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Menieres disease
Definition An inner ear disorder that causes one to experience periods of vertigo, dizziness, nausea, ear pressure, sensitivity to light and tinnitus. Causes Anatomical-abnormalities Genetic-autosomal dominant Immunological-immune complex deposition Viral-serum IgE to herpes simples virus types I and II, Epstein-Barr virus and CMV Vascular-associated with migraines Metabolic-potassium intoxication

Symptoms Periodic episodes of rotatory vertigo or dizziness Fluctuating, progressive, low-frequency hearing loss Tinnitus Fullness/pressure

Diagnosis The diagnosis of Meniere disease is made based on a careful history and physical exam. If the work-up is normal and the classic symptoms continue, the diagnosis of Meniere disease is made. History Most important part of the diagnosis Pattern of symptoms Association between hearing loss, tinnitus, and vertigo

Prepared by Navjot and Kawal, MSc 2nd year, Mai Bhago College of Nursing, Tarn-Taran

Physical examination: Examination results vary, depending upon the phase of disease. During remission, physical examination findings may be completely normal, particularly if the patient is symptom free. During an acute attack, the patient has severe vertigo. Patients are sometimes diaphoretic and pale. Vital signs may show elevated blood pressure, pulse, and respiration. Spontaneous nystagmus directed toward affected ear is typical during an acute attack. The Romberg test generally shows significant instability and worsening when the eyes are closed. The Weber tuning fork test usually lateralizes away from the affected ear. The Rinne test usually indicates that air conduction remains better than bone conduction. Complete neurologic evaluation is important. New-onset vertigo might be an early sign of stroke, migraine, or brainstem compression that may require emergent evaluation and care. Lab values: No lab studies are specific for Meniere disease. A CBC, urinalysis, chemistry panel, and alcohol and drug screening may be helpful if other causes are considered. If an infectious cause is suspected, consider blood cultures, urine culture, and a cerebral spinal fluid (CSF) examination. Imaging studies: Magnetic resonance imaging Brain scan should be done to rule out abnormal anatomy or mass lesions. Specifically, acoustic neuromas or other cerebellopontine angle lesions are sought. Other lesions, such as multiple sclerosis or Arnold Chiari malformations, also can be ruled out. Note that mass lesions rarely are found but are important to exclude.

Prepared by Navjot and Kawal, MSc 2nd year, Mai Bhago College of Nursing, Tarn-Taran

CT scans reveal dehiscent superior semicircular canals and/or widened cochlear and vestibular aqueducts Others Audiometry is particularly helpful to document present hearing acuity and to detect future change. -The patient may not notice a loss at specific frequencies. Low-frequency or mixed lowand high-frequency insufficiency may be observed. - Typically, the lower frequencies are affected more severely. This is due to preferential sensitivity of the apex to the hydrops. - Multiple hearing tests, which document fluctuating hearing loss, are helpful in diagnosing Mnire. Transtympanic electrocochleography (ECOG) Transtympanic electrocochleography (ECOG) specifically detects distortion of the neural membranes of the inner ear. This is presumably due to perilymph pressure fluctuations and can show evidence of cochlear involvement. ECOG measures the ratio of the summating potential (probably from the movement of the basilar membrane) and the nerve action potential in response to auditory stimuli. Hydrops is suggested when this ratio is greater than 35%. This is most accurate when Mnire is active.

Electronystagmography (ENG) Electronystagmography (ENG) is a test of the inner ear function (particularly the semicircular canals). It tests central and peripheral function and can help localize the site of lesion. Typically, Meniere disease causes a reduced vestibular response in the affected ear, although response may be increased secondary to an irritative lesion. The direction of the spontaneous nystagmus during or after an attack of Mnire is not a reliable indicator of the site of the lesion. An irritative phase may occur during the attack (fast phases directed toward involved ear) followed by a paretic phase (fast phases directed toward opposite ear).

Treatment Medical therapy is both symptomatic (ie, acute attacks) and prophylactic.

