Z- SERIES, OET READING PART – 1
Z-SERIES is mentioned to identify the oet materials without difficulty. Z-SERIES is given part by part for easy reading and learning.
Z- SERIES, OET READING PART – 1
OET Writing Practice Test
- Introduction to the Occupational Educational Test
- Speaking Sub Test Interview
- Structure of the Test
- General Test
- Recommended Reading for OET Speaking
OET READING PRACTICE TEST
Full reading practice test given
HYPOXIA PATIENTS
HYPOXIA Patients (Definition, Causes and Prevention)
HYPOXIA DEFINITION
It is the deficiency of an adequate supply of oxygen to the body tissues or cells.
ANOXIA DEFINITION
It is the total lack of oxygen to tissues.
DEFINITION HYPOVENTILATION
Hypoventilation is inadequate breathing leading to an increase of Carbon dioxide (hypercapnia) and hypoxaemia.
Apnoea means cessation of breathing in expiration.
CLASSIFICATION OF HYPOXIA
- Hypoxic Hypoxia: reduced oxygen entering the blood.
- Hypaemic/anaemic hypoxia: reduced capacity of blood to carry oxygen.
- Stagnant hypoxia: poor oxygenation due to circulation
- Histotoxic hypoxia: inability of cells to use oxygen.
COMMON CAUSES
Postoperative causes (usually hypoxic hypoxia)
- CNS depression, e.g. post-anaesthesia
- Airway obstruction, e.g. aspiration of blood or vomit, laryngeal oedema.
- Poor ventilation, e.g. abdominal pain, mechanical disruption to ventilation
- Loss of functioning lung, e.g. V/Q mismatch (pulmonary embolism, pneumothorax, collapse/consolidation)
GENERAL CAUSES
- Central respiratory drive depression, e.g. opiates, benzodiazepines, CVA, head injury, encephalitis.
- Airway obstruction, e.g. facial fractures, aspiration of blood or vomit, thyroid disease or head and neck malignancy.
- Neuromuscular disorders (MS, myasthenia gravis)
- Sleep apnoea (obstructive, central or mixed)
- Chest wall deformities
- COPD
- Shock
- Carboxyhaemoglobinaemia, methaemoglobinaemia
KEY DETAILS ABOUT HYPOXIA
- 80% of patients following upper abdominal surgery are hypoxic during the first 48 hours postoperatively. Have a high index of suspicion and treat prophylactically.
- Adequate analgesia is more important than the sedative effects of opiates – ensure good analgesia in all postoperative patients.
- Ensure the dynamics of respiration are adequate – upright position, abdominal support, humidified oxygen
- Acutely confused (elderly) patients on a surgical ward are hypoxic until proven otherwise.
- Pulse oximetry saturations 85% equate to an arterial Po2 8kPa and are unreliable in patients with poor peripheral perfusion.
CLINICAL FEATURES
In the Unconscious Patient
- Central Cyanosis
- Abnormal Respirations
- Hypotension
In the Conscious Patient
- Central Cyanosis
- Anxiety, restlessness and confusion
- Tachypnoea
- Tachycardia, dysrhythmias (AF) and hypotension
KEY INVESTIGATIONS
- Pulse oximetry saturations: monitors the percentage of haemoglobin that is saturated with oxygen – gives a guide to arterial oxygenation.
Very useful for patient monitoring
- Arterial blood gases (Pco2 Po2 pH base excess): respiratory acidosis, metabolic acidosis later.
- Chest X-ray: collapse/pneumothorax/consolidation.
- ECG: AF.
ESSENTIAL MANAGEMENT
Airway Control
- Triple airway manoeuvre (mouth opening, head extension and jaw thrust), suction secretions, clear oropharynx.
- Consider endotracheal intubation in CNS depression/exhausted patients (rising Pco2), neuromuscular failure.
- Consider surgical airway (cricothyroidotomy/minitracheostomy) in facial trauma, upper obstruction.
Breathing
- Position patient – upright
- Adequate analgesia
- Supplemental oxygen – mask/bag/ventilation
- Support respiratory physiology – physiotherapy, humidified gases, encouraging coughing, bronchodilators.
Circulatory Support
- Maintain cardiac output
- Ensure adequate fluid resuscitation
Determine and treat the cause.
EFFECT ON CELLS
Hypoxia causes the production of transcription factors (hypoxia – inducible factors; HIFs).
These are made up of alpha and beta subunits.
In normally oxygenated tissues, the subunits are rapidly destroyed.
