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Layer of the Heart:
Endocardium ( inner ) - facilitates blood flow,
contains valve & chambers
Myocardium ( middle ) - contracting muscle,
cardiac muscle
Pericardium ( outer )
o Layer of Pericardium

Visceral ( epicardium )

Pericardial ( 5-20cc of
fluid ) serves as cushion,



AV valves ( atrioventricular valves ) “Atria”
o 1 way flow of blood

Tricuspids ( right atria )

Bicuspids/ Mitral ( left
atria )
SL valves ( semilunar valves )

Pulmonary SL valve

Aortic SL valve
Ventricle contract : Semi Lunar valve open
( AV valve closed )
Ventricle relax : Semi Lunar valve closed ( blood filling )
( Av valve open )













Valves & Chambers:

Bundle of HIS

Intranodal tract

AV node

Bundle branches
Right Purkinje
Left Purkinje

Cardiac Cycle
Two main phase
o Systole : contraction / ejection
o Diastole : relaxation / refill

Difference between
Systolic & Diastolic is
( PP: 30 – 40cpm ) narrowed pulse – hypovolemia
( PP: 60cpm ) wided pulse – increased in Stroke volume

Fibrous layer


SA node

Coronary Artery



Conduction System
SA node ( sinoatrial node ) main pacemaker
of the heart : 60 – 100bpm
AV node ( atrioventricular node ) 2nd
pacemaker of the heart : 40 – 60bpm
Bachmann’s node ( node in the left atrium )

Branch out from ascending aorta
Right Coronary Artery – supplying the Right
Atrium / Right Ventricle / inferior portion of Left
Left Coronary Artery
o Circumflex – supplying the Left
Atrium / posterior portion of Left
o Left Anterior Descending Artery
(LADA) – supplying the Left
Ventricle /Apex
Electrophysiologic Properties
A – utomacity –
C – ontractility – transmit impulse
C – onductivity – contraction
E – xcitability – respond to stimuli
R – efractiones – ability to finish a response
before initiating another response.

Cardiac Output
Amount of blood pump by the heart
particularly by the left ventricle per minute
Stroke Volume (SV) – amount of blood pump by the
heart in every beat
amt (ml)
Contractility : ( Inotropic ) ability of cardiac
muscle to contract
Preload : amount of the blood from the
ventricle after the end of diastolic phase
(Frank Staring Law : the greater the stretch,
the better the pump)
o Venous returns
o Regurgitation of the blood
Afterload : resistance of LV must surpass as
the heart pump blood to the circulation
o Systemic resistance ( HPN )
o Blood viscosity ( DM. polycythemia
vera, multiple myeloma )
Heart Rate ( HR ) – number of heart beat per minute

Formula: Cardiac Output

amt (ml)



Autonomic Response
Symphatetic Nervous System ( SNS )
( Fight or Flight Response )
o Norepinephrine (adrenal gland)
o Dilated pupils(compensate)
o Constricted blood vessel
o Increased SV/HR
Parasymphathetic Nervous System ( PNS )
o Rest & Digest Response
o Pressure detectors ( common
carotid, right atrium, aortic arc )
o Chemical detectors ( O2, CO2, pH )
o Aortic arc, carotid bodies
o CO2 : 35 – 35mmHg ( normal )
volatile gas
o O2 : 80 – 100mmHg ( normal )
o CO2 + H2O = H2CO3 (carbonic acid )
increased pH level
o Stretch detectors ( tendons )
Electrocardiograph ( ECG )


Vertical : impulse
Horizontal : duration
Small box : 1mm/.04sec
Big box : 5mm / .2sec
Isoelectric line : straight/ middle line


Deflection : raise & falls of line ( wave )
Wave : line deviated from isoelectric line
( P wave )
Complex : group of continuous waves
( QRS complex )
Segment : isoelectric line between waves
( ST segment )
Interval : wave + segment ( PR interval )
P wave – atrial depolarization
PR segment – conduction delay from SA node – AV
QRS complex – ventricular depolarization
ST segment – early ventricular repolarization
PR – atrial depolarization + conduction delay of
SA node – AV node
T wave – ventricular repolarization
U wave – unknown

Assess for allergy ( seafoods : iodine/contrast
dye )
Assess for bleeding parameters
Assess for kidney function
Administer pre medication as ordered
Patient usually sedated ( valium )
CBR / monitor V/S
Prevent bleeding
Immobilized affected extremities
Do circulation assessment
Angiography / Arteriography
is a test that uses an injection of a liquid dye
to make the arteries easily visible on X-rays
Laboratories ( cardiovascular function )
Blood component

Electrode Placement
Right arm – white / Right leg - green
Left arm – black / Left leg – red
Chest Electrode Placement
1st Node – 4th ICS right of sternum
2nd Node – 4th ICS left of sternum
3rd Node – between the 2nd & 4th node
4th Node – 5th ICS left
5th Node – 6th ICS left
6th Node – axillary line
Holters Monitoring ( activity diary )
Stress Testing ( threadmill test )
Detection of level of activity
o Ischemic heart disease
o Chest pain
o Evaluate effectiveness of activity
o Develop cardiac rehab.program
Ultrasound of the heart
Supine position: HOB elevated 15 – 20 degree
Slightly turned to the left side
Chest Xray
Magnetic Resonance Imaging ( MRI )
The MRI scan uses magnetic and radio waves,
meaning that there is no exposure to X-rays
or any other damaging forms of radiation.
Cardiac Fluoroscopy
Cardiac Catherization
Introduction of radiopaque venous catheter
o Right radial / antecubital
o Left brachial / femoral

WBC ( leukocytes )
Platelets (thrombocytes )


Normal value ( mm )
4-6 million
150,0000- 450,000

Erythrocyte Sedimentation Rate ( ESR )
It is a common hematology test that is a nonspecific measure of inflammation
Male : < 15 – 20mm/hr
Female : < 25 – 30mm/hr
Blood Urea Nitrogen ( BUN )
10 – 20mg/dl ( normal )
Easily affected by hydration status
Blood Lipids
NPO ( 10 – 12hrs )
Serum cholesterol: < 200mg/dl
Triglycerides : 100 – 200mg/dl
Auscultation : ( Heart Sound )
S1 – apex – lubb – closure of AV valve (
contracting / ejecting ) systole phase
S2 – base – dub – closure of SL valve (
relaxation / refill ) diastole phase
S3 – above 30y.o – ventricular gallop ( rapid
ventricular refill )
S4 – atrial gallop ( resistance to ventricular
refill )
o Summation gallop ( S1, S2, S3, S4 )
Aortic – 2 ICS right sternum
Pulmonic – 2nd ICS left sternum
Mitral – 5 ICS midclavicular line
Tricuspid – 5 ICS left sternum

Diaphragm – hi pitch ( heart, lung ,
abdominal sound )
Bell – low pitch


Decubitus Angina : ( occurs when ever
standing or lying )
Silence Ischemia : ( no manifestation but
appear in laboratory test )


Paroxysm chest pain ( myocardial ischemia )
Pathogenesis: imbalanced in demand ( cardiac output )
& supply ( myocardial tissue perfusion )
Precipitating Factor:
Coronary Atherosclerosis – narrowing of
artery ( fatty deposit )
Coronary Thrombosis / Embolism
Hypertension ( HPN ) – increased in afterload
Decreased blood flow with shcok
Direct Trauma
Polycythemia Vera
Coronary Artery Spasm
Physical Exertion
Environment / Extreme Weather
Digestion Every Meal
Eating a heavy meal
Valsalva Maneuver
Emotion Stress
Sexual Excitation
Hot Bath or Shower
Types of Angina Pectoris
Stable / Exertional Angina : predictable
Unstable Angina : unpredictable (
Intermittent Coronary Syndrome )
Variant Angina : “ Prinzmetal” (even at rest)
Intractable Angina : chronic ( resistant to
medication / treatment )
Post Infarction Angina : ( myocardial
infarction )
Intractable Angina : ( more responsive to
medication )
Nocturnal Angina : ( occurs when sleeping )


Pain ( lactic acidosis )
o Substernal, crushing or squeezing
o Radiate from neck to arms up to
o Unaffected by inspiration /
Palpitation / Tachycardia
Dizziness / Faintness

DX test:
ECG, Stress Test, cardiac Catheterization,
Cardiac Enzymes
CBR ( decreased demand )
Lifestyle modification
o Nitrates ( nitroglycerine )
vasodialtion of coronary artery :
decreased demand & afterload (
heart ) : 3 – 6 months
o Calcium Channel Blocker ( VAND )
Verapamil, Anlodipine, Nicardipine,

calcium – innervating
muscular movement
o Antilipidemic – “statin” : prevent
o Beta Adrenergic Blockers “olol”
o Antiplatelet : ( ASA ) Acethy
Salicylic Acid
o Anticouagulant : Heparine
PTCA ( Percutaneous Transluminal Coronary
Angioplasty )
Vascular Stent
Laser Angioplasty
CABG ( Coronary Artery Bypass Graft )
Heart attack : formation of localized necrotic
areas in the myocardium

Risk factor:
CAD ( Coronary Artery Disease )
Elevated cholesterol level
Smoking ( damage the endothelium:
vasospasm ) nicotine
HPN, DM, stress ( increased the workload /
afterload )
Classification of MI
Transmural Infarct : starts in the myocardium
going to pericardium & endocardium
Sub endocardial Infarct : starts in the
myocardium going to endocardium
Intramural Infarct : isolated / patchy &
localized myocardium death
3 areas developed ( after MI )
Area of Infarction : O2 totally deprived (
damage is irreversible ) Q wave pathologic
Area of Injury : damage is reversible ( cell is
viable as long as collateral circulation is
present ) ST segment elevation
Area of Ischemia : blood circulation is only
reduced ( most of the time it is not damage )
T wave inverted
Prolonged pain ( > 3o min )
Unrelieved by Nitroglycerin
Crushing Severe Radiating Pain
Levines Sign
Anxiety / apprehension ( increased
restlessness )
Feeling of Doom
Pallor, Cyanosis, coolness of extremities
Mild fever ( hard to assess ), dyspnea,
Nausea & vomiting ( nasovagal stimuli )
Syncope ( sudden loss of consciousness )

.2 .35 . nausea & vomiting. o Peripheral edema o Hepatomegaly o Spleenomegaly. ( stimulate vagal response / bradycardia ) CONGESTIVE HEART FAILURE Inability of heart to maintain cardiac output Cause by impaired pumping activity Classification Types of CHF R-sided CHF L-sided CHF Forward failure Lungs System Backward failure Vena cava Lungs Ejection fraction : % of blood pump by the ventricle after a diastolic phase Manifestation: RSCHF: o JVD. - - - - - o Tissue Plasminogen Activator o Monitor patient for bleeding Benzodiazepine ( Anxiolytic ) o Diazepam/Lorazepam  Valium : ( relaxation )  Flumazenil : ( antidote ) Anticoagulant (prevent thrombus formation) o Heparin o Coumadin Anitplatellet o ASA : ( Acethyl Salicylic Acid ) platelet aggregation o Dipyridamole ( Persatin ) o Clopidogrel ( Flavix ) Beta Adrenergic Blockers ( SNS ) o Beta1 – heart ( Propanolol / Atenolol ) o Beta 2 – lungs Laxatives ( Lactulose ) prevent bowel straining o Valsalva Maneuver (contraindicated to HF ) o Rectal Temp. ASD( atrial septal defect ) IVF overload  Increased Afterload: aortic / pulmonary valve stenosis. HPN o Constriction of Left Ventricles  Pericarditis. restrictive cardiomyopathy ( HYDRATION STATUS : weight is the best indication ) TX: Promote oxygenation Promote rest & activity Facilitate fluid balance Providing skin care Promote nutrition Promote elimination Pharmacotherapy: Digitalis therapy: “ treatment of choice” o Digoxin ( Lanoxin ) . o Ascites (peritoneal cavity fluid) o Decreased urine output o Anasarca ( generalized edema) LSCHF: o Crackles/rales ( pulmonary edema ) o Increased ventilation o Cough o Dyspnea o Paroxysimal Nocturnal Dyspnea o Decreased urine output Direct damage to the heart o Myocarditis o Ventricular Aneurysm ( cells dilated / turn back to normal size ) o Ventricular Overload  Increased Preload: mitral / aortic regurgitation.. cardiac tamponade ( constriction of ventricle / rapid accumulation of pericardial fluid ). o Feeling of bloutedness.46u/L)(heart) LDH3 – LDH4 – LDH5 ( liver ) LDH1 > LDH2 (flipped) LDH1 < LDH2 (normal) Complication of MI Dysrrhythmia : Vtach ( emergency ) CHF : increased inotropic activity Cardiogenic Shock : pump failure ( #1 cause of death ) Post Infarction Angina Pericarditis : Transmural Infarct Pulmonary Edema : ( CHF ) TX: Goal: o Prevent further tissue injury o Decreased cardiac workload o Increased O2 NI: O2 ( nasal cannula ) CBR : 24 – 48hrs w/o bathroom Semi-fowlers ( immediate phase ) Monitor Cardiac function ( ECG ) o Continuous ECG monitoring o Blood pressure ( cardiogenic shock ) Lifestyle Modification ( diet.DX studies: Cardiac Enzymes ( most accurate ) CK ( Creatinine Phophokinase ) 26 -174u/L  CKmB ( myocardial ) O – 5% total ( normal )  CKmM ( damage muscle tissue )  CKbB ( reflects brain tissue damage ) LDH ( Lactate Dehydroginase ) 90 – 176u/L  LDH1 (. VSD ( ventricular septal defect).36u/L)  LDH2 (. Urokinase. exercise ) o Low salt – fat o Compliance to treatment Pharmacotherapy: Morphine Sulfate ( Opiate Analgesic ) o Severe pain – SNS – increased CW Nitroglycerin ( Nitrates ) o Vasodilation – decreased CW / Afterload ( dilation of coronary artery ) Thrombolytics ( dissolve clot / thrombus ) fibrinolysis process o Best given in the 1st 6hrs o Streptokinase.

syncope. chest pain Left Ventricular Hypertrophy LSCHF ( manifestation ) AORTIC REGURGITATION Manifestation: Corrigans ( water hammer pulse ) quick sharp pulse / suddenly collapse High pitch diastolic murmur Tricuspid Valve Disease TRICUSPID VALVE REGURGITATION / STENOSIS RSCHF like symptom Dyspnea. lymph Connective Tissue Disease ( SLE ) Systemic Lupus Erythematus Common Complication: Heart failure Cardiac tamponade Manifestation: Chest pain ( aggravated by supine position & relieve by sitting and leaning forward ) Pericardial Friction Rub ( scratchy high pitch sound ) Sign & symptoms of inflammation ( increased ESR.chronotropic effect ( dec.- - - MOA: + inotropic effect ( inc. blood. syncope PULMONIC VALVE DISEASE RSCHF like symptom Dyspnea. entero ) Tumor ( metastasis ) o Lungs. fever ) DOB & fatigue ( oxygenation problem ) MYOCARDITIS Caused by infection Manifestion: Murmur & Summation Gallop rhythm Sign of Infection / Inflammation DOB & fatigue Complication: Thrombus Heart failure Cardiomyopathy ( dysfunction of the heart/ myocardial defect-disease ) INFECTIVE MYOCARDITIS Manifestation: Signs of infection ( fever ) DOB & fatigue Splinter Hemorrhages ( strain blood in the nails ) Oslers nodes ( painful nodules in the fingers ) Janeways Lession ( flat macules : palm/soles ) pinkish – purflish TX: Promote oxygenation Facilitate proper rest activity pattern Administer medication ( CANADA ) o C-orticosteroid (anti-inflammatory) o A-ntiplatelet o N-SAID’s o A-ntibiotics o D-Igoxin o A-ntidysrhthmia .5 – 5mEq/L  Potentiates digitalis toxicity Vasodilators: ( Hydralizine ) o Calcium channel blockers ( VAND )  Verapamil  Amlodipine  Nicardipine  Diltiazem Symphatomemitics: o Dopamine / Dobutamine ( severe HF ) Diuretics therapy: o Loop diuretics ( Furosemide ) o K+ wasting diuretics  Best given in the morning monitor UO/BP VALVULAR HEART DISEASE Mitral Valve Disease MITRAL STENOSIS Narrowing of the mitral valve Manifestation: Initially assympthomatic Diastolic murmur ( abnormal heart sounds ) Dyspnea Atrial fibrillation / hypertrophy o Chamber quivering o Thrombus formation MITRAL REGURGITATION Incompetent mitral valves Manifestation: Dyspnea / fatigue Atrial fibrillation High pitch systolic murmur LSCHF ( manifestation ) - MITRAL VALVE PROLAPSED Manifestation: Dyspnea / fatigue Systolic click Chest pain & palpitation Aortic Valve Disease AORTIC VALVE STENOSIS Narrowing of the aortic valve Manifestation: Dyspnea. syncope TX: Depend on the clinical manifestation Valvular Repair o Commissurotomy ( commissure ) o Annuloplasty ( annulos ) o Chordoplasty ( chordate tindenae ) o Leaflet repair Valvular Replacement o Mechanical ( synthetic ) o Tissue ( living organism ) Valvular Graft / Tissue ( living organism ) o Xenograft / Heterograft (non human ) o Homograft ( human source ) o Isograft ( same person ) INFLAMMATORY DISEASE OF THE HEART PERICARDITIS Causes: Mechanical injury to the heart ( invasive ) Infection ( viral :HIV / bacteria : streptococcal. leukocytosis. Staphylococcal. SV ) . HR ) Maintenance drug: ( digitalis toxicity ) o Nausea & vomiting ( early stage ) o Visual disturbances : yellow – green halo vision ( snowy vision ) o Dysrhythmia / Arrhythmia (dangerous) o Assess:  PR: ( bradycardia ) +  K level ( hypokalemnia )  3.

CARDIAC DYSRHYTHMIA NORMAL SIGN RHYTHM Originate from SA node Atrial/ ventricular rate ( normal ) PR interval / QRS complex ( normal ) P : QRS ratio 1 : 1 SINUS BRADYCARDIA Sinus node creates / slower than normal rate ( 60bpm ) SA node PR interval / QRS complex ( normal ) Causes: o Metabolic rate ( hypothyroidism ) o Sleep decreased metabolic rate o Vagal stimuli ( valsalva. sunctioning increased ICP ) TX: Sinus Bradycardia that lead to Bradycardia o Atropine Sulfate ( anticholinergic ) . palpable pulse No respiration Need immediate treatment Causes: ( SSSCAT ) o S-evere hypoxia ( cerebral ) o S-evere electrolyte imbalance o S-hock o C-ardiac tamponade o A-cidosis o T-ension Pneumothorax TX: Artificial Cardiac Pacemaker Antiarrhythmic drugs CLASS I ( fast sodium channel blocker ) o CLASS IA . 3:1.) chronotropic Calcium Channel Blockers “ VAND ” Beta Adrenergic Blockers ( decreased contractility & HR ) “olols” MOST COMMON DYSRHYTHMIA ATRIAL FLUTTER SA node is not the main pacemaker Ectopic atrial focus captures heart rhythm Conduction defect on the atrium SAW TOOTHED ( atrial rate 250 – 400bpm ) PR interval is difficult to determine o P / QRS ratio 2:1.12sec/complex ) Risk for asystole VENTRICULAR ASYSTOLE Absence of QRS complex No heart beat. 4:1 so on…… ATRIAL FIBRILLATION Atrial quivers ( 300 – 600bpm ) Multiple rapid impulses ( many foci ) No definitive P wave PR interval cannot measured VENTRICULAR DYSRRHYTHMIA PVC ( premature ventricular contraction) Ectopic beat originating from ventricle Conducted before the next sinus PVC of 6 or more is life threatening (>6/min) Occurs in repetitive patterns / alternating repetitive pattern / continuous repetitive pattern o Bigeminy ( N-PVC ) 2nd turn rd o Trigeminy ( N-N-PVC ) 3 turn  Couplet ( 2x PVC )  Triplet ( 3x PVC ) QRS complex may be unifocal ( same foci ). impetigo Inflammatory disease of the heart ( valves is affected ) .moderate depression of depolarization but prolonged repolarization ( Procainamide ) - CLASS IB – minimal depression of depolarization but prolonged repolarization ( Lidocaine ) o CLASS IC – marked depression of depolarization / no effect on repolarization ( Propafenone ) CLASS II ( beta adrenergic blocker ) increased automacity /conduction CLASS III prolonged repolarization/ Amiodanone CLASS IV ( calcium channel blocker ) Pacemaker Indication: Permanent normal impulse / temporary slower than formation Pacing mode By demand ( if heart needs a demand ) By set ( settings ) Cardioversion Delivery of Electrical Current Synchronized with patient electrical event Send electrical impulse: QRS complex Elective procedure Starts with low voltage Client is awake ( sedated ) Defibrillation Immediate & synchronized Toc: V-fib & pulse less Emergency Starts with high voltage Unconscious ECG is monitored Conduction defects st 1 degree AV block ( impulse is send & receive ) in slower rate nd 2 degree AV block ( not all impulse is received ) if sympyomatic – treatment Atropine Sulfate rd 3 degree AV block ( totally no impulse is received ) sympyomatic – treatment Atropine Sulfate / pacemaker RHEUMATIC HEART DISEASE Preceded by GABHS infection o Sore throat. multi-focal ( came from different foci ) VENTRICULAR TACHYCARDIA Irritable focus on the ventricle ( emergency ) Ventricular rate ( 100 – 200 ) Ventricular no time to refill QRS complex prolonged ( .5mg – 3mg “ treatment of choice” Bradycardia ( IDEA ) o I-soprotenolol o D-opamine o E-pinephrine o A-tropine SINUS TACHYCARDIA SA node ( adult 100bpm ) Faster than normal Causes: Stress / hypermetabolic rate Medication ( aminophylline ) o IDEA o Illicit drugs ( shabu ) PR interval / QRS complex (normal) Rates exceed 100bpm TX: Digoxin (.