Prepared by Navjot and Kawal, MSc 2nd year, Mai Bhago College of Nursing, Tarn-Taran

If Mnire is due to a secondary cause (ie, Mnire syndrome), primary first-line management is the diagnosis and treatment of the primary disease (eg, thyroid disease). Vestibulosuppressants (eg, meclizine) decrease symptoms, but generally only mask the vertigo by decreasing the brain's response to vestibular input. Diuretics or diuretic-like medications (eg, hydrochlorothiazide) actually decrease the fluid pressure load in the inner ear. These medications help prevent attacks but do not help once an acute attack has started. Anti-inflammatory properties of steroids are helpful in endolymphatic hydrops. This is probably due to reduced endolymphatic pressure. Steroids actually can reverse vertigo, tinnitus, and hearing loss. Aminoglycosides are a class of antibiotics that were discovered serendipitously to be preferentially toxic to the vestibular end organ. Destruction of the vestibular end organ renders the brain insensitive to the fluctuations in the inner ear pressure during an acute Mnire attack. If given systemically, aminoglycosides affect both ears. Although these drugs can be used to treat extremely severe bilateral Mnire disease, they leave the patient with little or no balance function. The resulting Dandy syndrome, a complete loss of inner ear function, can be debilitating. During the quiescent phase, medical treatment of Mnire disease is tailored to each patient. Lifestyle and dietary changes are usually the first step. Avoiding trigger substances (eg, caffeine) alone may be sufficient. Smoking cessation also is recommended. In an acutely vertiginous patient, management is directed toward vertigo control. Intravenous (IV) or intramuscular (IM) diazepam provides excellent vestibular suppression and antinausea effects. Steroids can be given for anti-inflammatory effects in the inner ear. IV fluid support can help prevent dehydration and replaces electrolytes. Surgical Care: Surgical therapy for Mnire disease is reserved for medical treatment failures and is otherwise controversial. Surgical procedures are divided into 2 major classifications as follows: Prepared by Navjot and Kawal, MSc 2nd year, Mai Bhago College of Nursing, Tarn-Taran

Destructive surgical procedures Nondestructive surgical procedures Destructive surgical procedures Rationale to control vertigo: Endolymphatic hydrops causes fluid pressure accumulation within the inner ear, which causes temporary malfunction and misfiring of the vestibular nerve. These abnormal signals cause vertigo. Destruction of the inner ear and/or the vestibular nerve prevents these abnormal signals. As long as the opposite inner ear and vestibular apparatus function normally, the brain eventually will compensate for the loss of one labyrinth.

Problems with destructive procedures: Destruction of one inner ear depends on the adequate function of the opposite ear. Unfortunately, Mnire disease can be bilateral (7-50%), in which case this method is contraindicated. Since balance and hearing are closely intertwined within the labyrinth, destruction of the balance portion carries a high risk of hearing loss. Note that destructive procedures are irreversible and reserved for severe cases.

Nondestructive surgical procedures: These are directed toward improving the state of the inner ear. They are less invasive than destructive procedures and do not preclude the use of other treatment modalities. Discussion here is limited to the 4 most generally accepted management options: endolymphatic sac decompression or shunt vestibular nerve section Labyrinthectomy transtympanic medication perfusion. Endolymphatic sac decompression and/or shunt In theory, the endolymphatic sac procedure decreases endolymph pressure accumulation by removing the petrous bone, which encases the endolymph reservoir. This procedure allows the reservoir sac to expand more freely, thus dissipating pressure. A drain or valve from the endolymphatic space to either the mastoid or subarachnoid space can be inserted as another means of further reducing pressure. Success rates (in terms of controlling vertigo and stabilizing hearing acuity) with this procedure are reported at 60-80%.

Prepared by Navjot and Kawal, MSc 2nd year, Mai Bhago College of Nursing, Tarn-Taran

Vestibular nerve section For patients with useful hearing in the affected ear, sectioning the diseased vestibular nerve can be the ultimate solution. Although the hearing and balance functions are housed in one common chamber within the inner ear, their neural connections to the brain separate into distinct nerve bundles as they course through the internal auditory canal. This anatomical separation allows balance function to be isolated and ablated without affecting hearing function.

Labyrinthectomy This management option for Mnire disease has the advantage of a high cure rate (>95%) and is useful in the patient whose hearing on the diseased side has been destroyed already by Mnire disease. Labyrinthectomy involves ablation of the diseased inner ear organs. This procedure is less complex than vestibular nerve section because labyrinthectomy does not require entry into the cranial cavity. Labyrinthectomy is less invasive than vestibular nerve section.

