Wednesday, October 19, 2011


Instruction : download PDF please click on image

Ebook Content :
Chapter 1 The Physiology of Wound Healing 1
1.1 Introduction 1
1.2 Definitions associated with wounds 1
1.3 The structure of the skin 2
1.3.1 Dermis 2
1.3.2 Epidermis 2
1.4 Wound healing 3
1.4.1 Inflammation 4
1.4.2 Reconstruction 6
1.4.3 Epithelialisation 8
1.4.4 Maturation 9
1.5 Impaired wound healing 9
1.5.1 Hypertrophic scars 9
1.5.2 Keloids 10
1.5.3 Contractures 10
1.5.4 Acute to chronic wounds 10
1.6 Conclusion 11
Chapter 2 The Management of Patients with Wounds 13
2.1 Introduction 13
2.2 Physical care 13
2.2.1 Nutrition 13
2.2.2 Infection 19
2.2.3 Smoking 23
2.2.4 Diabetes mellitus 25
2.2.5 They physical effects of stress 26
2.2.6 Pain 27
2.2.7 Sleeping 30
2.2.8 Hypothermia 32
2.2.9 Steroids 33
2.2.10 Radiotherapy 34
2.3 Psychological care 35
2.3.1 Anxiety 35
2.3.2 Motivation and education 37
2.3.3 Body image 39
2.3.4 Other psychological problems 41
2.4 Spiritual care 43
Chapter 3 General Principles of Wound Management 56
3.1 Introduction 56
3.2 Wound assessment 56
3.2.1 Wound classification 56
3.2.2 The position of the wound 57
3.2.3 The environment of care 58
3.2.4 M = measure 58
3.2.5 E = exudate 61
3.2.6 A = appearance 62
3.2.7 S = suffering 69
3.2.8 U = undermining 70
3.2.9 R = re-evaluate 70
3.2.10 E = edge 71
3.3 Managing wounds 72
3.3.1 Moist wound healing 72
3.3.2 Wound bed preparation 72
3.3.3 Pain management 76
3.4 Documentation 77
3.5 Evaluating the dressing 78
Chapter 4 Wound Management Products 83
4.1 Introduction 83
4.2 The development of dressings through the ages 83
4.2.1 Early days 83
4.2.2 The Dark Ages and early Middle Ages 85
4.2.3 Late Middle Ages and Renaissance 86
4.2.4 The seventeenth, eighteenth and early nineteenth centuries 87
4.2.5 Mid-nineteenth and early twentieth century developments 88
4.2.6 The British Pharmaceutical Codices 89
4.3 Traditional techniques 90
4.4 The use of lotions 91
4.4.1 Antiseptics 91
4.4.2 Antibiotics 95
4.4.3 Honey 96
4.4.4 Saline 0.9% 97
4.4.5 Tap water 97
4.5 Clinical effectiveness of wound management products 97
4.5.1 Providing an effective environment 97
4.5.2 The handling qualities of an effective wound
management product 98
4.6 Modern wound management products 99
4.7 Advanced technologies 105
4.7.1 Growth factors 105
4.7.2 Protease-modulating wound management products 105
4.7.3 Hyaluronan-based products 106
4.7.4 Hyperbaric oxygen 107
iv The Care of Wounds
4.7.5 Topical negative pressure 108
4.7.6 Tissue culture 110
4.7.7 Tissue engineering 110
4.8 Alternative therapies and wound management 112
Chapter 5 The Management of Patients with Chronic Wounds 121
5.1 Introduction 121
5.2 The prevention and management of pressure ulcers 121
5.2.1 The cost of pressure ulcers 122
5.2.2 The aetiology of pressure ulcers 123
5.2.3 Prevention of pressure ulcers 128
5.2.4 Management of pressure ulcers 138
5.3 The management of leg ulcers 143
5.3.1 The epidemiology of leg ulcers 144
5.3.2 The cost of leg ulcers 144
5.3.3 The causes of leg ulcers 145
5.3.4 Venous ulceration 145
5.3.5 Arterial ulcers 152
5.3.6 Ulcers of mixed aetiology 155
5.3.7 Malignant leg ulcers 156
5.3.8 Leg ulceration in rheumatoid arthritis 157
5.4 Diabetic foot ulcers 158
5.4.1 Aetiology 158
5.4.2 Prevention 159
5.4.3 Management 160
5.5 Fungating wounds 162
5.5.1 Aetiology and incidence 163
5.5.2 Management of fungating wounds 163
5.6 Lymphoedema 165
5.6.1 Lymphoedema management 166
5.7 Conclusion 168
Chapter 6 The Management of Patients with Acute Wounds 179
6.1 Introduction 179
6.2 The care of surgical wounds 179
6.2.1 Management of surgical wounds 179
6.2.2 Managing complications 186
6.3 Traumatic wounds 194
6.3.1 Minor traumatic wounds 194
6.3.2 The management of specific types of traumatic wounds 196
6.4 The burn injury 199
6.4.1 Aetiology 200
6.4.2 Incidence 201
6.4.3 The severity of the injury 201
6.4.4 Burn oedema 203
6.4.5 First aid treatment of burns 203
6.4.6 The management of burn injuries 205
Contents v
6.5 Radiation reactions 209
6.5.1 Aetiology 210
6.5.2 The classification of radiation reactions 210
6.5.3 Preventive skin care 210
6.5.4 Managing radiation reactions 211
6.5.5 Care of the patient 212
Chapter 7 Clinically Effective Wound Care 218
7.1 Introduction 218
7.2 Evidence-based practice and clinical effectiveness 218
7.3 Searching and appraising the literature 218
7.3.1 Appraising the literature on wound care 221
7.4 Developing clinical guidelines 222
7.4.1 Guidelines in wound care 222
7.5 The clinical audit cycle 224
7.5.1 Auditing clinical practice 224
7.5.2 Dissemination of audit findings 225
7.6 Conclusions 225
Chapter 8 The Organisation of Wound Management 228
8.1 Introduction 228
8.1 Managing wounds in the community 228
8.2.1 Nurse prescribing 228
8.2.2 Community leg ulcer clinics 229
8.3 Nurse specialists in wound care 230
8.4 The management of pressure-redistributing equipment 232
8.4.1 Equipment stores 232
8.4.2 Total bed management 232
8.5 Wound-healing centres 233
8.6 Conclusions 234
Index 236