CM: HYPERTENSION ( HPN ) Shortness of breath Heart murmur Tachycardia Fever Subcutaneous nodules Erythema marginatum Chorea DX test: Elevated ASO titer ( anti streptolysin O ) Elevated ESR TX: CBR ( 24hr ) Increased CHO. gender. genetic factor. CHON Medication: ASA Corticosteroid Penicillin CARDIOMYOPATHY Form of cardiac dysfunction DCM ( Dilated Cardiomyopathy ) HCM ( Hypertropic Cardiomyopathy ) RCM ( Restrictive Cardiomyopathy ) ACM ( Arrhytmogenic Cardiomyopathy ) Unclassified CM: Sign & symptoms is progressive CHF ( manifestation ) Chest pain & palpitation Dizziness & syncope (+) S3 & S4 Enlarged heart Complication: Severe HF Lethal dysrrhythmia ( death ) TX: Identify /manage cause if possible Treat heart failure Low sodium diet Exercise & rest Anti dysrrhythmia / anticoagulant Surgical Management: Heart transplant RAAS ( renin angiotensin aldosteron system ) BP ( signals ) kidney ( renin ) Angiotensin 1 ( weak vasoconstriction ) ace inhibitors (lungs ) renin converts Angiotensinogen ( liver ) converts angiotensin 1 to Angiotensin 2 initiates ( strong vasoconstriction ) adrenal cortex ( to release ) Cathecholamines ( epinephrine / norepinephrin ) Glucocortecoid ( costisol ) blood sugar Mineralocortecoid ( aldosteron ) sodium reabsorption / potassium excretion sodium attracts H20 ( plasma ) CBV Abnormal elevation of BP SBP > 140 : DBP > 90 Systemic Hypertension Risk factor: Age. lifestyle. stress Determinants of BP BV – CBV ( increased BV – increased pressure) Peripheral Vascular Resistance ( afterload ) Cardiac Output Compliance of blood vessel( change in diameter of lumen ) Blood viscosity Blood pressure regulator Main factor of BP o CBV ( Circulating Blood Volume ) o Systemic Vascular Resistance o Intrinsic Regulators  RAAS ( renin angiotensin aldosteron system ) BP  ANP ( anti natriuretic peptide) ANP ( anti natriuretic peptide) BP atria is stretch ANP is release Kidney Excrete sodium sodium attracts ( H2O ) BP H2O ( plasma ) CBV  ADH (anti diuretic hormone) vasopressin ( target the kidney to increased the permeability of collecting tubules – reabsortion of H2O in the system – .

blurred vision ) Brain : ( hemorrhagic CVA. o decreased urine output ( concentrated )  pituitary gland / hypophysis  posterior/neuro hypophysis  anterior/adeno hypophysis Catecholamine (epinephrine / norepinephrine) emergency stress hormone (vasoconstriction : increased HR (tachycardia) increased SV = increased CO Classification of HPN: Primary HPN ( idiopathic ) no cause Secondary HPN ( resulted from a complication from existing disease Hypertensive Crisis o MAO inhibitor + Tyramine = HPN crisis Malignant HPN White coat HPN CM: Headache Epistaxis Dizziness.Increase contraction & vasodilation ( increase Calcium uptake of cell ) .Calcium initiate the Sliding Filament Theory  Verapamil  Amlodipine  Nicardipine  Diltiazem ACE Inhibitors Block Angiotensin 1 to convert to Angiotensin 2 ( pril )  Captopril  Enalapril  Lisinopril ARB’s .Angiotensin2 Receptor Blocker blocks Angiotensin2 receptors (sartan ) .Ask the client to rise up slowly or dangle feet Advise client to take drugs on REGULAR BASIS ( maintenance ) Always promote safety PERIPHERAL VASCULAR DISORDER DX: Venography – indirect visualization of vein ( contrast dye ) Angiopgraphy – indirect visualization of artery ( contrast dye ) . dysrrhythmia. gangrene TX: Healthy Lifestyle o Maintain IBW o Regular exercise o Stress reduction o Proper diet Advise to have regular consultation Pharmacologic Treatment Diuretics - Thiazide – affect the Nephron (kidney) Decreased CBV / Increased UO  Hydrochlorothiazide  Chlorothiazide  Methylchlorothiazide  affects the kidneys ( Distal Convulated Tubules ) – after the Loop of Henle o Loop Diuretics – Potassium Wasting Diuretics ( hypokalemia )  Furosemide  Bumetamide  Ethacrynic Acid  Affects the kidneys ( Ascending Loop of Henle ) o Potassium Sparing Diuretics (common effects hyperkalemia / dehydration)  Spironolactone  Amiloride Symphatolytics Destruction of Symphathetic Response o Beta Adrenergic Blockers decreased HR & contractility (olol) Types of Beta Adrenergic Blockers  Cardio Selective ( beta 1 ) Heart  Metraprolol  Atenolol  Besoprolol  Non Cardio Selective ( beta 2 ) Lungs  Propanolol  Tinolol Side Effects :  Hypotension  Bradycardia  Brochospasm  Fatigue  Weakness o Alpha Adrenergic Blockers o o o o o Blocks stimulation resulting to vasodilation . blurred vision Tinnitus Complication of HPN: Heart : ( MI. CHF. hemorrhagic ) Kidney : renal failure ( HPN 2nd leading causes of CRF ) hypertensive nephrosclerosis Peripheral Blood Vessel : aneurysm. thrombotic. unsteadiness. IHD ) Eyes : ( retinopathy.decreased BP  Lozartan  Irbesartan  Telmisartan NI: - Monitor S/E ( orthostatic hypotension ) .decrease BP ( zosin )  Doxazosin  Prazosin  Terazosin Direct Acting Vasodilator Relaxation of smooth muscle (tunica media)  Hydralizine  Monoxide Central Alpha 2 Agonist Decrease contractility / vasodilation  Methyldopa ( Aldomet )  Clonidine ( Catapress ) Calcium Channel Blockers ( VAND ) . stroke imbolic.

K ) o Monitors  PT ( 9 – 12sec )  1. arteriography TX: Goal: o Limit progression o Prevent rupture ( Dacron graft ) prosthesis NI: Antihypertensive drugs Surgical treatment ( Dacron Graft ) BUERGER DISEASE Throm Anginitis Obleterans Occlusive disease medium / small arteries & veins . swelling NI: Perform peripheral circulatory assessment (5P’s) - Instruct client to avoid precipitating environment ( exposure to cold environment) Avoid stress / smoking Pharmacotheraphy Vasodilators ( Calcium Channel Blockers ) (FUCKN ) F-emale ( high risk ) U-pper extremities C-yanosis K-( Cold ) N-numbness / tingling sensation AORTIC ANEURYSM Abnormal dilation of aorta Located along the aorta Types: Fussiform – dilation in both side Dissecting – separation of layer of arteries Saccular – aneurysm in 1 side Location: Thoracic Abdominal #1 predisposing factor ( atherosclerosis ) Most feared complication ( HPN rupture ) Assessment: Thoracic o Pain ( swallowing ) o Hoarseness of voice ( dysphagia ) o Syncope(sudden loss of consciousness) Abdominal o Pulsating mass in the abdomen o Pain ( abdominal .K ( per OREM ) o Antidote ( Vit. tingling.- Vascular Endoscopy – direct visualization of blood vessel - Assess allergy to Iodine ( seafood allergy ) Increase IFO Apply pressure function site ( prevent bleeding ) NI: DEEP VEIN THROMBOSIS Cause: VIRCHOWS TRIAD Vessel wall injury o Trauma o Substance abuse – nicotine Venous stasis o Stagnant blood o Prolonged standing / sitting Hypercoagubility of the blood o Pregnant o Women using pills ( fibrinogen ) CM: ( + ) Homan’s Sign o Outstanding sign o Pain in the Calves ( dorsiflex ) o Pathognomonic sign Warm skin / tender to touch Redness / Edema Pulmonary embolism ( dangerous ) emboli can impede pulmonary blood vessel ( phlegmonic cerulea dolens ) Massive edema ( ileu-femoral vein ) TX: CBR ( elevate legs ) Compression stocking ( morning / upon awakening / before rising in bed Perform peripheral circulatory assessment ( 5P’s) Pain/Pulse/Pallor/Paresthesia/Paralysis Do not massage affected leg Anticoagulant Heparin ( immediately effective ) o MOAdmission – subcutaneous or TIV o MOAction – inhibits action of thrombin o Antidote ( protamine sulfate ) o Monitor – PTT & APTT (20 – 39sec)  1.5 – 2. ultrasound.lower back ) o Bruit on the aorta DX: Ct scan.5X the higher laboratory control - Warparin ( 3 – 4 days effective ) o Inhibits synthesis of Vit.5 – 2X normal laboratory control  INR(1) normal  2–3 PTT – Partial Thromboplastin Time PT – Prothrombin Time APTT – Activated Partial Thromboplastin Time INR – International Normalized Ratio VARICOSE VEINS Distended – protruded veins Cause: Incompetent Valve Etiology: Hereditary Prolonged standing / sitting Venous hypertension Congenital CM: Dilated purplish – tortuous veins Edema – Pain Feeling of fullness / heaviness in the veins ( + ) Trendelenburg Test TX: Sclerotheraphy ( palliative treatment than curative ) Vein stripping / Ligation ( curative ) NI: Health teaching Use anti-embolitic stockings Avoid wearing restrictive clothing Avoid prolonged standing / sitting RAYNAUD PHENOMENON Vasospasm ( arteries / arteriols ) Assessment: Abnormal tissue discoloration Numbness. abd.

35 – 7.45pH ) ( 380C ) Plasma ( 90% water ) CHON – liver o Albumin ( osmotic / oncotic pressure ) o Fibrinogen ( clotting ) o Globulin ( immune system ) o Other substance  Nutrient  Waste / metabolic ( urea )  Hormone Blood elements ( formed cell ) o RBC ( biconcave / annucleated )  90 – 120 days expired 3  4 – 6 million / mm  Provide wider space for Oxygen  No ATP ( low consuming cellular activity )  M: 14 – 18g/dl  F: 12 – 16g/dl o Heme ( iron ) Globin ( protein ) o Hematocrit :  Can be affected by plasma ( decrease plasma – decrease hematocrit )  M: 42 – 52%  F: 35 – 47%  Hemoconcentration .- #1 precipitating factors ( tobacco ) - Brocks ( complete repair ) CM: Pain ( intermittent claudication ) Cool / numb Diminished pulse Complication: Ulceration Gangrenous foot Management: Eliminate smoking Medication: Calcium Channel Blocker Antiplatelet Surgery: Symphalectomy Amputation CONGENITAL HEART DISEASE ( Cyanotic / Acyanotic) Cyanotic: ( starts with letter T ) Right – Left Shunting ( deoxygenated blood is circulating in the systemic circulation ) Acyanotic: Left – Right Shunting ( oxygenated blood is going to the pulmonic circulation ) CYANOTIC HEART DISEASE Tetralogy of Fallot o 4 anomalies  P-ulmonic Stenosis  V-entricule Septal Defect  O-ver-riding of the Aorta  R-ight Ventricular Hypertrophy S/S: Cyanosis Polycythemia ( increase RBC ) Severe Dyspnea TET spell ( severe acute hypoxic attack ) Management: Oxygenation Knee – chest position Pharmacotheraphy Morphine Sulfate ( decrease oxygen consumption ) Surgery : Blalock – Taussig Procedure ( palliative ) TRICUSPID ATRESIA Ended in a blinded pouch S/S: Cyanosis Polycythemia DOB Management: FONTAN procedure TRANSPOSITION OF THE GREAT ARTERIES Largest arteries ( aorta / pulmonary ) S/S: Cyanosis Poycythemia DOB Management: Rashkind procedure ( palliative ) Mustard procedure ( complete repair ) TRUMCUS ARTERIOSUS Aorta / Pulmonary artery branch out ina single artery S/S: Cyanosis Polycythemia DOB Management: Modified Rastelli procedure ( surgical ) ACYANOTIC HEART DEFECT ASD / VSD Cyanosis appears in severe case DOB Murmur DX: Cardiac catheterization ECG MRI & CT scan Management: Open Heart Surgery ( ECMO ) PDA ( Patent Ductus Arteriosus ) CM: Continuous machinery murmur DX: Cardiac catheterization ECG MRI & CT scan Management: Indomethacin ( NSAID’s ) strong affinity to heart Ligation of PDA ( surgical ) inhibit steroids ( prostaglandin ) COARCTATION OF THE AORTA Narrowed portion of the aorta Manifestation: Weak / absent pulse ( lower extremities ) Strong pulse ( upper extremities ) BP changes DX: Cardiac catheterization ECG MRI & CT scan Management: Closed Heart Surgery BLOOD DISORDER ( Hematological ) Blood ( 4 -6 liter ) ( 7.

B12 Vit. antacid.Lymphocyte ( humoral mediated immune system) WBC ( white blood cell ) LEUKOCYTE Myeloid o WBC  Neutrophils ( 40 – 70% )  Active phagocytes  Eosinophil (1 – 4% )  Kill parasitic worms – stop chemical for inflammation  Basophil ( 0 – 1% )  Contain histamine ( activate inflammation )  Lymphocyte ( 20 – 45% )  T. B12 is responsible to RBC maturation Etiology: Total / Partial gastric surgery Malabsorption disorder Deficiency intake .  Hemodilution  Increase plasma/ decrease Hct Erythropoiesis ( erythropoietin ) process of producing RBC Reticulocyte ( immature RBC ) o 1 day circulating in the body & become matured Hematopoiesis Stem cell – (hemocrytoblast) – myeloid /lymphoid Myeloid o Reticulocyte o RBC.rare ( intrinsic factor ) DX test: CBC Schilling test ( for absorption of vit.animals o Non heme – plants Medical management: Blood transfusion as needed Administer iron supplement Iron supplement Oral: o Ferrous Sulfate – gastric irritation o Oral liquid – use straw Parenteral: ( Iron Dextran ) o Administer through Z track ( do not massage ) o Do not give tea. milk o Stool appear dark o Common Side Effects:  Constipation ( increase OFI – increase fiber ) FOLATE DEFICIENCY ANEMIA Deficiency of folic acid Macrocytic & Hyperchromic RBC o Folic acid is responsible for synthesis of RBC maturation Causes: Poor dietary intake / malnutrition ( folate ) Malabsorption disorder Alcoholism TX: Folic rich food Folic supplement 1mg / day ( PO ) PERNICIOUS ANEMIA ( Megaloblastic Anemia ) Decreased Vit. decrease plasma/ decrease Hct. platelet.Lymphocyte (cell mediated immune system)  B. B12 maintain integrity of myelin sheath TX: . WBC Lymphoid o Lymphocyte  T.Lymphocyte  B.Lymphocyte  Monocyte ( 4 – 8% )  Become macrophage (much greater than neutrophil) PLATELETS ( Thrombocytes ) 150.000 mm3 Granular fragments of megakaryocyte Prevent bleeding Platelet aggregation Platelet adhesion DISORDER OF THE BLOOD ( RBC ) ANEMIA Oxyhemoglobin ( oxygen connect to RBC ) bright red Primary problem: decrease availability of oxygen going to the tissue or fast hemolysis Common manifestation of Anemia: ( PWET ) P-allor o Oxygenation problem W-eakness o Decrease O2 E-asy fatigability o Decrease O2 T-achycardia o Compensation Severe: Chronic: - SOB Chest pain Koilonychia ( spoon shape nail ) Amenorrhea Brittle hair / nail IDA ( IRON DEFICIENCY ANEMIA ) Microcytic – smaller than normal Hypochromic – amount of RBC in the hemoglobin Causes: Blood lost Gastrointestinal malabsorption Dietary inadequate Increase metabolic demand TX: Nursing Intervention: Promote iron rich food o Heme .B12 ) 24hr urine collection CM: Red beefy tongue Manifestation of anemia Jaundice ( massive hemolysis ) Neurological impairment ( psychosis ) o Vit.000 – 450.

- Vit.B12 supplementation Blood transfusion APLASTIC ANEMIA Characteristic by bone marrow hypoplasia o Immature bone marrow Result to Pancytopenia ( decrease RBC / WBC / platelet ) Causes: Congenital Radiation Medication Infection DX: CBC Bone marrow aspiration CM Anemia Leukopenia ( recurrent infection ) Thrombocytopenia TX: Anemia: o Activity pacing ( promote oxygenation ) Prevent infection: o Provide isolation  Strict  Reverse Encourage hygiene Avoid raw / fresh fruit / vegetable Bleeding precaution: Avoid sharp object Minimize invasive procedure Avoid contract sport Medical management: Bone marrow transplant Blood transfusion SICKLE CELL ANEMIA Hgb is replace by Hgb S Inherited Resulting to severe chronic anemia Causes: ( DISH ) D-ehydration ( #1 causes ) I-nfection S-tress H-ypoxia Types of Sickle Cell: Vaso occlusive ( painful ) - Splenic Sequestration ( spleen ) Aplastic ( decrease RBC / WBC / platelet ) o Parnovirus ( decrease red bone marrow ) - Blood smear Sickle turbidity test Amniocentesis - Prevent DISH During crisis o Promote oxygenation during hydration DX: NI: THALASSEMIA Inherited group of hemolytic anemia Cause by few hemoglobin peptide chain Resulting to decrease Hgb & life span Common for Mediterranean blood 4 forms: Thalassemia Minor o Silent carrier Thalassemia Major o Very severe Thalassemia Intermedian o Moderate severe w/ hemolysis Thalassemia Tract o Mild microcytic anemia Sign & Symptoms: Frontal brossing Maxillary prominence Splenomegaly Hemosiderosis ( iron overload ) DX: PBS ( Peripheral Blood Smear ) Hgb electrophoresis CBC TX: Goal: Supportive Treatment No known cure Blood transfusion Admission of Deferoxime ( iron overload ) Spleenectomy OTHER DISORDER ( RBC ) POLYCYTHEMIA Increase RBC POLYCYTHEMIA VERA Primary ( hyperactive bone marrow ) Increase RBC / WBC / platelet SECONDARY POLYCYTHEMIA Release of erythropoietin Complication: Thrombosis Increased cardiac workload DISORDER OF WBC LEUKEMIA Malignant disorder characterized by rapid & unregulated proliferation of immature WBC Classification: ALL – Acute Lymphocyte Leukemia AML – Acute Myeloid Leukemia CLL – Chronic Lymphocyte Leukemia CML – Chronic Myeloid Leukemia Causes: Idiopathy ( cannot pin point causes ) Viral infection Familiar susceptibility ( carcinogenic genes ) Genetic disorder Radiation and Chemical Theories / CA ( cellular aberration ) Failure of the immune response theory Cellular transformation & dearrangement CM: Decrease mature WBC / RBC / platelet Bone pain & Arthalgia ( pain in the joint w/out inflammation ) Hepato – Spleenomegaly Abdominal pain Sign & symptoms of electrolyte imbalance DX test: Bone marrow aspiration PBS ( Peripheral Blood Smear ) CBC Medical management: Chemotherapy Bone marrow transplant BT NI: Prevent bleeding Prevent infection Promote oxygenation BLEEDING DISORDER DIC ( Dissimenated Intravascular Coagulation ) Acquired thrombotic / Hemorrhagic syndrome Abnormal activation of clotting & fibrolysis .

Causes: - Severe massive infection ( septicemia ) Obstetric complication Malignancy Hemolytic transfusion reaction Shock ABNORMAL CLOTTING Manifestation: Coolness / Cyanosis ( extremities ) Pain ( extremities ) Dyspnea / Adventitious breath sound Altered mental status Complication: Pulmonary Embolism (most feared complication) DVT ( deep vein thrombosis ) CVA ( cerebro vascular accident ) embolic MI ( myocardial infarction ) coronary artery ABNORMAL BLEEDING Manifestation: Internal / External bleeding DX: Decrease platelet / fibrinogen Prolonged PT & PTT Complication: Hemorrhage ( most common cause of death ) TX: Treat underlying cause Replacement therapy: FFP ( fresh frozen plasma ) Cryoprecipitate – platelet transfusion Anticoagulant HEMOPHILLIA ( specific ) Deficiency in specific coagulation factors Pattern of inheritance ( X linked recessive ) Male: manifest Female: carrier Most common type: Hemophilia A (deficiency in clotting factor 8) Hemophilia B (Christmas hemophilia) Hemophilia C (deficiency in clotting factor 11) Assessment: Sudden bleeding Abnormal bleeding during trauma Hemorthorosis ( bleeding of joints ) - Excessive bleeding - Same as the other bleeding disorder TX: NI: - WOF sign of bleeding Institute bleeding precaution Monitor vital sign ( hypovolemic shock )hypo tachy-tachy If already present ( control bleeding ) o I-ce o C-ompress o E-levate Medical management: Replacement therapy Antifibrinolytic medication ( stops dissolving of clot ) o Amicar o Tranexamic acid VON WILLEBRAND DISEASE Deficiency or defect on vWf o vWf – initiates platelet aggregation / adhesion – potentiates clotting factor CM: Bleeding especially in the mucus membrane Prolonged bleeding time Decrease vWf ( clotting factor 8 ) TX: Same as hemophilia Pharmacotherapy Humate P ( alphate ) ATP ( AUTO IMMUNE THROMBOCYTOPENIC PURPURA) Idiopathic Immune destruction of platelet Usually viral infection Suppressor T cell cannot stop immune response Destroy other cell Infected thrombocytopenic purpura (dengue) CM: Bleeding from gums & nares Bruising Petechiae Menorrhagia TX: Platelet transfusion - Immunesuppresant Bleeding precaution MULTIPLE MYELOMA Malignant disease of plasma cell Rapid B – cell proliferation CM: Normochromic / Normocytic anemia Back pain Decrease WBC / platelet Bone pain / fracture ( osteoclast – destruction ) o Bone ( hydroxyl apatite crystals ) Hypercalcemic ( renal failure ) Complication: Bleeding Anemia Infection Renal failure ( hypercalcemia ) DX procedure: (+) Bence Jones Protein ( urine / blood ) FNAB – fine needle aspiration biopsy o bone marrow TX: Chemotherapy Alpha interpheron Radiation Hydration ( viscos blood due to plasma ) Pain management RESPIRATORY SYSTEM PHYSIOLOGIC DEAD SPACE ( nares – bronchi ) Nares Nasal cavity Vestibule – inner portion of nasal cavity Vibrissae – tiny hair in the nasal cavity Pharynx Vasopharynx Oropharynx Laryngopharynx Larynx Voice box ( cartilagenious epithelium ) Epigloittis ( guardian of the airway ) Thyroid cartilage ( largest cartilage in the larynx ) “ adams apple “ Vocal chords ( vibration – phonation ) Trachea Wind pipe ( cartilage with smooth muscle ) .

phagocyte Respiratory Center Medulla Oblongata: primary center of respiration Pons: helps the regulation of respiration o Pneumotoxic center – responsible 5 o Apneustic center – deep & prolonged inspiration Chemoreceptor: detects the level of respiratory gases & blood pH Proprioreceptors: detects amount of stretch Lung Volume Tidal volume   o In & out of air with normal breath ( 500ml ) Inspiratory reserve volume o Amount of extra air that can be inhaled beyond the tidal volume ( 3100ml ) Expiratory reserve volume o Amount of air that can be exhaled of the normal breath ( 1200ml ) Residual volume o Amount of air that remain in the lungs after a forceful expiration ( 1200ml ) Assessment: Inspection: Signs of respiratory distress o Nasal flaring o Alteration of LOC o Rapid respiration o Skin discoloration o Used of accessory muscle  Sternocleidomastoid  Pectoris major / minor  Trapezius Rate & depth of respiration: Eupnea ( normal ) Bradypnea ( <12cpm ) Tachypnea ( >24cpm ) Hypoventilation ( decrease rates & depth ) Hyperventilation ( increase rates & depth ) hypercapnia / Kussmaul Respiration Apnea ( absence of breathing Cheyne stroke ( progress apnea prolonged ) Boit’s respiration Thoracic inspection: AP diameter to Lateral diameter ( 1: 2 ratio ) 4 main chest deformities: Barrel chest (1.surfactant o Type 3 .pulmonary edema Air passing to a fluid ( mucus ) Gurgles ( ronchi ) pneumonia Air passing to a narrowed passage w/ fluid Friction rub Inflammation of the pleural surfaces Wheezes ( asthma ) Voice sound ( ask the client to say ninety nine / eee ) Egophony Bronchopony Whispered pectoriloquy DX procedure: Chest Xray ( radiograph ) Sputum specimen o Sputum C & S ( identify pathogen / antibiotics ) o AFB staining ( detects TB bacilli ) o Cytologic examination Mantoux test o Read after 48 – 72hrs .Carina ( point were before trachea separates) Bronchi Right Left Segmental bronchi o Sub – segmental bronchi o Bronchioles o Terminal bronchioles o Respiratory bronchioles Basic Functional Unit ( Lungs ) ALVEOLI Alveolar duct Alveoli o Alveoli 1 ( gas exchange ) o Alveoli 2 ( surfactant production ) Muscle responsible for breathing: Diaphragm Intercostals’ muscle Pleura ( parietal ) – Outside cover of the lungs ( serous membrane ) Visceral pleura – Inside cover of the lungs Prinic nerve – innervations of the diaphragm RESPIRATION ( an act of breathing ) External ( lungs – environment ) Internal ( blood cells – capillaries ) 3 process: Ventilation: movement of air in & out of the lungs Diffusion: exchange of gas ( higher pressure – lower pressure ) Perfusion: availability / movement of blood for transport Pneumocytes: o Type 1 .increase AP diameter) COPD Funnel chest ( pectus excavatum ) Pigeon chest ( pectus carinatum ) Kyposcoliosis Thoracic Palpation & Inspection: Respiratory excursion ( 3 -5cm ) o Measure the symmetry / extent of lung expansion Tactile fremitus o Spoken voice transmit low frequency vibration  Abnormal findings Increase tactile fremitus  Consolidation of the lungs  Pneumonia  Tumor  Fibrosis Decrease tactile fremitus  Increase amount of air in the lungs  COPD  Pneumothorax Percussion tones Resonance / long-hollow /normal Flat / short extremely dull / pleural perfusion Dull / moderate /may indicate consolidation Tympanic / moderate drumlike / Hyperresonance / very long booming / COPD Auscultation: NORMAL BREATH SOUND Bronchial Bronchio Vesicular Vesicular Manubrium area (upper) Bronchi (mid) Base of Lungs Pitch High Amplitude Loud Moderate Moderate Low Low ADVENTITIOUS BREATH SOUND Crackles ( rales ) coarse / fine .1 ratio .located in the alveoli o Type 2 .

bronchitis normal resonance decrease intensity normal DX: COPD ( CHRONIC OBSTRUCTIVE PULMONARY DISEASE) Progressive chronic airway mutation that is not fully reversible Associated with abnormal inflammatory response ( structural changes ) Structural changes in COPD - - Pulmonary function test o FEV – false expiratory volume o FVC – functional vital capacity o RV – residual value ABG: o Decrease PO2 : increase PCO2 ( >45mmHg) . chemotherapy.#1 initial sign ) Environmental pollutant Chronic laryngitis Assessment: Persistent voice hoarseness Mass at the anterior part of the neck Persistent cough & sore throat Dyspnea / dysphagia ( burning sensation – swallowing ) Pain radiating to ear ( metastasis ) - TX: - Symptomatic treatment based on manifestation Treatment includes surgery. epigloittis. 3 tracheal ring - Proximal airways: o >2mm in diameter o Increase number of Goblet cell o Enlarged in submucosal gland Goblet gland grandular epithelium ) produce musin result to excessive mucus & decrease diameter in lumen of airways.o - - - - Result:  (+) induration of 10mm or more  (+) induration of 5mm or more ( HIV ) Bronchoscopy ( direct visualization – endoscope) o Consideration:  NPO ( check for gag reflex )  Pre op meds ( atropine sulfate )  WOF complication Bronchography ( visualization through the use of radiopaque o Consideration:  Check for allergy ( iodine )  NPO ( 8 -12 hrs before )  Pre op med ABG ( measure dissolve oxygen & carbon dioxide in the arterial blood ) Lung biopsy o Transbronchospic biopsy / bronchoscopy o Percutaneous needle biopsy o Open lung biopsy / chest surgery Pulse oximetry ( measure O2 saturation ) O2% in the capillary blood Lung scan o Intervention  Assess for allergy to dye SINUSITIS Inflammation of sinus Causes: URTI ( upper respiratory tract infection ) . Peripheral airways: o <2mm in diameter o Thickening of the air wall o Peribronchial fibrosis ( fibrous connective tissue ) Lung parenchyma ( functional unit ) o Decrease elastic recoil CHRONIC BRONCHITIS ( COPD ) Presence of cough & sputum production Increase mucus secreting cell Narrowing of the bronchial lumen Alveoli become damage ( fibrosis ) EMPHYSEMA ( BARREL CHEST ) COPD Abnormal destruction & distention of alveoli Impaired diffusion Increase dead space Reduction in the size of the capillary bed At high risk for the developing col pulmonade Col pulmonade – R-sided CHF related to pulmonary distention ( COPD ) Risk factors: Exposure to tobacco Air pollution Occupational exposure Genetic abnormalization Assessment: T. smoking. cricoids cartilage. allergic rhinitis Assessment: Pain: o Maxillary o Frontal o Ethmoid o Sphenoid Fever Cough & runny nose TX: NI: - Rest & increase OFI Warm pack ( pain ) Administer medication prescribed o Decongestant ( phenylephrine ) o Antihistamine ( chlorphenamine ) o Antipyretic ( paracetamol ) Surgical Intervention: FESS ( functional endoscopic sinus surgery ) Caldwell – Luc surgery Ethmoidectomy / Ethmoidotomy Sphenoidectomy Osteoplastic flap surgery - CANCER OF THE LARYNX Risk factor: Substance abuse ( smoking ) Voice abuse ( persistent voice hoarseness .fremitus Percussion Auscultation Emphysema decrease hyperresonance C. radiation Surgical Intervention: Laryngofissure-thyrotomy (partial laryngotomy ) o Removal of parts of larynx Total Laryngectomy o All laryngeal structures are remove includes the hyoid bone.

