cardiology and hematology ppt
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Cardiology and Hematology PptTRANSCRIPT
OXYGENATIONOXYGENATION
CARDIOVASCULAR CARDIOVASCULAR AND HEMATOLOGIC AND HEMATOLOGIC
SYSTEMSYSTEM
TERMINOLOGIESTERMINOLOGIES
VENTILATIONVENTILATION – MOVEMENT OF AIR IN & OUT OF THE – MOVEMENT OF AIR IN & OUT OF THE LUNGSLUNGS
RESPIRATIONRESPIRATION – EXCHANGE OF GASES : EXTERNAL & – EXCHANGE OF GASES : EXTERNAL & INTERNALINTERNAL
EXTERNAL EXTERNAL –– BET. ALVEOLI & PULMONARY CAPILLARIES BET. ALVEOLI & PULMONARY CAPILLARIES
INTERNAL INTERNAL – – BET. SYSTEMIC CAPILLARIESBET. SYSTEMIC CAPILLARIES
PERFUSION PERFUSION – AVAILABILITY & MOVEMENT OF – AVAILABILITY & MOVEMENT OF CAPILLARY BLOOD FOR EXCHANGE OF GASESCAPILLARY BLOOD FOR EXCHANGE OF GASES
CASE STUDYCASE STUDY
You are the Emergency Room nurseYou are the Emergency Room nurse
A patient came in, 48 y.o.,A patient came in, 48 y.o.,dyspneicdyspneic, , with the following vital signs : T= with the following vital signs : T= 38C, RR=50, CR=105, BP=160/110 38C, RR=50, CR=105, BP=160/110 mmHgmmHg
CASE STUDYCASE STUDY
You noted that the patient is You noted that the patient is jaundiced, with bipedal edema, and jaundiced, with bipedal edema, and prefer to sit than lie down.prefer to sit than lie down.
What is your immediate nursing What is your immediate nursing action even without the doctor’s action even without the doctor’s order?order?
CASE STUDYCASE STUDY
What nursing history would you ask ?What nursing history would you ask ?
What other nursing assessment What other nursing assessment would you do?would you do?
What is your plan for the patient?What is your plan for the patient?
CARDIOVASCULAR SYSTEM CARDIOVASCULAR SYSTEM
• Review of Anatomy & Physiology• Assessment : History and Physical
Assessment•Diagnostics•Planning
REVIEW OF ANATOMY AND REVIEW OF ANATOMY AND PHYSIOLOGY- PHYSIOLOGY- HeartHeart
StructuresStructures
Blood Supply – LCA, RCA, veinsBlood Supply – LCA, RCA, veins
Conductive System –Sino-atrial node Conductive System –Sino-atrial node AV node Bundle of His AV node Bundle of His Bundle branch Purkinje fibers Bundle branch Purkinje fibers
HEARTHEART
RA
RV
LUNGS
LA
LV
SYSTEMICCIRCULATION
SYSTEMICCIRCULATION
LUNGS
SYSTEMICCIRCULATION
CONDUCTION PATHWAYCONDUCTION PATHWAY
RA LA
RV LV
- SA NODE
AV NODE-
BUNDLE OF HIS
BUNDLEBRANCH
PURKINJE
PURKINJE
REVIEW OF ANATOMY AND REVIEW OF ANATOMY AND PHYSIOLOGY- PHYSIOLOGY- HeartHeart
Nervous System ControlNervous System Control
– SYMPATHETICSYMPATHETIC
– PARASYMPATHETICPARASYMPATHETIC
REVIEW OF ANATOMY AND REVIEW OF ANATOMY AND PHYSIOLOGY- PHYSIOLOGY- HeartHeart
Properties of the Heart:Properties of the Heart:– All or None PrincipleAll or None Principle– RhythmicityRhythmicity– ExcitabilityExcitability– RefractorinessRefractoriness– ConductivityConductivity– AutomaticityAutomaticity– ExtensibilityExtensibility
REVIEW OF ANATOMY AND REVIEW OF ANATOMY AND PHYSIOLOGY- PHYSIOLOGY- HeartHeart
STROKE VOLUME (SV) - STROKE VOLUME (SV) - amount of blood amount of blood pumped out with each contractionpumped out with each contraction
HEART RATE (HR)HEART RATE (HR)CARDIAC OUTPUT (CO)– CARDIAC OUTPUT (CO)– volume of blood volume of blood
pumped out per minutepumped out per minute
=SV x HR =SV x HR
PRELOADPRELOAD
AFTERLOADAFTERLOAD
REVIEW OF ANATOMY AND REVIEW OF ANATOMY AND PHYSIOLOGY – Blood VesselsPHYSIOLOGY – Blood Vessels
ArteriesArteries MicrocirculationMicrocirculation VeinsVeins Flow RegulationFlow Regulation
– Pressure gradientPressure gradient– Flow resistanceFlow resistance
Role of Blood Role of Blood vesselsvessels
Layers of the Blood Layers of the Blood Vessels:Vessels:
IntimaIntima MediaMedia AdventitiaAdventitia
REVIEW OF ANATOMY AND REVIEW OF ANATOMY AND PHYSIOLOGYPHYSIOLOGY
CIRCULATIONCIRCULATION SYSTEMICSYSTEMIC
PULMONARYPULMONARY
PORTALPORTAL
PULMONARY CIRCULATIONPULMONARY CIRCULATION
RA
RV
LUNGS
LA
LV
SYSTEMICCIRCULATION
SYSTEMICCIRCULATION
LUNGS
SYSTEMICCIRCULATION
SYSTEMIC CIRCULATIONSYSTEMIC CIRCULATION
RA
RV
LUNGS
LA
LV
SYSTEMICCIRCULATION
SYSTEMICCIRCULATION
LUNGS
SYSTEMICCIRCULATION
HISTORY AND PHYSICAL HISTORY AND PHYSICAL EXAMEXAM
Check for: Check for: – dyspnea, dyspnea, – jaundice, jaundice, – edema, edema, – hemoptysis,hemoptysis,– fatigue,fatigue,– syncope and syncope and
fainting,fainting,– cyanosiscyanosis,,
– abdominal pain abdominal pain and discomfort, and discomfort,
– clubbing of clubbing of fingers, chest fingers, chest pain, pain,
– palpitationspalpitations
HISTORY AND PHYSICAL HISTORY AND PHYSICAL EXAMEXAM
Heart –I P P A Heart –I P P A – aortic area,aortic area,– pulmonic area,pulmonic area,– tricuspid, tricuspid, – mitralmitral
Heart SoundsHeart Sounds S1- AV valve S1- AV valve
closure closure S2 semilunar S2 semilunar
v. closure v. closure S3 vent. S3 vent.
Gallop Gallop S4 atrial gallopS4 atrial gallop MurmursMurmurs rubsrubs
HISTORY AND PHYSICAL HISTORY AND PHYSICAL EXAMEXAM
Blood vesselsBlood vessels– Inspection Inspection
color:pallor, rubor, cyanosiscolor:pallor, rubor, cyanosis circulation of extremitiescirculation of extremities
– Palpation Palpation edema, pulsesedema, pulses
– Auscultation Auscultation bruitbruit
Diagnostic AssessmentDiagnostic Assessment NonInvasive NonInvasive
ECGECG
Dynamic ECG Stress Dynamic ECG Stress Test Test
Treadmill VectorTreadmill Vector CardiogramCardiogram
Phonocardiogram Phonocardiogram
EchocardiogramEchocardiogram
Chest Xray Chest Xray
Radionuclide Radionuclide Studies Studies
Venography Venography
UTZ – DOPPLERUTZ – DOPPLER
PletysmographyPletysmography
Diagnostic AssessmentDiagnostic Assessment
InvasiveInvasive
Cardiac Cardiac CatheterizationCatheterization
ArteriogramArteriogram
AngiocardiogramAngiocardiogram
Venogram Venogram
Lymphogram Lymphogram
Bone Marrow Bone Marrow Aspiration:Aspiration:
– SternumSternum– iliac crestiliac crest– tibia (infantstibia (infants))
Diagnostic AssessmentDiagnostic Assessment Blood and Urine Blood and Urine
StudiesStudies– CBC CBC – Hematocrit Hematocrit – Clotting time Clotting time – PT PT – PTT PTT – APTT APTT – ESR ESR
– lipid profilelipid profile– serum enzymes: serum enzymes:
SGOT, SGPT, SGOT, SGPT, LDH, CPK LDH, CPK
– VMA VMA – Renin Test Renin Test – Schilling’s TestSchilling’s Test
HEMODYNAMICS HEMODYNAMICS MONITORINGMONITORING
CVP n= 6 -12 cm water CVP n= 6 -12 cm water – Measures:Measures:
cardiac efficiency,cardiac efficiency, bld volume,bld volume, peripheral resistance,peripheral resistance, right ventricular pressure right ventricular pressure
– 0-pt be at mid axillary line, 5 cm below 0-pt be at mid axillary line, 5 cm below the sternum the sternum
– dc ventilator with readingdc ventilator with reading– = fluid overload, = hypovolemia= fluid overload, = hypovolemia
HEMODYNAMICS HEMODYNAMICS MONITORING MONITORING
Pulmonary Artery and Pulmonary Pulmonary Artery and Pulmonary Wedge Pressure Wedge Pressure – Swan Ganz catheterSwan Ganz catheter : :– floated at the right heart, floated at the right heart, – measures left side of the heartmeasures left side of the heart