Instruction : download PDF please click on image


Instruction : download PDF please click on image


The National Council Licensure Examination for registered nurses
(NCLEX-RN®) measures the knowledge and abilities necessary for entrylevel
■ It is administered by Computer Adaptive Testing (CAT), which
individualizes tests to match the unique competencies of each test taker.
■ Each exam adheres to the NCLEX-RN® Test Plan, which describes the
content and scope of RN competencies.
■ Practices basic to nursing (e.g., nursing process, caring, teaching,
learning, communication, documentation) are integrated throughout,
and most questions require application and analysis of information.

NCLEX-RN® Test Plan—Distribution of Content
Safe and Effective Care Environment
■ Management of Care 13%–19%
■ Safety/Infection Control 8%–14%
Health Promotion and Maintenance 6%–12%
Psychosocial Integrity 6%–12%
Physiological Integrity
■ Basic Care/Comfort 6%–12%
■ Pharmacological/Parenteral gfd Therapies 13%–19%
■ Reduction of Risk Potential 13%–19%
■ Physiological Adaptation 11%–17%

Taking the NCLEX-RN® Test on a Computer
■ First: You will receive general information about the exam and the testing
center. Your time spent on this will not count.
■ Second: You will take a tutorial on how to use the computer to answer the
questions on NCLEX-RN®. Your answers will not count toward your score,
but the time you take will be subtracted from the total 6 hours you have
for the exam.
■ Third: You will then be presented with real NCLEX-RN® items; there will
be between 75 and 265 items. The test ends when it is 95% certain your
ability is ↑ or ↓ the passing standard.