This procedure carries less danger of cerebrospinal fluid leak and meningitis since craniotomy is not required. Like those who undergo vestibular nerve section, patients require a few days of inpatient care. Accommodation to the surgical loss of one vestibular apparatus usually takes weeks or months. Vestibular rehabilitation during this time period is also helpful. Transtympanic perfusion of medication Medications for Mnire disease are applied through a myringotomy within the middle ear cavity, where they presumably are absorbed through the round window membrane into the inner ear. Transtympanic perfusion is a relatively low-risk, simple procedure that applies a high concentration of medicine with minimal systemic effects.

Diet:

Prepared by Navjot and Kawal, MSc 2nd year, Mai Bhago College of Nursing, Tarn-Taran

Dietary management is appropriate in patients not severely affected; patients avoid substances that may trigger or exacerbate fluid pressure buildup in the inner ear. Similar to managing systemic hypertension, the goal for Mnire disease is to reduce the total body fluid volume. This, in turn, may reduce the inner ear fluid volume. Since sodium seems to play a major role in fluid retention within the inner ear, avoiding salt (eg, pizza, preserved foods, smoked fish) is paramount.

Consult with a nutritionist to establish a rigid salt-restricted diet (1.5 g sodium per day). Avoiding other trigger substances (eg, caffeine, nicotine, alcohol, high-carbohydrate substances, high-cholesterol/triglyceride foods) also can help. Note that many preserved and smoked foods contain sodium nitrite, which can contribute to high sodium content. Activity: Endolymphatic hydrops does recommended in moderation. not preclude regular activity. Exercise is

Because of the unpredictable nature of the disease, balance-intensive, dangerous tasks (eg, especially climbing ladders) should be avoided.

Epilepsy
A chronic neurologic disorder manifesting by repeated epileptic seizures (attacks or fits) which result from paroxysmal uncontrolled discharges of neurons within the central nervous system (grey matter disease). Causes: Acute: Cortical damage Trauma Infections Alcohol and barbiturates withdrawl Extracranial disorders eg. DM, HTN, Septicemia,SLE Stroke hypoxia Hypoglycemia ACUTE CONGENITAL

Prepared by Navjot and Kawal, MSc 2nd year, Mai Bhago College of Nursing, Tarn-Taran

Dehydration Vascular diseases Neoplasm

Electrolyte imbalances Metabolic disturbances Autoimmune disorders (RASMUSSENS ENCEPHALITIS)

Congenital DYSGENESIS (FAILURE OF CORTEX TO GROW PROPERLY) VASCULAR MALFORMATIONS AT LEAST EIGHT SINGLE LOCUS GENETIC DEFECTS ARE ASSOCIATED WITH EPILEPSY. MOST FORMS INVOLVE INHERITING MORE THAN ONE LOCUS. (EXAMPLES: JUVENILE MYOCLONIC, PETIT MAL)

Epileptic seizure foci MOTOR CORTEX: CAUSE MOVEMENTS ON CONTRALATERAL SIDE ACCORDING TO THE SOMATOTOPIC LOCATION OF THE SEIZURE FOCUS. SOMATOSENSORY CORTEX: CAUSE AN EPILEPTIC AURA IN WHICH A SENSATION IS EXPERIENCED. ALSO DEPENDS ON WHICH PART OF SOMATOTOPIC REPRESENTATION HOLDS THE FOCUS. VISUAL CORTEX: CAUSE A VISUAL AURA (SCINTILLATIONS, COLORS). AUDITORY CORTEX: CAUSE AN AUDITORY AURA (HUMMING, BUZZING, AND RINGING). VESTIBULAR CORTEX: CAUSE A FEELING OF SPINNING. TEMPORAL LOBE: CAUSE COMPLEX BEHAVIORS. OLIFACTORY CORTEX: CAUSE MALODOROUS AURA. HIPPOCAMPUS: PARTICULARLY SUSCEPTIBLE AND A FREQUENT SOURCE OF EPILEPTIC ACTIVITY.