Intraarterial Blood PressureIntraarterial Blood Pressure : : – Radial Artery,Radial Artery,– Allen’s TestAllen’s Test
Planning for Health PromotionPlanning for Health Promotion
Modification of High Risk FactorsModification of High Risk Factors
Promotion of CirculationPromotion of Circulation
Prevention of Infection Prevention of Infection syphillis, syphillis, staph, strep, staph, strep, german measlesgerman measles
Genetic counsellingGenetic counselling
Role of nutritionRole of nutrition
Modification of High Risk Modification of High Risk FactorsFactors
dyslipedemiadyslipedemia
hypertension hypertension
smokingsmoking
sedentary sedentary lifestylelifestyle
obesityobesity
stress stress
glucose glucose intolerance,intolerance,
alcohol abusealcohol abuse
caffeinecaffeine pollutionpollution
Planning for Health Planning for Health Maintenance & Maintenance &
RestorationRestoration– Basic Life SupportBasic Life Support– Advanced Life SupportAdvanced Life Support
– Client With Client With Cardiac Surgery:Cardiac Surgery: Closed Heart surgeryClosed Heart surgery Open Heart SurgeryOpen Heart Surgery Heart TranspantHeart Transpant
Closed Heart Closed Heart surgerysurgery
– valvutomyvalvutomy
– mitral commisurotomymitral commisurotomy
Open Heart surgery (CABG)Open Heart surgery (CABG)
COMPLICATIONS COMPLICATIONS ::
DYSRHYTHMIASDYSRHYTHMIAS
THROMBOSIS THROMBOSIS AND PULMONARY AND PULMONARY EMBOLISMEMBOLISM
CARDIOGENIC CARDIOGENIC SHOCKSHOCK
BLEEDINGBLEEDING
WOUND INFECTIONWOUND INFECTION
RENAL FAILURERENAL FAILURE
ELECTROLYTE ELECTROLYTE IMBALANCEIMBALANCE
POST-OP POST-OP PSYCHOSISPSYCHOSIS
HEART TRANSPLANTHEART TRANSPLANTCRITERIACRITERIA
1. End Stage of Disease1. End Stage of Disease
2. Freedom from Chronic Disease2. Freedom from Chronic Disease
3. Family Support3. Family Support
4. Age < 50 yo4. Age < 50 yo
5. No psychological problem5. No psychological problem
IMPORTANTIMPORTANT1. Immunosuppressant & Steroids – 4 hrs prior1. Immunosuppressant & Steroids – 4 hrs prior
2. Donor-Recipient Compatibility – size, crossmatching2. Donor-Recipient Compatibility – size, crossmatching
3. Donor Heart – saline solution 4C up to 4 hrs3. Donor Heart – saline solution 4C up to 4 hrs
CARDIOVASCULAR CARDIOVASCULAR DISTURBANCESDISTURBANCES
CORONARY / ISCHEMIC HEART DISEASECORONARY / ISCHEMIC HEART DISEASE– Arteriosclerotic Heart DiseaseArteriosclerotic Heart Disease– Angina PectorisAngina Pectoris– Coronary InsufficiencyCoronary Insufficiency– Myocardial InfarctionMyocardial Infarction
CONGESTIVE HEART FAILURECONGESTIVE HEART FAILURE HYPERTENSIONHYPERTENSION PERIPHERAL VASCULAR DISEASEPERIPHERAL VASCULAR DISEASE DISORDERS OF THE BLOODDISORDERS OF THE BLOOD
ARTERIOSCLEROTIC HEART DISEASEARTERIOSCLEROTIC HEART DISEASE
Plaque formation and internal thickeningPlaque formation and internal thickening(intima)(intima)
Plaque formation and internal thickeningPlaque formation and internal thickening(intima)(intima)
Fibrosis and calcification (media)Fibrosis and calcification (media)Fibrosis and calcification (media)Fibrosis and calcification (media)
Narrowing and constriction of coronary arteriesNarrowing and constriction of coronary arteriesNarrowing and constriction of coronary arteriesNarrowing and constriction of coronary arteries
S/sx of ISCHEMIAS/sx of ISCHEMIAS/sx of ISCHEMIAS/sx of ISCHEMIA
ANGINA PECTORISANGINA PECTORIS
1. STABLE1. STABLE
2. UNSTABLE2. UNSTABLE
3. PRINZMETAL – coronary artery 3. PRINZMETAL – coronary artery spasm spasm
4. NOCTURNAL4. NOCTURNAL
5. DECUBITUS5. DECUBITUS
ISCHEMIA VS INFARCTIONISCHEMIA VS INFARCTION
ISCHEMIAISCHEMIA INFARCTIONINFARCTION
PAINPAIN SUBSTERNAL SUBSTERNAL PRESSURE/ PRESSURE/ HEAVINESSHEAVINESS
SQUEEZINGSQUEEZING
SUBSTERNALSUBSTERNAL
CONSTRICTIVE (+ SX CONSTRICTIVE (+ SX OF SHOCK)OF SHOCK)
DURATIONDURATION 3-5 MIN3-5 MIN > 5 MIN> 5 MIN
PRECIPITANTSPRECIPITANTS STRESS/ EXERTIONSTRESS/ EXERTION NONO
REST REST
NITROGLYCERINENITROGLYCERINERELIEVEDRELIEVED NOT RELIEVEDNOT RELIEVED
CARDIAC TISSUE CARDIAC TISSUE DAMAGEDAMAGE
NO PERMANENTNO PERMANENT PERMANENTPERMANENT
ANGINA PECTORISANGINA PECTORIS
DIAGNOSIS:DIAGNOSIS:Nitro Test 0.4mg Nitro Test 0.4mg
NURSING GOALS:NURSING GOALS:
1. 1. O2 to myocardiumO2 to myocardium
2. O2 demand2. O2 demand
3. Prevent future episodes of angina3. Prevent future episodes of angina
O2 to MyocardiumO2 to Myocardium::
AntiplateletsAntiplatelets
Calcium BlockersCalcium Blockers
Beta blockersBeta blockers
Whisky/BrandyWhisky/Brandy
Nitrates :Nitrates :RAPID-ACTING : RAPID-ACTING :
NitroglycerineNitroglycerine NitrostatNitrostat
AmylNitrateAmylNitrate
LONG-ACTING: LONG-ACTING: ISDN,ISMN,ISDN,ISMN,
Nitroglycerine Nitroglycerine ointment, ointment,
Transdermal, Transdermal, IVIV
O2 DemandO2 Demand
Limit activities – CBRLimit activities – CBR
Moderate ExerciseModerate Exercise
SedativesSedatives
WarmthWarmth
Prevent Future EpisodesPrevent Future Episodes DIET – low calorie, low saturated fatDIET – low calorie, low saturated fat
No tobaccoNo tobacco
Stress Reduction (Anger Stress Reduction (Anger Management)Management)
Coronary InsufficiencyCoronary Insufficiency
IMBALANCE BETWEEN :IMBALANCE BETWEEN :
OXYGEN SUPPLY OXYGEN SUPPLY
OXYGEN DEMANDOXYGEN DEMAND
MYOCARDIAL INFARCTIONMYOCARDIAL INFARCTIONIRREVERSIBLE CARDIAC DAMAGE FROM OCCLUSION OF 1 OR IRREVERSIBLE CARDIAC DAMAGE FROM OCCLUSION OF 1 OR MORE CORONARY ARTERYMORE CORONARY ARTERY
REVIEW OF ANATOMY AND PHYSIOLOGYREVIEW OF ANATOMY AND PHYSIOLOGY
E.C.G.E.C.G.Recent M.I. – ST elevation (injury)Recent M.I. – ST elevation (injury)
T wave inversion (ischemia)T wave inversion (ischemia)Previous M.I. – Q wave (necrosis / old infarct)Previous M.I. – Q wave (necrosis / old infarct)
BLOOD STUDIESBLOOD STUDIESTroponin T & ITroponin T & ILDHLDHCPK MBCPK MB
P Q
R
S
T
E.C.G.
P Q
R
ST
E.C.G.
ST SEGMENTELEVATION
P Q
R
S
T
E.C.G.
INVERTEDT - WAVE
P
Q
R
S
T
E.C.G.
Q wave
MYOCARDIAL INFARCTIONMYOCARDIAL INFARCTION
NURSING CARENURSING CARE1. Pain relief – 1. Pain relief –
Morphine ( + Morphine ( + preload & preload & afterload)afterload)
Demerol causes Demerol causes vomitingvomiting
2. Oxygen2. Oxygen
3. Inotropics3. Inotropics
4. Beta Blockers4. Beta Blockers
5. Antiarrhythmics5. Antiarrhythmics
6. No ice or very hot 6. No ice or very hot drinksdrinks
7. Anticoagulants7. Anticoagulants 8. ECG and CVP 8. ECG and CVP
monitoringmonitoring 9. Laxatives – 9. Laxatives –
LactuloseLactulose 10. PTCA10. PTCA 11. Thrombolytic 11. Thrombolytic
TherapyTherapyBEFORE CELLULAR BEFORE CELLULAR
DEATH, US. 6 HRS AFTER DEATH, US. 6 HRS AFTER THE ATTACKTHE ATTACK
CARDIAC ARRHYTHMIACARDIAC ARRHYTHMIA
Review Conduction PathwayReview Conduction Pathway
Review the Basics of Normal ECGReview the Basics of Normal ECG
CONDUCTION PATHWAYCONDUCTION PATHWAY
RA LA
RV LV
- SA NODE
AV NODE-
BUNDLE OF HIS
BUNDLEBRANCH
PURKINJE
PURKINJE
P Q
R
S
T
E.C.G.