However, in hypoxic cells, the factors dimerize with the beta subunit
The dimmers activate genes that produce angiogenic factors and erythropoietin
CAUSES OF HYPOXIA
Anemic Hypoxia
Carbon Monoxide Intoxication
Respiratory Hypoxia
Hypoxia Secondary to High Altitude
Hypoxia Secondary to Right-to-Left Extrapulmonary Shunting
Circulatory Hypoxia
Specific Organ Hypoxia
Increased Oxygen Requirements
Improper Oxygen Utilization
CAUSES OF HYPOXIA
- Hypoxic Hypoxia
- Inadequate oxygenation of blood in the lungs due to extrinsic causes
- Deficiency of oxygen in the atmosphere – Altitude; Mines
- Hypoventilation – Neuromuscular disorders; fatigue and depression of RC
TYPES OF HYPOXIA
There are four types of hypoxia such as
- Hypoxic Hypoxia
- Anaemic Hypoxia
- Stagnant/Ischemic Hypoxia
- Histotoxic Hypoxia
DEFINITIONS
Hypoxia/anoxia: it denotes a partial or complete lack of oxygen respectively, in one or more tissues of the body, including the blood stream.
Asphyxia: it is the state in which pulmonary or placental gas exchange is affected leading to progressive hypoxemia, which is severe enough to be associated with acidosis.
Ischemia: it is a reduction in or cessation of blood flow that arises from systemic hypotension, cardiac arrest, or occlusive vascular disease.
HYPOXIC HYPOXIA
It is due to reduced oxygen tension in arterial blood (Supply Problem)
Causes:
- Low oxygen tension in the inhaled air.
- Leaking mask, inadequate oxygen regulator function, and faulty hose connections.
- Impaired gas exchange in the lungs. E.g. Chronic Bronchitis and Emphysema
- Gross Ventilation/Perfusion Mismatch, as occur in high G forces
ANAEMIC HYPOXIA
It is due to decreased oxygen carrying capacity of the blood (Transport Problem)
Causes: CO POISONING, CHEMICALS/SULPHA DRUGS AND HAEMORHAGE/HEMOLYSIS AND ANAEMIA
STAGNANT HYPOXIA
It occurs when blood circulation through tissue is reduced. (Distribution Problem)
Causes: High G Forces, Syncope (Fainting), Heart Failure and Shock
HISTOTOXIC HYPOXIA
It is due to inability of the tissues to make use of the oxygen supplied to them (Utilization Problem)
Example:
Cyanide Poisoning – Cytochrome Oxidase
Alcohol and Barbiturate
Oxygen Toxicity – 100 % Oxygen for 8 to 10 hours
Inhibition of certain enzymes (Cytochrome Oxidase) Hampering Oxygen Metabolism
STAGNANT/ISCHEMIC HYPOXIA
Causes:
- Decreased cardiac output/sluggish blood flow due to heart failure, hemorrhage, circulatory shock and venous obstruction.
- Blood remains in tissues for longer time, so tissue extracts increased oxygen from blood – more arteriovenous difference of oxygen concentration.
- So PC02 increases, it facilitates unloading of oxygen from hemoglobin (shifts the oxy-hemoglobin association dissociation curve to right).
Three factors that develop the sensation of dyspnea:
- Abnormality of respiratory gases in body fluids (mainly hypercapnia and partly hypoxia)
- Work of ventilation by respiratory muscles
- State of Mind (Neurogenic/emotional dyspnea)
CAUSES OF HYPOXIA IN FLIGHT
- Ascent to altitude without supplemental oxygen.
- Breathing a gas mixture poor in oxygen
- Exposure of high G Forces
- Failure of oxygen equipment
- Loss of cabin pressurization
FACTORS INFLUENCING HYPOXIA
- Altitude
- Rate of ascent
- Duration of exposure to altitude
- Individual tolerance
- Physical fitness
- Psychological stresses
- Temperature
- Medication
- Hypoglycaemia
- Physical Activity
TIME OF USEFUL CONSCIOUSNESS
- Time interval between the reduction of oxygen tension in the inspired gas and the individual’s effective performance
- It is time available to the individual to take remedial action following the onset of hypoxia
SIGNS AND SYMPTOMS OF HYPOXIA
STAGES
- Indifferent Stage
- Compensatory Stage
- Disturbance Stage
- Critical Stage
SIGNS AND SYMPTOMS OF HYPOXIA
- Indifferent Stage – (0 to 10,000 feet breathing air, 40,000 feet on 100% oxygen)
- No symptoms usually
- Fatigue on long exposure
- Night vision is impaired
- Short term memory starts deteriorating at an altitude of 5000 feet
- Compensatory Stage: (10 to 15,000 feet breathing air, 40000 to 42000 feet on 100% oxygen)
- Little or no symptoms at rest
- When exposure is prolonged or physical activity is undertaken then headache, dizziness are experienced.