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Thursday, October 13, 2011

IV Med Notes PDF

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Infusion Assessment

Primary infusion fluid—Fluid that is infusing continuously.
Secondary infusion—Fluid that is infusing intermittently, usually
in a 50-250 ml IV bag infusing over 15 minutes to 2 hours.
Patient-controlled analgesia (PCA) pump—Infuses pain medication
and is usually connected to the primary line. Both the
primary line and PCA pump infuse concurrently.
HOT TIP: When assessing the infusions to check for incompatibilities,
the PCA pump can easily be overlooked!! Verify
the type of medication in the PCA pump, and ensure it is
Total parenteral nutrition (TPN)/Lipids—TPN usually infuses
continuously over 24 hours. Lipids usually infuse over 8, 10,
or 12 hours connected to the TPN IV line below the filter.
HOT TIP: Due to the additional components/medications in the
TPN solution, NO medication is to be given in the same line as
the TPN or the lipids.
Blood products—Include whole blood, packed red blood cells,
plasma, platelets, albumin, serum globulins.
HOT TIP: NEVER give any medication in the blood component
IV line. The only compatible solution is 0.9% normal saline

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Jones' Clinical Paediatric Surgery Diagnosis and Management PDF

Introduction, 1
1 Antenatal Diagnosis – Surgical Aspects, 3
2 The Care and Transport of the Newborn, 7
3 The Child in Hospital, 13

Neonatal Emergencies, 17
4 Respiratory Distress in the Newborn, 19
5 Diaphragmatic Hernia, 26
6 Oesophageal Atresia and Tracheo-Oesophageal Fistula, 30
7 Bowel Obstruction, 35
8 Abdominal Wall Defects, 44
9 Spina Bifi da, 49
10 Disorders of Sexual Development, 56
11 Anorectal Anomalies, 61

Head and Neck, 67
12 The Scalp, Skull and Brain, 69
13 The Eye, 79
14 The Ear, Nose and Throat, 91
15 Cleft Lip, Palate and Craniofacial Anomalies, 97
16 Abnormalities of the Neck and Face, 106

Abdomen, 115
17 The Umbilicus, 117
18 Vomiting in the First Months of Life, 121
19 Intussusception, 126
20 Abdominal Pain: Appendicitis?, 130
21 Recurrent Abdominal Pain, 136
22 Constipation, 139
23 Bleeding from the Alimentary Canal, 142
24 Infl ammatory Bowel Disease, 147
25 The Child with an Abdominal Mass, 153
26 Spleen, Pancreas and Biliary Tract, 157
27 Anus, Perineum and Female Genitalia, 162
28 Undescended Testes and Varicocele, 168
29 Inguinal Region and Acute Scrotum, 172
30 The Penis, 179

Urinary Tract, 185
31 Urinary Tract Infection, 187
32 Vesico-Ureteric Refl ux, 193
33 Urinary Tract Dilatation, 198
34 The Child with Wetting, 205
35 The Child with Haematuria, 211

Trauma, 215
36 Trauma in Childhood, 217
37 Head Injuries, 224
38 Abdominal and Thoracic Injuries, 231
39 Foreign Bodies, 236
40 The Ingestion of Corrosives, 241
41 Burns, 243

Orthopaedics, 247
42 Neonatal Orthopaedics, 249
43 Orthopaedics in the Infant and Toddler, 254
44 Orthopaedics in the Child, 259
45 Orthopaedics in the Teenager, 266
46 The Hand, 271

Chest, 275
47 The Breast, 277
48 Chest Wall Deformities, 279
49 Lungs, Pleura and Mediastinum, 283

Skin and Soft Tissues, 291
50 Vascular and Pigmented Naevi, 293
51 Soft Tissue Lumps, 298

Answers to Case Questions, 301
52 Answers to Case Questions, 303

Index, 311

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Users Guides to the Medical Literature A Manual for Evidence-Based Clinical Practice PDF

