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Altered HomeostasisAltered Blood Clotting

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Pulmonary embolism. Ischemic States. Hypocoagulation States. Excessive bleeding. Thrombocytopenia ... Therapies: Thrombosis/Embolism. Prevention. hydration ... – PowerPoint PPT presentation

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Title: Altered HomeostasisAltered Blood Clotting

1
Altered Homeostasis/Altered Blood Clotting
2
Homeostasis

Homeostasis is the regulation, formation,
retraction and dissolution of a clot.
Clot Formation/ Clot Lysing

3
Normal Clotting 3 Components

1. Vascular response
vasoconstriction, ? blood loss
2. Platelets
Sticky, Adhesive blood components
Platelet Aggregation
3. Plasma clotting factors
Always circulating
Become Active when stimulated/needed
Roman Numerals I-XII ( pg. 724 in text)

4
Homeostasis

A Balance between Procoagulation Factors and
Anticoagulation Factors
Keeps blood in a viscous, flowing state
Promotes Oxygen delivery to cells
Altered Homeostasis.
Too Much or Too Little
Inherited States Vs Acquired States of Altered
Homeostasis

5
Altered Coagulation.

Inherited
Hemophilia
von Willebrands disease
Acquired
D.V.T.
P.E.
Spontaneous Bleeding
DIC

6
Clotting Mechanisms

Happens along one of two Pathways, then to Common
pathway
Follows through a Cascade or Staged Process

7
Intrinsic Pathway

Within the Vessel
Begins with the rough surface created by a
ruptured vessel
Platelets adhere to the ruptured area
Platelets disintegrate and release their
coagulation factors into the plasma
CA is critical

8
Extrinsic Pathway

Cellular tissue outside the vessel
Tissue cell injury results in the release of
Thromboplastin, a coagulation factor
Thromboplastin , in the presence of CA reacts
with the clotting factorts to form the extrinsic
thromboplastin
Extrinsic thromboplastin and other factors are
necessary to convert prothrombin to thrombin

9
Clotting Studies
10
Disorders of Coagulation

Hypercoagulation States
Venous thromboembolism
Pulmonary embolism
Ischemic States
Hypocoagulation States
Excessive bleeding
Thrombocytopenia
Disseminated Intravascular Coagulation
( D.I.C.)

11
Hypercoagulation States

DVT, PE Most Common
At Risk Patients can be I. D., Treated
prophalactically
Advanced age
Prolonged immobility or paralysis
Prior venous thromboembolism
Cancer
Surgery
Obesity/Very Tall
Varicose veins
Known hypercoagulability disorder

12
Triad of Events (Virchows Triad)

Venous Stasis
Venous Endothelial injury
Hypercoagulability
Venous Stasis--Alteration of Blood Flow
Venous Endothelial Injury
--alteration in Platelet and coagulation factors

13
Venous Thromboembolism

Serious, sometimes fatal
Activated clotting factors and platelets
accumulate in vein cusps
A fibrin mesh is formed and occludes the vessel
Pulmonary Embolism can result

14
Thrombus Formation
15
Pulmonary Embolism

PE blocks pulmonary artery and chemically induces
arterial and bronchoconstriction
Lyses of these clots create secondary PEs
Symptoms can mimic MI with pain, respiratory
distress, impending doom, rapid, shallow
breathing, dysrhythmias
Can be life threatening 12 mortality rate
PEs most frequently happen down the line ,
Ex. 7-10 days Post Op

16
Related Physiological Concepts

Ischemia,
a condition in which
insufficient O2 is available to meet the
metabolic demands of the tissue involved
Heart, Brain, Mesenteric Artery

17
Clinical Therapies Thrombosis/Embolism

Prevention
hydration
positioning
foot dorsiflexion
compression devices
Treat underlying cause
Initiate anticoagulation therapy
Be aware of Risk Factors, Risk Timeline

18
Heparin

Interferes with conversion of prothrombin to
thrombin
Monitor APTT, Baseline-then want Therapeutic at
1.5-2.5 x Baseline
Antidote Protamine Sulfate
Adverse effects
hemorrhage thrombocytopenia, allergy
Short Term Therapy prevents further clotting
Lovenox - a low molecular weight heparin

19
Warfarin

AKA Coumadin
Oral therapy (P.O.)
Monitor PT, INR- therapeutic at 1.5-2.5 X
Baseline
More long term therapy, still designed to prevent
further clotting episodes
Alters synthesis of Vitamin K dependent
coagulation factors by the liver
Antidote
Vitamin K

20
Antiplatelets

Aspirin
blocks adhesion of platelets to exposed collagen
fibers
Dipyramidole ( persantine)
decreases platelet aggregation
Dextran 40
blocks coagulation factor activation
coats the surface of platelets
Plavix- new one

21
Thrombolytic Therapy

Clot Busters
Urokinase, streptokinase, TPA, TNK
Lyses clots
Contraindications
Risk hemorrhage

22
Bleeding Clinical Therapies

Prevention
Arrest cause
Replacement Fluids, Blood, Blood Components,
Iron supplements
Prevent tissue damage
Maintain body image
Labs Hct, Hgb, PT, APTT, Plt, electrolytes,
ABGS, FSP

23
ThrombocytopeniaNormal 150,000-400,000/mcl

Decreased Platelet Production
Increased Platelet Destruction
Abnormalities of Platelet function

24
Manifestations

Petechiae
Purpura Visual indicators, Skin Ecchymosis
Prolonged bleeding after routine procedures
Internal bleeding
Bleeding time prolonged

25
Nursing

Discourage OTC meds
Seek careepistaxis, petechiae, Assess for
changes
Acute Intervention
prevent and control hemorrhage
avoid SQ and IM injections
platelet administration
ITP
corticosteroids, high dose IV immunoglobulin,Splen
ectomyTransfusions

26
Disseminated Intravascular Coagulation (D.I.C.)

Results from abnormally initiated and accelerated
clotting at the capillary level
Subsequent decrease in clotting factors and
platelets which may lead to uncontrollable
hemorrhage
Always caused by an underlying disease
Labs Fibrin Split Products (FSP), D-Dimers
Life threatening

27
Disease States Associated With DIC