- Respiratory and CVS (Compensatory Response come into Play)
- Disturbance Stage: (15 to 20,000 feet breathing air, 42-45000 feet on 100% oxygen)
- Sign and symptoms develop even at rest
- Loss of will power
- Impairment of judgment
- Thinking is slowed
- Calculation unreliable
- Reaction time slows down
- Euphoric and Elated
- Impairment of muscular coordination
- Visual acuity decreased
- Tough and pain sensation decreased, hearing also decreased but it is last to go
- Tiredness
- Headache
- Cyanosis
- Critical Stage: (Above 20,000 feet breathing air, Over 45000 feet on 100% oxygen)
- All symptoms become severe even at rest
- Mental functions decline rapidly
- Unconsciousness generally comes on with little or no warning
- Unconsciousness occurs when oxygen tension falls below 30 mmHg
- If exposure is prolonged, death can occur due to cardiopulmonary failure
ALTITUDE TIME OF USEFUL CONSCIOUSNESS
22,000 10 MINUTES
25,000 5 MINUTES
28,000 2.5 TO 3 MINUTES
30,000 1.5 MINUTES
35,000 0.5 TO ONE MINUTE
40,000 15 SECONDS
65,000 9 SECONDS
PREVENTION OF HYPOXIA
- Increasing concentration/pressure of oxygen
- Cabin pressurization
- Price check before lowering canopy
P = PRESSURE
R = REGULATOR
I = INDICATOR
C = CONNECTIONS
E = EMERGENCY OXYGEN SYSTEM
- Periodic check of following systems
Regulator – all functions
Cabin Pressurization Systems
Pressure Suits (Anti G Suit)
- All Switches up – On, 100% Oxygen
- Mask On
- Check Regulator and Connections
- Control Breathing
- Notify Aircraft Commander
CARCINOMA MAXILLARY SINUS
Carcinoma Maxillary Sinus arises from lining of maxillary sinus. It occurs in middle aged male around 40 to 60 years old. Sinus remains silent for a long time or showing only symptoms of sinusitis. It destroys bony walls and invades the surrounding structures.
ETIOLOGY
- It is occupational – mainly due to inhalation of carcinogens
- Hard wood exposure increases the relative risk by 70 fold particularly ethmoids
- Soft wood exposure increases the risk of squamous cell carcinoma
- Nickel exposure increases the risk for SCC by 250 times
- Other factors are smoking, aflatoxins, formaldehyde, chromium, mustard gas, polycyclic hydrocarbons and thorotrast
PATTERNS OF TUMOUR SPREAD
- Anteriorly – cheek and skin
- Posteriorly – pterygomaxillary fossa, pterygoid plates, nasopharynx, sphenoid sinus, base of skull
- Medially – nasal cavity, NLD
- Superiorly – orbits, ethmoid sinuses
- Inferiorly – palate, buccal sulcus
- Intracranial – ethmoid and cribriform plates
- Lymphatic – submandibular, upper jugular, retropharyngeal nodes
- Systemic – lungs occasionally
CARCINOMA MAXILLARY SINUS – CLASSIFICATION
- OHNGREN’S Classification
- AJCC Classification
- Lederman’s Classification
OHNGREN’s CLASSIFICATION
Suprastructure: Poor prognosis
Infrastructure: Good Prognosis
LEDERMAN’S CLASSIFICATION
- 2 horizontal lines of sebileau pass through floors of orbits and maxillary sinus,producing:
- Supra structure: ethmoid, sphenoid and frontal sinuses: olfactory area of nose
- Mesostructure: Maxillary sinus and respiratory part of nose
- Infrastructure: Alveolar processes
TNM STAGING
Primary Tumor (T)
TX: Primary tumor cannot be assessed
TO: No evidence of primary tumor
Tis: Carcinoma in situ
T1: Tumor limited to maxillary sinus mucosa with no erosion or destructionof bone
T2: Tumor causing bone erosion or destruction including extension into the hard palate and/or the middle of the nasal meatus, except extension to the posterior wall of maxillary sinus and pterygoid plates
T3: Tumor invades any of the following: bone of the posterior wall of maxillary sinus, subcutaneous tissues, floor or medial wall of orbit, pterygoid fossa, ethmoid sinuses
T4a: Tumor invades anterior orbital contents, skin of cheek, pterygoid plates, infratemporal fossa, cribriform plate, sphenoid or frontal sinuses
T4b: Tumor invades any of the following: orbital apex, dura brain, middle cranial fossa, cranial nerves other than maxillary division of trigeminal nerve (V2), nasopharynx, or clivus
TNM STAGING OF MAXILLARY CARCINOMAS
Stage I: Limited to mucosa
Stage II: Bone Involvement (Not Posterior Wall)
Stage III: T3 lesion and T1 or T2 lesions with N1
Stage IV: T4 lesion and any T with N2/N3 or M1
STAGING – MAXILLARY SINUS CARCINOMAS
TX – Primary tumor cannot be assessed
T0 – No evidence of primary tumor
Tis – Carcinoma in situ
T1 – Tumor limited to the antral mucosa with no erosion or destruction of bone
T2 – Tumor with erosion or destruction of the infrastructure, including the hard palate and/or the middle nasal meatus
T3 – Tumor invades any of the following: skin of cheek, posterior wall of maxillary sinus, floor or medial wall of orbit, anterior ethmoid sinus
T4 – Tumor invades orbital contents and/or any of the following: cribriform plate, posterior ethmoid or sphenoid sinuses, nasopharynx, soft palate, pterygomaxillary or temporal fossae, or base of skull.