Types of seizures:

Prepared by Navjot and Kawal, MSc 2nd year, Mai Bhago College of Nursing, Tarn-Taran

Focal seizures (partial seizures)

simple partial seizures complex partial seizures partial seizures secondarily generalised

Generalized seizures

tonic clonic seizures atonic seizures myoclonic seizures abscence seizures tonic seizures clonic seizures

not included in any particular type

Unclassified seizures
Simple partial seizures: Motor, sensory, vegetative or psychic symptomatology ,

Typically consciousness is preserved

Complex partial seizures (= psychomotor seizures) ; Initial subjective feeling

(aura), loss of consciousness, abnormal behavior (perioral and hand automatisms) Partial seizures evolving to tonic/clonic convulsions secondary generalised tonic/clonic seizures (sGTCS)

Prepared by Navjot and Kawal, MSc 2nd year, Mai Bhago College of Nursing, Tarn-Taran

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Investigations: The concern of the clinician is that epilepsy may be symptomatic of a treatable cerebral lesion. Routine investigation: Haematology, biochemistry (electrolytes, urea and calcium), chest X-ray, electroencephalogram (EEG). Neuroimaging (CT/MRI) should be performed in all persons aged 25 or more presenting with first seizure and in those pts. with focal epilepsy irrespective of age. Specialised neurophysiological investigations: Sleep deprived EEG, video-EEG monitoring. Advanced investigations (in pts. with intractable focal epilepsy where surgery is considered): Neuropsychology, Semiinvasive or invasive EEG recordings, MR Spectroscopy, Positron emission tomography (PET) and ictal Single photon emission computed tomography (SPECT)

Surgery A proportion of the pts with intractable epilepsy will benefit from surgery. Epilepsy surgery procedures: Curative (removal of epileptic focus) and palliative (seizure-related risk decrease and improvement of the QOL) Curative (resective) procedures: Anteromesial temporal resection, selective amygdalohippocampectomy, extensive lesionectomy, cortical resection, hemispherectomy. Palliative procedures: Corpus callosotomy and Vagal nerve stimulation (VNS).

Prepared by Navjot and Kawal, MSc 2nd year, Mai Bhago College of Nursing, Tarn-Taran

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SYNCOPE
DEFINITION Syncope is the medical term for fainting, is precisely defined as a transient loss of consciousness and postural tone characterized by rapid onset, short duration, and spontaneous recovery due to global cerebral hypoperfusion that most often results from hypotension. CATEGORIES There are two broad categories of syncope, cardiogenic or reflex Cardiogenic forms are more likely to produce serious morbidity or mortality and require prompt or even immediate treatment. Although cardiogenic syncope is much more common in older patients, an effort to rule out arrhythmic, obstructive, ischemic, or cardiomyopathic causes of syncope and circulatory inadequacy is mandatory in each patient. Reflex syncope CAUSES Decreased blood flow to the brain can occur because 1) the heart fails to pump the blood 2) the blood vessels don't have enough tone to maintain blood pressure to deliver the blood to the brain 3) there is not enough blood or fluid within the blood vessels 4) a combination of reasons one, two, or three above. Electrolyte imbalance Electrolyte and hormone abnormalities may also be responsible for syncope; however, these causes are due to their effects on the heart and blood vessels. Other medications and drugs Other medications or drugs may also be potential causes of fainting or syncope including those for high blood pressure that can dilate blood vessels, antidepressants that can affect heart electrical activity, and those that affect mental status like pain medications, alcohol, and cocaine. Prepared by Navjot and Kawal, MSc 2nd year, Mai Bhago College of Nursing, Tarn-Taran

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Pregnancy Syncope is also related to pregnancy. Compression of the inferior vena cava (the large vein that returns blood to the heart) by the enlarging uterus and by orthostatic hypotension. Physical injury such as head trauma Central nervous system ischaemia Cardiac arrhythmias Obstructive cardiac lesion Low blood pressure, hypoglycemia, growth spurts high g-force, physical exercise in excess of the energy reserve of the body, emotional distress, and lack of sleep. Orthostatic hypotension TYPES

1. Vasovagal syncope
Vasovagal (situational) syncope, one of the most common types, may occur in scary, embarrassing or uneasy situations, or during blood drawing, coughing, urination or defecation. Other types include postural syncope (caused by a change in body posture), cardiac syncope (due to heart-related conditions), and neurological syncope (due to neurological conditions). There are many other causes of syncope, including low blood-sugar levels and lung disease such as emphysema and a pulmonary embolus. The vasovagal type can be considered in two forms:

Isolated episodes of loss of consciousness, unheralded by any warning symptoms for more than a few moments. These tend to occur in the adolescent age group, and may be associated with fasting, exercise, abdominal straining, or circumstances promoting vaso-dilation (e.g., heat, alcohol). The subject is invariably upright. The tilt-table test, if performed, is generally negative. Recurrent syncope with complex associated symptoms. This is so-called Neurally Mediated Syncope (NMS). It is associated with any of the following: preceding or succeeding sleepiness, preceding visual disturbance ("spots before the eyes"), sweating, light-headedness. The subject is usually but not always upright. The tilt-table test, if performed, is generally positive.