- CBC: o Polycythemia ( increase RBC ) CM: Chronic cough Sputum production Dyspnea on exertion Adventitious breath sound Weight loss Signs of respiratory distress Clubbing of fingernails Polycythemia Barrel chest Decreased tactile fremitus & hyperresonance Complication: Respiratory insufficiency Respiratory failure Pneumonia Atelectasis Pneumothorax TX: Avoid smoking and sir pollutant Increase OFI ( if not contraindicated ) to liquify mucus Promote rest Oxygen supplementation ( in times of exacerbation / 1-3LMP ) O2 narcosis CPT ( chest percussion therapy ) Pharmacotherapy: Antitussives ( suppress cough ) o Dextrometorphan ( Codeine )  s/e: drowsiness Expectorant & mucolytic Bronchodilator Antihistamine Steroids ( anti inflammatory ) Leukotrine inhibitors Antibiotic BRONCHIOSTATIS Chronic reversible dilation of the bronchi & bronchioles Predisposing factor: Airway injury / obstruction Recurrent / long term pulmonary infection Abnormal host defense Idiopathic cost CM: Chronic cough - Purulent sputum Hemoptysis Clubbing Recurrent pulmonary infection - - CT scan - DX: TX: Avoid cigarette & air pollutant Increase OFI ( if not contraindicated ) Promote rest Oxygen supplementation CPT Pharmacotherapy: Antitussives ( suppress cough ) o Dextrometorphan ( codeine )  s/e: drowsiness Expectorant & mucolytic Bronchodilator Antihistamine Steroids ( anti inflammatory ) Leukotrine inhibitors Antibiotic ASTHMA Chronic reversible and diffuse airways inflammation Hyper responsive of the airway resulting to o Bronchospasm o Mucosal edema o Mucus production CM: Cough Wheezing ( expiratory ) Chest tightness / dyspnea Other sign of respiratory distress Assessment: Tactile fremitus ( normal to decrease ) Percussion ( resonance to hyperresonance ) Auscultation ( wheeze ) TX: Identify / prevent precipitating factors Promote oxygenation Alleviate anxiety Pharmacotherapy: Inhaled corticosteroid ( acute attack ) o Busemide o Beclomethasone o Monetasone Systemic ( long term ) o Betaprednisolone o Prednisone o Prednisolone Methylxanthines ( bronchodilators ) o Theophylline Beta 2 agonist ( bronchodilators ) o LABA ( long acting beta adrenergic agonist )  Salveterol  Albuterol ( SR ) sustain release o SABA ( short acting beta adrenergic agonist )  Salbutamol  Metaproterenol  Terbutaline o Mast cell inhibitors ( histamine )  Cromolyn sodium o Leukotrine inhibitors  Zafirlukast  Montelukast o Anticholinergic ( decrease mucus secretion )  Ipatropium CYSTIC FIBROSIS ( Mucuvisidosis ) Chronic disorder resulting to hyperactivity of the exocrine gland Most common life shortening inherited Result: Chronic airway obstruction Infection Malabsorption CM: Failure to pass meconium ( meconium ilues ) Sign of respiratory distress Thick mucus production Cyanosis / clubbing Steatorrhea ( recurrent plug infection ) Recurrent long infection Frosting of the skin or salty taste sweat DX: Iontophoresis of Pilocarpine test ( sweat chloride test ) < 60meq/L TX: Promote effective airway CPT Reduce risk factor for respiratory infection Lifestyle modification .

stridor.nosocomial Aspiration Opportunistic ( immunocompromised ) Hypostatic ( prolonged bed rest ) Etiology: Bacterial pneumonia o Streptococcus pneumonia ( CAP ) o Staphylococcus aureus ( HAP ) o Pseudomonas aureginosa o Klebsiella pneumonia Non bacterial pneumonia o Mycoplasma pneumonia o Pneumocytic car inii ( HIV ) o Influenza parainfluenza virus Assessment: Rusty sputum Fever & chills Sign of respiratory distress Sign of URTI Anxiety & confusion Tactile fremitus increased Percussion: dull .o CM: Fever Nausea & vomiting Nasal flaring 1 – hoarseness. permanent cyanosis. cessation of breathing Laboratory study: ABG Throat swab Chest – neck Xray Causes: Parainfluenza virus Bacterial infection Management: Promote mucus secretion Steam inhalation Advise to rest Oxygen administration Pharmacotherapy: Corticosteroid Antibiotic Bronchodilator - Severe case : inhalation EPIGLOITTITIS Emergency condition of the URTI Resulting to airway obstruction Sign & symptoms: Sudden onset Pooling of the saliva Hoarseness Tripod position Leaning forward with tongue protrusion High fever Sign of respiratory distress Management: Comfortable position Do not use tongue depressor Steam inhalation Pharmacotherapy: Antibiotic Corticosteroid Vaccination: HIB ( humane influenza type B ) PNEUMONIA Inflammation of the lung parenchyma Resulting to consolidation of the alveoli space Classification: CAP HAP . use of accessory muscle 4 – intermittent respiration.cough or barky cough 2 – inspiratory stridor. intercoastal retraction 3 – lower rib retraction.Supplemental oxygen Pharmacotherapy: Antibiotic Anti inflammatory Leukotrine ( mast cell inhibitors ) PHARYNGITIS Painful inflammation of the pharynx Causes: Viral / bacterial CM: Fiery red pharyngeal membrane Enlarged & tender cervical lymphnodes Malaise / masalgia Fever Headache LARYNGITIS Inflammation of the larynx Causes: Voice abuse Exposure to dust & chemical Smoking GERD ( gastro esophageal reflux disorder ) Manifestation: Hoarseness of voice Aphonia Severe cough Subjective complain of tickling Management: Avoid irritants Rest the voice Steam inhalation Increase OFI Pharmacotherapy: Corticosteroid Antibiotic Expectorant Omeprazole ( proton pump inhibitor ) GERD / decrease HCl cheyne ATELECTASIS Collapse of alveoli Causes: Altered breathing pattern ( guillian baire syndrome ) shunt Retained secretion Prolonged supine positioning Reduced lung volume - Surgical procedure Accumulation of excessive pleural fluid CM: Progressive dyspnea Percussion flat Auscultation ( decreased to absent) DX findings: Xray Pulse oximetry & ABG Prevention: Frequent turning Early mobilization Strategies to expand the lungs Secretion management techniques Management: Endotracheal intubation Mechanic ventilation Treat underlying cause RESPIRATORY INFECTION LTB ( Laryngo – Tracheo Bronchitis ) Most common in infant & children less than 3 y.

general population o (+)5mm o DSSM ( direct sputum smear microscopy ) interpret Classification ( PTB ) Category 1 Type of PTB patient -New (-)DSSM -New(-)DSSM w/ extensive parenchymal lesion on CXR -EPTB Treatment intensive continuation RIPE RI 4 -Treatment failure -Relapse -New(-)DSSM w/ minimal parenchymal lesion on CXR -chronic/still smear positive after supervised retreatment RIPES RIE RIPE RI DOTS Management: Goal of treatment: Prevent spread of diseases Promote recovery Weight loss Medication: Rifampicin – red .- Auscultation: crackles Egophony Bronchopony Whispered pectoriloqy 2 3 TX: Promote thermoregulation Promote rest Promote sputum expectoration Promote infection control Antibiotic: Macrolide ( Azithromycin / clindamycin / erythromycin ) Cephalosporin Penicillin Flouroquinolone ( floxacin) PTB ( Pulmonary Tuberculosis ) Infectious diseases affecting the lungs parenchyma Mycobacterium ( anaerobe ) Sensitive to heat & UV ray CM: Fever Cough Night sweat Weight loss Shortness of breath Chest / back pain Risk factor: Close contact to patient w/ active PTB Immunocompromised status Substandard lungs Healthcare worker DX: CXR ( ideal ) Mantoux test ( Tb bacilli ) o (+) discoloration ( normal ) Isoniacid – increase vit.b6 ( pyridoxine ) causes peripheral neuritis Pyrazinamide – photosensitivity Ethambutol – optic neuritis Streptomycin – category 2 patient Hepatotoxicity / Ototoxicity Single dose ( separate preparation ) Fix ( single tablet medicine ) Fixcom/ Quadtab MDR ( multi drug regimen ) avoid develop PTB regimen – reduce side effect TB Cancer Chest pain / Trauma Assessment: Chest pain SOB Pleural friction rub DX findings: Xray Thoracentesis ( removal of fluid – pleura ) TX: TUC Promote comfort Promote oxygenation HISTOPLASMOSIS Systemic fungal disease Common in rural / Midwest / southern area Not spread from human to human ( chicken / dove ) o Fecal transmission Assessment: Similar to PTB & pneumonia Cough Joint pain Malaise DX: CXR Histoplasmin skin test TX: Antifungal ( Ampothericin B / Polymycin B ) PLEURAL EFFUSION Accumulation of excessive fluid ( pleura ) Type: Hemothorax ( blood ) Pyothorax ( emphysema ) pus/ inflammation Hydrothorax ( serous fluid ) Common cause: Pulmonary infection Iatrogenic Neoplastic tumor Trauma Connective tissue disease Complication: Atelectasis Hypovolemic shock CM: Sudden sharp chest pain Tachycardia / tachypnea Assessment: Tactile fremitus ( absent ) Percussion: dull to flat Auscultation: decrease to absent TX: C – hest drainage ( 5th – 6th ICS ) H – igh fowlers O – xygen P – ain management A – BG PLEURISY / PLEURITIS Inflammation of the pleura Causes: Pneumonia URTI PNEUMOTHORAX Accumulation of fluid in the pleural space CM: SOB Restlessness .

infection ) o Neuromascular dysfunction ( ALS – amyotropic lateral sclerosis / Guillan Barre Syndrome. granulomatous disease Hypersensitivity response to one or more exogenous agents Etiology: Idiopathic Pulmonary changes: Granuloma infiltration & fibrosis CM: . kyphosis ) Oxygenation failure ( COPD. high fowlers. lung infections ) o Constrictive lung disease ( pneumothorax. pleural effusion) CM: SORD Air hunger Tachycardia / Tachypnea Cyanosis Diaphoresis Alteration of LOC Complication: Respiratory arrest TX: TUC Oxygenation therapy Endotracheal intubation Mechanical ventilation Monitor respiratory status ACUTE RESPIRATORY DISTRESS SYNDROME Severe form of acute lung injury Caused by diffuse alveolar damage CM: Sudden & progressive pulmonary edema o Increased bilateral infiltrates in CXR o Hypoxemia unresponsive to oxygen therapy o Absence of elevated atrial pressure Common cause: Aspiration Drug overdose Hematologic disorder Shock / trauma Major surgery Embolism CM: Sudden ( 4 – 48hrs onset ) Severe dyspnea SORD Dry cough ( sticky ) Fine crackles DX: ABG ( decrease oxygen / increase carbon dioxide) CXR BNP ( brain natriaretic peptide ) / endocardiography TX: - Oxygen therapy Positioning ( orthopnic.Types: - o Sudden sharp chest pain Tracheal deviation Tachycardia / tachypnea Cyanosis Open pneumothorax o Penetrating chest injury o Wound is large enough to move air in / out o Tidal volume diminished ( decrease ventilation ) Tension pneumothorax o Accumulation of pressure o Disease or injury ( emphysema ) o Air is traped ( inspiration ) Complication: Lung collapsed Mediastinal shift ( dangerous ) Assessment: Signs & symptoms are bought by underlying diseases Tactile fremitus: decreased Percussion: hyperresonant Auscultation: absent breath sound Pleuritic pain SORD DX: - CXR Thoracentesis - TUC Promote oxygenation CHOPA TX: ACUTE RESPIRATORY FAILURE ( ARF ) Deterioration in the gas exchange function of the lungs Resulting to: Caused by failure in the ventilation / oxygenation mechanism Cause: Ventillary failure ( acute respiratory failure ) o Impairment CNS ( head trauma. malnutrition. semi fowlers ) Promote comfort Intubation / mechanical intubation Avoid anxiety PULMONARY EDEMA Excessive accumulation of fluid in the lung tissue / alveolar spaces CM: SORD Air hunger Frothy sputum Assessment: Tactile fremitus. M. gravis) - Muscular dysfunction ( chest trauma. CVA. normal Percussion: resonant Auscultation: crackles TX: Treat fluid volume excess Alleviate anxiety Promote oxygenation o Proper positioning o CPT o Oxygen therapy o Suctioning / coughing exercise In severe cases: o Intubation ( ET ) o Mechanical ventilation PULMONARY EMBOLISM Obstruction in the pulmonary artery Common cause: PVD ( peripheral vascular disease ) Fat embolism Multiple trauma Immobility Hypercoagubility SARCOIDOSIS Multi system.

Bone DX: TX: - - FLAIL CHEST Crushing chest injury ( 2 adjacent ribs ) Manifestation: Paradoxical breathing ( other part is not expanding when breathing ) Signs of SORD TX: Promote oxygenation Surgery ( chest surgery ) CARBON MONOXIDE POISONING CO takes up the space of O2 in the RBC resulting to hypoxia Exposure to inadequately vented combustion device CM: SORD - Headache Vertigo ( feeling that environment is moving ) Paralysis - Hyperbanic pressure Remove patient from immediate area of poisoning Initiate CPR immediately Administer oxygen Monitor VS Intubation / Mechanical ventilation TX: - RESPIRATORY MODALITIES Oxygen Therapy O2 concentration in room air ( 21% ) Factor related to O2 transport Cardiac output Arterial O2 content ( 96 – 100% O2 saturation).V-D-P Hg concentration ( decrease. O2 concentration in RBC – tissue ) Circulatory hypoxia ( blood flow ) CHD – PVD Anemic hypoxia ( anemia ) Histotoxic hypoxia ( certain substance ) cyanide Intervention: Continuous assessment Humidify O2 if indicated Reduce risk for fire ( O2 highly combustible gas ) OXYGEN ADMINISTRATION DEVICE Low flow system: Partial O2 Is Inspire Nasal cannula: 1 – 6 LPM ( 22% – 42% ) . Liver.< 12cpm o Site of metastasis  Brain. RBC ) Metabolic requirement ( increase metabolic rate & O2) Indication: Hypoxemia / Hypoxia Types of hypoxia Hypoxemia hypoxia ( dec.Depend on the system affected General manifestation: Anorexia Fatigue Fever Specific pulmonary manifestation: Dyspnea Cough / hemoptysis DX: X ray / CT scan Biopsy TX: Symptomatic treatment Corticosteroid Cytotoxic Immnunosuppressive PNEUMOCONIOSES Occupational diseases of the lung Non neoplastic alteration of the lungs Causes: Inhalation of mineral / inorganic dust o Asbestosis o Coal worker pneumoconiosis ( black lung ) Result: Pulmonary fibrosis Parenchymal changes Manifestation: SORD Cough Chest pain TX: Symptomatic treatment Avoid exposure to industrial dust LUNG CANCER Predisposing factor: Cigarette smoking Chronic exposure to industrial dust Emphysema ( pre cancerous cell ) Genetics Types: Squamous cell ( good prognosis ) Adenocarcinoma ( good prognosis ) Oat cell ( poor prognosis ) Undifferentiated ( poor prognosis ) Manifestation: Asymptomatic ( early stage ) - Cough Dyspnea Adventitious breath sound Chest pain SORD - CXR / CT scan Bronchoscopy Biopsy ( #1 ) - Surgical o Pneumonectomy (removal of the lung ) Unaffected side ( chest drainage ) o Lobectomy ( removal of the lobe ) o Segmentectomy o Wedge resection ( removal of the tumor regardless of the segment ) o Decortation ( stripping of the fibrous membrane – enclosing the lung ) Chemotherapy Promote oxygenation Radiation Alleviate pain o Narcan / Morphine ( narcotic antagonist ) monitor respiratory rate . Adrenal gland.

in mechanical ventilator Oxygen toxicity Risk: o Too high ( above 80% ) o Too long ( longer than 48hrs ) Result: inc. Ventilator Mechanical Ventilation Indication: during surgery.- Indication : need for low to medium O2 concentration Advantage: comfortable for longer period Disadvantage: drying of the nasal mucosa ( variable FiO2 ) fraction of inspired O2 Simple mask: 6 – 8 LPM ( 40% .75% ) Indication: moderate Non Rebreather: Reservoir bag + Additional valves: 12 LPM ( 80% -100%) Indication: high O2 concentration ( deteriorating O2 status ) High flow system: “ no room air “ Venturi mask: 4 – 5 LPM ( 24% .40% ) - T – Piece/Tracheostomy Collar: 8 – 10 LPM ( 30% 100% ) o o o o Indication: useful in weaning Pt. volume of air vary as the resistance or compliance change Time cycled o It delivers flow of air until it reaches preset time ( commonly used – infant/newborn ) o Volume of air receives is regulated by the length of inspiration Volume cycled o Most commonly used o Volume of air is preset o Constant/ adequate breath despite of varying pressure Non invasive positive pressure ventilation Mode of ventilation Controlled: o Tidal volume / rate is set o For patient who cannot initiate respiratory effort o Mechanical ventilator is in total control o If the client attempt to initiate breath the ventilator block it Assist Controlled: o Commonly used . severe head injury or inadequateventilation Types: Pressure cycled o It delivers flow of air until it reaches preset pressure ( commonly for short term ) o Limitation. E ) Oxygen narcosis / COPD Incentive spirometry ( method of deep breathing exercise / visual feedback ) encourage Pt. to breathe deeply & slowly Indication: Atelectasis ( risk ) Patient Education: Proper positioning: upright / semi fowlers Breathing exercise o 10x a day / 10 breaths each hour ( 3 sec. intervals ) allow coughing – best in waking hours o Splint incision ET ( Endotracheal Intubation ) most reliable / accurate Indication: precise FiO2 - Indication: any person who cannot maintain adequate airways Pt. need mech. O2 radicals ( anti radicals – anti oxidants / Vit. Ventilation Passes with the aid of Laryngoscope May be useful for not longer that 3 weeks Client cannot talk / increase secretion which is thicker Ensure 1 way flow of air o Tracheostomy Opening of the trachea ( temporary/permanent ) Indwelling tube is inserted Indication: by pass an upper airway obstruction / for long term use of mech.60% ) Indication: low to medium ( short term ) Advantage: able to gather O2 Disadvantage: uncomfortable ( variable FiO2) Partial Rebreather Mask: With Reservoir bag: 8 – 11 LPM ( 50% .