CARCINOMAS MAXILLARY SINUS – CLINICAL FEATURES
- Nasal stuffiness
- Blood-stained nasal discharge (These are early C/F)
- Facial paraesthesia or pain (Often misdiagnosed and treated as Sinusitis
- Epiphora
TREATMENT
- Stage 1 and 2 SCC – Surgery or Radiation
- Stage 3 and 4 SCC – Combined modalities
- Inoperable tumours – Chemoradiation
- Intra arterial Infusion of 5-Fluorouracil or Cisplatin
TREATMENT OPTION AVAILABLE FOR MAXILLARY SINUS CARCINOMAS
- Surgery
- Radiotherapy – definitive, pre op RT and post op RT
- Combined modality (Sx + RT)
- Chemotherapy – Neo Adjuvant and Concomitant
CHEMOTHERAPY
- Primary Systemic Therapy + Concurrent RT
- Cisplatin alone (preferred)
- 5-FU/hydroxyurea
- Cisplatin/paclitaxel
- Cisplatin/infusional 5-FU
- Carboplatin/infusional 5-FU
- Carboplatin/paclitaxel
- Cetuximab
ROLE OF CHEMOTHERAPY
- Neoadjuvant chemotherapy is sometimes offered in order to reduce tumor volume, which may permit removal of tumor with a less morbid resection or facilitate radiotherapy planning if shrinkage pulls away tumor from critical structures
- Chemotherapy may be given concurrent with radiotherapy in the management of inoperable tumors on the basis of improved results in more frequent head and neck carcinomas
Stage I/II (T1 – T2, N0)
- Surgical resection is the primary treatment
- If margins are free (1.5-2cm), Kept on regular follow-up without adjuvant therapy
- If there is perineural invasion by the tumor, Adjuvant Radiotherapy is needed
- If margins are positive, Re-surgery should be considered, after which, if margins comes negative, RT only; if margins come positive, Chemo + RT is recommended
SURGERY
Surgical approaches:
- Endoscopic
- Lateral rhinotomy
- Transoral/transpalatal
- Weber fergussen
- Midfacial degloving
- Combined craniofacial approach
Extent of resection
- Medial maxillectomy
- Inferior maxillectomy
- Total maxillectomy
RADIOTHERAPY
- Addition of RT to surgery improve 5-years survival (44%) when compared to RT alone (23%) or surgery alone
- Indications;
Definitive: medically inoperable or who refuse radical surgery or early lesions
Adjuvant
Palliative
- Pre- and postoperative radiation may result in similar control rates.
But post-operative RT preferred:
Preoperative radiation increases the infection rate and the risk of postoperative wound complications
Preoperative radiation may obscure the initial extent of disease-surgery can not remove the microscopic extensions of the tumor
- Postoperative radiation therapy is started 4 to 6 weeks after surgery
PROGNOSTIC FACTORS
- Patient-specific – age and performance status
- Disease-specific – location, histology, locoregional extent (reflected in TNM stage), perineural invasion
- Extensive local disease involving the nasopharynx, base of skull, or cavernous sinuses markedly increases surgical morbidity as well as the risk of subtotal surgical excision
- Tumor extension into the orbit may require enucleation, but minimal invasion of the floor or medial wal may be dealt with through resection and reconstruction, sparing the globe.
COMPLICATIONS
- ACUTE – mucositis, skin erythema, nasal dryness, xerostomia
- LATE – xerostomia, chronic keratitis and iritis, optic pathway injury, soft tissue or osteoradionecrosis, cataracts, radiation-induced hypopituitarism
NEPHROTIC SYNDROME
Nephrotic syndrome is classified as Primary Glomerular disease and Secondary Glomerular disease. Histopathologically, primary or idiopathic Nephrotic Syndrome are classified as:
- Minimal Change Nephrotic Syndrome
- Focal Glomerular Sclerosis
- Diffuse Glomerular Sclerosis
- Membranous Glomerular Nephrotis
- Mesangio Capillary Glomerular Nephrotis
- Mesangial Proliferative Glomerular Nephrotis
- Endo Capillary Proliferative Glomerular Nephrotis
- Other Chronic Sclerosing Lesion
- Other Unclassified Disease
THE PREVALENCE OF PRIMARY NEPHROTIC SYNDROME
(Due to primary glomerular disease according to Cameron and Co-workers is given below)
LESION % OF PREVALENCE
Minimal Change 83%
Focal Glomerular Sclerosis 8%
Membranous Glomerular 1%
Nephrotic
Mesangiocapillary Glomerular 5%
Nephrotic
Endocapillary and Crescentric 3%
Glomerular Nephritis
SECONDARY GLOMERULAR DISEASE
Infection:
Post infective Glomerular Nephrotitis, Infective Endocarditis, Hepatitis B Infection, Shunt Nephrotis and Malaria
Multisystem:
Henoch Schonlein Purpura, Systemic Lupus Erythmatosus and Polyarteritis Nodosa
Heredo Familial Neoplasm:
Alport Syndrome, Hodgkin’s disease, Leukemia and Wilm’s tumor
Medication:
Non Steroidal anti inflammatory drugs, Anti Convulsants Like phenytoin, Trimethadione, Pencillamine, Allergens, Serum Sickness Toxoid, Food allergens, Insect Bites.