Completely revised and updated with all new coverage of the basic issues in evidence-based medicine in patient care

Abundant real-world examples drawn from the medical literature are woven throughout, and include important related principles and pitfalls in using clinical research in patient care decisions

Edited by over 60 internationally recognized editors and contributors from around the globe

Also look for, a new interactive database for the best practice of evidence based medicine


1. How to Use the Medical Literature–and This Book–to Improve Your Patient Care
2. The Philosophy of Evidence-Based Medicine
3. What Is the Question?
4. Finding the Evidence
5. Why Study Results Mislead: Bias and Random Error
6. Therapy (Randomized Trials)
7. Does Treatment Lower Risk? Understanding the Results
8. Confidence Intervals
9. Harm (Observational Studies)
10. The Process of Diagnosis
11. Differential Diagnosis
12. Diagnostic Tests
13. Prognosis
14. Summarizing the Evidence
15. How to Use a Patient Management Recommendation

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Wednesday, October 12, 2011

ECG and arrhythmia classification

ECG and arrhythmia classification :

Narrow complex arrhythmias (arise above bifurcation of the bundle of His) – QRS duration <0.1s (2.5 small squares)
Broad complex arrhythmias (arise from ventricles or are conducted abnormally from a site above the ventricles so that a delay occurs (rarer). QRS duration is >0.1s (2.5 small squares).

Narrow complex arrhythmias

·         Sinus arrhythmia
·         Sinus tachycardia
·         Sinus bradycardia
·         Junctional tachycardia
·         Atrial tachycardia, Atrial flutter
·         Atrial fibrillation
·         Atrial ectopics

Broad complex arrhythmias

·         Ventricular ectopics
·         Ventricular tachycardia
·         Supraventricular tachycardia with BBB
·         Ventricular fibrillation

Sinus arrhythmia: Irregular spacing of normal complexes associated with respiration. The P-R interval is constant, but there are beat-to-beat changes in R-R interval. Normal, especially in young people.
- Because in inspiration, the negative pressure sucks more blood into the chest, which ­ cardiac output. This is detected by baroreceptors which ­ HR).

Sinus tachycardia: Rate over 100bpm. Normal P-QRS-T complexes are present.
Causes include:
·         Pain
·         Fever/sepsis
·         Hypovolemia
·         Anaemia
·         Heart failure
·         Thyrotoxicosis
·         Drugs – atropine, ether, ketamine, catecholamines

Management – correction of underlying disease.
·         b-blockers if tachycardia causes myocardial ischemia in patient with IHD

Sinus bradycardia: Heart rate of <60bpm. May be normal in athletic people, or with increased vagal tone.
·         Drugs - b-blockers, digoxin, anticholinesterase drugs, halothane
·         MI
·         Sick sinus syndrome (fibrosis of AV node)
·         Raised intracranial pressure
·         Hypothyroidism
·         Hypothermia

Management: Often not necessary in a fit young person (unless rate is <45-50bpm) and/or there is haemodynamic compromise. You may consider:
·         Correct underlying cause
·         Atropine

Arrhythmias due to re-entry

·         Where there is anatomical branching and re-joining of a conduction pathway.
·         If one limb is slower than the other, the impulse may pass normally down one limb but be blocked in the other. Where the pathways rejoin, the impulse can then spread backwards up the abnormal pathway. If it arrives at a time when the first pathway is no longer refractory to activation, it can pass right around the circuit repeatedly, activating it and resulting in tachycardia

·         Wolf-Parkinson-White syndrome (anatomical “accessory” pathway between the atria and ventricles) “Macro-reentry circuit” (Other macro re-entry circuits can exist in the atrial/ventricular myocardium and cause paroxysmal atrial flutter, AF, ventricular tachycardia).

·         In Junctional tachycardia, there are “micro re-entry” circuits within the AV node itself

Junctional tachycardia: Micro re-entry circuits in or near the AV node (or, as in W-P-W, from an accessory conduction pathway between the atria and ventricles).