Prepared by Navjot and Kawal, MSc 2nd year, Mai Bhago College of Nursing, Tarn-Taran

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2. Deglutition syncope Syncope may occur during deglutition. "Deglutition syncope is characterised by loss of consciousness on swallowing; it has been associated not only with ingestion of solid 3. Cardiac syncope a. Cardiac arrhythmias Most common cause of cardiac syncope. Two major groups of arrhythmias are bradycardia and tachycardia. Bradycardia can be caused by heart blocks. Tachycardias include SVT (supraventricular tachycardia) and VT (ventricular tachycardia). SVT does not cause syncope except in Wolff-Parkinson-White syndrome. Ventricular tachycardia originate in the ventricles. VT causes syncope and can result in sudden death. Ventricular tachycardia, which describes a heart rate of over 100 beats per minute with at least three irregular heartbeats as a sequence of consecutive premature beats, can degenerate into ventricular fibrillation, which requires DC cardioversion. b. Obstructive cardiac lesion Aortic stenosis and mitral stenosis are the most common examples. Aortic stenosis presents with repeated episodes of syncope. Pulmonary embolism can cause obstructed blood vessels. High blood pressure in the arteries supplying the lungs (pulmonary artery hypertension) can occur during pulmonary embolism. Rarely, cardiac tumors such as atrial myxomas can also lead to syncope. c. Structural cardiopulmonary disease These are relatively infrequent causes of faints. The most common cause in this category is fainting associated with an acute myocardial infarction or ischemic event.. Among other conditions prone to trigger syncope (by either hemodynamic compromise or by a neural reflex mechanism, or both), some of the most important are hypertrophic cardiomyopathy, acute aortic dissection, pericardial tamponade, pulmonary embolism, aortic stenosis, and pulmonary hypertension. d. Other cardiac causes Sick sinus syndrome, a sinus node dysfunction, causing alternating bradycardia and tachycardia. Often there is a long pause asystole between heartbeat. Adams-Stokes syndrome is a cardiac syncope which may occur with seizures caused by complete or incomplete heart block. Symptoms include deep and fast respiration, weak and slow pulse and respiratory pauses that may last for 60 seconds. Prepared by Navjot and Kawal, MSc 2nd year, Mai Bhago College of Nursing, Tarn-Taran

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Aortic dissection (a tear in the aorta) and cardiomyopathy can also result in syncope Various medications, such as -blockers, may cause bradycardia induced syncope.

e. Blood pressure
Orthostatic (postural) hypotensive faints are as common or perhaps even more common than vasovagal syncope. Orthostatic faints are most often associated with movement from lying or sitting to a standing position. The most susceptible individuals are elderly frail individuals, or persons who are dehydrated from hot environments or inadequate fluid intake. More serious orthostatic hypotension is often the result of certain commonly prescribed medications such as diuretics, -adrenergic blockers, other anti-hypertensives (including vasodilators), and nitroglycerin. In a small percentage of cases, the cause of orthostatic hypotensive faints is structural damage to the autonomic nervous system due to systemic diseases (e.g., amyloidosis or diabetes) or in neurological diseases (e.g., Parkinson's disease). SIGN AND SYMPTOMS Early warning symptoms of a faint
o o o o o o o o o

Lightheadedness (presyncope) Feeling like you will pass out Sweating Weakness Dizziness Nausea Rapid breathing vertigo muffled hearing and tingling sensations in the body.

