risk factors for ↓ plt

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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) - PowerPoint PPT Presentation

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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 CELLSWHITE BLOOD CELLS

Segmented Segmented Neutrophil (60%)Neutrophil (60%)

Lymphocytes(30%)Lymphocytes(30%) Monocytes(6%)Monocytes(6%) Eosinophils(3%)Eosinophils(3%) Basophils(1%)Basophils(1%)

SEGMENTED SEGMENTED NEUTROPHILNEUTROPHIL

11STST line of defense line of defense Normal 50-70%Normal 50-70% Survive 1-2 DAYSSurvive 1-2 DAYS

LYMPHOCYTESLYMPHOCYTES

2 Types by 2 Types by appearance: Large appearance: Large granular and smallgranular and small

Large granular are Large granular are NK cellsNK cells

Small are T & B cell Small are T & B cell T cell mediated T cell mediated

immunityimmunity B cell humoral B cell humoral

immunityimmunity

MONOCYTEMONOCYTE

5-10 % Circulating 5-10 % Circulating WBCsWBCs

When stimulated When stimulated become become Macrophages and Macrophages and dentritic cells in dentritic cells in the tissuethe tissue

Clean up the Clean up the debrisdebris

EOSINOPHILEOSINOPHIL

1-5% Circulating 1-5% Circulating WBCSWBCS

Involved in Involved in parasitic infectionsparasitic infections

Involved with Involved with mechanism mechanism associated with associated with allergy and asthmaallergy and asthma

↑↑In case of w.w.w.In case of w.w.w.

BASOPHILBASOPHIL

< 1% circulating < 1% circulating WBCSWBCS

Involved with Involved with allergic and allergic and inflammatory inflammatory responseresponse

Release histamines Release histamines and cytokinesand 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 PTTPT AND PTT

PT (PROTIME) Test the extrinsic PT (PROTIME) Test the extrinsic pathwaypathway

PTT Tests the intrinsic pathwayPTT Tests the intrinsic pathway COUMADIN (WARFARIN) Affects the COUMADIN (WARFARIN) Affects the

Vitamin K factors (II,VII,IX,X ) of which Vitamin K factors (II,VII,IX,X ) of which factor VII is the most labilefactor VII is the most labile

Hemophilia is a factor VIII deficiencyHemophilia is a factor VIII deficiency INR: Method for standardizing Protimes. INR: Method for standardizing Protimes.

It is a ration of tested results : controlIt is a ration of tested results : control

COAGULATION COAGULATION PRODUCTSPRODUCTS

Fresh Frozen PlasmaFresh Frozen Plasma Cryoprecipitate: Factor VIII, Cryoprecipitate: Factor VIII,

FibrinogenFibrinogen Activated Products: Factor IXActivated Products: Factor IX

Chemistry TestsChemistry Tests

Liver Function StudiesLiver Function Studies Renal FunctionRenal Function Electrolytes—Na, K, Ca, Mg, Po4, Electrolytes—Na, K, Ca, Mg, Po4,

Co2Co2

LIVER FUNCTIONLIVER FUNCTION

Hepatocelluar Enzymes: Hepatocelluar Enzymes: AST AST (ASPARTATE AMINOTRANSFERASE) (ASPARTATE AMINOTRANSFERASE)

ALTALT (ALANINE AMINOTRANSFERASE) (ALANINE AMINOTRANSFERASE)

SGGT (very specific) SGGT (very specific) LDH (Lactate Dehydrogenase)LDH (Lactate Dehydrogenase)

LIVER FUNCTIONLIVER FUNCTION

ALKALINE PHOSPHATASE-AP not specific to ALKALINE PHOSPHATASE-AP not specific to liverliver

AP= LARGE COMPONENT IN BONE AP= LARGE COMPONENT IN BONE

BILIRUBIN -2 TYPESBILIRUBIN -2 TYPES DIRECT OR CONGUGATED AND DIRECT OR CONGUGATED AND

INDIRECT OR INDIRECT OR UNCONGUGATED.UNCONGUGATED.

AP / BILIRUBIN the first enzymes AP / BILIRUBIN the first enzymes to rise with liver GVHDto rise with liver GVHD

INDIRECT BILIRUBIN associated INDIRECT BILIRUBIN associated with hemolysiswith 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.

RENALRENAL

BUN BUN (BLOOD UREA NITROGEN)(BLOOD UREA NITROGEN) Elevated with:Elevated with: Kidney Kidney dysfunction, Dehydration, excess protein in dysfunction, Dehydration, excess protein in blood such as TPN, High protein diet, GI blood such as TPN, High protein diet, GI bleedingbleeding

Creatinine: Creatinine: chemical waste is generated chemical waste is generated from muscle metabolism. Creatinine is from muscle metabolism. Creatinine is produced from creatine, a molecule of major produced from creatine, a molecule of major importance for energy production in importance for energy production in muscles. Creatinine is transported through muscles. Creatinine is transported through the bloodstream to the kidneys. The kidneys the bloodstream to the kidneys. The kidneys filter out most of the creatinine and dispose filter out most of the creatinine and dispose of it in the urine.of it in the urine.

CREATININE CREATININE CONT.CONT.

The ratio of BUN : creatinine determines The ratio of BUN : creatinine determines renal dysfunction VS pre-renal dysfunction renal dysfunction VS pre-renal dysfunction such as dehydrationsuch as dehydration. .