CARDIAC ARRHYTHMIACARDIAC ARRHYTHMIA
Sinus Tachycardia – Sinus Tachycardia – P wave precede each P wave precede each QRS >100 bpmQRS >100 bpm
Sinus Bradycardia – Sinus Bradycardia – P wave precede each P wave precede each QRS <60 bpmQRS <60 bpm
Atrial Fibrillation: Atrial Fibrillation: P wave = f waves; QRS = P wave = f waves; QRS = normalnormal
P Q
R
S
T
E.C.G.
CONDUCTION PATHWAYCONDUCTION PATHWAY
RA LA
RV LV
- SA NODE
AV NODE-
BUNDLE OF HIS
BUNDLEBRANCH
PURKINJE
PURKINJE
CARDIAC ARRHYTHMIACARDIAC ARRHYTHMIA
Premature Ventricular Contraction: Premature Ventricular Contraction: P P wave normal: early QRSwave normal: early QRS
Ventricular Tachycardia : Ventricular Tachycardia : 3 or more PVCs3 or more PVCs
Asystole – Asystole – no cardiac activityno cardiac activity
P Q
R
S
T
E.C.G.
CONDUCTION PATHWAYCONDUCTION PATHWAY
RA LA
RV LV
- SA NODE
AV NODE-
BUNDLE OF HIS
BUNDLEBRANCH
PURKINJE
PURKINJE
CARDIAC ARRHYTHMIACARDIAC ARRHYTHMIA
Nursing ManagementNursing Management– OxygenOxygen– Complete Bed RestComplete Bed Rest– Cardioversion/ defibrillationCardioversion/ defibrillation– Administer antiarrhythmics as prescribed:Administer antiarrhythmics as prescribed:
AtropineAtropine Beta blocker- propanololBeta blocker- propanolol LidocaineLidocaine Epinephrine Epinephrine
CONGESTIVE HEART CONGESTIVE HEART FAILUREFAILURE Review of Anatomy and PhysiologyReview of Anatomy and Physiology
Backward Failure Backward Failure Forward FailureForward Failure Left-SidedLeft-Sided Right SidedRight Sided Hypermetabolic FailureHypermetabolic Failure Clinical Manifestations according to:Clinical Manifestations according to:
– Tissue AnoxiaTissue Anoxia– Pulmonary HypertensionPulmonary Hypertension– Systemic congestionSystemic congestion
C.H.F.C.H.F.
RA
RV
LUNGS
LA
LV
SYSTEMICCIRCULATION
SYSTEMICCIRCULATION
LUNGS
SYSTEMICCIRCULATION
LV
CONGESTIVE HEART CONGESTIVE HEART FAILUREFAILURE Review of Anatomy and PhysiologyReview of Anatomy and Physiology
Backward Failure Backward Failure Forward FailureForward Failure Left-SidedLeft-Sided Right SidedRight Sided Hypermetabolic FailureHypermetabolic Failure Clinical Manifestations according to:Clinical Manifestations according to:
– Tissue AnoxiaTissue Anoxia– Pulmonary HypertensionPulmonary Hypertension– Systemic congestionSystemic congestion
CONGESTIVE HEART CONGESTIVE HEART FAILUREFAILURE DiagnosticsDiagnostics
Nursing Management Nursing Management – Goals :Goals :
1.1. CARDIAC LOADCARDIAC LOAD – REST AND SEDATIONREST AND SEDATION
2. 2. CARDIAC CONTRACTILITYCARDIAC CONTRACTILITY– CHRONOTROPICS – CHRONOTROPICS – DIGITALIS DIGITALIS
– Increase in force of contraction Increase in force of contraction – monitor serum K, monitor serum K, – C/I if HR </= 60 bpm,C/I if HR </= 60 bpm,– DIGITALIS TOXICITYDIGITALIS TOXICITY
CONGESTIVE HEART CONGESTIVE HEART FAILUREFAILURE
3.3. SODIUM REABSORPTION AND FLUID SODIUM REABSORPTION AND FLUID RETENTION RETENTION
--DIURETICS ( Thiazide, Loop, K-sparing)DIURETICS ( Thiazide, Loop, K-sparing) -measure UO-measure UO
-weigh patient-weigh patient-watch for s/sx of electrolyte imbalance-watch for s/sx of electrolyte imbalance--DIET : DIET : Sodium Restricted (0.5gm/day)Sodium Restricted (0.5gm/day)
CONGESTIVE HEART CONGESTIVE HEART FAILUREFAILURE
4.4. PREVENTION OF COMPLICATIONS:PREVENTION OF COMPLICATIONS:– Intractable HFIntractable HF– Pulmonary edemaPulmonary edema– Pulmonary InfarctionPulmonary Infarction– Myocardial InfarctionMyocardial Infarction– Digitalis ToxicityDigitalis Toxicity– Cardiac ArrhythmiaCardiac Arrhythmia– PneumoniaPneumonia
PULMONARY EDEMAPULMONARY EDEMA Emergency!Emergency! Fluid into the alveoli, bronchi & Fluid into the alveoli, bronchi &
bronchiolesbronchioles
S/SX:S/SX: ……of CHFof CHF DyspneaDyspnea Cough with pink frothy sputumCough with pink frothy sputum
PULMONARY EDEMAPULMONARY EDEMA MANAGEMENT:MANAGEMENT:
– OxygenationOxygenation
– Assist in Intubation Assist in Intubation
– Rotating tourniquetRotating tourniquet
– PhlebotomyPhlebotomy
– CVP monitoringCVP monitoring
HYPERTENSIONHYPERTENSION
IN SYSTOLIC PRESSURE >140IN SYSTOLIC PRESSURE >140 IN DIASTOLIC PRESSURE > 90IN DIASTOLIC PRESSURE > 90
CLASSIFICATION : CLASSIFICATION : – PRIMARY PRIMARY
BENIGN- GRADUAL BENIGN- GRADUAL MALIGNANT -ABRUPT ONSET ;SHORT COURSE MALIGNANT -ABRUPT ONSET ;SHORT COURSE
– SECONDARY: SECONDARY: Renal patho, Adrenal patho, Renal patho, Adrenal patho, GeneticsGenetics
HYPERTENSIONHYPERTENSION
CATEGORYCATEGORY SBP mmHgSBP mmHg DBP mmHgDBP mmHg
NormalNormal <120 and<120 and <180<180
PreHPNPreHPN 120-139 or120-139 or 80-8980-89
HPN, Stage 1HPN, Stage 1 140-159 or140-159 or 90-9990-99
HPN, Stage 2HPN, Stage 2 >=160 or>=160 or >=100>=100
HYPERTENSIONHYPERTENSION Assess for Major CVD Risk FactorsAssess for Major CVD Risk Factors Assess for Identifiable Causes of Assess for Identifiable Causes of
Hypertension:Hypertension:– Sleep apneaSleep apnea– Drug-Induced relatedDrug-Induced related– Chronic Kidney DiseaseChronic Kidney Disease– Primary AldosteronismPrimary Aldosteronism– Renovascular DiseaseRenovascular Disease– Cushing’s Syndrome/steroid TherapyCushing’s Syndrome/steroid Therapy– PheochromocytomaPheochromocytoma– Coarctation of the AortaCoarctation of the Aorta
HYPERTENSIONHYPERTENSION
DiagnosticsDiagnostics Nursing Care : Nursing Care :
– Teach about: modification of Lifestyle, Teach about: modification of Lifestyle, diet, avoidance of stimulants and coffeediet, avoidance of stimulants and coffee
– Administer meds as prescribed: Administer meds as prescribed: ANTIHYPERTENSIVES AND DIURETICSANTIHYPERTENSIVES AND DIURETICS
– Hypertensive Crisis : Hypertensive Crisis : DIAZOXIDE (Hyperstat), DIAZOXIDE (Hyperstat), NaNITROPRUSSIDE (Nipride)NaNITROPRUSSIDE (Nipride)
PERIPHERAL VASCULAR PERIPHERAL VASCULAR DISEASEDISEASE
ISCHEMIA OF THE PERIPHERAL VESSELSISCHEMIA OF THE PERIPHERAL VESSELS Review of Peripheral Vascular Review of Peripheral Vascular
StructuresStructures Signs and Symptoms of IschemiaSigns and Symptoms of Ischemia
– ColdnessColdness– PallorPallor– RuborRubor– CyanosisCyanosis– Pain ( Intermittent Claudication)Pain ( Intermittent Claudication)
ISCHEMIA OF THE PERIPHERAL ISCHEMIA OF THE PERIPHERAL VESSELSVESSELS
Nursing ManagementNursing Management1.1. Increase Arterial Blood Flow or Increase Arterial Blood Flow or
Venous returnVenous return
2.2. Promote VasodilationPromote Vasodilation
3.3. Prevent and Treat Vascular Prevent and Treat Vascular OcclusionOcclusion
Increase Arterial Blood Flow Increase Arterial Blood Flow or Venous returnor Venous return
