUM
 POTASSIUM
 CALCIUM
 PHOSPHORUS
 MAGNESIUM
 CO2
 SODIUM/POTASSIUM
 SODIUM
/POTASSIUM
MEMBRANE PUMP
 CALCIUM/PHOSPHORUS
 DIRECT
INTERACTION
 IF GIVEN
CONCOMBINETLY:
NaPO4 + CaCO3 =
 CALCIUM
 Calcium in plasma is bound to Albumin. If
Albumin is low, you get a falsely low serum
calcium.
 2 ways to get a more accurate Calcium:

IONIZED CALCIUM
CORRECTED CALCIUM
 CORRECTED Calcium:
[(4.0 – serum alb) x 0.8 ] + s Ca = corrected Ca
 MAGNESIUM
 Very important for Cardiac, Nervous and GI
systems.
 Interacts with calcium and Potassium.
 Difficult to get a Normal serum level of
Potassium if Mg is low.
 CO2
 Gives a rough idea of pH and buffer system in
blood
 Infections typically have low venous CO2
 Bone marrow Biopsy-aspirate
 Used in Identi. metastatic Dz, esp hematological
malignancies
 Assess iron stores
 Assess megaloblastic maturation, in Vit B12 and
folate deficiencies or in MDS
 Assess fat atrophy, aplasia or fibrosis
 Other tests done in Hem/Onc
 Fractionated bilirubin—to differentiate cause of
hyperbilirumia
 Stool guaiac--? bleeding
 Coombe’s test—direct/indirect
 Haptoglobin level—to detect hemolytic anemia
 Hgb electropheresis----
 MICROBIOLOGY
 BACTERIA
 VIRUS
 FUNGAL/YEAST
 PROTOZOAN
 BACTERIA
 CATAGORIZED BY SHAPE AND
STAINING PROPERTIES
 GRAM’S STAIN
 SHAPES ARE COCCI, RODS, AND
SPIROCHETES
 BACTERIAL SHAPES
 COCCI
 RODS
 SPIROCHETES
 GRAM’S STAIN
 INTERACTS WITH THE BACTERIAL
MEMBRANE AND STAINS IT EITHER BLUE OR
RED
 BLUE IS GM (+)
 RED IS GM (-)
 GRAM POSITIVE
 COCCI: 1. STAPHALOCOCCUS
EITHER COAGULASE (-) OR (+)
COAG NEG=STAPH EPID.
COAG POS= STAPH AUREUS

2. STREP, ENTEROCOCCUS
 RODS: BACILLUS, LISTERIA,
CORYNEBACTERIA DIPTHERIA
Staph aureus
 GRAM NEGATIVE
 COCCI: NEISSERIA, MORAXELLA,
ACINETOBACTER
 RODS: E.COLI, PSEUDOMONAS,
SHIGELLA, SALMONELLA, KLEBSIELLA,
PROTEUS, ENTEROBACTER, VIBRIO
Gram Negative rods
 FUNGUS
 MOLDS:
ASPERGILLUS ,
MUCOR,
 YEAST AND YEAST-
LIKE: CANDIDA,
TORULOPSIS,
HISTOPLASMOSIS,
CRYPTOCOCCUS,
BLASTO.
FUNGUS
 VIRUS
 CYTOMEGALOVIRUS
 EPSTEIN-BAR
 BK
 ADENOVIRUS
 INFLUENZA A & B
 PARAINFLUENZA
 RSV
 PNEUMOCYSTIS CARINII
 PREVIOUSLY
CONSIDERED A
PROTOZOAN BUT
NOW IN FUNGUS
CLASS
 References
 Demetri, G. (2001) Anemia and its functional consequences in cancer pts, current
challenges in management & prospects for improving therapy. British
Journal of Cancer,84,31-37
 Dessypris, E, Erythropoiesis (1988). Lee G R, Foster J, Lukens J, Wintrobe M M,
eds.Wintrobe’s clinical hematolology. Pa: Lippincott Williams & Williams 1998.
169-192.
 Ludwig H, & Strasser K.(2001) Symptomatology of anemia. Seminars in oncology, 28,
7-10
 Means, R. (1999). The anemias of chronic disorders. Lee GR, Foerster J, Lukens J,
Paraskeras F, Greer J P, Rodgers GM, eds. WIntrobe’s Clinical hematolgoy.10th
ed, Pa. Lippincott Williams & Wilkin;1999:1011-1021
 National Comprehensive Cancer Network (2007). Cancer and treatment related
anemias, version 3.2007
The End
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