Tidal volume / ventilator rate is
o When the client initiates breath the
ventilator deliver the preset tidal
Synchronized Intermittent Mandatory
o Tidal volume / ventilator is preset
o Allows the patient breath on his
own effort and the tidal volume is
between the ventilator and client

High pressure alarms
o When ventilator receives resistance


Displaced tube

When the clients cough,
gags or bite the tube
Low pressure alarms
o Detects fast flow of air

Ventilator disconnection

Leak on ventilator of
patient cuffs
Chest Physio Therapy ( Cpt )
Postural drainage
Chest percussion
Decrease bronchial secretion
Coughing Exercise
Position: sitting
Inhale slowly through the nose, exhale
through purse lips and cough twice during
Note: for splint incision area to prevent
dehiscence / evisceration

Chest Drainage


After thoracic surgery
Pneumothorax / pleural effusion
Remove excess fluid / air
Re expand the lungs
Restore negative pressure
Collection Chamber
Blood / Fluids
Maintain ( - ) pressure
Monitor / Report
o 100ml / Hr
o Sudden increase in bright red color
Water Seal Chamber
Note for patency
No bubbling ( leak )
Stop flanctuation
o Obstruction / Full expansion
Suction Controlled Chambers
With 20mm of sterile NSS
With gentle continuous bubbling
Absent of bubbling
o Not enough suctioning
o Vigorous leakage

80% TBW ( infant )
60% TBW ( male )
50% TBW ( female )
Function of fluid
Maintain blood volume
Transport gas & nutrients
Chemical cellular function
Eliminate waste ( urea )
Intake & Output
Intake ( 2600ml)
o Oral
o Water in food
o Metabolism
Output ( 2600ml )
o Urine
o Stool
o Insensible


Movement of body fluids
Colloid oncotic & osmotic pressure
Pulling force ( moving in )
Plasma ( oncotic ) albumin ( CHON )
Solutes ( osmotic ) sodium
Osmolarity ( mOsm/L ) / Osmolality (
mOsm/kg )
o Measures the concentration of the
o 270 – 300mOsm/L ( kg )
Hydrostatic pressure
Pushing force ( moving out )
Fluid regulation
Main organ for excretion & regulation of F&E
( urine )
3 process:
o Glomerular filtration
o Tubular reabsorption
o Tubular secretion
ANP ( Anti Natriuretic Peptide ) sodium
Atrium of the heart( stretch )
Potent diuretic / reduce thirst
Thirst mechanism ( earliest sign of FVD )
o Dry mouth ( xerostamia )
o Hyperosmolarity
ADH ( Anti Diuretic Hormone) - vasopressin
Released by Neurohyphopysis
Synthesize in the Hypothalamus

Amount & Composition:
Intracellular: ( 2/3 fluid )
Extracellular :
Intravascular ( 3L ) plasma ( 90%)
Interstitial ( 11 – 12L ) lymphatic fluid
Transcellular (1L ) specific function
o Cerebrospinal, pericardial,
pancreatic, pleural, intraocular,
biliary, peritoneal, synovial fluid


Increase serum osmolarity. ADH is produced
– collecting ducts become permeable
RAAS ( Renin Angiotensin Aldosterone System )
Juxtaglomerular cell of the kidney initiates
Baroreceptors ( pressure detectors )
Osmoreceptors ( osmolarity detectors )


Active chemicals in the plasma ( ions )
Maintaining fluid balance
Acid base regulation
Transmitting neuromuscular reaction
Dynamic transport of F&E
Passive ( - )ATP
o Diffusion ( H – L ) particles
o Osmosis ( L – H ) water
o Filtration ( H – L movement of
F & E in a semi permeable
Active ( + )ATP
o Sodium – Potassium pump (
balance the potassium )
Fluid volume deficit
When loss of ECF exceed the intake of fluid
Fluid not sufficient to meet the fluid needs of
the body
Inadequate fluid intake
Impaired mental status
Lack of access of fluid ( rare )
Abnormal fluid loss
GI suctioning
Excessive sweating
Disorder that increase fluid loss
DI ( decrease ADH )

o Polyfagia
o Polydypsia
o Polyuria
ARF ( diuretic phase )
o Increase metabolic rate
o Diaphoresis
Adrenal insufficiency
o Addisons disease.
o Regulate



Third space fluid shifting
Fluid accumulate in a certain parts of the
body which is not necessary ( non functional )
o Pathologic in origin
o Disease
o Burns edema
o Electrolytes loss equals to Fluid
o Electrolyte loss less than or equals
to Fluid loss
Hypertonic ( most common )
o Fluid loss greater than Electrolyte
Decreased skin turgor
Weight loss
Oliguria / concentrated urine
o 1.02 – 1.025cc/hr
Weal / rapid HR
Flattened neck vein
Delayed capillary refill
Warm, dry skin
Muscle weakness & cramps
Sunken fontanels & eyeballs
Assessment & DX findings
Blood osmolarity
Hematocrit ( decrease in plasma )
Urine specific gravity
Low central venous pressure
( 2 – 6mmHg )
Changes in V/S ( hypo-tachy-tachy )


Fluid replacement


Promote safety
Oral care & skin care
Encourage OFI ( mild – moderate )
Monitor for V/S, I & O, weight & LOC


No dehydration

Mild dehydration

5 – 10% TBW


Moderate dehydration
(Insatiable thirst)

10% TBW


Severe dehydration
(too weak to move )

< 5%TBW

Fluid volume excess
Result from either:
o Increase in water / sodium
o Decrease in water / sodium
o Electrolytes equals to Fluid
o Electrolyte greater than Fluid
Hypotonic ( most common )
o Electrolyte less than or equals to
Excessive IVF therapy ( fluid overload )
Renal failure ( oliguric phase ) CRF – ESRD
Long term corticosteroid ( Na+ reabsorption )
Distended neck vein
Abnormal lung sounds
Polyuria ( diluted urine ) except SIADH
Assessment & DX findings:
Blood osmolarity


BUN ( renal function test)
Urine specific gravity
Bounding pulse rate
Increase BP


Prevent further fluid overload


Restrict fluid & Na+ intake
Monitor V/S ( bp ), I & o, weight & LOC
WOF complication





135 – 145meq/L ( normal )
Primary determinant of Osmolarity
Responsible for excitability of the
neuromuscular junction
Regulated by ADH, ANP, RAAS & thirst
Less than 135meq/L
Inadequate intake
Increased excretion
o Vomiting, diarrhea, excessive
diaphoresis & dieresis of fluid /
Water excess ( dilutional hyponatremia )
o Excessive intake of hypotonic fluids
o Disorders that result to water
Anorexia, Nausea & Vomiting
Headache & Dizziness
Alteration of LOC
Muscle cramps & Weakness
Edema & Low BP
Laboratory findings
Serum sodium
Urine sodium
Urine specific gravity
Sodium replacement
o Hyper Osmolar Demyelination
(complication of Na+ replacement)
<12meq/L for 24hrs

Water restriction for dilutional
Enforce high sodium diet
o Avoid SPC ( sauce, process food,
canned goods
Promote safety

Greater than 145meq/L
Causin crenation ( shrinking of cell )
Decreased sodium excretion
o Corticosteroid
o Cushing syndrome ( hyper activity
of adrenal gland )
o Conn’s disease
Increased sodium intake
Decreased water intake
Increased water loss
Dry sticky mucus membrane
Flush skin ( hyperemia )
Peripheral / pulmonary edema
Increase deep tendon reflexes
Alteration of LOC
Laboratory findings
Serum sodium
Urine sodium
Urine specific gravity
Increase fluid
Restrict sodium
Promote sodium excretion
Promote safety
Monitor V/S and I & O
3.5 – 5meq/L
Major intracellular cation
Important for neuromuscular function
Regulated by kidney & aldosteron
Below 3.5meq/L

Decreased potassium intake
Excessive potassium loss
o Use of diuretics / corticosteroid
o Vomiting & diarrhea
o Disorder that increase K+ excretion
Movement from ECF to ICF
o Alkalosis
o Hyperinsulinism
o Weak, Thready pulse & Hypotension
o Dysrhythmia
o Shallow & Ineffective respiration
o Confusion, Lethargy & Coma
o Muscle weakness, Leg carmaps &
o Deep Tendon Hyporeflexia
Gastro Intestinal
o Decreased motility
ECG changes
o Flat or inverted T wave
o Low ST segment
o High U wave
Metabolic alkalosis
Respiratory failure
Potassium replacement
o Encourage intake of K+ ( ABCPOT )

Avocado / Apricot


Carrot / Cantalope



Administer K+ supplement
Provide sympthomatic treatment
WOF complication
Remember: UNANO
U – rine output greater than 30cc/hr
N – ever via Bolus
A – ssess IV site ( phlebitis )
N – not more than 1meq/10cc (PNSS)

99% bone ( hydroxyl apatite crystals ) Bone strength / density Calcium is inversely proportional to Phosphorus Function - Forms: - Transmission of nerve impulse Necessary for blood coagulation Cloting factor #4 Decreases cellular membrane permeability o Decrease Serum Ca+ stimulate the Parathyroid gland to secrete PTH which will trigger Osteoclastic activity o Increase serum Ca+ stimulate Parathyroid gland to secrete Calcitonin which trigger Osteoblastic activity Ionized: (4. flaccid & paralysis Gastro Intestinal o increased motility DX: findings ECG changes o Tall peaked T wave o Wide QRS complex o Prolonged PR intervals o Flat P wave Complication Dysrhytmia Metabolic acidosis Respiratory failure TX: Restrict K+ intake Dialysis WOF complication Pharmacotherapy Potassium excreting diuretics Polysterine Sulfonate ( Kayexalate ) Na+ resin exchange Regular insulin & IV glucose Calcium Gluconate Sodium Bicarbonate CALCIUM IMBALANCE ( CA+ ) 8.1mg/dL ) 50% physiologic active Bound / Complexed ( citrate/phosphate ) HYPOCALCEMIA Less than 8.2meq/dl ( serum) Regulated by PTH & Calcitonin ( thyroid ) 1% serum . D Malabsorption (Cronhs disease/ulcerative colitis) ESRD Disorder resulting to Steatorrhea Hypoparathyroidism Increase Ca+ excretion Renal disease ( diuretic phase ) Massive blood transfusion ( citrate ) anticoagulant Hyperphosphatemia Pancreatitis ( lipolysis ) increase FFA – Ca+ binds to FFA CM: Fast & High CNS: Tingling sensation & Seizures GI: Increased peristalsis CV: Dysrhytmia RESP: Laryngospasm MUSCOSKELETAL: Muscle spasm.6 – 10.` O – n cardiac monitor if greater than 10meq/hr HYPERKALEMIA Greater than 5meq/L Causes: Excessive intake of K+ rich food/ medication Decreased K+ excretion o Use of Potassium Sparing Diuretics o Renal failure o Adrenal failure Movement of K+ from ICF – ECF o Tissue damage o Acidosis CM: Cardiovascular o Dysrhythmia Respiratory o DOB ( late ) Neuromuscular o Early  Muscle twitching & spasm o Late  Muscle weakness. & Tetany ( + )Trousseaus & Chvostek sign Risk for: TX: - Osteoporosis Bone fracture Bleeding High Ca+ diet Calcium supplementation Promote safety Monitor Cardio – Respiratory function ( dysrhytmia ) Pharmacotherapy Calcium Gluconate 10% Aluminum Hydroxide ( Amphogel ) phosphate binding agent HYPERCALCEMIA Greater than 10.2mg/dL Causes: Increase Ca+ absorption / intake Decrease Ca+ excretion Increase Ca+ resorption o Hypothyroidism o Malignancy ( ectopic PTH ) o Immobility stimulate Osteclast (physical stress stimulate Osteoblast ) o Hemoconcentration o Use of Thiazide Diuretics CM: Low & Slow Decrease neuromuscular activity o Muscle weakness o Diminished ( absent of deep tendon reflex ) o Lethargy & Coma ECG changes Gastro Intestinal disturbances o Anorexia. nausea & Vomiting o Decrease Bowel movement Formation of Renal Calculi Decrease Bone density .5 – 5.6mg/dL Causes: Decrease Ca+ absorption Inadequate intake of Ca+ Inadequate intake of Vit.

Hasselbach equation ) 20 : 1 . HCO3 ) REGULATORY SYSTEM OF BLOOD PH Carbonic Acid – Bicarbonic System Normal ratio: 20:1 ( Henderson .TX: Decrease calcium in diet WOF complication of hypercalcemia Increase OFI Pharmacotherapy PNSS Phosphorus Calcitonin Mithracin (antineoplastic antibiotic) decrease serum Ca+ MAGNESIUM IMBALANCES ( MG+ ) 1.45pH ( alkalosis ) o Respiratory alkalosis ( dec H2CO3 ) o Metabolic alkalosis ( inc.7meq/L = NaCl  ( Less than 9% is hypotonic )  .45pH ) < 7.3meq/L Causes: Excessive intake of Mg+ Decreased Mg+ excretion Assessment: Low & Slow - - Neuromuscular o Hypoflexia o Drowsiness / Lethargy o Skeletal muscle weakness Cardiovascular o ECG changes o Bradycardia / hypotension Respiratory depression TX: Decrease Mg+ in diet D/C of Mg+ based antacid Pharmacotherapy Diuretics Calcium Gluconate ( antidote to Mg+ toxicity) IV Therapy Purpose: Replacement therapy ( F & E ) Provide vascular access ( blood products medication ) Types of solution Colloids ( Albumin / Dextran ) Increasevascular volume rapidly Tonicity ( strength to provide osmotic forces ) o Isotonic ( same osmolarity as body fluids ) 154meq/ L ( Na+/CL+ )  9% NaCl  PNSS ( plain normal saline solution ) o Hypotonic ( lower osmolarity – fluid moves out to ICF – cell will swell – Lysis ( rupture ) 7.< 1 month ) o PICC ( Peripheral Inserted Central Catheter ) > 1 month ( antecubital vein) x ray PPN Small concentration ( < 10% CHO ) Short term PN ( < 1 week ) Arm Complication H – yperglycemia A – ir embolism ( ask patient to perform valsalva maneuver P – neumothorax I – nfection ACID – BASE IMBALANCE Concentration of H+ ion ( 7. heart failure.3meq/L Necessary for Carbohydrates & Protein metabolism Inhibits the production of Acethylcholine ( muscular contraction ) HYPOMAGNESEMIA Less than 1. HCO3 ) > 7. cerebral edema.35 – 7.6meq/L ( vasoconstriction ) Causes: Insufficient Mg+ intake Increase Mg+ secretion Assessment: High & Fast Cardiovascular o ECG chages o Tachycardia ( hypertension ) Neuromuscular o (+) Trousseaus & Chvostek sign o Hyperreflexia o Tetany & Seizures o Muscle twitching TX: Increase Mg+ diet Promote safety WOF complication Pharmacotherapy Mg+ sulfate ( IV ) o B – lood pressure o U – rine output ( oliguria: 30cc/hr ) o R – espiratory rate ( <12cpm ) o P – atellar reflex ( absent ) HYPERMAGNESEMIA Greater than 2.35pH ( acidosis ) o Respiratory acidosis ( inc. H2CO3 ) o Metabolic alkalosis ( dec.45%NaCl ( half strength) NSS  25% dextrose in water  2% dextrose in water  Precaution: pulmonary edema.6 – 2. increase ICP o Hypertonic ( higher osmolarity – increase osmotic pressure )  3% NaCl ( 513 me/L of NaCl )  5% NaCl (856meq/L of NaCl )  Lactate Ringer – cell shrink – Crenate Lactate Ringer ( Hartman Solution ) Na+: 130meq Cl+: 109meq Lactate 28meq K+: 4meq Ca+: 3 meq Parenteral Nutrition Least desire option Nutrition via Vein Indication Severely dysfunctional or non functional GI Need to rest GI ( severe abdominal surgery ) Need to meet high nutritional requirement Types of PN ( 5 – 70% vary CHO ) TPN Large concentration of CHO >10% Long term PN ( > 1 week insertion ) Intrajugular / Subclavian ( > 1 week .

HCO3 ( Kidney ) Hour / Days - o o o o H2CO3 ( Lungs regulates amount of CO3 ) Seconds / Hours Carbonic acid is controlled by retention or excretion of carbon dioxide Bicarbonate is released / excreted by kidney Potassium plays an exchange role H+ exchange to potassium (compensation ) Plasma – Protein System Have the ability to attract or release hydrogen ions ( albumin – strongest ) Respiratory Acidosis Carbonic acid excess Cause: Carbon dioxide retention Disorder that result to respiratory disorder o B-rain trauma o A-sthma o H-ypoventilation o A-telectasis o P-neumonia o E-mphysema o P-ulmonary edema o U-se of CNS depressants CM: Increase Blood pressure.23 ( acidosis ) PCO2: 21 ( acidosis ) PCO3: 27 ( alkalosis ) nd 2 Identify etiology Check for the same value of pH pH 7.35 ) o Alkalosis ( > 7.45 ) PCO2 ( 35 – 45mmHg ) o Acidosis ( > 45mmHg ) o Alkalosis ( < 35mmHg ) PHCO3 ( 22 – 26mmHg ) o Acidosis ( < 22mmHg ) o Alkalosis ( > 26mmHg ) Steps: 1st Analyze the data: Ex.45pH ) o Acidosis ( < 7. Repsiratory rate Increase ICP ( cerebral vasodilation ) acidosis Depression of CNS o Disorientation o Drowsiness  Monroe Kellie Hypothesis ( cranium close cavity )  Brain Herniation (dangerous ) NI: TUC Promote / Monitor oxygenation Monitor electrolyte value Prepare for ET / Mechanical ventilation WOF complication Respiratory alkalosis Carbonic acid deficit Cause: Carbon dioxide over excretion Disorder resulting to respiratory alkalosis o Hyperventilation Hysteria & Anxiety Fever Pain Over ventilation by mechanical ventilation CM: - Light headedness ( initial ) Sign of hypokalemia Tachycardia Tetany / Muscle twitching Seizures ( over stimulated CNS ) - Alleviate anxiety Encourage proper breathing pattern Promote CO2 breath Monitor electrolytes NI: METABOLIC ACIDOSIS Bicarbonate acidosis or deficit Cause: Diabetic Ketoacidosis ( faster than ketone rate oxidation ) Excessive ingestion of ASA Insufficient CHO metabolism Malnutrition Renal failure Severe diarrhea CM: Kussmaul Respiration (increase rate / depth) Sign of hyperkalemia Drowsiness / Lethargy Coma TX: Fluid replacement Promote safety Pharmacotherapy Sodium Bicarbonate o TUC o WOF complication METABOLIC ALKALOSIS Bicarbonate excess Cause: Excessive vomiting Gastrointestinal suctioning Hyperaldosteronism Massive blood transfusion ( citrate repel / bind to H+ ) CM: Hypoventilation - Sign of hypokalemia Tetany & muscle twitching Seizures TX: Safety Pharmacotherapy NaCl ammonium chloride Carbonic Anhydrase Inhibitors o Identify & TUC o WOF complication ABG ( ARTERIAL BLOOD GAS ) Normal values: PO2 ( 80 – 100mmHg ) pH ( 7.23( acidosis) PCO2(acidosis)= respiratory acidosis 3rd Check or identify compensation (if normal) PCO2: 21 ( acidosis ) PCO3: 27 ( alkalosis ) Compensated th 4 Identify the degree ( totally / partially ) If the pH is normal ( totally ) GENITO – URINARY SYSTEM Maintain homeostasis by regulating fluid component & volume . Heart rate.35 – 7. pH: 7.

but not blood Proximal convoluted duct o The portion of the renal tubule in the nephron between the Bowman's capsule and the . urea. and other small molecules found in blood Filtration o The process by which filtrate enters the renal tubule without allowing blood Glomerulus o A ball of capillaries that secretes filtrate into the Bowman's capsule Juxtamedullary nephron o A nephron whose loop of Henle extends past the cortex and well into the medulla Loop of Henle o A long. narrow portion of the renal tubule which extends into the deeper tissue of the kidney Peritubular capillaries o The capillaries that weave around and between the proximal and distal convoluted tubules Podocytes o Selectively permeable cells on the capillaries of the glomerulus that allow water and small solutes into the Bowman's capsule. salts.branch into the renal pelvis ( basin like cavity ) Adrenal glands ( located in the top of the kidney ) Nephrons ( urine formation ) basic functional unit of the kidney - - - - - - - 3 parts of kidney Parts: - - - Afferent arteriole o The artery that subdivides into the capillaries that compose the glomerulus Bowman's capsule o The cup-shaped capsule that encompasses the glomerulus and draws filtrate from the blood Brush border - Microscopic protrusions that increase the surface area for reabsorption Cortical nephron o A nephron whose loop of Henle does not extend past the cortex Distal convoluted duct o The portion of the renal tubule in the nephron between the ascending limb of the loop of Henle and the collecting duct Efferent arteriole o The artery that is formed when the capillaries in the glomerulus converge Filtrate o The fluid in the renal tubule which consists of water.2 ½ inches ( female ) o Risk for UTI Bladder Reservoir of urine Detruser muscle / smooth muscle ( excreting urine ) 1000cc maximum capacity ( disorder ) 400 – 500cc ( physiologic ) 200 – 250cc ( void reflex ) Stretch receptor stimulate detruser muscle Cortex o Superficial parts of the kidney Medulla o Innermost part of the kidney that contains the renal/medullary pyramids o Contains calyces that collects urine  Calyces .o - - - Kidney - Ureter - T12 – L3 vertebra ( costovetebral angle ) Retroperitoneal area Enclosed by fibro renal capsule ( shiny appearance – fatty layer – adipose tissue ) attach to muscular wall 25 – 30mm Transport urine ( renal pelvis – bladder ) Obliquely inserted ( ureterovesicular sphincter ) urinary reflux Urethra 5 – 7 inches ( male ) o Posteriorly – Lateraly to prostate 1 ½ .

Most accurate in malignancy & cancer. ptt. urea.2mg/dl o Stomatitis & GI bleeding o Urineferous breath o Hyperpigmentation ( increase urochrome ) o Uremic frost ( severe dryness/ itchiness of the skin ) o Decrease libido Complication Renal Encephalopathy Inability to secrete erythropoietin o Severe & Chronic Anemia Inability of the kidney to regulate fluid & electrolyte o Oliguria o Edema o Hyperkalemia o Hypermagnesemia . pc ) Mild sedation is done Prone position Local anesthesia Ask client to hold breath After: Bed rest Monitor for bleeding & V/S ( hypo-tachytachy Increased oral fluid intake Risk: Bleeding Infection Function of kidney Remove waste Regulate fluid &electrolyte Restore pH balance Nephrotoxic agent A – minoglycoside N – SAIDs T – etracycline A – ntineoplastic V – ancomycin A – mpothericin B Type of shock Cardiogenic Anaphylactic Septic Hypovolemic Neurogenic - Distributive DISORDER OF GENITO-URINARY TRACT RENAL FAILURE CHRONIC RENAL FAILURE ( CRF ) Gradual & progressive loss of renal function Irreversible Cause: DM ( diabetic nephropathy ) HPN ( hypertension nephrosclerosis ) Chronic Glomerulonephritis Autoimmune disorders ( incompetent suppressor T-cell ).SLE / Lupus nephritis Advancement of acute renal failure Staging: CRF ( old ) Renal impairment 40 – 50% GFR Renal insufficiency 20 – 40% GFR Renal failure 10 – 20% GFR ESRD <10% GFR ( new ) Stage I > 90ml/min Stage II 60 – 89ml/min Stage III 30 – 59ml/min Stage IV 15 – 29ml/min Stage V < 15ml/min CM: Inability to excrete metabolic waste o Increased BUN & serum creatinine  BUN: 10 – 20mg/dl  Creatinine: . apt. Bladder & Urethral opening using a cystoscope NI: Before: Must secure a consent Lithotomy position After: Increase fluid intake ( to promote urination ) Assess urine output ( pink tinged color is normal within 24hrs ) Relieve discomfort ( hot seat bag / warm compress ) KUB ( kidney.6 – 1. bladder x-ray visualization ) NI: Bowel preparation as ordered o Laxative ( night before procedure ) o Enema ( morning before procedure) Assure that the procedure is painless IVP ( intravenous pyelography ) Indirect visualization with contrast medium NI: Before: Written consent Assess for allergy to iodine o Antihistamine – allergy o Epinephrine – anaphylactic shock Bowel preparation After: Increase fluid intake ( for excretion of dye ) Assess voiding pattern ( to determine excretion of dye ) UTZ ( ultrasound ) Soundwave Deyecys tumor. excess fluids & electrolytes ) Clean blood ( renal veins to circulation ) Process: Glomerular filtration Tubular reabsorption Tubular secretion Cystoscopy – direct visualization of Urethra. NI: Before: Check for bleeding parameters ( inr. obstruction & cyst NI: Bowel preparation Distend the bladder ( drink 2 – 3 glass of water 3omin before procedure ) Renal biopsy – removal of living renal tissue for microscopic examination. urethra.descending limb of the loop of Henle Reabsorption o The movement of substances from the filtrate back into the interstitial fluid so as to be readmitted into the blood stream Renal tubule o The tube through which filtrate passes as it is converted into urine in the nephron Secretion o The addition of plasma solutes into the filtrate from the interstitial fluid How does kidney works? Kidney – blood supplied – renal arteries – nephrons ( separate waste – clean bloods ) Waste ( ammonia.