Proper positioningProper positioning
ExerciseExercise Short walksShort walks Buerger Allen Routine Buerger Allen Routine Oscillating BedOscillating Bed Circoelectric BedCircoelectric Bed
Buerger Allen RoutineBuerger Allen Routine
1. FEET UP , 3 MIN 1. FEET UP , 3 MIN
2. SIT ON BED & DO FOOT EXERCISE,3 MIN2. SIT ON BED & DO FOOT EXERCISE,3 MIN
3. LIE DOWN 5 MIN3. LIE DOWN 5 MIN
Increase Arterial Blood Flow Increase Arterial Blood Flow or Venous returnor Venous return
Patient educationPatient education
Decrease wieghtDecrease wieght
Avoid prolonged standingAvoid prolonged standing
Never wear constricting garmentsNever wear constricting garments
Never cross legsNever cross legs
Promote VasodilationPromote Vasodilation
– WarmthWarmth
– No nicotineNo nicotine
– Vasodilators : papaverine HCl, vasodilanVasodilators : papaverine HCl, vasodilan
– Moderate alcoholModerate alcohol
– sympathectomysympathectomy
Prevent and Treat Vascular Prevent and Treat Vascular OcclusionOcclusion
- - avoid prolonged bedrestavoid prolonged bedrest
-increase fluids-increase fluids
-proper positions-proper positions
-anticoagulant therapy & fibrinolytics-anticoagulant therapy & fibrinolyticsHeparin - Heparin - APTT- Protamine SO4APTT- Protamine SO4
Dicumarol- Dicumarol- PT - Vit KPT - Vit K
ARTERIAL DISEASEARTERIAL DISEASE ARTERIOSCLEROSIS OBLITERANSARTERIOSCLEROSIS OBLITERANS
– – LATE STAGE OF ATHEROSCLEROSIS WITH PARTIAL OR LATE STAGE OF ATHEROSCLEROSIS WITH PARTIAL OR COMPLETE OCCLUSION BY ATHEROMA WITH THROMBOSISCOMPLETE OCCLUSION BY ATHEROMA WITH THROMBOSIS
RAYNAUD’S DISEASE – RAYNAUD’S DISEASE – PERIODIC SPASM OF PERIODIC SPASM OF THE ARTERIESTHE ARTERIES
ANEURYSMS – ANEURYSMS – LOCALIZED OR DIFFUSED ARTERIAL LOCALIZED OR DIFFUSED ARTERIAL DILATIONDILATION
EMBOLUS/THROMBUSEMBOLUS/THROMBUS
VENOUS DISEASEVENOUS DISEASE THROMBOPHLEBITISTHROMBOPHLEBITIS – –
– INFLAMMATION OF THE VEIN WITH CLOT FORMATIONINFLAMMATION OF THE VEIN WITH CLOT FORMATION– HOMAN’S SIGNHOMAN’S SIGN
PHLEBOTHROMBOSISPHLEBOTHROMBOSIS– CLOTS WITHOUT INFLAMMATIONCLOTS WITHOUT INFLAMMATION
VARICOSE VEINSVARICOSE VEINS– TRENDELENBERG’S TEST – NORMAL VEIN FILLS FROM BELOWTRENDELENBERG’S TEST – NORMAL VEIN FILLS FROM BELOW
DISEASE OF ARTERIES AND DISEASE OF ARTERIES AND VEINSVEINS
BUERGER’S DSE / Thromboangitis BUERGER’S DSE / Thromboangitis ObliteransObliterans– RECURRING INFLAMMATION OF ARTERIES & VEINSRECURRING INFLAMMATION OF ARTERIES & VEINS– SMOKINGSMOKING– INTERMITTENT CLAUDICATIONINTERMITTENT CLAUDICATION
A-V FISTULAA-V FISTULA– ABN COMMUNICATION BETWEEN A. & V.ABN COMMUNICATION BETWEEN A. & V.– TRAUMATIC/ CONGENITALTRAUMATIC/ CONGENITAL– BRUITBRUIT
NURSING CARE OF PATIENTS NURSING CARE OF PATIENTS WITH AMPUTATIONWITH AMPUTATION
1.1. Control Bleeding – BandageControl Bleeding – Bandage
2.2. Prevent Edema – elevate 1Prevent Edema – elevate 1stst 24 hrs 24 hrs
3.3. Relieving Phantom Limb Pain – Relieving Phantom Limb Pain – hypnosis, destructionhypnosis, destruction
4.4. Assume Body Alignment – Prone 30 Assume Body Alignment – Prone 30 min 2x a day to prevent flexion min 2x a day to prevent flexion contracture ; AKA –contracture ; AKA –HIP FLEXION AND HIP FLEXION AND
ABDUCTION, EXTERNAL ROTATION ABDUCTION, EXTERNAL ROTATION BKA – BKA – KNEE KNEE FLEXIONFLEXION
NURSING CARE OF PATIENTS NURSING CARE OF PATIENTS WITH AMPUTATIONWITH AMPUTATION
Trochanter roll against the hip along Trochanter roll against the hip along the outer side to prevent outward the outer side to prevent outward rotation rotation
5.5. Preparing for LocomotionPreparing for Locomotion– Stump care : wash with soap and water Stump care : wash with soap and water
onlyonly– Exercise : quad setting, isometricExercise : quad setting, isometric– Crutch walking : weight- palms, stairs : Crutch walking : weight- palms, stairs :
GOOD LEG FIRST TO HEAVEN; BAD LEG FIRST TO HELLGOOD LEG FIRST TO HEAVEN; BAD LEG FIRST TO HELL
The acute nursing management of a The acute nursing management of a client with CHF will include all of the client with CHF will include all of the following goals following goals except:except:
a.a. Increase in cardiac outputIncrease in cardiac output
b.b. Elevation in renal blood flowElevation in renal blood flow
c.c. Reduction in the heart’s workloadReduction in the heart’s workload
d.d. Decrease in myocardial contractilityDecrease in myocardial contractility
REVIEW OF ANATOMY AND REVIEW OF ANATOMY AND PHYSIOLOGY – Blood and PHYSIOLOGY – Blood and
LymphaticsLymphatics Composition of the bloodComposition of the blood
RBC, WBC, Platelets, PlasmaRBC, WBC, Platelets, Plasma RBC RBC
normal erythropoeisis requires : normal erythropoeisis requires : pyridoxine, Vit B12, pyridoxine, Vit B12, folic acid, protein, copper, cobalt;folic acid, protein, copper, cobalt;
HEMOBGLOBIN : HEMOBGLOBIN : Iron; Oxygen transport; Acid-base Iron; Oxygen transport; Acid-base bufferbuffer
WBC WBC granulocytes –neutrophils, eosinophils, basophilsgranulocytes –neutrophils, eosinophils, basophils agaranulocytes –lymphocytes (T,B), monocytesagaranulocytes –lymphocytes (T,B), monocytes
Plasma Plasma albumin, water, clotting factors, antibodiesalbumin, water, clotting factors, antibodies
REVIEW OF ANATOMY AND REVIEW OF ANATOMY AND PHYSIOLOGY – Blood and PHYSIOLOGY – Blood and
LymphaticsLymphatics Role of the Bone MarrowRole of the Bone Marrow
– Production of all blood componentsProduction of all blood components Major Roles of the Blood Major Roles of the Blood
– homeostasis homeostasis – transport of nutrients and electrolytes transport of nutrients and electrolytes – distribute hormones and electrolytesdistribute hormones and electrolytes
Major Role of Lymphatics Major Role of Lymphatics – brings back blood to the circulation brings back blood to the circulation – immune antibody productionimmune antibody production
HEMATOLOGIC HEMATOLOGIC DISTURBANCESDISTURBANCES
DISORDERS OF THE BLOODDISORDERS OF THE BLOOD– RBCRBC : : IDA, PERNICIOUS ANEMIA, APLASTIC ANEMIA, IDA, PERNICIOUS ANEMIA, APLASTIC ANEMIA,
HEMOLYTIC ANEMIA, POLYCYTHEMIA VERAHEMOLYTIC ANEMIA, POLYCYTHEMIA VERA
– WBC and Plasma CellWBC and Plasma Cell : LEUKEMIA, MULTIPLE : LEUKEMIA, MULTIPLE MYELOMAMYELOMA
– Lymph Nodes and SpleenLymph Nodes and Spleen : : LYMPHOMA, LYMPHOMA, INFECTIOUS MONONUCLEOSIS, SPLENIC RUPTURE, INFECTIOUS MONONUCLEOSIS, SPLENIC RUPTURE, HYPERSPLENISMHYPERSPLENISM
– Hemorrhagic DisordersHemorrhagic Disorders : : PURPURA PURPURA
– Altered CoagulationAltered Coagulation : : HEMOPHILIA, HEMOPHILIA, HYPOPROTHROMBINEMIA, D.I.C.HYPOPROTHROMBINEMIA, D.I.C.