During the episode, when the person is unconscious, there may a few twitches of the body which may be confused with seizure activity. The person may have some confusion after wakening but it should resolve within a few seconds. After a syncopal episode, there should be a quick return to normal mental function, though there may be other signs and symptoms depending upon the underlying cause of the faint. DIAGONSTIC TESTS A hemoglobin count may indicate anemia or blood loss. Prepared by Navjot and Kawal, MSc 2nd year, Mai Bhago College of Nursing, Tarn-Taran

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An electrocardiogram (ECG) records the electrical activity of the heart. It is estimated that from 20%-50% of patients will have an abnormal ECG. However, while an ECG may identify conditions such as atrial fibrillation, heart block, or a new or old heart attack, it typically does not provide a definite diagnosis for the underlying cause for fainting. Holter monitor may be used. This is a portable ECG device that can record the wearer's heart rhythms during daily activities over an extended period of time. Since fainting usually does not occur upon command, a Holter monitor can provide a better understanding of the heart's activity during fainting episodes. The Tilt table test is performed to elicit orthostatic syncope secondary to autonomic dysfunction (neurogenic). For patients with more than two episodes of syncope and no diagnosis on routine testing, an insertable cardiac monitor might be used. It lasts 14 to 18 months. Smaller than a pack of gum, it is inserted just beneath the skin in the upper chest area. The procedure typically takes 15 to 20 minutes. Once inserted, the device continuously monitors the rate and rhythm of the heart. Upon waking from a fainting spell, the patient places a hand held pager size device called an Activator over the implanted device and simply presses a button. This information is stored and retrieved by their physician. San Francisco syncope rule The San Francisco syncope rule was developed to isolate patients who have higher risk for a serious cause of syncope. Anyone with high risk criteria needs to be further investigated. They are summed up by the CHESS mnemonic: congestive heart failure, hematocrit <30%, electrocardiogram abnormality, shortness of breath, or systolic blood pressure <90 mm Hg. MANAGEMENT Neurocardiogenic syncope is most often treated with a combination of increased salt and water intake in conjunction with drugs that regulate blood pressure. It is important for patients to recognize potential triggers and heed warning signs. Treatment can broadly be divided into two categories: 1. General Measures:

The first step in treating this problem is to increase fluid intake. We cannot stress this enough. Patients who drink fluids regularly throughout the day seem to do better than those who don't take this task seriously. If low salt intake is an issue, we recommend an increase in the amount of salt for patients to add to their food. For some individuals with mild symptoms, an increased intake of salt and fluids may be all that is needed. Most of those with chronic fatigue syndrome and more severe symptoms require one of several medications in addition to the increased salt and fluid intake. The increased salt and fluid intake continue regardless of which of these medications is added. To be successful, though, the increased salt intake must be Prepared by Navjot and Kawal, MSc 2nd year, Mai Bhago College of Nursing, Tarn-Taran

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accompanied by a sufficient increase in the intake of water and other fluids (minimum of 2 liters of fluid per day). Where practical, avoid circumstances that might bring on symptoms. o Shop at non-peak hours to avoid long lines o Take shorter showers and baths and aim for a cooler water temperature o Avoid saunas, hot tubs, and lying on a hot beach o Avoid standing still for prolonged periods in hot environments, and on very hot days o Flex your leg muscles and shift your weight when you are standing still, or better still, walk around. o Avoid alcohol because it leads to dilation of the veins and arteries, and this can steal blood away from the central circulation o Reduce caffeine intake Certain postures and physical maneuvers are helpful in raising blood pressure when sitting for a prolonged time, mainly by helping use contraction of the leg muscles to pump blood back to the heart and by compressing the abdomen to reduce the amount of blood that pools in the intestinal circulation. The helpful maneuvers include: o standing with one's legs crossed o squatting o standing with one leg on a chair o bending forward from the waist (such as leaning over a shopping cart) o sitting in the knee-chest position o sitting in a low chair o leaning forward with hands on the knees when sitting o elevate the head of the bed slightly by 10-15o, a position that appears to help the body retain fluid at night rather than lose fluid into the urine o waist-high support hose can prevent some of the excessive pooling of blood in the legs (knee-high support socks may not work as well Exercise is important in regaining the effects that fitness brings in counteracting neurocardiogenic syncope. Because exercise can initially make symptoms worse, it must be done carefully at first.

2. Medications: beta-blockers (e.g., atenolol) fludrocortisone (Florinef) disopyramide (Norpace) fluoxetine (Prozac) sertraline (Zoloft) midodrine ephedrine pseudoephedrine theophylline methylphenidate (Ritalin) Prepared by Navjot and Kawal, MSc 2nd year, Mai Bhago College of Nursing, Tarn-Taran