Target weight Assess for bleeding ( heparin bolus ) Provide adequate nutrition ( first 2hrs patient can eat anything ) Complication Air embolism ( rare ) Infection ( reprocessing or reuse of dialyzer ) Painful muscle cramps ( incompliant patient ) Dialysis encephalopathy ( aluminum toxicity / dialyzate solution is not good ) Disequilibrium syndrome ( CNS disturbances ) st o 1 timer ( decrease duration of HD ) PERITONEAL DIALYSIS No dialyzer Peritoneum acts as a dialyzing membrane Dialyzate solution ( sterile ) Indication Susceptible to rapid fluid . femoral ) Dialyzate solution ( non sterile ) Indication Acute renal replacement ( temporary ) Chronic renal replacement ( permanent ) Types of vascular access AV graft o Surgical connection ( synthetic blood vessel ) GORETEX o For geriatric patient with inadequate blood vessel ( 1 month ) External AV graft o Outside the body o Silastic cannula AV fistula o Most common form o Anastomosis ( 1 – 2 months ) Subclavian / intrajugular / femoral vein catheter o 6 weeks ( risk for infection ) Nursing care: Arm precaution on patient with AV access Assess for patency of AV access o Bruit ( auscultate ) o Thrill ( palpate ) Monitor V/S & LOC ( q30 ) Omit hypertensive medication ( 24hrs ) Promote comfort ( 3 – 4hrs / 2 – 3weeks ) Monitor weight o Actual weight . BUN.Na+. creatinine >Pulmonary edema >fluid volume excess >decrease BP >Hypovolemic Shock >fluid volume deficit Hypercalcemia Hyperphosphatemia Hyperparathyroidism Hyperosteodysthropy TX: - - - - Fluid restriction ( 800cc/day ) Electrolyte control Proper diet o Increase CHO o Decrease CHON.K+ & fluid Treat complication o Anemia ( epoitin alfa / epogen alfa – subQ ) o GI disturbances o CHF o HPN Dialysis Renal transplant o GVHD – graft vs. electrolyte imbalances 2 types: Coupling ( 1x use ) Reprocessing ( 4x use – ideally ) ( 6x maximum ) HEMODIALYSIS Requires vascular access ( subclavian.- o Sodium imbalances o Metabolic acidosis Inability to activate Vit. electrolyte & metabolic changes duing HD ( 36 – 48hrs ) Insertion Site: 3 – 5cm below umbilicus ( avascular ) TENCKHOOF CATHETER Nursing care 1st few bottle will have pink tinged drainage Warm the dialyzate ( to promote vasodilation ) removal of extra waste & avoid abdominal cramping WOF peritonitis ( cloudy drainage If drain stops put patient in side lying position Process: Infusion ( introduce dialyzate ) 5 – 10min Dwelling ( solution stay in the peritoneum membrane ) 20 – 30min Drainage ( drain the solution ) 10 – 20min o Clamp ( regulator ) o Dialyzate ( increase dextrose content ) o Every 1 cycle – 2L CAPD( continuous ambulatory peritoneal dialysis ) URINARY CALCULI Stone in the urinary tract 70% of stone formed in the kidney . intra jugular.D Urine output Electrolyte Urine < 4L/day Oliguric phase >Dilutional hyponatremia >Hyperkalemia concentrated 4L/day Diuretic phase >True hyponatremia >Hypokalemia diluted o o o o >Increase BP. host disease ( immunosuppressant ) – cyclosporin ( prograft/prednisone ) Promote comfort ACUTE RENAL FAILURE Sudden loss of renal function Reversible Cause: Pre renal ( decrease renal perfusion – before kidney ) Renal artery obstruction Infarction Cardiac disorder Hypovolemia Shock Intra renal ( inside the kidney ) Pigment nephropathy Acute tubular necrosis Acute glomerulonephritis Acute pyelonephritis Nephrotoxicity Post renal ( obstruction of renal outflow ) Benign prostatic hyperplasia Blood clots Calculi Tumor Phase: Onset: from exposure to precipitating factor Oliguric / Anemic phase ( 1 – 3 weeks ) Diuretic phase ( 1 week ) Recovery phase ( 1 – 2 years ) 80% recovery DIALYSIS Acute renal failure & chronic renal failure with severe fluid excess.

prunes ) o Low calcium/phosphate diet Calcium oxalate stones o Acid ash diet o Low calcium / oxalate diet Struvite o Acid ash diet o Low phosphorus diet Uric acid stones o Alkaline ash diet  Fruits except CPP o Low purine diet Cystine stone o Alkaline ash diet Medical intervention Pharmacotherapy Calcium stones o Aluminum Chloride / Calcibind Phosphate stones o Amphogel Uric stones o Allupurinol Stone removal Extracorporeal Shockwave Lithotripsy Surgery Nephrolithotomy Pyelolithotomy Ureterolithotomy NEPHROTIC SYNDROME Caused by glomerular drainage / increased glomerular permeability Risk factor Not a specific disease ( complication ) Malignancy DM / HPN Toxins CM: Proteinuria ( albuminemia ) Microscopic or no hematuria Hypoalbuminemia Edema Elevated serum cholesterol o Breaking down of lipoprotein Malaise / easy fatigability Irritability / headache TX: Medical management o Bed rest o High protein diet o Low sodium diet Pharmacotherapy o Anitlipidemics ( statin ) o Diuretics o Plasma / volume expanders NI: - Monitor hydration status Promote safety GLOMERULONEPHRITIS Inflammation of glomerular capillaries Cause Post infection ( GABHS ) Auto immune disorders o Antigen antibody complex Type Acute ( 2 – 3 weeks after streptococcal infection) Chronic ( slow progression) Assessment Proteinuria Periorbital / facial edema Cloudy smoky urine Pallor Irritability / lethargy Hypertension Severe sign of ARF ( oliguric phase ) Laboratory findings Elevated Aso titer Increased BUN / creatinine NI: Monitor V/S & hydration status Limit activity / provide safety measure WOF complication Pharmacotherapy Diuretic Antihypertensive ( ACE inhibitors ) Anitibiotics PYELONEPHRITIS Inflammation of renal pelvis ( basin like ) Cause Ascending infection ( urine ) Systemic spread of infection ( blood ) 2 types Acute pyelonephritis ( enlarge kidney / interstitial infiltration ) .Types of stone Alkaline stone o Calcium phosphate 75% o Calcium oxalate o Struvite . plums.staghorn  Magnesium  Ammonia  Phosphate  Urease splitting microorganism  Klebsiella  Pseudomonas  Staphylococcus  Streptococcus Acidic stone o Uric acid ( hyperuricemia )  Gout ( inherited disorder of urine metabolism ) o Cystine stone ( malabsorption of cystine ) Most common causes Hypercalcemia Urinary stasis Dehydration Elevated uric acid UTI Diagnostic procedure KUB IVP CT scanning Renal UTZ CM: Renal colic ( sudden severe sharp pain from lumbar – abdominal – testicle ) GI disturbances ( nerve plexus – genito intestinal reflex ) o Anorexia / vomitting o Diarrhea / constipation Changes in bladder pattern o Dysuria o Urine frequency TX: Increase oral fluid intake Strain all urine Pain management Nutritional therapy Calcium phosphate stones o Acid ash diet ( cranberries.

- Chronic pyelonephritis ( contracted & scar kidney ) CM: Fever & chills Leukocytosis Bactenuria & Pyuria Flank pain Dysuria ( kidney punch ) DX procedure UTZ CT scan IVP TX: Usually on outpatient basis ( if not complicated ) Increase oral fluid intake Antibiotic ( 2 weeks ) o Fluoroquinolone o Cotrimaxazole o Cephalexin Uralgesic ( phenizopyridine ) pyridium o Red orange urine ( normal o Absence of pain to test efficiency WILMS TUMOR Encapsulated tumor of the kidney Rapid proliferation of the rhinoblast Assessment Non tender mass Hematuria Lethargy Anorexia DX: UTZ CT scan MRI TX: Surgical removal of tumor o Chemotherapy / radiation  Before . hesitancy Increased residual urine Decreased projectile force of the urine Hematuria DX: Cystoscopy UTZ Digital rectal examination .for tumor to shrink  After – to prevent metastasis or recurrent URINARY TRACT INFECTION Urethra ( urethritis ) Ureter ( ureteritis ) Baldder ( cystitis ) Female is high at risk E. coli ( most common causative agent ) Risk factor Incomplete bladder emptying Immunosuppresion ( iatrogenic/pathogenic ) Instrumentation DM Pregnancy CM: F-requency U-rgency C-hills K-( cloudy urine ) E-levated temperature D-ysuria S-uprapubic pain DX: Routine urinalysis o Increase WBC o Bacteruria o Pyuria Urine C&S NI: Increase oral fluid intake Acidify urine ( CPP) Relieve pain ( pyridium ) 4W o Water therapy o Wash after sex o Wear cotton underwear o Wife ( front to back ) Avoid urinary stasis Empty bladder after sex Pharmacotherapy Uralgesic ( phenazopyridine ) Urinary antiseptic Antibiotic o Fluoroquinolone ( floxacin ) o Sulfonamides ( sulfadiazine ) At risk : Steven Johnson Syndrome ( crystanuria ) Exposure to radiation Common site of metastasis Liver Bones Lungs Assessment Painless hematuria ( initial sign / most characteristics ) Dysuira ( late sign ) Urinary frequency Urgency DX: Bladder wash specimen Biopsy NI: Treatment for cancer ( surgical intervention ) Cystectomy ( urinary diversion ) o ILEAL CONDUIT ( ileum is cut and connected through anastomosis Cutaneous ureterostomy Indiana pouch (straight catheter for draining) BLADDER CANCER Papillomatous growth ( pre cancerous ) Undergoes malignant change Infiltrate bladder cell wall Common among males Predisposing factors Cigarette smoking Exposure to industrial chemicals TX: Surgical intervention Transurethral resection of the prostate o Continuous bladder irrigation Suprapubic prostectomy Retropubic prostectomy Perinial prostectomy BPH ( BENIGN PROSTATIC HYPERPLASIA ) Prostate enlargement Cause is unknown Resulting to comprehension of the urethra Complication Renal failure UTI Renal calculi Assessment Nocturia Frequency. urgency.

stroke.infection Pharmacotherapy Desmopressin acetate ( DDVAP ) Vasopressin ( pitressin ) Clofibrate ( antilipidemic medication) SIADH Excessive water retention Cause Brain trauma ( increase ICP ) Cushing triad hyper brady brady Ectopic ADH production o Some cell are capable of producing hormone ( lung carcinoma. a hormone that affects the modulation of wake/sleep patterns and seasonal functions. It produces the serotonin derivative melatonin. trauma ) CM: Edema Weight gain HPN Hyponatremia Signs of hypovolemia Decrease urine output ( concentrated ) TX: Fluid restriction Monitor V/S Assess cardio respiratory function Assess neurological assessment o Cerebral edema .Responsible fpr production of TSH Adrenocorticoid hormone Stimulates adrenal cortex MSH ( melanocyte stimulating hormone ) Signals to the brain have effects on appetite and sexual arousal. Gonadtropic hormone TSH & LH Development of secondary hormone HYPERPITUITARISM Hyper function of adenohypophysis Related disorder Acromegaly / Gigantism Gigantism ( increase GH before closure of epiphyseal plate / lengthening of the bone ) o Epiphyseal line – not active Acromegaly ( increase GH after closure of epiphyseal plate / widening of the bone ) Cushing syndrome Galactorrhea ( excessive milk production ) Hormonal imbalances TX: Surgery Transphenoidal hypophysectomy o Removal of pituitary – lifetime hormone replacement therapy  Insition site ( between upper lip & upper gum Pharmacotherapy Bromocriptine ( Parlodel ) only effective in inhibiting growth hormone HYPOPITUITARISM Hypo function of anterior pituitary gland SSTT & CNS infection Related disorder Pituitary dwarfism . CHON & fat metabolism Antagonizing effect of insulin ( hyperglycemia Prolactin Necessary for breast development and lactation TSH ( thyroid stimulating hormone ) T3 & T4 . surgery stroke. Pituitary Gland o Located at the selia turcica inferiorly of the hypothalamus ( controlled ) Composed of 2 parts Anterior ( adenohypophysis ) glandular Posterior ( neurohypophysis ) nervous (+ feedback mechanism ) o Oxytocin  Milk let down reflex  Increase uterine contraction o ADH ( vasopressin )  Controlled osmolarity  Controlled water reabsorption DIABETES INSIPIDUS Decrease ADH Inability of the renal tubules to retain water DX: Water deprivation test o No water intake ( 8 – 12 hours) Polyuria Polydypsia Constipation Signs of FVD TX: - Fluid replacement Monitor V/S & LOC Monitor hydration status TUC o Tumor. CNS infection.most feared o Cushing triad o Widen pulse pressure Monitor hydration status TUC Pharmacotherapy Demeclocycline ( Declomycin ) o Antagonize effect of ADH in the kidney Diuretics ( loop diuretics ) ADENOHYPOPHYSIS Samatotropin ( growth hormone ) Stimulates growth Affect CHO.ENDOCRINE 2 types CM: o o - Exocrine ( w duct ) Endocrine ( w/ out duct ) Pineal Gland is a small endocrine gland in the vertebrate brain. trauma.

4mu/ml )’ o Primary hypothyroidism ( problem is in the thyroid gland itself ) – decrease T3 – T4 / increase TSH assay o Secondary hypothyroidism or (problem is in the stimulation ) – increase T3 – T4 / decrease TSH o Hyperthyroidism – increase T3 – T4 / decrease TSH assay T3 : 80 – 230ng/dL (decrease hypothyroidism) T4 : 5 – 12mcg /dL (increase hyperthyroidism) Radioactive iodine uptake Iodine123 ( radionuclide isotope ) o Measure the absorption of iodine isotope o Normal value:  3 – 10% at 24hour urine specimen - GOITER Thyroid scan o Radio isotope of iodine is administered before scanning o Identify nodules ( hot & cold areas ) using gamma camera  Hot ( hyperactivity )  Cold ( hypoactivity ) - Enlargement of thyroid gland due to increase TSH My occur with o Hyperthyroidism & hyperplasia of thyroid cell o Hypothyroidism : Hyperthropy o Euthyroidism .- Panhypopituitarism ( Simon disease ) Post partum pituitary necrosis o Post partal hemorrhage ( Shechan disease ) - HRT ( hormonal replacement therapy ) TUC TX: THYROID GLAND T3 ( triiodothyronine ) T4 ( thyroxine ) o Regulate metabolism o T3 ( 5x more potent than T4 ) steady metabolic rate o Stimulates SNS response CNS underdevelopment ( neurological & psychological disturbance ) Thyrocalcitonin Inhibits osteoclastic activity DX: TSH assay ( .2 – 5.decrease intake of iodine Common types of Goiter Endemic Goiter Goiter belt area: o ( far from sea ) no seafoos w/c is rich in iodine o Mountainous regions ( goitrogenic foods )  Cabbage  Radish  Turnips  Sweet potato  Spinach Sporadic Goiter Goitrogenic drugs o Antithyroid hormones o Lithium . palpitation. hypertensive crisis TX: Safety High calorie diet Eye care ( exopthalmos & dalyrimple signs ) Rest Environment cool Fluid & electrolytes replacement Monitor V/S and LOC Thyrotoxicesis – all clinical manifestation Pharmacotherapy Anti thyroid medication o Iodides – inhibits the release of thyroid hormones  Mix with H2O or juice. use straw ( prevent teeth stain )  SSKI ( saturated solution of potassium iodide ) Lugols solution o Thiomides – inhibits synthesis of thyroid homones  PTU ( proyl thio uracil )  Topazole ( methimazole carbimazole ) o Antihypertensive Surgery Subtotal thyroidectomy ( 5/6 areas of thyroid ) o Pre op medication – Lugols solution ( to shrink the size of thyroid gland / decrease blood supply thyroid gland o Post operation – ensure V/S are stable / support neck .manic patients Attention Deficit Hyperactive Disorder o Methyl Phynedate o ASA ( acethyl salicylic acid ( inhibits the production of TSH ) HYPERTHYROIDISM Increase T3 – T4 & metabolic rate Metabolism – sum of all biochemical reaction inside the body Hypersecretion of thyroid Incidence higher in females Graves disease Most common form Related to: Stress and infection Cause: Idiopathic CM: High – fast – wet except men ( amenorrhea ) High Increase neurologic status Increase BP Increase temperature Fast Fast heart rate Fast respiratory rate Wet Stool & skin Other manifestation Heat intolerance Enlarged thyroid gland Exopthalmos ( bulging of eyes ) fatty pads behind the eyes Dalyrimple sign ( thyroid stare ) infrequent blinking / the eyeballs irreversible THYROID STORM ( thyroid crisis ) Severe uncontrolled hyperthyroidism Hyperpyrexia ( 41 C ) – extreme nervousness.

CHON & fat metabolism Cause Exact cause is still unknown Predisposing factor Stress Heredity ( diabetes induced gene ) Obesity Autoimmune Types of DM Type 1 Insulin dependent Juvenile onset ( < 30 y/o ) Pathologic etiology o Absolute deficiency / no insulin produced Insulin treatment Acute complication o Diabetic Ketoacidosis Type 2 Non insulin dependent Adult onset ( > 30 y/o ) Pathologic etiology o Lack of insulin o Insulin resistance ( not recognized by the cell ) Oral hypoglycemic agent treatment Complication o Hyperglycemic Hyperosmolar Non Ketotic Coma CM: Cardinal sign ( 3-P ) o Polyuria ( due to hyperosmolar diuresis) o Polydypsia ( due to hyperosmolar dehydration ) o Polyphagia ( cellular starvation ) - Associated sign ( 3W ) o Weight loss ( due to prolonged cellular starvation ) o Wound ( slow to heal )  Diabetic foot ( poor circulation ) slow to heal because protein is utilized – slow tissue repair o Warm & dry . sardines.dry except men ( menorrhagia ) Low Low neurologic status Low BP Low temperature Slow Heart rate Respiratory rate Dry Stool & skin Other manifestation Cold fatigue Fatigue Hyperlipidema Loss of memory ( forgetfulness ) Myxedema Coma – extreme severe stage Risk for respiratory failure & coma TX: Low calorie diet Assess LOC Warm environment Monitor V/S and daily weight Pharmacotherapy Thyroid replacement therapy – shynthetic thyroid hormone o Levotherapy ( morning to prevent insomnia / empty stomach ) DISORDER OF THE PARATHYROID GLAND HYPOTHYROIDISM Hyposecretion of parathyroid gland S/S: Hypocalcemia Hyperphosphatemia TX: Hypocalcemia o Spinach. anchovies.Slow .o o WOF complication  Injury of the larynx ( speak every hour )  Mild hoarseness ( normal )  Severe hoarseness ( report )  Hemorrhage  Hypocalcemia ( larygospasm)  Thyoid storm ( deadliest ) Radiation  Radioactive iodine ( I131) NI: - Place client on isolation for few days Do not use in pregnant women Pregnancy should be delayed for 6 months HYPOTHYROIDISM Hyposecretion of thyroid gland CM: Low . o Calcium gluconate in D5W Cause - - Congenital ( decrease T3 – T4 ) slow CNS development Autoimmune ( myxedema ) o Cretinism ( hypothyroidism in children) o Hashimoto disease ( autoimmune ) Thyroidectomy Radioactive thyroid HYPERTHYROIDISM Hypersecretion of parathyroidism gland S/S: Hypercalcemia Hyperphosphatemia TX: Hypercalcemia o Galium nitrate DISORDER OF THE PANCREAS DIABETES MELLITUS Chronic disorder of the CHO.

Bones. Cartilage together with the bones Bones: 206 ( adults ) . PVD Diabetic nephropathy Diabetic retinopathy ( impair retinal circulation ) Diabetic neuropathy ( erectile dysfunction ) DX: Measurement setting Normal value Fosting blood sugar 70 – 110mg/dl Oral glucose tolerant / challenge test 30min 2hrs Remember DASAL: Down phenomenon – occurs due to nocturnal release of GH w/c antagonize insulin o Diurnal variation ( body clock ) o Night ( increase GH ) o Pre breakfast hyperglycemia Allergic response – local allergy o Pruritus o Itchiness at IV site Somogye phenomenon Normal blood sugar Hypoglycemia ( 2 – 3 am ) Increase intrinsic hyperglycemic hormone o GH o Norepinephrine / epinephrine o Glucagon o Glucocorticoids  All are potent that insulin 110 – 170mg / dl 80 – 110mg / dl Dextrose anhydrase intake check blood every 2hr Glycosylated hemoglobin ( <7% reflects the pt. Tendons.54cm apart or 1 inch from the previous site o Do not massage injection site it may lead to rapid absorption o Administered insulin at room temperature Diet - Low calorie diet High fiber diet More complex than simple CHO Activity & exercise Increase glucose uptake Monitor glucose Acute complication Diabetic Ketoacidosis ( life threatening complication of DM type 1 Cause Underdose of insulin Illness or intection Stress of injury Clinical manifestation Kaussmaul Acetone breath Nausea & vomiting Abdominal pain TX: Insulin – insu. HPN.High risk for ( 3-I ) Infection ( conclusive for bacterial growth ) Inadequate circulation ( atherosclerosis ) Impotent ( impaired circulation in the genital) Complication CAD.blood sugar for the past 3 – 4 months / percentage of glucose attached to the cell TX: Medication ( type 2 ) Oral Hypoglycemic Agent ( OHA ) teratogenic ABS o Alpha glucosidase inhibitor  Moa: decreased absorption of CHO  Acarbose o Biguanides  Moa: decrease insulin resistance  Glucophage ( Metformin ) o Sulfonulureas  Moa: stimulates beta cell  “ ide “  Glipizide  Glimepiride  Glypuride  Chlorpropramide Insulin ( type 1 ) regular insulin through IV Rebound hyperglycemia Tx: Decrease evening dose of insulin or midnight snack - - Aypoglycemia ( hypoglycemia ) o Very long insulin ( humalog ) o Rapid acting ( humalin R ) o Intermediate ( NPH normal neutral hagedorn ) o Long acting ( ultra lente ) Assessment: Tired / Tachycardia Irritability Restlessness Excessive hunger Diaphoresis ( skin cold & moist ) Lipodystrophy – hardening of the subcutaneous tissue o drip IV rehydration ( PNSS isotonic – to prevent hyperglycemic rebound ) Sodium bicarbonate HHNK ( Hyperglycemic Hyperosmolar Nonketotic ) Life threatening complication on patient with type 2 DM Severe hyperglycemia without ketoacidosis Manifestation Severe hyperglycemia and dehydration TX: Same with DKA ( except sodium bicarbonate ) Thyroid gland o Adams apple / thyroid cartilage Parathyroid gland o Side / back of the thyroid Thymus gland o Mediastinal spaces Adrenal glands o Top of the kidney ( suprarenal ) Pancreas o Near the stomach Ovary & testicle MUSCOLUSKELETAL SYSTEM Consist: Muscle.

stirrups ) Composition of Bone structures Cancellous Bone ( spongy ) has a small needle like of bone ( located at epiphysis of a long bone) o Trabeculae: irregular layers and surrounded by red / yellow bone marrow ( add strength to the bone ) o Haversian systems / Osteon: ( Basic unit of the Bone ) - Compact bone . Ca+ Calcitonin Hypocalcemic o o Lamellae: ( thin sheets of extracellular matrix ) calcified / mineralized matrix Lacunae: ( opening between lamellae where osteocytes is located ) Canaliculus ( tiny canal ) passage way of blood Osteoclast Dec. Ca+ PTH Hypercalcemic Bone to Serum ( bone resorption ) Serum to Bone ( bone absorption ) Osteoclast ( bone resorption cell ) release of calcitonin and phosphate from bone Osteocytes ( mature bone cells ) maintenance of bone matrix Skeletal System according to Location: Axial skeleton: o Form a longitudinal axis ( skull.80% are H2O ( tough. shoulder blades ) Irregular ( vertebrae. shoulder girdle & pelvic girdle Types of Bones according to Shape Long ( L > W ) femur. tarsals Flat ( skull. knee etc ) .o Skeletal ( dried up ) Function: Locomotion / Skeletal movement ( voluntary) Protection Support and Lever Blood cell production Storage 2 major components: Non Living Intracellular Materials: Mineral ( calcium / phosphorus ) o Ca + Ph = hyaline apatite crystals Bone matrix o Collagen – Mucopolysaccharides Living Cell: Osteoblast ( bone building cell / formation of bone matrix ) Stimuli Activated by Effect Osteoblast Inc. vertebra ) Appendicular skeleton: o Consist of extremities. smooth.Dense ( smooth appearance ) o Osteon o Lamellae  Concentric ( inside osteon)  Circumference ( outside osteon )  Instertitial ( in between osteon ) o Haversian Canal / Central Canal ( parallel to the bone ) o Volksmann Canal / Perforating Canal ( perpendicular to the bone ) *Periosteum: outer layer of the bone ( fibrous connective tissue ) Long bone Epiphysis: ( ending of the bone ) - o Compact ( outside ) o Spongy ( inside ) o Articular cartilage: o Endosteum Diaphysis: ( shaft ) o Medullary cavity is located o Periosteum: o Medullary cavity: Red Bone Marrow Hematopoietic Tissue Produce stem cell ( hematoblast ) Location in adults ( Central Bone Cavity ) Function: Formation of RBC. WBC. cushion ) JOINTS: Hold the bones together Gives the rigid skeletal mobility Major classification: Synarthroses ( fibrous ) o Not movable ( suture of skull ) Amphiarthroses ( cartillagenous ) o Little movement ( intervertebral ) Diarthroses ( synovial ) o Full movement ( hip. hips. bony thorax. humerus Short ( cube ) carpal. Platelets CARTILAGE: Dense connective tissue consist of fibers embedded in a strong like gel substance 3 types Elastic: ( elastin in each intracellular substance ) Hyaline: ( pearly white color ) most abundant – articulary cartilage ( end of the bones ) Fibrocartilage: 65% .