·         Narrow complex tachycardia with rate of 150-200bpm
·         SHORT P-R
·         Slurred upstroke on the R wave (Delta wave in V4 in WPW)
·         Inverted T waves in V2-5 are characteristic

Management: This arrhythmia may be associated with severe circulatory disturbance
·         If they are haemodynamically compromised -cardioversion
·         Carotid sinus massage (rarely converts to sinus rhythm, but slows the rate and will reveal the underlying rhythm if in doubt) (helps differentiate from atrial flutter/AF)
o    The carotid sinus is a small dilatation of the proximal part of the internal carotid artery at the level of the superior border of the thyroid cartilage. It is vagally innervated and is involved in the control mechanism for causing a fall in HR and CO in response to rise in arterial pressure. Gentle pressure here may result in slowing of the heart and occasionally, termination of re-entry SVT. Never do on both sides or it can cause asystole and occlusion of the main arterial blood supply to the brain.
·         Adenosine (slows AV conduction so is useful for terminating re-entry SVTs of the WPW type)
·         Verapamil, b-blockers, amiodarone, flecainide may control the rate of convert to sinus rhythm

Atrial tachycardia and Atrial flutter: Due to an ectopic focus depolarising from anywhere within the atria. They contract faster than 150bmp and P waves can be seen superimposed on T waves of the preceding beats.
·         AV node conducts at a maximum of 200bpm, so if the atrial rate is faster, AV block will occur (Typically see ventricular rate as 150bpm with atrial flutter)
·         If the atrial rate is >250bpm, there is no flat baseline between P waves and you get “sawtooth” pattern
·         Can occur with any type of block (2:1, 3:1, 4:1)
·         Atrial tachycardia is typically a paroxysmal arrhythmia with intermittent tachycardia and palpitations (may be precipitated by many factors – stress, alcohol, caffeine)
o    With 2:1 block = characteristic of digitalis toxicity

Management: Very sensitive to direct current cardioversion (almost 100% success rate), so should be used first line if there is haemodynamic compromise
·         Carotid sinus massage and adenosine ® slow AV conduction and reveal underlying rhythm and block if there is doubt
·         Other drug treatment as for AF

Atrial fibrillation: Very common. It is a chaotic and uncoordinated atrial depolarisation (absence of P waves), with an irregular baseline and completely irregular ventricular rate. The ventricular response rate will normally be rapid – about 120-200 bpm.
Common causes:
·         Ischaemia
·         Myocardial disease/pericardial disease
·         Mitral valve disease
·         Sepsis
·         Electrolyte disturbance (esp. Hypokalaemia or hypomagnesaemia)
·         Thyrotoxicosis
·         Thoracic surgery

Since contraction of the atria contributes 30% to ventricular filling, the onset of AF may result in significant ¯ in CO. Fast AF may precipitate cardiac failure, pulmonary oedema and myocardial ischaemia and systemic thromboembolism may occur if blood clots in the fibrillating atria form.

Management: Treatment is aimed at restoration of sinus rhythm if possible and if not, maintaining the rate to <100bpm and prevention of embolic complications. Management depends on how long it has been present.
·         Correct precipitating factors where possible
·         DC cardioversion (for recent onset)
·         Digoxin – to slow ventricular rate
·         Amiodarone – to restore sinus rhythm
·         Verapamil – control ventricular rate
·         b-blockers – sometimes used to control ventricular rate
·         Aim to control ventricular rate to <100bpm – allows time for adequate ventricle filling and maintains CO
·         Digitalisation
·         b-blockers of verapamil
·         Amiodarone

When AF has been present for more than a few hours, anticoagulation is necessary before cardioversion to prevent the risk of embolisation. (Usually warfarin for 3 weeks prior to elective DCC)

Atrial ectopic beats: An abnormal P wave is followed by a normal QRS. The P wave is not always easily visible
·         “Ectopic” indicates that depolarisation originated in an abnormal place – get an abnormally shaped P wave
·         If the focus depolarises EARLY, the beat produced is an extrasystole (premature) and may be followed by a compensatory pause
·         If the underlying SA node is slow, sometimes an atrial focus takes over – escape beat as it occurs after a SMALL DELAY
·         Any heart disease
·         Ischaemia, hypoxia
·         Light anaesthesia
·         Sepsis
·         Shock
·         Anaesthetic drugs

Management: Correction of underlying cause and treatment is not necessary unless runs of atrial tachycardia occur.