HEMATOLOGIC HEMATOLOGIC DISTURBANCESDISTURBANCES
RBCRBC : : IDAIDA PERNICIOUS ANEMIA PERNICIOUS ANEMIA APLASTIC ANEMIAAPLASTIC ANEMIA HEMOLYTIC ANEMIAHEMOLYTIC ANEMIA POLYCYTHEMIA VERAPOLYCYTHEMIA VERA
NUTRITIONAL ANEMIANUTRITIONAL ANEMIA
IRON DEFICIENCY ANEMIAIRON DEFICIENCY ANEMIA
PERNICIOUS ANEMIAPERNICIOUS ANEMIA
IRON DEFICIENCY ANEMIAIRON DEFICIENCY ANEMIA
Composition of the bloodComposition of the blood RBC, WBC, Platelets, PlasmaRBC, WBC, Platelets, Plasma
RBC RBC normal erythropoeisis requires : normal erythropoeisis requires : pyridoxine, Vit B12, pyridoxine, Vit B12,
folic acid, protein, copper, cobalt;folic acid, protein, copper, cobalt;
HEMOBGLOBIN : HEMOBGLOBIN : IRONIRON; Oxygen transport; ; Oxygen transport; Acid-base bufferAcid-base buffer
WBC WBC granulocytes –neutrophils, eosinophils, basophilsgranulocytes –neutrophils, eosinophils, basophils agaranulocytes –lymphocytes (T,B), monocytesagaranulocytes –lymphocytes (T,B), monocytes
Plasma Plasma albumin, water, clotting factors, antibodiesalbumin, water, clotting factors, antibodies
IRON DEFICIENCY ANEMIAIRON DEFICIENCY ANEMIA HEMOGLOBIN LEVEL FALLS BELOW NORMALHEMOGLOBIN LEVEL FALLS BELOW NORMAL
CAUSES:CAUSES:
1.1. Poor intake if iron rich foodsPoor intake if iron rich foods
2.2. Poor absorption & utilization of iron Poor absorption & utilization of iron from foodsfrom foods
3.3. Acute / chronic blood lossAcute / chronic blood loss
Poor intake if iron rich foodsPoor intake if iron rich foods
increased requirement : increased requirement : – infants after 6 mos, infants after 6 mos, – children & adolescents children & adolescents – women of reproductive age women of reproductive age – pregnant & nursing women pregnant & nursing women
Erroneous food practices Erroneous food practices Respiratory & GI conditions Respiratory & GI conditions Substandard living conditionSubstandard living condition
IRON DEFICIENCY ANEMIAIRON DEFICIENCY ANEMIA
CAUSES:CAUSES:
1.1. Poor intake if iron rich foodsPoor intake if iron rich foods
2.2. Poor absorption & utilization of iron Poor absorption & utilization of iron from foodsfrom foods
3.3. Acute / chronic blood lossAcute / chronic blood loss
Poor absorption & utilization of Poor absorption & utilization of iron from foodsiron from foods
Form of Iron- Form of Iron- hemosiderin: from animal foodhemosiderin: from animal food
more readily absorbed more readily absorbed than than from plants from plants (nonheme iron)(nonheme iron)
Effects of other foods Effects of other foods – inhibit absorption of iron:inhibit absorption of iron:
tea, unpolished rice, veges: bulaklak ng tea, unpolished rice, veges: bulaklak ng kalabasa, sampalok, mustasakalabasa, sampalok, mustasa
Poor absorption & utilization of Poor absorption & utilization of iron from foodsiron from foods
Host factors : Host factors :
– poor iron absorption in:poor iron absorption in: severe protein-energy malnutrition & severe protein-energy malnutrition &
repeated diarrhea repeated diarrhea Infections Infections Delibitating diseaseDelibitating disease
IRON DEFICIENCY ANEMIAIRON DEFICIENCY ANEMIA
CAUSES:CAUSES:
1.1. Poor intake if iron rich foodsPoor intake if iron rich foods
2.2. Poor absorption & utilization of iron Poor absorption & utilization of iron from foodsfrom foods
3.3. Acute / Chronic blood lossAcute / Chronic blood loss
Acute / Chronic blood lossAcute / Chronic blood loss
Acute hemorrhageAcute hemorrhage Chronic or repeated Blood loss:Chronic or repeated Blood loss:
– WHIPWORMWHIPWORM 0.005 ML OF BLOOD PER WORM PER DAY0.005 ML OF BLOOD PER WORM PER DAY
– HOOKWORMHOOKWORM 0.2 ML OF BLOOD PER WORM PER DAY0.2 ML OF BLOOD PER WORM PER DAY
– SCHISTOSOMIASISSCHISTOSOMIASIS– MALARIAMALARIA– PEPTIC ULCERPEPTIC ULCER– EXCESSIVE MENSTRUAL FLOWEXCESSIVE MENSTRUAL FLOW
IRON DEFICIENCY ANEMIAIRON DEFICIENCY ANEMIACLINICAL FEATURES:CLINICAL FEATURES: Asymptomatic Asymptomatic
– inability to respond to increased iron demandinability to respond to increased iron demand
Normal Hgb levels but with s/sx :Normal Hgb levels but with s/sx :– lack of energy, fatiguability, reduced power lack of energy, fatiguability, reduced power
and concentrationand concentration
Severe anemia : Severe anemia : – difficulty in breathing, difficulty in breathing, – palpitation, palpitation, – headache, headache, – faintness faintness – loss of appetiteloss of appetite
IRON DEFICIENCY ANEMIAIRON DEFICIENCY ANEMIA
ASSESSMENT:ASSESSMENT: Lab: Lab:
DECREASED HEMOGLOBIN & HEMATOCRIT DECREASED HEMOGLOBIN & HEMATOCRIT LEVELLEVEL
MICROCYTIC, HYPOCHROMIC RBCMICROCYTIC, HYPOCHROMIC RBCDECREASED RETICULOCYTE COUNTDECREASED RETICULOCYTE COUNT
Clinical MethodClinical MethodHISTORYHISTORYCLINICAL EXAMINATION - PALLORCLINICAL EXAMINATION - PALLOR
IRON DEFICIENCY ANEMIAIRON DEFICIENCY ANEMIA
TREATMENT:TREATMENT:
IRON ADMINISTRATION:IRON ADMINISTRATION: ORAL ORAL
– ADULT : 100-120 mg/day ADULT : 100-120 mg/day – INFANTS AND CHILDREN : 3mg/kg/dayINFANTS AND CHILDREN : 3mg/kg/day
PARENTERAL IRON DEXTRAN PARENTERAL IRON DEXTRAN – IM :IM :250 MG FOR EACH gm% LOWER THAN THE 250 MG FOR EACH gm% LOWER THAN THE
NORMAL VALUENORMAL VALUE
– IV: IV: 100-300 mg in 500ml SALINE SOLUTION100-300 mg in 500ml SALINE SOLUTION
ORAL IRON ORAL IRON ADMINISTRATIONADMINISTRATION
ABSORPTION :ABSORPTION : GREATEST DURING THE FIRST MONTH OF TX, GREATEST DURING THE FIRST MONTH OF TX,
AND DECREASES WHEN IRON STORES ARE INCREASINGAND DECREASES WHEN IRON STORES ARE INCREASING EMPTY STOMACH: EMPTY STOMACH: GOOD ABSORPTION, MORE G.I. S/EGOOD ABSORPTION, MORE G.I. S/E
ADMINISTER DURING OR PCADMINISTER DURING OR PC ASCORBIC ACID ASCORBIC ACID BETTER ABSORBED IN FERROUS BETTER ABSORBED IN FERROUS THAN IN FERRIC THAN IN FERRIC
FORMFORM FERROUS SULFATE FERROUS SULFATE IS THE CHEAPEST AND READILY IS THE CHEAPEST AND READILY
ABSORBABLE FORMABSORBABLE FORM DOSE: DOSE: CALCULATE THE ELEMENTAL IRONCALCULATE THE ELEMENTAL IRON
– FERROUS SULFATE HAS 36.74% ELEMENTAL IRONFERROUS SULFATE HAS 36.74% ELEMENTAL IRON
ORAL IRON ORAL IRON ADMINISTRATIONADMINISTRATION
DURATION:DURATION: 2 MOS, 2 MOS, ANEMIA IS ALREADY ALLEVIATEDANEMIA IS ALREADY ALLEVIATED
5 MOS, 5 MOS, FOR IRON STORESFOR IRON STORES
PREGNANT : PREGNANT : 2424THTH WK TO TERM WK TO TERM
SIDE EFFECTS:SIDE EFFECTS: CONSTIPATION/DIARRHEACONSTIPATION/DIARRHEA NAUSEANAUSEA EPIGASTRIC PAIN / HEART BURNEPIGASTRIC PAIN / HEART BURN