Cellular Proliferation Granular tissue formation – white blood vessel & cartilage over lie the fracture Callus form as mineral and deposited to organize network fiber for the new bone ( fiber & cartilage ) 3.D Bursae: Fluid filled sac ( around the joint ) Reduces friction & facilitate movement Synovium: ( synovial membrane ) Line the capsule Synovial fluid: Secreted by synovium Bone Formation: ( Osteogenesis ) Ossification o Bone matrix is formed o Hardening materials is deposited (collagen fibers) Endochondral formation o Most of the bones o Osteoid ( cartillage like tissue ) Intramembrous formation o Flat bones Bone Healing: Kidney reabsorb of Ca+ urinary excretion of phosphorus activation of Vit.Callus Ossification ( 2 – 6 weeks ) Callus form the initial clinical union of the bone & provides enough stability to prevent movement when bones are gently stress 4. D o Increase amount of Ca+ in the blood by promoting Ca+ absorption in the GI o Facilitates mineralization of osteoid tissue Calcitonin: ( serum to bone ) PTH: ( bone to serum ) Parathyroid gland ( PTH ) Bone release Ca+ Calcium concentration in the extracellular fluid Intestine reabsorption of Ca+ via activate Vit.Bone Remodelling Consolidation & Remodeling Complete healing ( 3 – 6 months ) Continued bone healing provides gradual return of the injured bone to its pre injury shape & structural strength Factors affecting time required for healing: Age Displacement Site of fracture Nutritional level Blood supply to the area of injury MUSCLES: Skeletal muscle o Voluntary – Striated Cardiac muscles o Involuntary – Striated Smooth / Visceral muscles o Involuntary _ Non striated Tendons connect bone to muscles. Muscle is composed of numerous .D 1.    Ball & socket (to all direction – full movement) Ellipsoidal ( gliding joint) to all direction – limited Hinge ( elbow – knee ) bending – in one direction Pivot ( rotation movement ) Bone Maintenance: Weight bearing ( local stress ) o Activate osteoblast o Stimulate bone formation/ remodeling o Prolonged bed rest bone losses calcium ( resorption ) & becomes osteopenia & weak Calcitrol: o Activated form of Vit.Hematoma Formation & Inflammation Bone is damage – hematoma is precedes new tissue formation – production of new bone substance 2. Epimysium / Fascia cover the muscles.

Functional Property of Muscle Fibers Irritability : ability to react to a stimuli ( nerve impulse ) voluntary Contractility: ability to shorten with force (adequate stimuli ) Nerve Stimulus Motor unit: o 1 motor neuron + all the muscle correspond to it> o Action potential  Electrical impulses that controls bodily process SKELETAL MUSCLE Energy is consumed during muscle contraction Consume too much energy Muscle fatigue: ( work > 02 supply ) unaerobic respiration Depletion of glycogen / energy stored Accumulation of lactic acid Aerobic respiration: 36 ATP  6 oxygen 6 carbon dioxide Unaerobic respiration: 2 ATP + Lactic Acid Fascia: ( surrounded and divide muscle ) Tendons: ( fibrous connected tissue / tough ) decrease blood supply – slower healing Ligaments: ( fibrous connected tissue / dense & flexible ) connect bone to another bone – decrease in blood supply HEALTH HISTORY INJURY Genetic / Familial Disposition Congenital Talipes Equinovarus Marfan syndrome Osteoporosis Osteogenesis Imperfecta Concurrent Health Condition Communicable o Leprosy o TB of the bone Non Communicable o COPD o CAD o Asthma o CVA Physical Activities o Daily activity pattern o Occupation o Exercise pattern  F-requency  I-ntensity ( moderate )  Mild ( <50% )  Moderate ( 50% – 70% )  Highly ( 70% )  T-ime ( 30mins / Session ) - Recreation Alteration in Sensation o Pain  P-allative / Provocative  Q-uality  R-egion  S-everity  Pain Scale ( adult ) Wong – Baker ( pedia )  T-ime Paresthesia  Tingiling sensation ( impaired circulation / compression of nerves ) Nutritional Status o Dietary intake o Weight / Height ( IBW ) o - PHYSICAL EXAMINATION Posture Stand straight ( spinal curvature ) Abnormalities Kyphosis ( increase convexity of vertebrae ) Lordosis ( sway back/exaggeration of lumbar region ) Pride of pregnancy Scoliosis Lateral curvature of the spine Idiopathic Congenital Damage of Paraspinal Muscle o Polio Muscle Assessment Size ( atrophy ) Symmetry ( compare ) Tonicity ( palpation ) Muscle Strength o Method  Elbow flexion / extension  Wrist flexion / extension  Grip test Grade 5 4 3 2 1 Description Normal muscle strength Full ROM that can be overcome w/ increase examiner resistance Full ROM of muscle against gravity only is overcome w/ slight examiner resistance Weak movement of muscle but insufficient to overcome gravity Slight visible / palpable contraction ( . Each sarcomere contains Actin & Myosin ( myofilament ). Inside the muscle fibers is the basic structural and functional unit of muscle called Sarcomere. A fasciculus is composed of several Muscle Fibers ( contains nuclei / capillary ).visible bundles called Muscle Fasciculi which is surrounded by loose connective tissue called Perimysium. Each is surrounded by Endomysium. It also contains Z disk ( anchors the actin myofilament ) & M disk ( anchors the myosin myofilament ).) movement .

Create lumbar puncture ( shrimp position ) L3 – L 4 ( subarachnoid space ) 5 – 10ml for exchange with contrast dye o Hot flushes & metallic taste is normal 2.evaluate the stage cancer of the bone Uses contrast radioactive materials ( irritating to bladder ) o Galium o Thalium o Technetium Before: Remove jewelry During: Proper positioning ( supine – patient must be steady still ) Promote safety After: Increase OFI ( facilitate excretion ) patient should urinate within 4 hours after procedure DEXA ( Dual Energy Xray Absorptiometry ) Procedure that measure BONE MINERAL DENSITY Commonly used Low dosed radiation No special preparation only remove jewelry Quantitative ultrasonography Quantitative computed tomography Roentgenography ( X-ray ) 2 types: Bone X-ray Joint X-ray Other types: Multiple X-ray ( multiple views ) APL Serial X-ray ( to identify healing process ) Contraindicated to pregnancy Myelography Identify – locate tumor in spinal column X-ray of subarachnoid space 1.Intervention Before: Check allergy to iodine On NPO ( after liquid breakfast ) After: Oil dye ( flat on bed – to avoid spinal headache ) easily excreted ( 8 – 12hrs ) Water dye ( amipaque ) HOB elevated (semifowler ) 30 – 45hrs to avoid Seizures cause by Meningeal irritation Precaution: Before: Padded side rails Tongue guard Decrease height of the bed During: Put patient in side lying position Arthrography Identify tear in joint capsule / ligaments & tendons Indirect visualization of joints Intervention Assess for contraindication .0 Complete paralysis Gait Ask the client to walk straight Stance face Genu Varum ( sakang ) Genu Valgum ( piki ) Abnormal gait due to neurological disorder Spastic Hemaparesis ( stroke ) Steppage Gait ( lower motor neuron disease ) Shuffling Gait ( Parkinson disease ) Joint Assessment ROM Active / Passive ( form of intervention ) goniometer Inflammation o Dolor ( pain )  Compression of nerve endings ( release prostaglandin ) o Rubor ( redness )  Hyperemia o Callor ( heat )  Hyperemia o Tumor ( swelling )  Increase capillary permeability Laesa Function ( loss of function ) Effusion ( joint effusion ) Accumulation of excessive fluid o Ballon sign o Ballottement sign Identify presence of o Snap ( slipping of ligament in a bony prominent ) o Crepitus ( crackling / grating sound) ROM ( range of motion ) Head Protraction / Retraction Rotation Flexion / Extension / Hyperextension Arm Abduction ( away the midline ) Adduction ( toward the midline ) Circumduction Hand Foot 6P’s - Pronation ( palm down ) Supanation ( palm up ) Dorsiflex Plantar flexion Inversion Evesion External rotation Internal rotation Pain Pallor Paralysis Paresthesia Pulselessness Poikilothermia (inability to sustain temperature) Bone Marrow Aspiration ( biopsy ) Red bone marrow Leukemia / Aplastic Anemia Sternum / Hip bone ( posterior – superior iliac crest ) 1 – 2ml specimen Side lying position / Prone Before: Secure consent Check bleeding parameter After: WOF bleeding Apply pressure Bone Scan Identify .

Pain Subjective assessment manifested by Objective cues Assess Patient perception to pain Provide non – pharmacologic treatment to pain Provide pharmacologic treatment to pain o NSAID’s Assessment of effectiveness to pain measurement 2.) or < 1:40 Rheumatoid Factor ( specific ) Determine presence of auto antibody ( + ) RF is suggested of RA < 40 IU/ml Muscle Enzyme Test Cretinine Phospokinase ( cK3 / cKmm ) F: 30 – 135 U/L M: 55 – 170 U/L Alkaline Phospoknase ( ALP – 2 ) Normal: 20 – 90 IU/L Elevated indicates: o Paget’s disease o o o o o o Osteomalasia Cancer of the bone MUSCULOSKELETAL SYSTEM Nursing management 1.2 – 7mg/dl ( M )  4.2 – 8mg/dl ( F ) ANA ( Anti Nuclear Antibody ) Identify autoimmune disorder o Measures amount of antibody that destroys the nucleus of a normal tissue Normal value: o ( .MRI ( Magnetic Resonance Imaging ) better view Both are use to identify damage into tendons & ligaments Assess bone & soft tissue Assess for “ Claustrophobia“ Both are contraindicated to metal inplant ESR ( Erythrocyte Sedimentation Rate ) Non specific for inflammation M: <20mm/hr F: <30mm/hr Uric acid: Gout ( inborn error in metabolism ) o Normal:  2.- Perform ROM after injecting contrast dye (contrast dye leak into the tear of the joint ) After: Pain management ( NSAIDs ) Avoid bleeding ( ice ) Crackling sounds ( normal – 3 days ) Bone / Muscle Biopsy Use to identify cancer Intervention Local anesthesia Check PT – PTT Give coagulant ( 2 – 3 days ) before & after the procedure ( Amicar / Transxenamic Acid ) antifibrolytic medication Apply pressure CT scan ( Computed Tomography ) .Assistive: o Active – Resistive: ( apply resistance ) increase muscle power ( weight ) Provide support in ambulation w/ assistive devices Turn the patient every 2hrs to avoid bed soars Encourage mobility Facilitate exercise o Isotonic exercise ( change in muscle length & tension ) o Isometric exercise ( alternate contraction & relaxation of muscle 3.Self – Care deficit Assess functional level of the patient Assist patient w/ difficulty in bathing & hygiene o Assist W bath only when patient has difficulties o Provide ample time for patient to finish the activity Provide support for feeding problem o Proper positioning ( high fowler ) Provide assistive device Supervise meal time Offer finger foods Keep suction equipment available TRAUMA TRAUMATIC CONDITION CONTUSION Soft tissue injury cause by blunt trauma Skin is intact Extravasation ( blood under the skin due to rupture blood vessel ) S/S: Bleeding ( internal ) Swelling ( edema ) Pain ( compression of nerve ending ) Management: Elevate parts Cold compress in the 1st 24hrs & apply warm compress after 24hrs Apply pressure bandage STRAINS Over stretching of the muscle / tendons Types: Acute ( recent injury of muscle / tendon classified by degree ) Chronic ( repeated use of the muscle beyond physiologic needs ) Degree of acute strain First degree ( feels stiff & sore locally ) Second degree ( tenderness over the area ) Third degree ( burning sensation ) Assessment of Strain 1 st Assessment Tenderness Muscle spasm ROM No loss Edema No / Little   2   nd Slight ( loss pain ) Develops early rd 3   Cannot move Extreme .Impaired Physical Mobility Perform ROM exercise Types: o Active: ( allow patient to do ROM ) enhances joint mobility and muscle bone o Passive: ( nurse do the ROM ) enhances joint mobility and prevent contractures ( comatose / paralyzed patient ) o Active .

ompression E – levation FRACTURES A break in continuity of bone Types of Fractures rd 3   NSAID. muscle relaxant Needed rd 3   NSAID. muscle relaxant Needed - SPRAIN Greater than strain Over stretching of the ligament Assessment of Sprain Assessment Tearing of ligament Edema / Hematoma Loss of function Weakening of joint Pain st nd 1 Minimal 2 Up to half Localized Increase None decrease None intact Mild Mild Increase rd 3 Complete ruptre Severe Dramatic decrease Loss of integrity Severe pain Management 1 st nd Elevation Ice Drugs   analgesics 2   NSAID. muscle relaxant Physical therapy Compression Isometric Needed Bandage Restoration None Protective splint None General management for Strain / Sprain R .Ecchymosis No / Little Develops later - edema Delayed - Management 1 st   Elevation Ice Drugs None Physical therapy Not needed nd 2   NSAID. prolonged or abnormal stress Avulsion o Pulling away of a fragment of bone Factors Extrinsic factor ( stress ) Force Rate of loading ( speed / momentum ) Intrinsic factor ( bone strength ) speed > strength Bone capabilities o Age o Pre existing disease Behavioral factor High risk activities Nutrition Assessment of Fracture Pain Sudden / Severe Pain ( release of inflammatory mediator ) prostaglandin Compression & damage ( pain receptor ) Aggravated by movements Loss of function Compression / Damage to the nerve that innervates Deformity Obvious changes Edema formation Disalignment of the bone Shortening of the bone Disalignment ( cause by muscle spasm ) Crepitation Crackling / Grating sounds Edema ( 24 hrs ) Hyperpermeability of surrounding blood vessels Numbness Absence of sensation Damage to the sensory nerve Motor weakness .est I .ce C . muscle relaxant Needed - Casting - Surgery - - - Closed fracture ( simple fracture ) o No break in the skin Open fracture ( compound / complex ) o ( + ) skin breakage o Risk for infection Complete fracture o Entire cross section Incomplete fracture o Only portion of the bone Greenstick o One side portion of the bone is broken and the other portion is bend Comminuted o Several bone fragment Depressed o Fragment is driven down / inward Impacted o Bone is driven into another bone (bone to bone ) Transversed o Break straight across the bone Oblique o Angle across Spiral o From oblique to long shaft Compressed o Bone has been compressed Stress o Caused by repeated.

RR & slight oliguria ) normal BP  LOC. UO (oliguria phase) lethargy Late ( irreversible )  Bradycardia  (-) bradypnea. palpatory BP ( systole )  Unconscious  Sever schemia  Metabolic acidosis  Multiple organ failure  Anuric phase - - Pharmacological treatment o Cortecoisteroid ( decrease damage to the lungs ) o Morphine ( pain management ) SNS response. brain. low blood volume 15% blood loss Most common cause of death for patient with severe & multiple trauma Non progressive o Early compensatory stage  ( increase HR. Classical triad: Hypoxemia o Decrease perfusion.Ecchymosis ( after 24 hrs ) Evaluate if edema subside (ruptured capillary) Abnormal circulation Poor capillary refill time (-) pulse Cyanosis DX procedure Xray is enough ( presence of fracture ) Emergency management Immobilized any suspected fracture Support ( splint / sling ) Do not attempt to reduce the fracture Place clean sterile gauze Intervention Reduction Cast Fixation Traction Complication of fracture Early: Shock Compartment syndrome Infection Fat embolism Avascular necrosis Thrombos formation Late: Delayed union / non union / mal union Angulation Fixation reaction SHOCK Stages - - Hypovolemic shock . irritable & restlessness Progressive o Intermediate stage  Hypo – tachy – tachy ( release of catecholamine )  o Decrease BP . increase pressure pulmonary circulation Petechial rash o Chest / Neck - Neurological alteration o Sudden confusional stage o Chest pain / Dyspnea o Tachycardia Intervention Support respiratory function COMPARTMENT SYNDROME Increased tissue pressure within compartment Myofascia compartment o Low ability to expand  Blood vessel  Nerve  Muscle Edema & Hemorrhage ( fascia ) o Increase pressure compress myofascia compartment Assessment Pain Pallor Edema Pulselessness Paresthesia Medical / Nursing management Frequent assessment Elevate the extremities Reduce cast pressure ( Bivalbing ) Surgical: FASCIOTOMY INFECTION OSTEOMYELITIS Most common Assessment Fever Leukocytosis Elevated ESR Erythema Pain Intervention Proper handling of open fracture Long term antibiotic therapy Surgery: . kidney etc. increase oxygen consumption Institute preventive measure o Immobilization o Avoid manipulation Surgical: EMBOLECTOMY TX: - - - - - Positioning o Divert blood to vital organs  Tredelenburg / Modified tredelenburg position Respiratory and Support o Large concentration of oxygen  Mechanical ventilation  Intubation IV infusion o PNSS / LRS o 3%nacl Blood transfusion o Blood compatibility o Whole blood Emergency meds o Dopamine o Epinephrine o Atropine sulfate o Dobutamine o Sodium bicarbonate FAT EMBOLISM Release of fat globule ( fracture ) Stock to the lungs.

Prevent complication of mobility. Single hip spica – for hip and 1 femur. Maintain skin integrity – “petalling” Do neurovascular checks such as skin color. Shoulder spica – for humerus and shoulder joint. 1 and ½ spica mold – for hip and femur with compound affectation. 29. Types of Cast. 13. 19. 17. cast or traction CAST Types: Function - Is a temporary immobilization. Single hip spica mold – for pelvic fracture with callus formation. 7. 31. Night splint – for post polio. 24. mobility and pulse. Rizzer’s jacket – for scoliosis 26. Fiber glass or the plaster cast Characteristic of a good cast White / Shiny Odorless Light weight Properly fit Resonant on percussion Contraindications Pregnancy Skin disease Swelling Open wound Infection Handle wet cast with palms of hands. Cylindrical leg cast – for fractured patella. not fingers. Body cast – for lower dorso-lumbar spine affectation. Double hip spica cast – for fracture of hip and femur. Airplane cast – for humerus and shoulder joint with compound fracture. Short arm posterior mold – for wrist and fingers with compound affectation. Quadrilateral (ischial weight bearing) cast – for shaft of femur with callus formation. 34.3 day ) Fiber glass ( 30 min ) To promote healing and early weight bearing.Pallor / Cyanosis Temperature . 20. 11.Tingling / Numbness Mobility . Molds And Indications 1. 10.- SEQUESTRECTOMY ( sequestrium ) dead bone BONE GRAFT NI: - AVASCULAR NECROSIS Bone death due to disrupted blood supply Assessment Continuous pain Decrease sensation NI: Continuous assessment Removal of necrotic tissue FRACTURE MANAGEMENT REDUCTION Restore the bone to proper alignment Types Closed reduction o Client is under anesthesia o Cast may be applied Open reduction o Treated with internal / external fixation. Pantalon cast – for pelvic bone fracture 23. Observe “hot spot” and musty odor. 8. Cast should be allowed to air dry. Cast assessment Assessment WOF Color . 18. 30. sensation. Double hip spica mold – cervical affectation with callus formation. 25.Distal Paralysis Pulse . Collar cast – for cervical affectation. maintain and protect realigned bone. To prevent or correct deformity To immobilize Cast Application Apply the stockinette. 28. 4. Short leg circular cast – for ankle and foot fracture. 9. 33. Short leg posterior mold – for ankle and foot with compound affectation. 1 and ½ hip spica – for hip and femur. 5. o L – ow cool dryer o E – expose the cast o T – urn to promote equal drying Elevate the cast on one or two pillows during drying. 6.Cold Skin / Hot Spot Sensation . 12. Long arm circular cast – for fractured radius or ulna 16. Hanging cast – for fractured shaft of the humerus. Assess for vascular occlusion. Functional cast – for fractured humerus with abduction and adduction. Minerva cast – for upper dorsal or cervical affectation. Basket cast – for severe leg trauma with open wound or inflammation. 3. Apply the wadding sheet. 14. Long arm posterior mold – for fractured radius or ulna with compound affectation. 2. 22. To support. 32. which is signs and symptoms of infection. Long leg circular cast – for fractured tibiafibula. 15. Munster cast – for fractured radius or ulna with callus formation. Adhesive tape petals reduce irritation at cast edges. Cast brace – for fracture of femur (distal curve) with flexion and extension. Plaster of paris ( 1. skin temperature. Patella tendon bearing cast – for fractured tibia-fibula with callus formation. Delbit cast – for fracture of tibia or fibula. 21. Internal rotator splint – for post hip operation. 27. Short arm circular cast – for wrist and fingers. Frog cast – for congenital hip dislocation.Absent Cast procedures Petalling o Smoothening of cast to prevent rupture skin - Windowing o Removal of a part of a cast Bivalving o Splitting of the cast ( xray ) Other cast complication Compartment syndrome . Long leg posterior mold – for fracture tibiafibula with compound affectation. Boot leg cast – for hip and femoral fracture.

Left crutch and right foot together then the 2. Move the stronger part 2 point crutches gait Indication Weakness in both legs on poor coordination Pattern sequence 1. Right foot 3. Advance both crutches forward while bearing swing all weight down through both crutches. Right crutch and left foot together then repeat Swing to gait Indication Patients w/ weakness of both lower extremities Pattern sequence 1.- Cast syndrome o N&V o Abnormal pain / Bloatedness o ( . 2. Swing both legs forward at the same time – past the crutches Other Treatment Modalities Traction Fulling force in two opposite side Essential components Traction Forward force Countertraction Backward force Friction Purpose Reduce muscle spasm To immobilize Principles of traction Client should properly positioned For every traction there is a countertraction Line of full should be aligned with the deformity . down with the bad Going upstairs o Good leg up and crutch with weaker leg Going down o Bad leg then good leg 4 point crutch gait Indication Use if weight bearing is allowed Pattern sequence 1. Left foot then repeat 3 point crutches gait Indication - Partial weight bearing or no weight bearing on affected leg Pattern sequence 1.) bowel sound Plaster sores o Itchiness / burning sensation o Severe pain Equipment in removal Cast cutter Cast spreader Bandage scissor Fixation Alignment of the bone fragments More freedom of movement Outer Reduction & Internal Fixation ( ORIF ) Outer Reduction & External Fixation ( OREF ) Types: Internal Fixation May include removal of a damage Provide immediate bone strength o Screw o Skeletal pin  Inside the bones o Medullary rods o Plates External Fixation Use of a rigid external support Indication: Massive Tissue Trauma PIN care is necessary External frame Connect skeletal pin ( outside the bones ) 6 – 8 weeks Nursing management Check dressing for bleeding and infection Empty Hemovac – evacuation of blood Turn every 2 hours Avoid weight bearing on affected extremities Hypercalcemia Constipation Hypostatic pneumonia Assisted devices Walkers Level of the hip 4 -6 inches away to feet 15 -30 degrees flexion to elbow Lift & walk technique Lift walkers and walk across the walker Going up put the walker at the back Put the walker in front Cane Rubber tip C-ane O-pposite A-ffected L-imb NI: Inspect the device Proper positioning Proper handling o Greater trochanter to the femur o 5 cm below the hips o 4 -6 inches. Swing both legs forward at the same time ( not to pass ) the crutches Swing through gait Indication Inability to fully bear weight on both legs Pattern sequence 1.5 – 5cm /12 inches between crutches & armpit 30 degrees flexion Crutch palsy o Brachiocephalic paralysis 6 inches – 1 foot o Gives the client broader base The hand grip should be at waist level Standing with crutch Sit near the edge of the chair Unaffected part must be near the chair Stand using the unaffected part Then separate the crutch Up with the good. Move both crutches and leg 2. The weaker lower limb forward then bear all your weight down through the crutches 3. Left crutch 2. 15 – 30 degrees Proper movement The cane and the affected leg must moves at the same time Prosthesis Crutches 2-3 fingers width 2. while bearing all weight down through both crutches. Right crutch 4. 2. Advance both crutches forward then.