ETIOLOGY
Etiology of Idiopathic Nephrotic Syndrome is obscure.
PATHOGENESIS
Lymphocytoxins, Immune Complexes, Lymphokines and Vasoactive Amines – They are responsible for increasing the glomerular permeability and Proteinuria
T Cell – Dysfunction is the modern thinking. It is observed in Hodgkin’s disease
In Focal Glomerular Sclerosis – Immune Complexes, IgM and C have been identified
MCNS – has been linked with HLA B12, HLA B8 and HLA DR7
In Membrane Proliferative Nepthritis the role of Hepatitis B antigens in have been demonstrated
MCNS – Electron Microscopy reveals the glomeruli appear normal on
Minimal increase in mesangial cell and matrix
Retraction of the epithelial cell foot process
FGG – Focal Glomerular Sclerosis
- Majority of glomerulo appear normal or manifest mesangial proliferation
CLINICAL FEATURES
- In children the commonest form of N.S. is primary nephritic syndrome
- Among these the MCNS is the most frequent
- Insidious onset of odema
- Mild fever and Cold
- Many children have recurrent episodes of such transient edema for many months
- Physical examination shows
Edema – The edema is initially noted around the eyes and in the lower extremities where it pitting in nature, with time edema becomes generalized and may associate with weight gain and the development of ascites, pleural effusion and decreased urinal output
Pallor
White nails with red bands (leukonychia)
Normal Blood Pressure
No evidence of Renal Failure
PATHOPHYSIOLOGY
MASSIVE PROTEINURIA:
- Increased permeability to proteins
- Selective proteinuria to proteins
Low molecular weight proteins are excreted e.g. Albine
High molecular weight proteins e.g. Lipoproteins are not excreted
HYPOALBUMINAENIA:
- Because more proteins are lost in the urine
EDEMA
Fluid movements across capillary is normally the result of a balance between filteration and reabsorption, due to changes in capillary and tissue hydrostatic and oncotic pressure. It is still the pathogenesis of edema in NS is not well understood.
Because of the hypoalbuminaenia, there is reduction in plasma oncotic pressure leads to leak of fluid in to the interstitial compartment or accumulation of fluid secondary to sodium due to internal defect
The major sites involved in the edema formation are:
Capillaries – where there is disruption of starling equilibria
Kidney – where there is primary salt retension
According to the classical view
Vascular underfill hypothesis
Vascular overfill hypothesis
Vascular underfill hypothesis is responsible for the formation of edema
VASCULAR OVERFILL HYPOTHESIS
- Primary intra renal defect in sodium handling is responsible for occurrence of edema
- This results in decreased filteration per nephron, increase in tubular reabsorption and decreased sensitivity to atrial netriuretic peptide leading to fluid retension
Finally the human body is equipped with defence mechanism that limits excessive capillary fluid filteration
These defense mechanism includes increased interstitial hydrostatic pressure and lymph flow, decreased interstitial oncotic pressure and reduced permeability of the capillaries to protein.
EDEMA RESULTS WHEN THESE ADOPTIVE MECHANISMS ARE
- Inadequate
- It is suggested that vascular underfill is responsible for most cases in edema in MCNS. Other mechanisms might be important in patients with non MCNS.
- There is increasing evidence of hypoalbumia and the inability of the renal distal tubules to excret sodium are not only factor responsible for the occurrence of edema.
- Internal vascular capillary permeability related to the release of vascular permeability factor and other cytokines may also play a important role in the pathogenesis of NS.
INVESTIGATIONS
Hb %
TC
DC
Mx
Urine Examination
Urine Culture and Sensitivity
X Ray Chest
USG Abdomen
Serum Proteins
Urinary Proteins
Spot Urine Test
Serum Cholesterol
Selective Proteinuia
Kidney Biopsy
COMPLICATIONS DUE TO DISEASE
- Loss of Proteins
Albumin – Edema
Transferrin – Anemia
TMG – Biochemical hypothyroidism
Vit. D Binding Globulin – Hypocalcemia (Along with loss of Chole calciferol)
Immunoglobulin – Infection
Coagulation factors – Hypercoagulable state
- Infection:
Loss of Immunoglobulin – Acute
Depressed CMI – Chronic
- Hypercoagulable State: Due to alteration in coagulation factors, associated infections, sepsis, Hypovolemia.
Renal Vein Thrombosis
Peripheral Vein Thrombosis
Cerebral Vein Thromobosis
Chronic Renal failure
- Renal Failure
- Convulsions
TREATMENT
- Hospitalization is necessary in the presence of gross oedema,
Respiratory distress
Pleural effusion
Peritonitis
Unexplained fever
- Bed rest is essential in gross edema
- Salt and fluid restriction depend upon oedema
- Diuretic is a double edged weapon, so it should be used with caution
- Hydrochlorthizide would suffice in mild and moderate edema given as 4 mg/kg in a single dose.
- Spiranolactone should be combined with these diuretics.
