BASIC HEMATOLOGY - VCU Massey Cancer Center

Download Report

Transcript BASIC HEMATOLOGY - VCU Massey Cancer Center

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 YEASTLIKE: 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
Shortcut to DSC03990.lnk