- For traction to be effective it must be continuous Types of traction Halo Femoral Traction 90 – 90 degrees Balanced Skeletal Traction (BST) Overhead Crutchfield Tongs Supracondylar area Hemo-femoral Severe cases of scoliosis 90-90 traction Subtrochateric Fracture of the femur Types of Traction BUCKS EXTENSION RUSSELL TRACTION BRYANT TRACTION SKULL TONG / TURNING FRAME LATERAL SKELETAL TRACTION BALANCED TRACTION 1. 8. 7. Observe the patient foot drop 6. arterial insufficiency Post Op Intervention Monitor V/S & stump dressing Elevate stump for 12 – 24 hours Teach client about PHANTOM LIMB SENSATION ( after 24 hrs ) o Stimulation of the remain limb o Neural nerves in the brain Provide stump care o Maintain elastic bandage ( shrink / shape ) When wound is healed. The line of pull must be in line with deformity Braces Immobility Proper body alignment Support Treat fracture Amputation Removal of a body part ( limb ) Cause Trauma ( accidental amputation ) Surgical amputation Types Related to preservation of the joint Peripheral disease o BKA – below the knee amputation o BEA – below the elbow amputation Extensive trauma / Disease o AEA – above the elbow amputation o AKA – above the knee amputation Mostly Due to trauma. Balanced Suspension Bucks extension traction Bryant traction Bootcast traction Cotrel traction 6. 4. Ensure that the pulleys and ropes are properly functioning 5. wash the stump daily ( avoid oil ) maceration - Apply pressure to the end of the stump Encourage client to move the stump to promote circulation Place client with a lower extremities amputation in a prone position twice daily Figure of 8 method To wrap your residual limb ARTHRITIS 35 -45y. Always ensure that the weights hang freely 2. 5. 9. malignancy. 2. Cervical traction Dunlops traction Hammocks traction Pelvic girdle NI: Traction: General Principles 1. Observe for DVT 7.atigue o E-xtreme C-old o S-tress o I-nfection Immune response ( joint ) Neutrophil ( attract ) Collagen ( breakdown ) . Maintain proper body alignment 4. 3. Never remove the weights 3. Provide pin care for clients in skeletal traction 8.o ( female ) Inflammation of the joint Types: RHEUMATOID ARTHRITIS Inflammatory changes of the joint Chronic / Systemic Connective Tissue Disease Affect the Peripheral / Synovial membrane Factors Genetic predisposition Autoimmune A/E: o F. Promote skin integrity 9.

morning ) after a long period of inactivity Joint swelling / stiffness Sign of inflammation Fever & weight loss Anemia Spongy tissue Related disorder Sjorgen syndrome o Decrease activity of glands  Skin  Lacrimal  Salivary Felty syndrome o Rheumatoid Arthritis o Neutropenia o Splenomegaly DX test Xray o (+) bony erosion Blood studies o (+) rheumatoid factor.inhibitor ) Cox ( prostaglandin synthesis ) o Cox1 ( stomach lining ) o Cox2 ( inflamed area ) Chryotherapy / Gold Therapy o Gold Na+ Thromalate ( IM ) 36months / Auranofin ( PO ) Complication: o Kidney damage o Bone marrow depression Steroids o Prednisone / Cortisone Surgical Anthroplasty Synovectomy Nursing Management Relieve Pain / Discomfort Immobilized Suggest application o Cold / heat application Promote balance in activity & rest Increase patient mobility ( safety ) Provide diet therapy o Increase protein / caloric diet Prevent deformity o Use flat / firm mattress o Use one pillow under the head o No pillow under the joints o Lie prone several times OSTEOARTHRITIS Degenerative joint disease Destruction of cartilage Affects weight bearing joints Risk factors Increased age ( above 50 yo ) wear & tear Obesity Repetitive use of joints Genetic susceptibility Hyperactive chondrocytes ( cell in the jint capable of destroying cartilage) Assessment Functional joint limitation Bonchard Nodes ( thicken bone growth ) Heberdens Nodes ( terminal interphallegeal joint ) Joint pain o Assymetrical  Not systemic  Weight bearing joint Stiffness o Esp. elevated ESR.ANA & CRP (C-reactive protein) Arthrocentesis o Cloudy. nodules. fever. stiffness -Rest the joint -Cold/ Heat modalities -Medication GOUTY ARTHRITIS Systemic disease caused by disposition of uric acid crystal Cause Primary Gout ( error in purine metabolism ) Secondary Gout ( caused by pre existing disease ) Assessment Severe pain Inflammation of the joint TOPHI formation PODAGRA ( big toe because of gout ) Fever & malaise Body weakness & headache Renal stones DX test Serum uric acid Uric acid stones in the kidney (+) Urates crystal in the synovial fluid Medication Management Allopurinol o Taken after meal o WOF: allergy Colchicines . stiffness -Rest the joint -Cold/ Heat modalities -Medication Osteo -Onset is late -Non systemic -Involve the cartilage -Joint is unilateral -No other symptoms -Crepitus.- Destruction of synovial lining Inflammation of synovial membrane ( Fibrous antylosis ) Panus formation ( bone antylosis ) (development of tissue with blood vessel ) Fibrous antylosis – shortening of connective tissue Bone antylosis – fusion of the bone Assessment finding Pain ( esp. anemia -SubQ. milky & dark yellow o (+) WBC Medical management Pharmacotherapy NSAID’s ( non selective cox . morning o Decreases with movement DX findings Xray NI: Provide relief of pain Advise patient to reduce weight o Aerobic exercise o Walking Administer prescribed medication o NSAID’s Position the client to prevent flexion / deformity Surgical Intervention Synovectomy Arthrodesis – fusion of a joint o Artificial antylosis ( palliative ) Reconstructive surgery Comparison: Rheumatoid -Onset is early -Chronic systemic -Involves the synovium -Joints are symmetrical -Malaise.

intake daily Diet high in protein UV radiation therapy HERNIATED DISK Nucleus Pulposus forces through the weaker / torned outer fibrous ring Cause Trauma Strain Joint degeneration Assessment finding Back pain o Radiates to the buttocks. leg & feet Motor & sensory loss DX test Laseque test o 30 -70 degrees ( dorsiflex ) o Xray o CT Scan o MRI NI: Bed rest for several days Heat application Promote exercise on bed Pelvic traction application Provide the drugs as order o Muscle relaxants Provide care for Lamonectomy Surgical LAMONECTOMY o Removal of the protruding disk o Usually accompanied by insertion of metal plates Post operatively Maintain bed rest - Log rolling technique Never lie on prone Hemovac drainage system Straight back chair OSTEOMYELITIS Acute / Chronic infection of the acid surrounding soft tissue DX test CBC ESR Blood culture Reason Open fracture Sepsis CM: Fever & malaise Inflammation Difficulty with weight bearing Drainage from wound site Management Analgesic as prescribed COD Maintain proper body alignment Immobilization of affected part Surgery if needed Proper diet o High caloric / protein diet PAGET’S DIET Oteitis Deformans Slow progressive Familial Rapid osteoclastic activity ( bone resorption ) Abnormal bone formation Assessment Assymptomatic initially Musculoskeletal o Bone deformity ( bowing of the bone ) skull. femur. tibia & vertebra .- o Acute attack Probenecid o Uricosuric drugs - Provide proper diet Increase OFI Provide alkaline ash diet Provide bed rest during arly attack of gout NI: METABOLIC BONE DISORDER OSTEOPOROSIS Decrease in the bone mass & density Types Primary osteoporosis o Above 55 yo ( female ) o Menopause ( estrogen ) Secondary osteoporosis o Pathologic ( renal failure ) o Iatrogenic ( long term steroid therapy ) Risk factor Sedentary lifestyle ( immobility ) Age Poor diet Post menstrual Genetics ( Caucasian / Asian ) Assessment findings Low stature ( Dowagers back ) Bona pain High risk for fracture Laboratory findings DEXA ( Dual Energy Xray Absorptiometry ) Xray Medication management Diet therapy Hormone replacement therapy Biphosphonate ( Alendronate ) decrease osteoclastic activity Moderate weight bearing exercise Management of fracture OSTEOMALACIA Delayed mineralization Kyphosis / Lordosis Assessment History Muscle & Skeletal Physical Examination Gait o Wide stance o Waddling gait Muscle weakness Cones o Deformities of the spine o Bone breaks easily DX testing Radiographic resting Laboratory studies Serum calcium ALP Management Ca+ Gluconate Vitamin D.

- o Bone pain even without activity Fracture DX - Radiographic findings ( pathologic fracture ) sclerotic bones Laboratory analysis Increase ALP Increase Urine Hydroxy Proline o Substance similar structure to amino acid only found on collagen Increase serum level ORTHOPEDIC SURGERY TOTAL HIP REPLACEMENT Replacement of both articular surfaces of hip joint Indication Osteoarthritis Rheumatoid Arthritis Femoral neck fracture Avascular necrosis ( head & neck of femur ) Post op care WOF for bleeding ( 24-48 hours / 500ml blood ) o After 48 hrs – 1 week ( minimal bleeding ) 100 -200cc Pain management o PCA ( patient control analgesia ) narcotic morphine ( 48-72hrs )  After 72hrs ( non narcotic analgesia ) NI: st 1 post op week ( use abductor device ) Use bed pan Client therapy o Use assistive device o Methods to prevent dislocation o Sexual activity Avoid -External rotation -Prevent hip flexion -Adduction -Do not bend -Do not cross the legs Do’s -Place trochanter walls -Use high chair -Used Abduction splint -Use slip on shoes -Keep feet flat TOTAL KNEE REPLACEMENT Hinged joint Metal or Acrylic prosthesis Indication Osteoarthritis Rheumatoid Arthritis Trauma Flexion failure Wrong insertion Manifestation Unable to flex the knee ( 1st week ) NI: 1st 48hrs ( apply ice ) Wound drainage ( 200ml / 8 hrs ) 3rd day no bleeding Physical therapy ( aggressive ) after 8 hrs – prevent flexion Prescribe CPM ( control passive machine ) Keep leg elevated Pain management ( NSAID’s ) Monitor limb neurovascular status ( 6P) Monitor for complication NEUROSENSORY SYSTEM Lacrimal Apparatus Hyperactive Lacrimal Gland Chemical irritation Foreign object Emotional stress 6 Extra Occular Muscle 1 2 3 5 4 6 Cranial Nerve 3 1. Inferior Rectus 3. Superior Rectus 2. Superior Oblique Layer Of The Eye Lacrimal gland Produce tears ( diluted salt ) Tears - Outer layer ( fibrous tunic ) Lysozyme ( protects & moisten the eye ) . Inferior Oblique Cranial Nerve 6 5. Lateral Rectus 6. Medial Rectus 4.

- - Sclera is the opaque. protective. fibrous. heterotropia & squint Retinoscopy Direct visualization of the eye Perimetry Test for peripheral vision Corneal Reflex Light touch to the corneal / Blinking reflex Blinking reflex is loss in times of : o Coma o Anesthesia o Death COMMON EYED DISORDER INJURIES Chemical injury ( any chemical that irritate the eye ) NI: Immediately wash the eye IOFB ( intraocular foreign body ) First Aid Wash the eye ( 15mins ) Never attempt to remove foreign body manually . pupil. Ciliary body attach the lens and responsible for accomodation Iris is the colored part of the eye & responsible for papillary reflex Inner layer ( nervous tunic ) o Rods ( dim vision ) o Cones ( colored vision )  Fovea centralis ( bundle of cones ) Cavities Of The Eye Anterior cavity ( aqueous ) Refract lights ( provide nourishment to cornea ) Drained through Trabecular Meshwork & Canal Of Schlemm Intraocular pressure ( 10 – 21 ) Posterior cavity / Vitreous cavity Contains gel like substance ( maintain the shape of the eyeball Attachment of 3 layers Refract lights Lens BICONVEX ( transparent ) Located posteriorly behind cornea & iris Accommodation – ability of the lens to change shape according to object distance. and anterior chamber.C to Pt. ( 20ft ) Denominator : -Distance wher eye can read the same letter 20/200 ( legal blindness ) OD ( ocular dexter ) . Cornea is the transparent front part of the eye that covers the iris. Middle layer ( vascular tunic ) Choroid provides oxygen and nourishment to the outer layers of the retina. Distant vision – flatten Near vision – rounded ( risk for eye strain ) Refraction of light / Bend of light Orbit Bony structure of the skull which contains the eyeball Orbital Cavity Space between eyeball & orbit Retina is a light-sensitive tissue lining the inner surface of the eye Optic Nerve - Bundle of axons Optic Chiasm Intersection of medial nerve Optic Tract Joining of medial & lateral nerve Visual Area Of The Thalamus Were nerve meet / receives optic tract Visual Cortex Interpret stimuli ( occipital lobes ) DX procedure: Snellen Chart Visual acuity ( sharpness of vision ) o Ability to distinguish in details through your eyes Numerator : -Distance of S.right OS ( ocular sinister ) – left Ishiwara Colored Plate Use to diagnosed color blindness Tonometer Indirect measurement for IOP ( indirect ocular pressure ) 12 -21 mmhg Increase IOP ( glaucoma ) Gonioscopy Bio microscopic examination of the eye Provide information regarding to the angle of the anterior chamber Use for glaucoma Opthalmoscope Visualizes ( direct ) fundus of the eye Visualize retina Visualize fovea centralis Slit Lamp Beam of light passes through the eye ( small frequency light ) & then direct examination follow Done to visualize small part of the eye Visualize different layer of the eye Cover – Uncover Test Diagnostic procedure for strabismus. outer layer of the eye containing collagen and elastic fiber. Rich in melanin.

Erythromysin. Erythromysin. Tetramycin CORNEAL INFLAMMATION Keratitis Cause Infection. Physical Chemical agent Assessment Pain – sharp radiating to frontal portion of the head Photophobia Lacrimation Blepharospasm ( sharp .BLUNT TRAUMA Injury in the eye due to blunt object First Aid: Apply ice ( prevent swelling ) Manifestation Non painful red rounded mass Cause Staphylococcus aureus PENETRATING EYE INJURY Injury due to sharp object NI: Put eye cover 7 rush to the hospital SYMPHATETIC OPTHALMIA ( feared complication) day – years after PEI INFECTION EYE LID DISORDER BLEPHERITIS Inflammation of the eye lid margin DISORDR OF CONJUNCTIVA CONJUNCTIVITIS Inflammation of conjunctiva ( red eye ) Viral in origin / bacterial ( self limiting ) Manifestation Red eye Lacrimation Eye discharge ( purulent ) Manifestation Burning sensation Irritation Itching Eye lashes fall apart Cause Bacterial / Viral Fungal ( rare ) HORDEOLUM Pustular infection of eyelash follicle Manifestation Painful red rounded mass Cause Staphylococcus aureus CHALAZION Inflammation of meibonian gland TRACHOMA Severe case of conjunctivitis Chronic eye disorder Conjunctivitis of the eyelid TX: C&S Sulfonamides. deficiency ( ACE ) At risk: AIDS Syphilis Systemic Lupus Erythematus Sarcoidosis TB Complication Corneal scarring ( perforation-severe ) Intraocular infection ( rare but severe ) Corneal opacity ( blindness ) TX: Corneal Transplantation ( Keratoplasty ) Treatment for corneal perforation / opacity Must remove 2 – 4hrs from the eye ( 4o C) 48hrs ( sterile normo saline solution ) 8 – 12hrs ( refrigerate without sterile ) UVEAL TRACT DISORDER Uveal Tract Middle layer ( vascular tunic ) responsible for dissemination of blood supply Easily inflamed ( phlebitis ) UVEITIS Cause - Iritis ( Iris ) Iridocyclitis ( Iris & Cyliary body ) Choroiditis ( Choroid ) Choroirentinitis ( Choroid + Retina ) Local or systemic disease o SLE o AIDS o Sarcoidosis Injury Unidentified factors Assessment . Tetramycin Manifestation Painful when blinking Redness to eyelid SCLERITIS Inflammation of sclera Manifestation Very red eye ( hyperemia ) Painful when blinking or movement of the eyeball TX: Sulfonamides.frequent blinking of the eye ) Decreased vision TX: - Bacterial : MOXIFLOXIN ( fluoroquinolones ) Viral : o TRIFLURIDINE ( Viroptic ) anti viral o IDOXURIDINE ( IDU ) herpes Severe cases: Mechanical / Chemical Intervention CORNEAL ULCERATION Cause Trauma Infection ( systemic ) o Vit.

- Pain ( radiating pain ) from eye to frontal & temporal ) Blurred vision Photophobia Redness of the eye Small pupil Lacrimation Collaborative management Mydriasis ( atropine drops ) o Relaxation of iris o Prevent adhesion of anterior structure ( lens. IO bleeding Miotics as prescribed o Carbotic ( Carbachol ) o Humorsol ( Demeconium Bromide ) o Isopto Carpine ( PIlocarpine HCl ) o Floropryl ( Isoflurophate ) CATARACT Opacity of the lens Transparent of opaque Etiological Factor: Chemical changes & structural changes of protein in lens Degeneration of epithelial layers of lens (older people ) Changes in density of the lens o Low molecular weight lens protein to high molecular weight – high dense Increase oxidation ( free radicals ) Classification Primary / Senile Cataract ( 70 – 75 yo ) o Older people Traumatic ( blunt trauma ) o Children Congenital Cataract o Infant acquired during pregnancy st o Exposure to teratogens ( 1 tri )  TORCH T-oxoplasmosis O-thers R-ubella C-ytomegalovirus H-erpes simplex Secondary o Pre existing disease (DM common) Ss/ Sx: .ydriasil o A – tropine sulfate o C – yclopentolate EXTRAOCULAR DISORDER STRABISMUS ( squint ) Uncoordinated extraocular muscles Unilateral Types: Esotropia both eyes turns inward - Exotropia the eyes are deviated outward Hypertropia upward Hypotorpia downward Collaborative Management Corrective Eyeglasses Surgery: o Tenotomy o Resection Tucking EYE SURGERY General Pre Op Care Orient ( to promote safety ) Practice covering the eyes for pediatric patients ( 5 -7 days eye cover ) Before surgical intervention give Mydriatics Post Op Care - Position ( supine or towards the unaffected side ) Burning sensation ( 1hr after the procedure decreases gradually after 8hrs ) Eye patch & Eye shield o To rest the eye ( 5 – 7 days ) after procedure o Eye patch every night for 1 month Sensation of pressure within the eye and sharp pain in the eye If pressure occurs during 16hrs ( notify physician ) it may indicate increase IOP.copolamine o M . iris & cornea ) Steroids ( anti inflammatory ) Dark glasses ( reduce photophobia ) Analgesics ( reduce pain ) RETINAL DISORDER RETINITIS Inflammation of the retina ( large portion of the retina ) Assessed through opthalmoscopy ( direct visualization of fundus of the eye ) Usually associated with chroinditis Rare fungal retinitis CYTOMEGALOVIRUS ( herpes group )common viral agent Protozoan ( toxoplasmosis gondvi ) Staphylococcus aureus ( bacteria ) Assessment Reduced visual acuity Changes in visual field ( narrowing ) Eye discomfort ( pain is provoked by exposure to light / pain is slightly removed by rest ) Photophobia Collaboration management Rest the eye Protects eye from light Mydriatics ( SMAC ) o S .

from the eye o TX: lens ( bifocal lens ) Astigmatism / Distorted sight o Abnormal curvature of lens o Due to variation of refractive ability o Eyeglass ( special cylindrical lens ) MACULAR DEGENERATION Loss of central vision o Macular Lutea (responsible for central vision) .- Dimness in visual acuity Refraction error ( rapid & marked changes ) HAZY VISION ( blurred vision ) - - Intracapsular cataract extraction ( ICCE ) o Removes lens & capsule Extracapsular cataract extraction ( ECCE ) o Removes lens only Cryoextraction (probe is inserted in 0oC temp) Phacoemulsification – probe vibrates Contact lens - Aphakic glasses – cataract glasses TX: - - Intraocular lens – synthetic distant vision for aphakic patient GLAUCOMA May result to irreversible damage Cause Increase Intra Ocular Pressure ( normal 12 – 21 ) Infection ( uvitis ) Injury ( blunt trauma ) Hereditary – thickening of trabecular meshwork resulting to obstruction of passage way of aqueous humor Narrowing of the Canal of Schlemm TYPES CHRONIC o Hereditary ( similar to open angle glaucoma ) o Narrowing of the canal of schlemm o It will take time to develop o Obstruction in the excretion of aqueous humor Ss/Sx: Tunnel vision ( loss of peripheral vision ) Difficulty in adjusting to darkness Colored vision disturbances - Headache Halo light surrounded by a concentric shape (rainbow color ) Dull eye pain Management Conservatives o Miotics ( papillary constriction ) o Acetazolamide ( decrease aqueous production )  Drug class: Carbonic Anhydrase Inhibitor  MOA: decrease acqueous humor production o Avoid excessive fluid Aggressive o Principle: Improve Drainage of Aqueous ( will create a permanent fistula ) o Indectomy ( passage way in the Iris) o Selerectomy ( passage way in the sclera ) o Trabeculotomy / ectomy o Corneoscleral therapy o Laser therapy ACUTE Aqueous humor imbalance o Increase production rather than drainage Displacement of Iris ( Iris blocked the aqueous humor ) Infection Injury or trauma Ss/Sx: Sever eye puss N&V Halo around light Dilated pupils Increase IOP Management Miotics Diamox Surgery Avoid: mydriatics Long term care: No restriction on the use of the eyes No fluid restriction Medical follow up ( for life ) RETINAL DETACHMENT - Causes - Ss/Sx: - Separation of: o Epithelial pigment – layer of rods and cones ( nervous layer of retina ) o Retina ( choroid ) rare Trauma Intra Ocular Hemorrhage Aphakia ( absence of lens ) Sudden severe exertion Floating spots ( dark pigment ) Head position Photo coagulation .increase coagulation with use of light ( adhere the detached retina ) Cryotherapy ( cold application using instruments ) Surgical Scleral Buckling o Re adhere the detach retina o Synthetic silicon Refractive errors Common errors Myopia o Light rays focus in front of retina ) o Due to : wide AP dimension o Near sightedness o Eye glasses ( concave ) long refraction Hyperopia / Far sightedness o Eye ball AP dimension too short o Light rays focus behind the retina o Good vision for far distances o Convex lenses Presbyopia / Far sightedness of old age o Gradual loss of accommodation (loss of elasticity ) o Inability to read without holding the material more 13ft.

bone” N = positive: “ air conduction is better “ ABN = negative : “ bone conduction is better” Conductive hearing loss Weber’s test Sound heard: normal ear vs.o Fovea centralis ( inside macula lutea ) sharpest vision Most common type : AGE related macular degeneration ( at risk : above 60 yo ) 2 types Dry macular 80 – 90% of incidence Non exudative Non neo vascularization DRUSEN ( yellow patches on retinal layer ) o No Ss/Sx if Drusen does not enter Macula Lutea Wet macular Low incidence 10 – 20 % (+) neo vascularization Symptomatic Ss/ Sx: Decrease visual acuity Blurred vision ( starting at central vision ) Central scotoma ( partial or totalblindness in certain areas ) TX: Wet: Anti-Angiogenesis o Macugen ( given once a month or twice ) o MOA: decrease progress of neo vascularization Dry: Lutein Omega 3 ( fishes ) DX: Amster grid o Consist of geometric square with a central fixation point o Ask the patient to look at the point o Blind spot – common to dry macular degeneration o Curves – common to wet macular degeneration Injection of Fluorescent Dye ( WET ) o Angiography o Evaluates macular edema neo vascularization & macular capillary Retinal photography ( black & white )( DRY ) EAR Auricle / Pinna ( elastic cartilages ) Collect sound waves Auditory canal / Meatus Transmit sound wavws from pinna to tymphanic membrane It has a protective function ( cerumen ) Tymphanic membrane / Ear drum Vibrates the 3 ossicles o Mallius o Illcus o Stapes Mastoid Air filled cavity & relieves pressure Eustanician tube/Auditory tube From middle ear going to nasopharynx Opening during yawning & swallowing Oval window Enter the sound wave & transmit Round window Relieves pressure Vestibule & Semi Circular Canal Rich in vestibular nerves Responsible for balance It is compose by: o Utericle o Saccule Cochlea Consist of Organ of Conti ( responsible for hearing ) Rich in auditory nerves Vestibular + Auditory = Vestibular Cochlear Nerve ( CNVIII ) transfer in temporal nerve ( interpretation of hearing ) HEARING TEST Accuracy or degree of hearing loss Whisper or Spoken voice test 2 ft. Twenty ) Audiometer Cannot measures accuracy but degree of hearing loss only Pure tone: o Increase decibels = Increase hearing loss Speech: o Degree of hearing loss with interpretation - Watch tick test: AUDITORY ASSESSMENT Test to localize cause of deafness Rinne’s test Sound heard better: “ air vs. behind the patient Cover 1 ear Say 2 syllable word ( eg. affected ear Better to detect : sensory neural hearing loss Better in affected ear ( conductive ) Normal: equal laterization Symptoms of Ear Diseases Deafness Varies in severity o Conductive ( rinne’s test ) o Sensorineural ( weber’s test ) o Mixed type Pain From ear itself or adjacent side o Otalgia ( ear ache ) inflammation o Otitis externa o Otitis media o Otitis interna Ear discharges May be o Mucoid ( inflammation – hyper active mucosa ) o Purulent ( infection ) o Bloody ( damages ) Vertigo Form of dizziness characterized by moving environment Tinnitus Noise in the ear ( ototoxicity ) OTOSCLEROSIS Conductive hearing loss Normal bone is replaced by spongy bone Ankylosis of the foot plate of the strapes Impaired vibration system Assessment Gradual hearing loss Difficulty hearing a whisper Paracusis : form of distortion to hearing DX: Rinne’s test .