CALCULATED CREAT. CLEARANCE:CALCULATED CREAT. CLEARANCE:

in ml/min---CRCL=(140-AGE) x ideal B.W./Scr. in ml/min---CRCL=(140-AGE) x ideal B.W./Scr. x 72 (x 0.85 for females)x 72 (x 0.85 for females)

ELECTROLYTESELECTROLYTES

SODIUMSODIUM POTASSIUMPOTASSIUM CALCIUMCALCIUM PHOSPHORUSPHOSPHORUS MAGNESIUMMAGNESIUM CO2CO2

SODIUM/POTASSIUMSODIUM/POTASSIUM

SODIUM SODIUM /POTASSIUM /POTASSIUM MEMBRANE MEMBRANE PUMPPUMP

CALCIUM/PHOSPHORUSCALCIUM/PHOSPHORUS

DIRECT DIRECT INTERACTIONINTERACTION

IF GIVEN IF GIVEN CONCOMBINETLYCONCOMBINETLY:: NaPO4 + NaPO4 + CaCO3 =CaCO3 =

CALCIUMCALCIUM

Calcium in plasma is bound to Albumin. Calcium in plasma is bound to Albumin. If Albumin is low, you get a falsely low If Albumin is low, you get a falsely low serum calcium. serum calcium.

2 ways to get a more accurate Calcium: 2 ways to get a more accurate Calcium:

IONIZED CALCIUMIONIZED CALCIUM CORRECTED CALCIUMCORRECTED CALCIUM

CORRECTED Calcium: CORRECTED Calcium: [(4.0 – serum alb) x 0.8 ] + s Ca [(4.0 – serum alb) x 0.8 ] + s Ca = corrected Ca= corrected Ca

MAGNESIUM

Very important for Cardiac, Nervous Very important for Cardiac, Nervous and GI systems.and GI systems.

Interacts with calcium and Interacts with calcium and Potassium.Potassium.

Difficult to get a Normal serum level Difficult to get a Normal serum level of Potassium if Mg is low.of Potassium if Mg is low.

CO2CO2

Gives a rough idea of pH and buffer Gives a rough idea of pH and buffer system in bloodsystem in blood

Infections typically have low venous Infections typically have low venous CO2CO2

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----

MICROBIOLOGYMICROBIOLOGY

BACTERIABACTERIA VIRUSVIRUS FUNGAL/YEASTFUNGAL/YEAST PROTOZOANPROTOZOAN

BACTERIABACTERIA

CATAGORIZED BY SHAPE AND CATAGORIZED BY SHAPE AND STAINING PROPERTIESSTAINING PROPERTIES

GRAM’S STAINGRAM’S STAIN SHAPES ARE COCCI, RODS, AND SHAPES ARE COCCI, RODS, AND

SPIROCHETESSPIROCHETES

BACTERIAL SHAPESBACTERIAL SHAPES

COCCICOCCI RODSRODS SPIROCHETESSPIROCHETES

GRAM’S STAINGRAM’S STAIN INTERACTS WITH THE BACTERIAL INTERACTS WITH THE BACTERIAL

MEMBRANE AND STAINS IT EITHER MEMBRANE AND STAINS IT EITHER BLUE OR REDBLUE OR RED

BLUE IS GM (+)BLUE IS GM (+) RED IS GM (-)RED IS GM (-)

GRAM POSITIVEGRAM POSITIVE

COCCI: 1. STAPHALOCOCCUS COCCI: 1. STAPHALOCOCCUS EITHER COAGULASE (-) OR EITHER COAGULASE (-) OR

(+)(+) COAG NEG=STAPH COAG NEG=STAPH EPID.EPID. COAG POS= STAPH COAG POS= STAPH

AUREUSAUREUS

2. STREP, 2. STREP, ENTEROCOCCUSENTEROCOCCUS

RODS: BACILLUS, LISTERIA, RODS: BACILLUS, LISTERIA, CORYNEBACTERIA CORYNEBACTERIA

DIPTHERIADIPTHERIA

Staph aureusStaph aureus

GRAM NEGATIVEGRAM NEGATIVE

COCCI: NEISSERIA, MORAXELLA, COCCI: NEISSERIA, MORAXELLA, ACINETOBACTERACINETOBACTER

RODS: E.COLI, PSEUDOMONAS, RODS: E.COLI, PSEUDOMONAS, SHIGELLA, SALMONELLA, SHIGELLA, SALMONELLA, KLEBSIELLA, PROTEUS, KLEBSIELLA, PROTEUS, ENTEROBACTER, VIBRIOENTEROBACTER, VIBRIO

Gram Negative rodsGram Negative rods

FUNGUSFUNGUS

MOLDS: MOLDS: ASPERGILLUS , ASPERGILLUS , MUCOR, MUCOR,

YEAST AND YEAST-YEAST AND YEAST-LIKE: CANDIDA, LIKE: CANDIDA, TORULOPSIS, TORULOPSIS, HISTOPLASMOSIS, HISTOPLASMOSIS, CRYPTOCOCCUS, CRYPTOCOCCUS, BLASTO.BLASTO.

FUNGUSFUNGUS

VIRUSVIRUS

CYTOMEGALOVIRUSCYTOMEGALOVIRUS EPSTEIN-BAREPSTEIN-BAR BKBK ADENOVIRUSADENOVIRUS INFLUENZA A & BINFLUENZA A & B PARAINFLUENZAPARAINFLUENZA RSVRSV

PNEUMOCYSTIS PNEUMOCYSTIS CARINIICARINII

PREVIOUSLY PREVIOUSLY CONSIDERED A CONSIDERED A PROTOZOAN BUT PROTOZOAN BUT NOW IN FUNGUS NOW IN FUNGUS CLASSCLASS

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

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