DIET
Salt restriction is important to reduce edema. Idli, idiyapam, rice puttu, sweet pongal, coconut rice, curd rice, lemon rice, beet-root, chappathi, dhal, sugar candy, boiled potato, carrot, cabbage, tomato and onion are accepted. Start with salt free diet in the presence of edema and then slowly add salt.
WATER
Along with salt restriction, water restriction is necessary to prevent dilutional hyponatremia. In mild edema, intake is restricted to the urine output. In moderate edema, intake is restricted to insensible water loss. In massive edema fluid intake is restricted to milk only equivalent to insensible water loss.
POTASSIUM
- Serum potassium abnormalities are infrequent in NS without renal failure
- Hypokalemia is the consequence of indiscriminate diuretics
- Add oral potassium in the presence of excessive tiredness or muscle weakness
- Periodic serum potassium level estimation will be useful
PROTEIN
Normal protein diet is advised. In case of malnutrition increased protein is recommended
CALORIES
In the acute phase of Nephrotic syndrome nutritional intake is reduced. In malnutrition, caloric supplementation is necessary.
LIPID
HDL levels are elevated in MCNS. Abnormal coagulability and glomerulus necrosis are consequence of lipid abnormalities. Weight control is essential. Diet should contain cholesterol less than 250 mg/day
CALCIUM
Secondary to hypoalbuminemia, there is low ionic calcium, which is responsible for cramps and tetany. Hence calcium intake of 800 mg/day either by diet or tabet with Vit. D is necessary.
IRON AND ZINC
Iron supplementation is necessary in microcytic hypochromic anaemia. Rarely, Zinc may be needed in the presence of deficiency symptoms.
Glucocorticoid has some influences on glomerular permeability. It blocks the action of migratory inhibiting factor (MIF) and chemotactic factor, inhibits the endothelial adherence of macrophages and leukocytes, blocks the antigen processing function of macrophage, stabilizes lysosomal membrane and prevents the increase in capillary permeability and diapedesis.
INITIAL THERAPY
Prednisolone 2 mg/kg as a single or divided doses for 4 weeks then give 2 mg/kg as single dose in the morning on alternative days for the next 4 weeks. Then taper prednisolone by 10 mg every 2 weeks. If there is persistent proteinuria even after four weeks of daily therapy of steroid, continue the same dose for the next 4 weeks. If there is no remission even after 8 weeks of full dose of steroids, then label the child as steroid resistant. In this type of cases, steroids should be tapered to 0.5 mg/kg. simultaneously add cyclophosphamide in a dose of 2 mg/day. Care should be taken to have weekly W.B.C count.
In case of steroid response but when there is frequent relapse prednisolone is to be given as 2 mg/kg for 4 weeks and then as a single dose in the morning on alternate day for 4 weeks. After 8 weeks of steroid therapy, it should be tapered but slowly so that the entire course lasts for 6 months. When the child is resistant to Predinosolone and Cyclophosphamise, Chlorambucil, 2 to 3 mg/kg is given for 10 weeks.
COMPLICATIONS OF DRUGS
- Steroids
Pseudo tumor cerebri
Cataract
Cushingoid facies
Unmasking of tuberculous focus
Peptic ulcer
Diabetes mellitus
Hypertension
Aseptic necrosis of femoral head
- Frusemide
Hypokalemia
Hyponatremia
Hyperuricemia
Hypercalciuria
Hypocalcemia
Hypovolemia
Tinnitus
Deafness – Permanent, Temporary
Acute Interstitial nephritis
- Cyclophosphamide
Haemorrhagic Cystitis
Bone Marrow Depression
Alopecia
EXAMINATION OF RESPIRATORY SYSTEM
SIGNIFICANCE
Clinical examination of the respiratory system is carried out to assess the functional status of the respiratory tract and lungs
GENERAL
EXAMINATION
Before doing the examination of the respiratory system, a general examination relevant to the respiratory system should be carried out.