Ventricular ectopic beats: Depolarisation spreads from a focus in the ventricles by an abnormal (\slow) pathway, so the QRS is wide and abnormal. (T wave is also abnormal in shape).
·         Usually benign if there is no structural heart disease
·         May be associated with abnormalities – Hypokalaemia, light anaesthesia (with halothane), raised CO2, intracranial pressure

The onset of runs of VT should be taken seriously where:
·         There is a bigeminal rhythm (one ectopic beat with every normal beat)
·         If they occur in runs of 2 or more (or more than 5/minute)
·         Where they are multifocal (arising from different foci – hence having different shapes)
·         Where the R wave is superimposed on the T wave

·         Small dose of b-blocker
·         If underlying sinus rhythm is slow, increase the rate with IV atropine (as ventricular ectopics could be a form of escape beat)
·         Lignocaine is the drug of choice
·         Alternatives – amiodarone

Ventricular tachycardia: A focus in the ventricular muscle depolarises at high frequency. Excitation spreads through the ventricles by an abnormal pathway. There are no P waves, wide QRS which may be slightly irregular/vary in shape.
Can be triggered by:
·         Hypoxia
·         Hypotension
·         Fluid overload
·         Electrolyte imbalance (low K, Mg)
·         Myocardial ischaemia
·         Adrenaline injection

·         Synchronised direct current cardioversion if the patient is haemodynamically unstable
·         If they relapse back into VT – lignocaine, amiodarone can sustain sinus rhythm
·         NOT verapamil

Supraventricular tachycardia with bundle branch block: Where there is abnormal conduction from the atria to the ventricles, a SVT may be broad complex if there is a BBB. Sometimes it can be due to ischaemia.

BUT – all tachycardias should be treated as VT if there is any doubt.
·         RBBB : V1 looks more at the right side of the heart, so if the right ventricle is the last to depolarise due to a block, you see  the last deflection in V6 will be negative (going away from the left of the heart) and the last deflection in V1 will be positive (going towards the right of the heart)
·         LBBB (much more common): V6 looks at the left heart, so if the left ventricle is the last depolarising due to a block, you see last deflection in V6 will be positive and the last deflection in V1 will be negative (going away from the right of the heart)
Ventricular fibrillation: This results in cardiac arrest. There is chaotic and disorganised contraction of ventricular muscle and no QRS complexes can be identified on the ECG.

Management: Immediate DCC


First degree block: PR interval is >0.2s (delayed). Usually benign, but can progress to 2nd degree block.

Second degree block – Mobitz type I (Wendebach): Progressive lengthening of the PR interval and then failure of conduction of an atrial beat. This is followed by a conducted beat with a short PR interval. The cycle then repeats
·         Common with inferior MI, tends to be self-limiting and doesn’t tend to require treatment

Secondary degree block – Mobitz type II: When excitation intermittently fails to pass through to the ventricles. Most beats are conducted normally, but occasionally, there is atrial contraction without a subsequent ventricular contraction
·         Often progresses to complete heart block

Second degree block – 2:1 type: Where there is alternate conducted and non-conducted beats resulting in 2 P waves for every QRS. A 3:1 or 4:1 block may also exist.
·         May herald complete heart block

Third degree (complete) heart block: Complete failure of conduction from the atria to the ventricles, so the ventricles are excited by an escape mechanism (slow) from a focus in the ventricles. There is no relationship between the P waves and the QRS complexes and the QRS complexes are abnormally shaped.
·         May be transient due to vagal stimulation (responds to IV atropine)
·         Acute inferior MI (due to AV nodal ischaemia)
·         Anterior MI – indicates more extensive damage, including the His-Purkinje system