wrist extender. chew gum or cover mouth when talking to hearing impaired clients Other types of ear surgry Myringoplasty Tymphanoplasty Ossiculoplasty Stapedectomy Post op: Ear surgery Inform client o Head still during surgery  Consciously sedated o Get out of bed with assistance o Avoid nose blowing ( 1 week ) o Change cotton ball ( daily ) o Lie on unoperated part Complication of ear surgery Facial nerve involvement o Facial paralysis Meningitis Bleeding NEUROLOGICAL SYSTEM Nervous System Central Nervous System o Brain o Spinal Cord Peripheral Nervous System o Motor Neuron  Somatic Nervous System  Autonomic Nervous System  Symphathetic Nervous System  Parasymphathe tic Nervous System o Sensory Neuron  Somatic Neuron System  Visceral Neuron System Cranial nerve ( 12 ) CN 1 – olfactory ( se ) CN 2 – optic ( se ) CN 3 – oculomotor ( mo ) CN 4 – trochlear ( mo ) CN 5 – trigeminal ( mi ) CN 6 – abducen ( mo ) CN 7 – facial ( mi ) CN 8 – auditory ( se ) CN 9 – glossopharyngeal ( mi ) CN 10 – vagus ( mi ) CN 11 – accessory ( mo ) CN 12 – hypoglossal ( mo ) Symphathetic Fight or Flight Dilated pupil Increase HR & contractility Bronchodilation Vasoconstriction Decrease peristalsis o Conversion of glycogen – glucose Inhibit bladder response Parasymphathetic Rest & digest Constricted pupil Decrease HR Bronchoconstriction Vasodilation Increase digestion – secretion of enzymes Constrict bladder Kernicterus ( jaundice ) deadly BILIRUBIN PRODUCTION : RBC Heme o Fe o Protoporphylin ( indirect bilirubin ) fats soluble  Glucorine transferase (convert to )  Direct bilirubin ( water soluble ) Globin Spinal Nerve / Peripheral Nervous System ( 31 ) Cervical ( 8 ) o Head . neck. hands Thoracic ( 12 ) o Chest & abdominal muscles Lumbar ( 5 ) . diaphragm.deltoid. biceps. triceps.Intervention Hearing aid Surgery o Stapedectomy ( primary ) o Fenestration ( create opening ) MENIERE’S DISEASE Endolymphatic Hydrops Chronic Increase in endolymphatic pressure (endolymphatic fluid ) Assessment Tinnitus ( earliest ) Hearing loss Vertigo ( most common ) Intervention Conservative : Pallative o Bed rest o Medication  Sedatives  Diuretics ( Diamox )  Antiemetic (Metoclopromide ) Diet o Low sodium ( limit fluids ) exacerbation Planning & Implementation Surgery o Labyrinthectomy o Endolymphatic Sac Decompression o Vestibular nerve section Inflammatory mediators ( nerve irritating substance ) Fever Provide environment not conducive to bacteria Fast metabolic rate Potentiates interferon response Assessment in a client with hearing loss Turns up volume Ask for repetition Inappropriate answer Leans forward to hear better Dominates conversation Abnormal articulation Communicating with hearing impaired clients Talk directly - Use gestures with speech Do not shout Use short phrases Do not whisper in front of hearing impaired clients Do not smile .

Chemoreceptor Trigger Zone ( CTZ ) +Cerebellum o Posture. Temporal  Hearing  Short term memory (anterograde amnesia)  Wernick’s area 3.branch out  Posterior part of forebrain  Thalamus ( rely of impulses / sensation) Spinothalamic Tract  Hypothalamus  Center for thirst  Satiety( insulin )  Osmoreceptor  Pituitary gland(controls)  Center for thermoregulator Brain Stem o Mid Brain( CN 3-4 )  Rely of impulses o Pons ( CN 5 – 8 )  Respiratory rhythm / depth o Medulla Oblongata ( CN 10 – 12 )  Controls HR. Parietal lobe  Sensory impulses  PPTT  Pain  Pressure  Temperature  Touch 4. Gait & Balance o Muscle Tonicity Cerebellar Test o Romberg’s Test  Normal anatomical position (20 – 30sec ) o Fingers to nose test . RR & vomiting  Center for cardio receptor . Occipital  Vision 5. GI tract o Stable ( regenerate for a limited time )  Liver. Frontal lobe:  Sense of humor  Abstract thinking  Primitive reflex inhibited  Hypothalalmus central  Broca’s area 2. libido. Rhiencephalon  Smell.long term memory ( retrograde amnesia ) Basal Ganglia o Parts of extrapyramidal tract o Release of dopamine DOPAMINE Decrease Parkinson & Huntington disease Increase Diencephalon ( CN 1 – 2 ) . lungs o Permanent Neuroglia Nerve glue ( group of cell ) o Support o Depend o Nourishes Not capable in transmitting impulses Types: Astrocytes o Nourishment of neurons o Barrier in neuron & brain cell( 75% of glucose ) o Forming the blood brain barrier (semi permeable / selective ) Toxins can pass through B&B: o B-ilirubin o L-ead o A-mmonia o C-arbon monoxide o K-etones Oligodendrocytes o Facilitating rapid transmitting of nerve impulses o Responsible in production of myelin sheath Migrolia o Engulf bacteria / cellular debris o Macropage of CNS - Brain: ( Microglia ) Blood: ( Monocytes / Macropages ) Liver: ( Kupfter Cell ) Lungs: ( Alveolar Macropage ) Subcutaneous: ( Histrocytes ) Intracranial Compartment: 80% ( brain mass ) 10% ( CSF ) 10% ( blood ) Brain Mass Grey matter – outer cortex o Integrative / Interpretation White matter – inner o Conduction of impulses Cerebrum Function: o S-ensory o I-ntegrative / Interpretation o M-otor 1. kidney.o Leg muscles Sacral ( 5 ) Coccyx ( 1 ) o Bowel.bladder. sexual function CNS ( central nervous system ) Neuron Excitability ( ability to response to stimuli ) o External o Internal Permanence ( cannot regenerate ) Regenerative capacity of the cell o Labile ( still regenerate )  Skin. respiratory tract.

and the legs are extended.6 ( 3 ) Occulomotor ( 4 ) Trochlear ( 6 ) Abducen o Motor o Movement of extraocular muscles o ( CN 3 ) pupillary reflex & accomodation Deviation: o Opthalmoplagia ( paralysis of EOM) o Diplopia ( double vision ) Cranial Nerve 5 ( Trigeminal ) Mixed o Eyes o Mandible o Maxillary Largest cranial nerve Sensation o Skin of the face o Corneal reflex Motor o Open mouth o Move jaw Cranial Nerve 7 ( Facial ) Mixed Facial sensory Sense of taste Motor o Facial expression o Close the eyelid Cranial Nerve 8 ( Vestibulocochlear ) Sensory Hearng acuity Balance Cranial Nerve 9 ( Glossopharyngeal ) Mixed Sensory ( posterior 1/3 of the tongue ) Motor o Swallowing o Gag reflex Cranial Nerve 10 ( Vagus Nerve ) Mixed Sensory o Throat. 4 . Sensory: Body parts to brain Motor: Brain to body parts Odynophagia ( painful swallowing ) Vagal nerve increase peristalsis / heart rate Decorticate posturing present with the arms flexed. and the legs extended and feet turned inward. or bent inward on the chest. Abdominal & Thoracic vicera Motor o PNS response of GI & Heart Cranial Nerve 11 ( Accessory ) Motor Movement of sternocleidomastoid &m trapezius Headache Cranial Nerve 12 ( Hypoglossal ) Motor Movement of the tongue Assess the motor function Assess the muscle tone & strength o Grading of muscle strength  5/5 – movement against gravity with strong resistance  4/5 – movement against gravity with some resistance . A hallmark of decerebrate posturing is extended elbows. the arms are extended by the sides. Peripheral Confrontation Test ( Visual Field Test ) Cranial Nerve Function: Cranial Nerve 1 ( Olfactory ) Sensory Sense of smell Shift & identify aromatic subs Cranial Nerve 2 ( Optic ) Sensory Impulses of Vision Check: o Visual acuity ( Snellen Chart ) o Visual field ( PCT ) Cranial Nerve 3. o Identifies Dysmetria (+FTNT) Alternate Pronation & Suponation  Dysdiadokinesia Assessment of the Neurologic System Physical examination 5 categories Cerebral function Cranial nerve Motor function Sensory function GLASGOW COMA SCALE ( Level of Consciousness ) Eye opening 4 – spontaneous 3 – to voice 2 – to pain 1 – no response Verbal Response 5 – oriented 4 – confused 3 – inappropriate voice 2 – incomprehensive 1 – none Motor Response 6 – obeys command 5 – localize pain 4 – withdraw to pain 3 – decorticate posture ( corticothalamic tract ) 2 – decerebrate posture ( pons ) 1 – none GCS Scoring 15 – 14 Conscious 13 – 11 Lethargy 10 – 8 Stupos 7 Coma 3 Deep Coma Decerebrate posturing. the head is arched back. the hands are clenched into fists.

) stimuli Obtunded Client remain drowsy when awaked Stupor Respond to a strong stimulus ( pain ) Confusion Has short attention span React to stimuli Coma Poor response / totally no response to stimuli V/S maybe stable Cerebral death Vital sign must be maintained artificially V/S unstable ( .) respond .increased ++++ .present but diminished ++ .absent + .hyperactive Assessment of Brain Stem Test for the Oculocephalic reflex o Doll’s eye test ( eye movement towards the opposite side ) Test for Oculovestibular reflex o Caloric test  Assess patency of the ears  Semifowlers position  Irrigate the ear  C – old  O – pposite  W – arm  S – ame side Diagnostic Procedure EEG ( Electroencephalogram ) Records electronic activity generated in the brain especially in the grey matter Identify seizure disease Identify brain death Nursing Consideration Advise to shampoo hair before procedure Recommend the patient not to sleep Withhold medication that affect brain function ( 24 – 48hrs prior ) o Antiseizure ( Penetol ) o Tranquilizer ( major / minor ) o Brain stimulant ( Amphetamine ) o Caffeine o Methylpenedate o Sedatives Alpha – awake ( calm ) Beta – awake ( alert ) Delta – children Theta – deep sleep CT Scan Scan the body part in successive layer Uses narrowed xray beams Asses allergy for contrast dye Identify: Intracranial bleeding Pressure of lesion tumor Identify changes in brain structure o Brain atrophy o Cerebral edema Ares of refraction Brain herniation MRI Uses magnetic waves Contraindicated to a patient with: Pacemaker Orthopedic metal prosthesis Implanted Cerebral Angiography Visualization of cerebral artery o Brachial / Femoral - Give patient a rest after procedure / Maintain pressure dressing o To avoid bleeding Lumbar Puncture Ensure consent Determine ability to lie still o Side lying position with knee & head flex o 500ml CSF ( choroid flexus ) o Subarachnoid space ( L3 – L4 ) o 150ml ( aspirate ) Contraindicated to a patient with increase ICP o Brain herniation Keep flat on bed after procedure ( 6 – 12 hrs ) Increase fluid intake after procedure Indication: Obtain CSF analysis Cerebrospinal Gross Analysis o Normal color ( colorless ) o Abnormal ( pinkish color ) Measure & reduce CSF pressure ( 70 120mmHg ) Use to administer medication Quekenstedt Test Subarachnoid block ( assess ) Normal ( CSF pressure is increased ) Slow rise and fall in pressure indicates a partial block Alteration in the level of consciousness Delirium ( acute confusional state ) Disoriented – agitated Even without stimuli o Hallucination ( .normal +++ . - - - 3/5 – movement against without resistance  2/5 – movement cannot resist gravity  1/5 – trace movement  0/5 – no movement Assessing the motor function of cerebellum o Test for balance o Test for coordination Assessing the sensory function o Evaluate symmetric areas of the body o Ask the patient to close eyes Materials:  Used test tubes  Blunt / sharp object  Use wisp of cotton Assessing the reflexes o Deep tendon / muscle stretch reflexes  Bicep  Tricep  Patellar  Brachioradialis o Superficial / Cutaneous reflexes  Abdominal  Cremasteric ( inner thigh ) ascend scrotum/ testes  Gag o Pathologic / Primitive reflexes  Babinski Grading of reflex 0 .) EEG ( .) reflex ( .

INCREASED ICP (8 – 20 mmHg ) Predisposing factor Increased size of brain mass o Tumor o Edema Intracranial bleeding o Intracerebral o Subarachnoid o Epidural hematoma o Subdural hematoma Inflammatory condition o Meningitis o Encephalitis CSF flow problem o Hydrocephalus Ss/Sx.P Nursing Management for increased ICP Proper positioning o Semi/ High Fowler ( neck properly aligned ) Close monitoring ( GCS q1 – PERRLA papillary reflex ) Promote oxygenation Promote safety Decrease environmental stimuli Limit fluid intake Prevent ICP Instruct the patient to avoid this: Valsalva maneuver Excessive cough Excessive vomiting Lifting heavy object Bleeding Administer meds as ordered Fast drip Osmotic diuretic ( Mannitol ) o Cerebral decompression Loop diuretic o Onset 15 – 30 mins prior to administration Corticosteroid Antipyretic Anticonvulsant Analgesic PARKINSON DISEASE Idiopathic Chronic progressive disease by CNS Predisposing factor Poisoning ( lead monoxide ) Hypoxia Encephalitis Ss/Sx: Resting tremor Propulsive gait Rigidity Drooling Shock Decrease temp.P - D ysphagi a M onotono us speech Bradykinesia o Micropphagia o Hypomimia o Hypophonia Pharmacotherapy Dopamine agonist o Controls of voluntary movement o Inhibits excitability of neuro muscular junction o Levodopa ( L –dopa ) o Carbedopa ( Sinemet ) inhibits dopamine carboxillation Artane ( minimize muscle rigidity ) Antihistamine ( decrease tremors ) Amantadine HCl ( symmetrel ) increase availability of dopamine in the brain Nursing management Passive ROM exercise Maintain good nutrition o High protein o High carbohydrates o Increase oral fluid intake o Increase fiber Safety precaution Promote ambulation MULTIPLE SCLEROSIS Demyelization of neuron White matter Ss/Sx: Visual disturbances o Blurring of vision o Diplopia & nystagmus o Scotoma Impaired sensation o Paresthesia Impaired motor function Urinary bowel disturbances o Constipation o Spastic bladder o Flaccid bladder Decrease sexual capacity . Increase RR Increase HR Decrease BP Narrowed P. Decrease RR Decrease HR Increase BP Widened P. Early sign: Alteration of LOC o Awaken coherent o Restlessness – agitated o Confusion o Lethargy o Obtunded o Stupor o Coma Visual problem o Blurring of vision o Diplopia Headache Late sign: Change in V/S Cushing triad ( hyper – brady – brady ) o Increase BP ( systolic ) o Decrease RR o Decrease HR o Increased heart volume Projectile vomiting Pupil changes Changes in motor function o Spasm o Paralysis ( transient ) Increase ICP Increase temp.

S I-ntentioanl tremors N-ystagmus A-taxia DX: CSF analysis MRI ( + ) Lhermittes sign ( caudal portion) Medication Muscle relaxant Immunosuppressive medication Urinary cholinergics ( Bethanechol ) Urinary antispasmodic Clonazepam ( reduce ataxia ) NI: Promote safety Provide eyepatch for diplopia Establish regular exercise-rest pattern Proper diet Promote independence ( degree of flexion ) SPINAL CORD INJURY Result from disruption of nerve tract and neuron May result to partial or complete loss of motor sensation & reflex Cause: Contusion ( blunt ) Laceration ( penetrating ) Fracture of vertebrae NI: Enhance activity rest pattern Facilitate normal nutrition Facilitate spinal revery Pharmacotherapy Corticosteroid Baclofen Dantrolene sodium Level of injuries Cervical injury o Respiratory difficulty o Quadriplegia Thoracic o Paraplegia o Bladder / Bowel dysfunction Lumbar & Sacral o Paraplegia o Erectile dysfunction Complication Spinal Shock ( Neurogenic ) o Sudden onset o Muscles are paralyzed o Negative reflex o Sign of shock o Medical emergency Autonomic dysreflexia / Hyperflexia o Gradual onset (Hypertensive stroke) o Caused by injured above T6 o Triggered by visceral distention (Full bladder / Constipation) o Sign of SNS stimulation o Medical emergency MYASTHENIA GRAVIS Auto immune disorder Low Acethylcholine ( Neurotransmitter ) o Excitability of NMJ High production of Acethylcholinesterase Decrease receptor site Presence of resistance in receptor site Ss/Sx: Ptosis ( dropping of eyelid ) Diplopia Dysphagia Weakening of Laryngeal muscle Muscle weakness DX test for MG: Edrophonium Chloride o Tensilon Test ( Confirmatory ) o CSF Analysis  Increase Cholinesterase Monitor for 2 types of crisis Mysthenia Crisis o Causes  Under Medication  Stress  Infection o Management  Give Anticholinesterase Cholinergic Crisis o Over Medication o Ss/Sx:  Salivation ( Thialism )     o Lacrimation Urination Diarrhea Body weakness  Evident Sign Depolarization of Neuroplates Management  Give Anticholinergic  Atropine Sulfate (Antidote) TRIGEMINAL NEURALGIA ( Tic Douloureux ) Sensory disorder of the 5th cranial nerve Assessment Severe recurrent sharp pain along the tract of the 5th CN o Cheeks o Superficial layer of the nose o Lips o Gums Triggering factors o Direct pressure o Washing of the face o Chewing o Intake of foods or fluid ( Extreme temperature ) o Exposure of cold environment NI: Diet modification Avoid factor that triggers pain Chew on the unaffected side Pharmacotheraphy Baclopen Carbemazepine o Relieves neuralgia Surgical Intervention Microvascular Decompression o It relocates the artery that compresses nerves & blood vessels BELL’S PALSY Facial Nerve ( CN7) Cause Lesion on lower motor neuron Unilateral facial paralysis Predisposing factors Infection ( CNS ) Tumor .Late stage: ( psychiatric disturbance ) Depression Apathy Euphoria Forgetfulness Triad of M.

Neglect Syndrome ( Unilateral Neglect ) o Homonyniuos Hemanopsia Neglect Syndrome ( Unilateral Neglect )  Approach on intact vision o o o o o o o o Encouraged client to scan environment Aphaxia  Receptive  Expressive  Provide alternative ways for expression  Put extra patience  Simple phrases Agraphia  Inability to write Alexia  Inability to comprehend Ataxia  Unsteady / Jerky movements Speech changes  Dyarthria Decreased sensation Bowel & Bladder dysfunction Nuchal rigidity DX procedure CT scan Angiography ( perfusion of blood vessel ) Management for CVA Acute phase Promote oxygenation BP maintenance at 140/90mmHg Suction secretion as needed WOF increased ICP ( herniation of medulla oblongata ) Proper positioning ( semifowlers ) Post Acute phase Maintain patent airways Elevate head of the bed Monitor V/S. MI Valvular Heart Disease ( valvular stenosis ) Post Heart Surgery ( valvular replacement ) Lifestyle o Smoking o Sedentary Lifestyle o Hyperlipidemic o Prolonged use of Contraceptives  Abdominal pain  Chest pain  Headaches  Eye problem  Severe leg cramps Stages of CVA 1. GI infection ) –Polyneuritis Form of an autoimmune disorder o Damage Myelin Sheath (Polyneuritis) Ss/Sx: Clumsiness ( Initial ) Paresthesia Ascending muscle weakness Dysphagia Arrhythmic Respiratory failure ( #1 complication ) DX: CSF analysis NI: Maintain patient airway Continuous monitoring Promote safety Plasmapherisis o Extracorporeal treatment ( outside the body – antecubital vein )  Cell separator (Centrifugal force) separates plasma Pharmacotherapy Corticosteroids ( SAWSO ) Anti arrhythmia CVA ( Cerebro Vascular Accidents ) Disrupted cerebral blood flow Common location Middle Cerebral Artery ( MICA ) Internal Carotid Artery ( ICA ) Types: Thrombolic ( Ischemic Stroke ) o Form inside the cerebral blood vessel Embolic ( Ischemic Stroke )  o Form outside the cerebral blood vessel Hemorrhagic ( Hypertensive Stroke ) o Rupture of aneurysm Risk Factors: Atherosclerosis ( narrowing ) HPN. neurocheck Prevent complication of immobility Prevent aspiration ( thicken fluid ) Alternative means of complication Maintain side rails Pharmacotheraphy Osmotic diuretic Loop diuretic Corticosteroid . Nausea & Vomiting o Dysphagia Late sign: o Cheyne Stroke Respiration ( hyper capnea with period of apnea ) Other Ss/Sx: (+) Kernigs & Brudzinki ( hemorrhagic ) o Meningeal Irritation Neurological Deficits o Hemiplagia . Transient Ischemic Attack Reversible : Ss/Sx subside in 2hr Same as CVA ( causes. Stroke in evolution o Progressive Ss/Sx of stroke 3. DM. affectation ) o Headaches o Dizziness o Numbness o Tinnitus o Visual / Speech Disturbances 2. Complete stroke o Paralysis o Anorexia. effect. I&O.Trauma Assessment Facial Paralysis o Unilateral ( 2 weeks ) Loss of taste o anterior 2/3 of tongue Intervention Protect eyes from dryness Instruct client to chew on affected side GUILLAIN BARRE SYNDROME ( Spinal nerve ) Acute ( sudden onset ) -Post -Infection ( Resp.

Epileptic spasm without interval of consciousness o Acute – Severe Exacerbation (30mins of continuous episode of epilepsy) Drug Of Choice ( DIAZEPAM ) Predisposing factors Head injury due to birth trauma Carbon monoxide poisoning Brain tumor Genetics Physical Stress Sudden withdrawal of convulsant Types of Seizures Generalized Tonic – Clonic Seizures o With or without AURA  Epigastric pain  Halo vision  Burning sensation  Tactile aura  Ringing sensation  Epileptic cry o Tonic phase ( 10 -20 sec ) o Stiffining or rigidity o Clonic phase ( 30 sec ) o Jerking movement o Hyperventilation Absence Seizures ( Petit Mal ) o May or may not lose consciousness - - Partial - - Seizures may occur several times during the day o Blank stare o Decreased blinking Myoclonic o Brief generalized seizures o Clonic phase Atonic / Akinetic ( drop attack ) o Sudden momentary loss of muscle tone Complex Partial ( Temporal damage ) o Psychomotor seizures o Drastic change in behavior Simple Partial o Confined into a specific area NI: - Note time and duration of seizures Assess for AURA If the client is standing. place client on the floor Support ABC During Seizures: Do not place anything in the client mouth Do not restrain the client .- o Mild analgesic Thrombolytics ( Ischemic stroke ) o Prevent blood clot Anticoagulant o Maintenance Antiplatelet o Prevent platelet adhesion & aggregation o Before meals CONVULSIVE DISORDER CONVULSION Seizure – Abnormal excessive uncontrolled electrical activity of the brain Epilepsy – Characterized by chronic seizure activity Acute febrile seizure – ( Cytoplasmic Reticulum Alteration ) Hyperpyrexia Status Epilepticus .