Appearance
Pallor
Cyanosis
Clubbing (Excessive curvature of the nail)
Venous pulses
Lymph node enlargement
Examination of the respiratory system is carried out by:
- Inspection
- Palpation
- Percussion
- Auscultation
EXAMINATION OF THE CHEST
INSPECTION
- Shape of the chest
The normal chest is bilaterally symmetrical and elliptical in cross section
The transverse diameter – anterioposterior diameter
Common Abnormalities of Shape
Kyphosis – forward bending of vertebral column
Scoliosis – lateral bending of vertebral column
Barrel shaped chest – increase in anteroposterior diameter flattening
INSPECTION
- Rate and Rhythm of respiration
Rate of respiration in health (adult) 12 to 14 breaths/min
- Measurement of chest expansion
Chest expansion can be measured with a tape measure around the chest just below the nipples in a healthy adult it is about 3 to 5 cm
- Symmetry of chest expansion
Chest expansion of a healthy adult should be equal on both sides
- Movements of the chest wall
Presence of intercostals recessions or the use of accessory muscles
PALPATION
Before making a systemic examination palpate any part of the chest where the patient complains of pain or where there is a swelling
- Position of the Apex beat and Trachea
In normal subjects the trachea is in the midline and can be palpated in the suprasternal notch
The apex beat ( the lowest and outermost point of definite cardiac pulsations) can be usually palpated in the 5th intercostals space withing the midclavicular line
Displacement of the apex beat and trachea indicates that the position of the mediastinum has been altered. This may be due to diseases of the heart, lungs or pleura
PALPATION
- Expansion of the chest
Symmetrical or asymmetrical chest expansion can be assessed by palpation
Vocal fremitus
Vocal fremitus is the vibration detected by palpation with the pal of the hand on the chest, when the patient is asked to repeat ‘ninety nine’ or ‘anunavaya’
In a normal healthy adult, the vibrations felt in the corresponding areas on the two sides of the chest are equal in intensity
PERCUSSION
The middle finger of the left hand is placed on the chest and middle phalanx is struck with the tip of the middle finger of the right hand
Compare the percussion note (resonant) with that of the corresponding area on the opposite side of the chest
A resonant sound is produced during percussion. The sound and feel of resonance over a healthy lung has to be learned by practice
AUSCULTATION
- Breathing sounds
There are 2 types of breath sounds (vesicular breath sounds and bronchial breath sounds)
Vesicular breath sounds
These originate in the larger airways and are produced by the passage of air in and out of normal lung tissue
In good health, they can be heard all over the chest
- The inspiration is longer than expiration
- The inspiratory sound is intense and louder than the expiratory sound
- It is a low pitched rustling sound
- There is no gap between inspiration and expiration
Vesicular breathing with prolonged expiration
Example: airway obstruction (asthma)
AUSCULTATION
- Bronchial breath sounds
These are produced by the passage of air in the trachea and larger bronchi
In good health, they can be heard only over the trachea
In disease, bronchial breathing may be heard over the area of lung that is affected (lung collapse, fibrosis or when there is cavity)
- The expiration is long as or longer than inspiration
- The pitch and sound of the expiration is loud or louder than the inspiratory sounds
- There is a gap between inspiration and expiration
AUSCULTATION
- Vocal Resonance
the resonant sound that is heard with the stethoscope when the patient is asked to repeat ‘ninety nine’ or ‘anunavava’
This depends on the loudness and the depth of the patients voice and the conductivity of the lungs
AUSCULTATION
- Added sounds
These are abnormal sounds that arise in the pleura or lungs
Rhonchi – wheezing sound (asthma)
Crepitations – bubbling or crackling noises
Pleural rub – creaking or rubbing noises associated with pain
ROLE OF NURSE IN CARE OF MECHANICALLY VENTILATED PATIENT
HAND HYGIENE
Wash hands before direct contact. 40% of infections are transmitted by the hands of hospital staff
Use sterlium or alcohol based hand rub in between procedure
RECORDING OF VITAL SIGNS
Record vital signs (Assess for hypotension, tachycardia, tachypnoea)
Observe respiratory pattern and auscultate lung sounds
Observe for breathing pattern in relation to ventilatory cycle
Assess for changes in mental status and LOC
Continuous pulse oximetry
Observe ABG for abrupt changes or deterioration as required
ENDOTRACHEAL TUBE CARE
Introduce an oropharyngeal airway
Maintain inflation of the cuff at 15 to 20 mmHg
Institute Endotracheal suctioning as appropriate
Administer humidified oxygen before suctioning to loosen secretions
Change Endotracheal tapes every 24 hours
Inspect the skin and oral mucosa
Stop feeding during 30 to 60 minutes before suctioning and chest physiotherapy
Observe the type, color and amount of secretion,notify the changes
Avoid drawing of arterial blood sample immediately after suctioning
Watch for side effects: hypoxemia, bradycardia, and hypotension
ORAL HYGIENE
Provide careful oral hygiene
Apply lubricant to lips to prevent drying, cracking and excoriation
Rotate the ET tube from one corner of mouth to the other side at least every 24 hours
ARTERIAL BLOOD GAS ANALYSIS
ABG reflects oxygenation adequacy of gas exchange in the lungs and acid base status
Avoid taking sample immediately after suctioning, nebulisations and baging
While drawing blood prevent entry of air in syringe
Send immediately ABG sample to laboratory
MAINTAIN NUTRITIONAL NEED
Basal energy expenditure calculation (Harris Benedict Equation)
Men: 66.477 + (13.75 multiply W) + (5 multiply H) – (6.76 multiply A) Kcal/Day
Female: 65.51 + (9.56 multiply W) + (1.58 multiply H) – (4.68 multiply A) Kcal/Day
(W = weight of Pt., H = Height of Pt., A = Age of Pt.)
High protein, high fat and low carbohydrates diet can be beneficial
Add mineral supplements to the diet expecially magnesium and phosphorus. These are essential for energy production and respiratory muscle function
POSITIONING
Turn and reposition the patient every 2nd hourly
Positioning prevents complications such as pneumonia and atelectasis
PERSONAL HYGIENE
Frequent oral hygiene must be done
Eye care to be given every 4th hourly to prevent corneal ulcers and dryness of conjunctiva
Provide skin care
Provide catheter care using sterile technique
ALLAYING ANXIETY AND FEAR
Explain all the procedures to the patient and relatives to win their confidence
Talk and clear the doubts of patient and attainders. Never ignore their feelings.