PARENTERAL IRON PARENTERAL IRON ADMINISTRATIONADMINISTRATION
INDICATIONS:INDICATIONS: SEVERE DEFICIENCYSEVERE DEFICIENCY ORAL PREPARATIONS FAILORAL PREPARATIONS FAIL CONDITION DO NOT PERMIT ORAL CONDITION DO NOT PERMIT ORAL
ADMINISTRATIONADMINISTRATION
ABSORPTION:ABSORPTION: RAPIDRAPID
THERAPEUTIC RESPONSETHERAPEUTIC RESPONSE SAME WITH ORALSAME WITH ORAL
PARENTERAL IRON PARENTERAL IRON ADMINISTRATIONADMINISTRATION
ADVANTAGE:ADVANTAGE: S/E ARE AVOIDEDS/E ARE AVOIDED PROBLEMS WITH ABSORPTION IS PROBLEMS WITH ABSORPTION IS
AVOIDEDAVOIDED
DISADVANTAGE:DISADVANTAGE: COSTLYCOSTLY TOXICITY IS POSSIBLETOXICITY IS POSSIBLE ALLERGIC REACTIONALLERGIC REACTION
PARENTERAL IRON PARENTERAL IRON ADMINISTRATIONADMINISTRATION
PRECAUTION:PRECAUTION: GIVEN UNDER CLOSE SUPERVISION GIVEN UNDER CLOSE SUPERVISION
BY PHYSICIANBY PHYSICIAN Z-TRACK METHOD Z-TRACK METHOD TISSUE STAINING & IRRITATIONTISSUE STAINING & IRRITATION
IRON TOXICITYIRON TOXICITY
VERY RARE IN ORALVERY RARE IN ORAL SIDEROSIS SIDEROSIS
– HEMOSIDERIN IN TISSUESHEMOSIDERIN IN TISSUES HEMOCHROMATOSIS HEMOCHROMATOSIS
– END POINT OF SIDEROSIS, END POINT OF SIDEROSIS, – DAMAGE TO LIVER AND PANCREASDAMAGE TO LIVER AND PANCREAS
PREVENTION: PREVENTION: – ADMIN IN DIVIDED DOSES ADMIN IN DIVIDED DOSES – KEEP OUT OF CHILDREN’S REACHKEEP OUT OF CHILDREN’S REACH
MEASURES TO MINIMIZE MEASURES TO MINIMIZE IRON REQUIREMENTSIRON REQUIREMENTS
PARASITE CONTROLPARASITE CONTROL– ADMINISTER MEDS FOR PARASITISMADMINISTER MEDS FOR PARASITISM– MINIMIZE RISK OF REINFESTATION:MINIMIZE RISK OF REINFESTATION:
REGULAR DEWORMING – EVERY 4-6 MOSREGULAR DEWORMING – EVERY 4-6 MOS FOOTWEARFOOTWEAR PROPER USE OF LATRINEPROPER USE OF LATRINE
FAMILY PLANNINGFAMILY PLANNING– DECREASE THE # OF PREGNANCIES AND DELIVERIESDECREASE THE # OF PREGNANCIES AND DELIVERIES– IUD – INCREASED MENSTRUAL LOSSESIUD – INCREASED MENSTRUAL LOSSES
POST-DELIVERY MEASURESPOST-DELIVERY MEASURES– LATCH ON – OXYTOCIN RELEASELATCH ON – OXYTOCIN RELEASE– CUT THE CORD AFTER PULSATION STOPSCUT THE CORD AFTER PULSATION STOPS
MEASURES TO DIRECTLY MEASURES TO DIRECTLY AUGMENT IRON STORESAUGMENT IRON STORES
SUPLEMENTATIONSUPLEMENTATION– PREGNANT 24 WKS TO TERMPREGNANT 24 WKS TO TERM– NURSING MOTHERSNURSING MOTHERS– MALNOURISHED INFANTS & MALNOURISHED INFANTS &
PRESCHOOLERSPRESCHOOLERS– PRETERM INFANTSPRETERM INFANTS
FORTIFICATIONFORTIFICATION
EDUCATIONEDUCATION
Burger King guest
PERNICIOUS ANEMIAPERNICIOUS ANEMIAREVIEW OF ANATOMY & PHYSIOLOGY : REVIEW OF ANATOMY & PHYSIOLOGY :
STOMACHSTOMACH Stores and mixes food with gastric juices & Stores and mixes food with gastric juices &
mucus producing chemical & mechanical mucus producing chemical & mechanical changes in the bolus of foodchanges in the bolus of food
Sphincters: cardiac and pyloricSphincters: cardiac and pyloric Divisions: fundus, body, antrumDivisions: fundus, body, antrum Secretions:Secretions:
– Pepsinogen : by chief cellsPepsinogen : by chief cells– HCl:HCl: by parietal cells by parietal cells
– Intrinsic factor : by parietal Intrinsic factor : by parietal cellscells
– mucoidmucoid
PERNICIOUS ANEMIAPERNICIOUS ANEMIA Composition of the bloodComposition of the blood
RBC, WBC, Platelets, PlasmaRBC, WBC, Platelets, Plasma
RBC RBC normal erythropoeisis requiresnormal erythropoeisis requires : : pyridoxine, pyridoxine,
Vitamin B12Vitamin B12, , folic acid, protein, copper, cobalt; folic acid, protein, copper, cobalt; HEMOBGLOBIN : Iron; Oxygen transport; Acid-base HEMOBGLOBIN : Iron; Oxygen transport; Acid-base
bufferbuffer WBC WBC
granulocytes –neutrophils, eosinophils, basophilsgranulocytes –neutrophils, eosinophils, basophils agaranulocytes –lymphocytes (T,B), monocytesagaranulocytes –lymphocytes (T,B), monocytes
Plasma Plasma albumin, water, clotting factors, antibodiesalbumin, water, clotting factors, antibodies
PERNICIOUS ANEMIAPERNICIOUS ANEMIANo INTRINSIC FACTORNo INTRINSIC FACTOR
VIT B 12 cannot be absorbedVIT B 12 cannot be absorbed
Alteration in DNA synthesis Alteration in DNA synthesis needed for cell divisionneeded for cell division
Delayed cellular division, altered nuclear pattern Delayed cellular division, altered nuclear pattern
MEGALOBLASTMEGALOBLAST
Ineffective erythropoeisisIneffective erythropoeisis : increased : increased serum bilirubin & urobilinogen excretionserum bilirubin & urobilinogen excretion
PERNICIOUS ANEMIAPERNICIOUS ANEMIA
OTHER TISSUES AFFECTED BY VIT B12 OTHER TISSUES AFFECTED BY VIT B12 DEFICIENCY:DEFICIENCY:
MOUTHMOUTH STOMACHSTOMACH VAGINAVAGINA MYELIN SHEATHMYELIN SHEATH
PERNICIOUS ANEMIAPERNICIOUS ANEMIAS/SX:S/SX: WEAKNESS, FATIGUE, PALLOR, WEAKNESS, FATIGUE, PALLOR,
JAUNDICEJAUNDICE SORE MOUTH, SMOOTH BEEFY SORE MOUTH, SMOOTH BEEFY
TONGUETONGUE ATROPHY OF THE GASTRIC MUCOSAATROPHY OF THE GASTRIC MUCOSA PERIPHERAL NERVE DEGENERATION : PERIPHERAL NERVE DEGENERATION :
TINGLING, NUMBNESS OF HANDS AND TINGLING, NUMBNESS OF HANDS AND FEETFEET
LOSS OF COORDINATION, LOSS OF COORDINATION, +ROMBERG’S+ROMBERG’S
PERNICIOUS ANEMIAPERNICIOUS ANEMIA
DIAGNOSIS:DIAGNOSIS:
PERIPHERAL SMEAR : PERIPHERAL SMEAR : MACROCYTIC MACROCYTIC CELLSCELLS
(+) ROMBERG’S(+) ROMBERG’S GASTRIC ANALYSIS GASTRIC ANALYSIS
– (diagnex blue test) – (diagnex blue test) – ACHLORHYDRIA from ACHLORHYDRIA from thinning of mucosa – HCl is also produced by thinning of mucosa – HCl is also produced by parietal cells of the stomachparietal cells of the stomach
SCHILLING’S TESTSCHILLING’S TEST – – B12 IN 24 HRS B12 IN 24 HRS URINE SPECURINE SPEC
SCHILLING’S TESTSCHILLING’S TEST DEFINITIVE TEST DEFINITIVE TEST FOR PERNICIOUS ANEMIAFOR PERNICIOUS ANEMIA
DETECT DETECT LACK OFLACK OF INTRINSIC FACTOR INTRINSIC FACTOR
MEASURES ABSORPTION MEASURES ABSORPTION OF OF RADIOACTIVE RADIOACTIVE VIT B12 VIT B12 BOTH BEFORE & AFTER PARENTERAL BOTH BEFORE & AFTER PARENTERAL
ADMINISTRATION OFADMINISTRATION OF INTRINSIC FACTOR INTRINSIC FACTOR
FASTINGFASTING CLIENT IS GIVEN CLIENT IS GIVEN RADIOACTIVE VIT RADIOACTIVE VIT B12 BY MOUTH AND NONRADIOACTIVE VIT B12 BY MOUTH AND NONRADIOACTIVE VIT B12 IMB12 IM
SCHILLING’S TESTSCHILLING’S TEST
24-48 HR URINE 24-48 HR URINE OBTAINED & TESTED FOROBTAINED & TESTED FOR VIT B 12VIT B 12
AFTERAFTER 1 WK, FASTING CLIENT IS GIVEN 1 WK, FASTING CLIENT IS GIVEN RADIOACTIVE VIT B 12 RADIOACTIVE VIT B 12 ORALLY WITH ORALLY WITH
