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Hematology Donna  O’Niell Hematology Donna  O’Niell

Hematology Donna O’Niell - PowerPoint Presentation

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Hematology Donna O’Niell - PPT Presentation

RN Evy Warmbier MSN RN CNE Objectives To Identify the Basic Hematological Components To Understand the Clotting Cascade To Relate the Fibrinolytic Systems Regarding Medication Administration ID: 920994

hematology heparin patients anticoagulants heparin hematology anticoagulants patients platelet clotting asa blood platelets days normal 000 cells thrombocytopenia dose

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Slide1

Hematology

Donna O’Niell, RNEvy Warmbier, MSN, RN, CNE

Slide2

Objectives

To Identify the Basic Hematological ComponentsTo Understand the Clotting CascadeTo Relate the Fibrinolytic Systems Regarding Medication AdministrationTo compare this knowledge when caring for a patient with upper GI bleed.

Slide3

Three Basic Components of Hematology

The Bone Marrow

The Spleen

Slide4

Hematology Basics – 1. Bone Marrow

The bone marrow makes stem cells Myeloid stem cells produce Erythrocytes (red blood cells)

Thrombocytes (platelets)

Lymphoid stem cells produce

B & T cells for the immune system

Slide5

Hematology Basics – 2. Liver

The liver does many things including:Synthesis of AlbuminCoagulation factors

Removes nonfunctioning erythrocytes

Slide6

Hematology Basics – 3. Spleen

The spleen Removes damaged erythrocytes from the blood

Slide7

Hematological Homeostasis

Definition: The ability or tendency of an organism or cell to maintain internal equilibrium by adjusting its physiological processes.Example 1:

Erythropoetin

is released by the kidneys in states of hypoxemia which makes the bone marrow produce more erythrocytes to carry the oxygen to the tissue.

Example 2:

If a vessel is injured, platelets rush to the site to form a plug, then cytokines are released to stimulate the production of more platelets

Example 3:

Forming clots (the clotting cascade) & dissolving clots (thrombolytic effect)

Slide8

The Clotting Cascade

See handout for Blood Coagulation Factors

Slide9

The Clotting Cascade

Slide10

Hematology - Platelets

Definition: Platelets are the smallest of the three major types of blood cells. The principal function is to prevent bleeding.  Overview:

Normal count 150,000 - 350,000 per

microliter

of blood

8 to 10 day lifespan

10 % are consumed daily in normal body repairs

30% are stored in the spleen for injury

Starts the clotting process after injury

In ITP,

spleenomegaly

, up to 70% may be stored in the spleen

They contain proteins on their surface that allow them to stick to breaks in the blood vessel wall and also to stick to each other.

Slide11

Hematology – Platelet Inhibitors

Aggrenox : (ASA with extended release)Used in patients post TIA or ischemic CVAAspirin: inhibits platelet aggregation for the life of the platelet

Can be given chewable, regular or enteric coated

Given to patients with arterial or vascular diseases such as MI, CVA, post PCI, chronic angina, & peripheral vascular diseases

Can have non-responders to the ASA if taking enteric, switch to regular

Clopidogril

: (

plavix

), 75 mg

po

daily

Give 600 mg

p.o

. with the start of PCI

Normal platelet function returns in about 4 days

10 % of patients may not respond to

plavix

, may need to switch to

ticlid

Ticlopidine

: (

ticlid

), 250 mg bid

Can cause thrombocytopenia,

neutropenia

delayed onset,

Return to normal platelet within 7 days

Slide12

Hematology – Platelet Inhibitors

Eptifibatide: (intergrilin) IIb/

IIIa

inhibitor

Bolus with 180 mcg/kg IV and then 2 mcg/kg/min IV 12 to 24 hours

Lower dose by ½ in pts with

creatinine

> 2.0

Given with ASA, heparin prior to start of PCI

Give 12 to 24 hours for acute MI

Half life 2.5 hours

Abciximab

: (

reoPro

)

IIb

/

IIIa

inhibitor

Bolus with 0.25mg/kg IV,

then 0.125 mcg/kg/min for 12 hours

Can cause severe thrombocytopenia

Given with ASA and heparin prior to the start of PCI

Half life 10 min.

Slide13

Anticoagulants

Warfarin

Unfractionated

Heparin

Low Molecular Weight Heparin

Slide14

Anticoagulants –

Warfarin/Coumadin cont.

Action:

Inhibitor of Vitamin K which is essential to the hepatic synthesis of clotting factors II, VII, IX and X

Uses to prevent embolism in patients with:

Thrombophlebitis

Porcine heart valve

Mechanical heart valve

Atrial

fibrillation

Myocardial infarction

Slide15

Anticoagulants –

Warfarin/Coumadin cont. Contra-indications

Recent stroke, active internal bleeding

Recent

neuro

and eye or major surgery

Severe hypertension

Renal or hepatic insufficiency

Thrombocytopenia

Pregnancy

Intracranial tumor

Pericarditis

Recent spinal puncture

Dose to increase

prothrombin

time (PT)

Normal PT is 11 – 14 seconds

Desired dose PT 1.5 to 2.5 times normal

or INR = 2 - 3

Slide16

Anticoagulants –

Warfarin/Coumadin cont. Effects are Potentiated by

Drugs such as:

ASA,

Quinidine

, Sulfonamides, Chloral hydrate,

Amiodarone

,

Chloramphenicol

, antibiotics,

thrombolytics

Check the PDR

Physical conditions such as:

Carcinoma,

Vit

K deficiency, Scurvy, CHF, infectious hepatitis

Effects are Decreased by

Drugs such as:

Antacids, estrogen, oral contraceptives, thiazide diuretics, barbiturates, corticosteroids

Physical conditions such as:

Hypothyroidism, diabetes mellitus

Slide17

Anticoagulants –

Warfarin/Coumadin cont. Teach Patient

Periodic testing

2% of patients/year on Coumadin have GI bleeds

Have INR checked every 4 – 6 weeks

Report excessive anticoagulation

Severe nosebleed, headache, black/bloody stools, blood in urine, coughing up blood, easy bruising

Keep diet constant

Avoid foods high in vitamin K

Slide18

Anticoagulants – Unfractionated

Heparin

Make sure you have the correct concentration!

Slide19

Anticoagulants – Unfractionated

Heparin

Action

Inhibits conversion of

prothrombin

to thrombin

Inhibits

formed thrombin

Inhibits

the aggregation of platelets

Uses:

To treat or prevent

thromboembolism

for patients with:

ACS,

atrial

fibrillation, PE, DVT

To prevent

thromboembolism

in patients undergoing:

Reperfusion

treatment with

fibrinolytics

PCI or CABG

To diagnose and/or treat DIC

Slide20

Anticoagulants – Unfractionated

Heparin

Monitor

aPTT

:

Obtain baseline

aPTT

, normally it is 25 to 35 seconds

Dose is adjusted to increase the

aPTT

to 1.5 to 2 times the control (to 45 to 70 seconds)

Recheck

aPTT

q6 hours

IV Bolus

60 – 80 U/Kg (maximum is 100 units/

kg) or 5,000 U total

IV

Infusion

12

– 18 U / Kg / hr or 1250 U/hr

See PDR for

increase and decrease in infusion rate

Antidote:

Protamine

sulfate IV

1 mg

protamine

to neutralize 100 units heparin bolus

½ mg

protamine

to neutralize 100 units heparin

gtts

Slide21

Anticoagulants – Low Molecular Weight Heparin

Description:

Fractionated heparin that is 1/3 the size

Inhibits activated clotting factor X

Advantage:

More predictable anti-thrombin response and longer half-life

Does not affect

aPTT

. Lab monitoring not required

Less risk of HIT

More cost effective

Decrease dose for elderly

Disadvantages:

Reversal is difficult

Protamine

sulfate is not the best agent.

Heparinase

may be effective

Slide22

Anticoagulants – Low Molecular Weight Heparin

For DVTEnoxaparin

(

Lovenox

): 1 mg/kg SC bid

+ ASA 325 mg / d x 2 – 8 days.

Is the only FDA approved LMWH for DVT prophylaxis

For Unstable Angina / non Q wave AMI

Enoxaparin

1 mg/kg SC q 12 hrs

+ ASA 325 mg / d x 2 – 8 days

Or

Dalteparin

(

fragmin

): 120 IU / kg, not to exceed 10,000 IU Q 12 hr + ASA 75 – 165 mg / day for 5 – 8 days

Treat VTE

Lovenox

1

jmg

/ kg SC q 12 h; or 1l5 mg / kg SC daily.

Not to

exceet

180 mg

Antidote:

reversal is difficult as these meds have a long half-life

Protamine

1 mg IV per 1 mg of

lovenox

given will partially reverse, may add FFP

Slide23

Heparin-Induced Thrombocytopenia

HIT Type I:Most common, seen in up to 30 % of patients receiving heparin therapy

Seen within a few days after heparin started

Platelet depletion is moderate, 100,000/mm

3

Condition is transient, DC heparin not required

HIT Type 2:

Immune-mediated response

Seen in 3 to 5% of patients receiving

unfractionated

heparin

Also seen after exposure to LMWH

Severe thrombocytopenia, platelets down to 50,000/mm

3

Onset 5 to 14 days after exposure to heparin or within minutes after

rexposure

Mortality rate as high as 30%

Slide24

Heparin-Induced Thrombocytopenia

Pathophysiology

Formation of platelet antibody complexes (allergic reaction) which release factor 4 (PF4).

Activated platelet complexes stimulates the release of thrombin and therefore forms platelet clumps

Patients are at a greater risk of developing thrombosis rather than bleeding

. Leads to vessel occlusion ->

stroke, AMI, limb amputation, and even death.

Signs and Symptoms

Relates to where the vessel is occluded ->Cardiac, vascular, pulmonary, renal, gastrointestinal, neurologic

Nursing Management

Discontinue all heparin or

heparinized

products

Drugs:

Lepirudin

&

Argatroban

Educate patient to avoid another Heparin reaction

Slide25

The

Fibrinolytic SystemFibrin degradation products

Fibrinogen

Fibrin-clot

Plasmin

Plasminogen

T-PA

F

XIIa

HMWK

Kallikrein

Urokinase

Streptokinase

Clotting Cascade

Biomaterials Research

Manfred Mann

Slide26

Slide27

Bibliography/References

Thelan, Critical Care Nursing, 6th EditionLippincott Williams & Wilkins, Critical Care Challenges, __________ , High Acuity Nursing, _____

http://www.hematology.org/education/teach_case/

http://emedicine.medscape.com/hematology

www.manfred.maitz-online.de