Use therapeutic touch
Encourage the family members to visit the patient as per hospital policy
CARE OF VENTILATOR CIRCUIT
Keep the water level in humidifier in normal limit
Humidification during mechanical ventilation required to prevent hypothermia, inspissations of airway secretions, destructions of airway epithelium and atelectasis
A heated humidifier should be set to deliver an inspired gas temperature of 33 -/+ 2 Degree Celcius
The temperature of inspired gas should not exceed 37 degree celcius at the airway threshold
Sterile water should be used only
Condensation from the patient circuit should be considered infectious waste and should never be drained back in to the humidification reservoir
Change the circuit when it is visibly soiled or mechanically malfunctioning
Bacterial filters should not be used for more than 48 hours
Use universal precautions when involved in circuit changes
CARE OF VENTILATOR ALARMS
Never Shut Alarms Off – Alarm system must be activated and function at all time. It is acceptable to silence alarms for a preset delay while suctioning and during oxygen flush before suctioning
If equipment failure is suspected and unable to determine the cause of alarm, manually ventilate the patient with resuscitation bag until the problem is corrected
VENTILATOR CARE BUNDLE
According to IHI ‘bundle’ is a group of evidence – based care components for a given disease that, when executed together, may result in better outcomes than if implemented individually.
It includes:
DVT Prophylaxis (unfractioned heparin, elastic stockings, pneumatic compression, elevation of affected extremity, gentle foot and leg exercise, fluid administration)
GI prophylaxis (H2 blocker/proton pump inhibitor)
Head of bed elevated to 30 to 45
Daily sedation vacation/daily spontaneous breathing trial
Skin safety (manage pressure, adequate nutrition, wound assessment and wound care)
Fall prophylaxis
ROLE OF NURSE IN CARE OF MECHANICALLY VENTILATED PATIENT PDF
URETEROCELE – Classification and Management
DEFINITION
Ureterocele is a congenital anomaly (present at birth) that affects girls more than boys. It is simply a swelling limited to the end of the ureter as it enters the bladder.
Ureterocele is saccular out-pouching of the distal ureter into the urinary bladder
It arise from abnormal embryogenesis with anomalous development of the intravesical ureter, the kidney, and the collecting system
Ureterocele may be asymptomatic or may cause a wide range of clinical signs and symptoms, from recurrent cystitis to bladder outlet obstruction
ETIOLOGY
Several theories exist, including:
- Obstruction of the ureteral orifice
- Incomplete muscularization of the intramural ureter
- Excessive dilatation of the intramural ureter during the development of the bladder and trigone
Obstruction of the ureteral orifice during embryogenesis, with incomplete dissolution of the Chwalla membrane
- The most commonly accepted theory behind ureterocele formation
Chwalla Membrane
- Primitive thin membrane that separates the ureteral bud from the developing urogenital sinus
- Failure to completely perforate during development of the ureteral orifice is thought to explain the occurrence of a ureterocele
CLASSIFICATION OF URETEROCELE
Types of ureteroceles classified by their association with the renal unit
- Single-sytem ureteroceles
- Associated with a single kidney, a single collecting system, and a solitary ureter
- Duplex-system Ureteroceles
- Associated with kidneys that have a completely duplicated collecting system and 2 ureters
- Orthotopic Ureterocele
- Orifice is located in a normal anatomic (orthotopic) position within the bladder
- Usually arises from a single renal unit with one collecting system and is more common in adults
- Ectopic Ureterocele
- Orifices are located in an ectopic position, such as the bladder neck or urethra
- Arise from the upper pole moiety of a duplicated collecting system and are more common in the pediatric population
CLINICAL MANIFESTATION
Urinary tract infection
Urosepsis
Obstructive voiding symptoms
Urinary retention
Failure to thrive
Hematuria
Cyclic abdominal pain
Ureteral calculus
URETEROCELES DIAGNOSIS
Before the advent of prenatal U/S, most diagnosed clinically
Most common presentation of UTI or urosepsis
Palpable abdominal mass
Ureterocele may prolapsed out of urethra
COMPLICATIONS OF URETEROCELE
Infection – it is the most common presentation
Obstruction – Hydroureteronephrosis
Stone Formation – Hematuria
Incontinence of Urine – Ectopic ureterocele drain beyond the bladder neck. It is more common in females
Acute Bladder Neck Obstruction – Ectopic or prolapsing ureterocele
URETEROCELE TREATMENT
Single-system ureterocele:
Initial management is usually endoscopic incision of the ureterocele, which can be followed by surgical ureteric reimplantation to preserve renal function and prevent influx
Duplex-system ureterocele:
Treatment options vary with the individual and include endoscopic incision, upper pole nephrectomy for a poorly functioning unit with ureterectomy (Heminephroureterectomy), or, when there is useful renal function, ureteropyelostomy can be performed.