PARENTERALPARENTERAL HUMAN INTRINSIC FACTOR HUMAN INTRINSIC FACTOR
URINE TEST URINE TEST IS REPEATEDIS REPEATED
PERNICIOUS ANEMIAPERNICIOUS ANEMIAMANAGEMENT:MANAGEMENT: NO CURE; NO CURE; VIT B12 IM FOR LIFEVIT B12 IM FOR LIFE
DIET: DIET: MEAT & DAIRYMEAT & DAIRY
HCL : HCL : – 11STST WK; WK; – DILUTE WITH WATER; DILUTE WITH WATER; – ADMINISTER WITH STRAWADMINISTER WITH STRAW
AVOID SEASONED FOODSAVOID SEASONED FOODS
PERNICIOUS ANEMIAPERNICIOUS ANEMIA
MANAGEMENT:MANAGEMENT:
MOUTH CARE: MOUTH CARE: SOFT TOOTHBRUSHSOFT TOOTHBRUSH
AVOID HEATING PADS – AVOID HEATING PADS – DECREASE IN DECREASE IN SENSATIONSENSATION
AFTER 2-3 DAYS TX, AFTER 2-3 DAYS TX, INCREASE IN INCREASE IN RETICULOCYTE COUNTRETICULOCYTE COUNT
REHAB & PT FOR NEURODEFICITSREHAB & PT FOR NEURODEFICITS
APLASTIC ANEMIAAPLASTIC ANEMIA
DEPRESSION OF ALL BLOOD FORMING ELEMENTS DEPRESSION OF ALL BLOOD FORMING ELEMENTS FROM BONE MARROW DESTRUCTIONFROM BONE MARROW DESTRUCTION
IDIOPATHIC IDIOPATHIC
SECONDARYSECONDARY
APLASTIC ANEMIAAPLASTIC ANEMIA
CAUSE:CAUSE:
ANTINEOPLASTIC DRUGS & RADIATIONANTINEOPLASTIC DRUGS & RADIATION IMMUNOSUPPRESIVE DRUGSIMMUNOSUPPRESIVE DRUGS CHLORAMPHENICOLCHLORAMPHENICOL SULFONAMIDESSULFONAMIDES TOXIC SUBSTANCES: TOXIC SUBSTANCES: BENZENE ,DDT, THIAZIDE, BENZENE ,DDT, THIAZIDE,
DIURETICS GOLDDIURETICS GOLD
APLASTIC ANEMIAAPLASTIC ANEMIA
ASSESSMENTASSESSMENT::
S/SX OF ANEMIAS/SX OF ANEMIA INCREASED SUSCEPTIBILITY TO INCREASED SUSCEPTIBILITY TO
INFECTIONINFECTION BLEEDING TENDENCIES & BLEEDING TENDENCIES &
HEMORRHAGEHEMORRHAGE
APLASTIC ANEMIAAPLASTIC ANEMIA
LAB:LAB: NORMOCYTIC ANEMIANORMOCYTIC ANEMIA GRANULOCYTOPENIAGRANULOCYTOPENIA THROMBOCYTOPENIATHROMBOCYTOPENIA
BONE MARROW BIOPSY:BONE MARROW BIOPSY: FATTYFATTY VERY FEW DEVELOPING CELLSVERY FEW DEVELOPING CELLS
HEMOLYTIC ANEMIAHEMOLYTIC ANEMIA EXCESSIVE RBC DESTRUCTIONEXCESSIVE RBC DESTRUCTION
CAUSES:CAUSES:
ACQUIREDACQUIRED– SNAKE VENOMSNAKE VENOM– BURNSBURNS– BT BT
INCOMPATIBILITYINCOMPATIBILITY– MALARIAMALARIA– TOXOPLASMOSISTOXOPLASMOSIS
CONGENITALCONGENITAL– HEREDITARY HEREDITARY
SPHEROCYTOSISSPHEROCYTOSIS– G6PD G6PD
DEFICIENCYDEFICIENCY– THALASSEMIATHALASSEMIA– SICKLE CELLSICKLE CELL
POLYCYTHEMIA POLYCYTHEMIA
INCREASE IN CIRCULATING BLOOD CELLS IN THE INCREASE IN CIRCULATING BLOOD CELLS IN THE BLOOD DUE TOBLOOD DUE TO BONE MARROW BONE MARROW OVERGROWTHOVERGROWTH
FORMS: FORMS: POLYCYTHEMIA VERA POLYCYTHEMIA VERA SECONDARY POLYCYTHEMIA SECONDARY POLYCYTHEMIA RELATIVE POLYCYTHEMIARELATIVE POLYCYTHEMIA
POLYCYTHEMIAPOLYCYTHEMIA
ASSESSMENTASSESSMENT:: RUDDY COMPLEXIONRUDDY COMPLEXION HYPERTENSIONHYPERTENSION SYMPTOMS OF CHFSYMPTOMS OF CHF THROMBUS FORMATIONTHROMBUS FORMATION BLEEDINGBLEEDING HEPATOSPLENOMEGALYHEPATOSPLENOMEGALY GOUTGOUT
PHLEBOTOMYPHLEBOTOMY
CLINICAL CARE OF PATIENTS CLINICAL CARE OF PATIENTS WITH ANEMIAWITH ANEMIA
RESTREST SKIN CARE SKIN CARE
– DECUBITUS ULCER FROM CELL HYPOXIADECUBITUS ULCER FROM CELL HYPOXIA DIET DIET
– 6 SMALL EASILY DIGESTIBLE MEALS6 SMALL EASILY DIGESTIBLE MEALS– NO HOT & SPICY FOODSNO HOT & SPICY FOODS
MOUTH CAREMOUTH CARE TRANSFUSION NOT A ROUTINETRANSFUSION NOT A ROUTINE OXYGENOXYGEN
CLINICAL CARE OF PATIENTS CLINICAL CARE OF PATIENTS WITH ANEMIAWITH ANEMIA
PROTECTION FROM INJURYPROTECTION FROM INJURY– BURNS and CHILLINGBURNS and CHILLING
ISLOLATION BY:ISLOLATION BY:– REVERSE ISOLATIONREVERSE ISOLATION– LIFE ISLAND- BED ENCLOSED IN PLASTIC LIFE ISLAND- BED ENCLOSED IN PLASTIC
CANOPYCANOPY– LAMIANR AIRFLOW LIMIT – UNIT WITH LAMIANR AIRFLOW LIMIT – UNIT WITH
MICROFILTERMICROFILTER
Don’t look at me…
HEMATOLOGIC HEMATOLOGIC DISTURBANCESDISTURBANCES
WBC and Plasma CellWBC and Plasma Cell ::
LEUKEMIALEUKEMIA
MULTIPLE MYELOMAMULTIPLE MYELOMA
LEUKEMIALEUKEMIA
FATAL NEOPLASTIC DISEASE THAT INVOLVES THEFATAL NEOPLASTIC DISEASE THAT INVOLVES THE BLOOD FORMING TISSUESBLOOD FORMING TISSUES OF THE: OF THE: – BONE MARROWBONE MARROW– SPLEEN SPLEEN – LYMPH NODESLYMPH NODES
UNCONTROLLED & DESTRUCTIVEUNCONTROLLED & DESTRUCTIVE PROLIFERATION PROLIFERATION OF ONE TYPE OF OF ONE TYPE OF WBCWBC & & ITS PRECURSORSITS PRECURSORS
LEUKEMIALEUKEMIA
INFILTRATE:INFILTRATE:– LIVERLIVER
– SKINSKIN
– KIDNEYS KIDNEYS
– LYMPH TISSUESLYMPH TISSUES
TYPES:TYPES:
MYELOGENOUSMYELOGENOUS
LYMPHOCYTICLYMPHOCYTIC
LEUKEMIALEUKEMIA
S/SX:S/SX:– ANEMIAANEMIA– THROMBOCYTOPENIATHROMBOCYTOPENIA– INFECTIONINFECTION– PETECHIAEPETECHIAE– HEPATOSPLENOMEGALY & LYMPH NODE HEPATOSPLENOMEGALY & LYMPH NODE
ENLARGEMENTENLARGEMENT– ARTHRALGIA & BONE PAIN ARTHRALGIA & BONE PAIN FROM FROM
EXPANSION OF BMEXPANSION OF BM
LEUKEMIALEUKEMIA
LAB:LAB: INCREASED WBCINCREASED WBC ANEMIAANEMIA THROMBOCYTOPENIATHROMBOCYTOPENIA INCREASE ALKALINE PHOSPHATASEINCREASE ALKALINE PHOSPHATASE
– OSTEOBLASTIC ACTIVITYOSTEOBLASTIC ACTIVITY
BONE MARROW BIOPSYBONE MARROW BIOPSY
LEUKEMIA – NURSING CARELEUKEMIA – NURSING CARE
PROVIDE ADEQUATE REST PROVIDE ADEQUATE REST INCREASED METABOLIC RATE FROM INCREASED METABOLIC RATE FROM OVERPRODUCTION OF LEUKOCYTESOVERPRODUCTION OF LEUKOCYTES
PAIN CONTROL PAIN CONTROL ASA, CODEINE, DEMEROLASA, CODEINE, DEMEROL
ADEQUATE FOOD & FLUID ADEQUATE FOOD & FLUID INTAKEINTAKE HIGH CALORIE DIET VITAMIN HIGH CALORIE DIET VITAMIN SUPPLEMENTS 3-4 L OF FLUID PER DAYSUPPLEMENTS 3-4 L OF FLUID PER DAY
LEUKEMIA – NURSING CARELEUKEMIA – NURSING CARE
MOUTH CARE MOUTH CARE H2O2 LEMON & GLYCERINEH2O2 LEMON & GLYCERINE
PREVENT INFECTION PREVENT INFECTION PROTECT PATIENT PROTECT PATIENT FROM HIS OWN FLORA – NEOMYCINFROM HIS OWN FLORA – NEOMYCIN
CHEMOTHERAPY CHEMOTHERAPY GOAL- INDUCTION OF COMPLETE REMISSION GOAL- INDUCTION OF COMPLETE REMISSION
TOLERABLE LEVEL OF TOXICITY – CRITERION FOR TOLERABLE LEVEL OF TOXICITY – CRITERION FOR LIMITATION OF INDUCTION PHASELIMITATION OF INDUCTION PHASE
MULTIPLE MYELOMAMULTIPLE MYELOMA MOST COMMON NEOPLASTIC DISORDER OF THE MOST COMMON NEOPLASTIC DISORDER OF THE
PLASMA CELLPLASMA CELL BONE MARROW MALIGNANCYBONE MARROW MALIGNANCY
REVIEW OF PLASMA CELL AND ITS REVIEW OF PLASMA CELL AND ITS PRODUCTSPRODUCTS
S/SX:S/SX:– BACK PAIN, BACK PAIN, – FATIGUE, WEIGHT LOSS,FATIGUE, WEIGHT LOSS,– OSTEOPOROSISOSTEOPOROSIS– HYPERCALCEMIAHYPERCALCEMIA
MULTIPLE MYELOMAMULTIPLE MYELOMA
LABS:LABS:– BLOOD: DECREASED WBC, HGB & PLATELET; BLOOD: DECREASED WBC, HGB & PLATELET;
INCREASED SERUM INMMUNEGLOBULINSINCREASED SERUM INMMUNEGLOBULINS
RADIOLOGYRADIOLOGY– DIFFUSE BONE LESIONSDIFFUSE BONE LESIONS