Bundle branch block: If the impulse from the SA and AV nodes reaches the IV septum normally, the PR interval will be normal, but if there is a subsequent delay in depolarisation of the L/R bundle branches, there will be a delay in depolarisation of part of the ventricular muscle and the QRS complex will be wide and abnormal
·         RBBB – often found in normal, may indicate right heart problems
·         LBBB – often indicates heart disease

Wednesday, October 5, 2011


NANDA International (formerly the North American Nursing Diagnosis Association) is a professional organization of nurses standardized nursing terminology that was officially founded in 1982 and develops, researches, disseminates and refines the nomenclature, criteria, and taxonomy of nursing diagnoses. In 2002, NANDA relaunched as NANDA International in response to the broadening scope of its membership. NANDA International published Nursing Diagnosis quarterly, which became the International Journal of Nursing Terminologies and Classifications in 2002.Other related international associations are AENTDE (Spanish), AFEDI (French language) and JSND (Japan)

In 1973 the First National Conference on the Classification of Nursing Diagnoses was held in St. Louis, Missouri which created the National Conference Group, a task force to standardize nursing terminology. In 1982 NANDA was formed including members from the United States and Canada.

NANDA developed a nursing classification to organize nursing diagnoses into different categories. Although the taxonomy was revised to accommodate new diagnoses, in 1994 it became apparent that an overhaul was needed. In 2002 Taxonomy II, which was a revised version of Gordon's functional health patterns, was released.

In 2002, NANDA became NANDA International in response to requests from its growing base of membership from outside North America. The acronym of NANDA was retained in the name because of the name recognition, but it is no longer merely "North American", and in fact boasts members from 32 countries as of 2010.

Taxonomy II
The current structure of NANDA's nursing diagnoses is referred to as Taxonomy II and has three levels: 13 domains, 47 classes, and 205 diagnoses.

* 1982-1988 Dr. Marjory Gordon
* 1988-1993 Jane Lancour
* 1993-1996 Dr. Lois Hoskins
* 1996-1998 Dr. Judith Warren
* 1998-2000 Dr. Dorothy A. Jones
* 2000-2002 Kay Avant
* 2002-2004 Mary Ann Lavin
* 2004-2006 Martha Craft-Rosenberg
* 2006-2008 Dr. Heather Herdman
* 2008-2012 Prof. Dickon Weir-Hughes


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Tuesday, October 4, 2011

The Intensive Care Manual PDF

"This is an excellent and most complete guide for the broad range of physicians dealing with patients with epilepsy and psychiatric disorders. It gives neurologists and psychiatrists working in practice settings tools essential for correct diagnosis and treatment. The book also provides outstanding teaching material for academic neurologists and residents

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Monday, October 3, 2011

Brunner & Suddarth's Textbook of Medical Surgical Nursing, 10th edition PDF

Medical-surgical nursing is a nursing specialty area concerned with the care of adult patients in a broad range of settings. The Academy of Medical-Surgical Nurses (AMSN) is a specialty nursing organization dedicated to nurturing medical-surgical nurses as they advance their careers. Traditionally, medical-surgical nursing was an entry-level position that most nurses viewed as a stepping stone to specialty areas. Medical-surgical nursing is the largest group of professionals in the field of nursing. Advances in medicine and nursing have resulted in medical-surgical nursing evolving into its own specialty.

Many years ago a majority of hospital nurses worked on wards, and everyone was a medical-surgical nurse. Today licensed medical-surgical nurses work in a variety of positions, inpatient clinics, emergency departments, HMO’s, administration, out patient surgical centers, home health care, humanitarian relief work, ambulatory surgical care, and skilled nursing homes. Some military medical-surgical nurses serve on battlefields.

Registered Nurses can become certified Medical-Surgical Nurses though the American Nurses Credentialing Center. (wikipedia)

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