DIAGNOSIS: DIAGNOSIS: BENCE-JONES PROTEINBENCE-JONES PROTEIN GLOBULIN IN THE URINEGLOBULIN IN THE URINE
HEMATOLOGIC HEMATOLOGIC DISTURBANCESDISTURBANCES
Lymph Nodes and SpleenLymph Nodes and Spleen : :– LYMPHOMALYMPHOMA
– INFECTIOUS MONONUCLEOSISINFECTIOUS MONONUCLEOSIS
– SPLENIC RUPTURESPLENIC RUPTURE
– HYPERSPLENISMHYPERSPLENISM
LYMPHOMALYMPHOMA
HODGKIN’S & NON HODGKIN’S HODGKIN’S & NON HODGKIN’S DISEASE DISEASE
LYMPHOSARCOMALYMPHOSARCOMA
BURKITT’S LYMPHOMABURKITT’S LYMPHOMA
HODGKIN’S DISEASEHODGKIN’S DISEASE
MALIGNANT NEOPLASM OF THE LYMPHOID TISSUEMALIGNANT NEOPLASM OF THE LYMPHOID TISSUE
ENLARGEMENT OF THE LYMPH NODESENLARGEMENT OF THE LYMPH NODES
NIGHT SWEATSNIGHT SWEATS
BODY MALAISEBODY MALAISE
WEIGHT LOSSWEIGHT LOSS
REED-STERNBERG CELLS IN LYMPHNODE BIOPSYREED-STERNBERG CELLS IN LYMPHNODE BIOPSY
NONHODGKIN’S DISEASENONHODGKIN’S DISEASE
MALIGNANT NEOPLASM OF THE LYMPHOID TISSUEMALIGNANT NEOPLASM OF THE LYMPHOID TISSUE
ENLARGEMENT OF THE LYMPH NODESENLARGEMENT OF THE LYMPH NODES
MORE FATAL & DIFFICULT TO CONTROLMORE FATAL & DIFFICULT TO CONTROL
UNDIFFERENTIATED CELLS IN LYMPH NODE UNDIFFERENTIATED CELLS IN LYMPH NODE BIOPSYBIOPSY
INFECTIOUS INFECTIOUS MONONUCLEOSISMONONUCLEOSIS
AKAAKA: GLANDULAR / KISSING DSE: GLANDULAR / KISSING DSE
S/SX:S/SX: PAINFUL ENLARGEMENT - LYMPHNODESPAINFUL ENLARGEMENT - LYMPHNODES
LYMPHOCYTOSISLYMPHOCYTOSIS
FEVERFEVER
INFECTIOUS INFECTIOUS MONONUCLEOSISMONONUCLEOSIS
CAUSE:CAUSE: EPSTEIN-BARR VIRUS EPSTEIN-BARR VIRUS
CONTACT:CONTACT: KISSING KISSING
DIAGNOSISDIAGNOSIS: PAUL-BUNNEL : PAUL-BUNNEL HETEROPHIL HETEROPHIL TEST TEST
COMPLICATIONCOMPLICATION: SPLENIC RUPTURE: SPLENIC RUPTURE
SPLENECTOMYSPLENECTOMYINDICATIONS:INDICATIONS:
RUPTURERUPTURE OF THE SPLEEN OF THE SPLEEN FROM FROM TRAUMA, INFECTIOUS MONONUCLEOSISTRAUMA, INFECTIOUS MONONUCLEOSIS
HYPERSPLENISMHYPERSPLENISM – – EXCESSIVE SPLENIC EXCESSIVE SPLENIC DAMAGE OF CELLULAR BLOOD COMPONENTSDAMAGE OF CELLULAR BLOOD COMPONENTS
SPLENECTOMYSPLENECTOMY
NURSING CARE:NURSING CARE:
PREOP PREOP PNEUMOCOCCAL VACCINEPNEUMOCOCCAL VACCINE
POSTOPPOSTOP MONITOR FOR BLEEDING & SHOCKMONITOR FOR BLEEDING & SHOCK FEVER WITHOUT INFECTION IS COMMONFEVER WITHOUT INFECTION IS COMMON PROPHYLACTIC ANTIBIOTICPROPHYLACTIC ANTIBIOTIC
Hemorrhagic Disorders : Hemorrhagic Disorders : PURPURAPURPURA
EXTRAVASATION OF SMALL AMTS OF BLOOD INTO THE EXTRAVASATION OF SMALL AMTS OF BLOOD INTO THE TISSUES AND MUCUS MEMBRANETISSUES AND MUCUS MEMBRANE
VASCULAR PURPURAVASCULAR PURPURACAUSES : CAUSES :
1.1. HEREDITYHEREDITY2.2. ALLERGY (HENOCH-SCHONLEIN)ALLERGY (HENOCH-SCHONLEIN)3.3. DRUGS (TOXIC PURPURA)DRUGS (TOXIC PURPURA)4.4. POOR NUTRITIONPOOR NUTRITION5.5. INFECTIONINFECTION6.6. HPNHPN
THROMBOCYTOPENIC PURPURATHROMBOCYTOPENIC PURPURA
Disorders of Altered Disorders of Altered CoagulationCoagulation
– HEMOPHILIAHEMOPHILIA
– HYPOPROTHROMBINEMIAHYPOPROTHROMBINEMIA
– D.I.C.D.I.C.
HEMOPHILIAHEMOPHILIA
Deficit in one of the clotting factorsDeficit in one of the clotting factors
A A – Factor VIII – Factor VIII
BB- Factor IX - Factor IX
C-C- Factor XI Factor XI
HEMOPHILIAHEMOPHILIAS/SX:S/SX:– PROLONGED BLEEDING AFTER MINOR INJURY:PROLONGED BLEEDING AFTER MINOR INJURY:
CUTTING OF CORD CUTTING OF CORD CIRCUMCISION CIRCUMCISION IMMUNIZATIONIMMUNIZATION
– HEMARTHROSISHEMARTHROSIS– PERIPHERAL NEUROPATHY – PERIPHERAL NEUROPATHY – BLEEDING NEAR BLEEDING NEAR
PERIPHERAL PERIPHERAL NERVESNERVES
LAB:LAB:PROLONGED PTTPROLONGED PTTNORMAL PLT CTNORMAL PLT CTANEMIAANEMIA
HYPOPROTHROMBINEMIAHYPOPROTHROMBINEMIA
LIVER FAILURELIVER FAILURE
BLEEDING EPISODESBLEEDING EPISODES
VITAMIN KVITAMIN K
D.I.C.D.I.C.2 CONFLICTING SETS OF 2 CONFLICTING SETS OF
MANIFESTATIONS:MANIFESTATIONS:
DIFFUSE FIBRIN DEPOSITIONDIFFUSE FIBRIN DEPOSITION WITHIN WITHIN ARTERIOLES AND CAPILLARIES ARTERIOLES AND CAPILLARIES THROUGHOUT THE BODYTHROUGHOUT THE BODY
BLEEDINGBLEEDING INTO THE KIDNEYS, BRAIN, INTO THE KIDNEYS, BRAIN, ADRENAL, HEART AND OTHER ORGANSADRENAL, HEART AND OTHER ORGANS
D.I.C.D.I.C.
DIFFUSE FIBRIN DEPOSITION WIHIN DIFFUSE FIBRIN DEPOSITION WIHIN ARTERIOLES AND CAPILLARIESARTERIOLES AND CAPILLARIES
DIFFUSE FIBRIN DEPOSITION WIHIN DIFFUSE FIBRIN DEPOSITION WIHIN ARTERIOLES AND CAPILLARIESARTERIOLES AND CAPILLARIES
WIDESPREAD CLOTTINGWIDESPREAD CLOTTINGWIDESPREAD CLOTTINGWIDESPREAD CLOTTING
DEPLETION OF CLOTTING FACTORSDEPLETION OF CLOTTING FACTORSDEPLETION OF CLOTTING FACTORSDEPLETION OF CLOTTING FACTORS
D.I.C.D.I.C.
CAUSE:CAUSE: UNKNOWNUNKNOWN CRITICAL ILLNESS:CRITICAL ILLNESS:
– TOXEMIA OF TOXEMIA OF PREGNANCYPREGNANCY
– CANCERCANCER– SURGICAL SURGICAL
PROBLEMSPROBLEMS– HEMOLYTIC DSEHEMOLYTIC DSE
ASSESMENT:ASSESMENT: PETECHIAE, PETECHIAE,
ECCHYMOSISECCHYMOSIS PROLONGED BLEEDINGPROLONGED BLEEDING ARFARF CONVULSIONSCONVULSIONS COMACOMA
LAB:LAB: FIBRIN SPLIT FIBRIN SPLIT
PRODUCTSPRODUCTS
A.I.D.S.A.I.D.S.
Severe deficit in cellular immune functionsSevere deficit in cellular immune functions HIV virus- infects T helper cellsHIV virus- infects T helper cells Transmission Transmission Antiretroviral drugsAntiretroviral drugs Assessment:Assessment:
– Flulike s/sxFlulike s/sx– Hypoxemia from pulm infectionHypoxemia from pulm infection– Progressive weight loss Progressive weight loss – Temp elevations; night sweatsTemp elevations; night sweats– Neurologic dyfxnNeurologic dyfxn– Opportunistic infectionsOpportunistic infections
•Laboratory :
•ELISA•Western Blot•Anemia•Leukopenia•thrombocytopenia
A.I.D.S.A.I.D.S.
NURSING INTERVENTION:NURSING INTERVENTION: Administer medsAdminister meds Monitor resp, neurologic, F & E balanceMonitor resp, neurologic, F & E balance Monitor nutritional intakeMonitor nutritional intake Inspect oral cavity for ulcerationsInspect oral cavity for ulcerations Observe s/sx of infectionObserve s/sx of infection Severe leukopenia – neutropenic Severe leukopenia – neutropenic
precautionprecaution Blood & body fluid precautionBlood & body fluid precaution Emotional supportEmotional support
The nurse should understand that a The nurse should understand that a heparin order for a client with DIC is heparin order for a client with DIC is given to:given to:
a.a. Prevent clot formationPrevent clot formation
b.b. Increase blood flow to target organsIncrease blood flow to target organs
c.c. Increase clot formationIncrease clot formation
d.d. Decrease blood flow to target Decrease blood flow to target organsorgans